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Journal articles on the topic 'Branching factor'

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Published: 4 June 2021
Last updated: 5 February 2022

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1

Simian, Marina, Yohei Hirai, Marc Navre, Zena Werb, Andre Lochter, and Mina J. Bissell. "The interplay of matrix metalloproteinases, morphogens and growth factors is necessary for branching of mammary epithelial cells." Development 128, no. 16 (August 15, 2001): 3117–31. http://dx.doi.org/10.1242/dev.128.16.3117.

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The mammary gland develops its adult form by a process referred to as branching morphogenesis. Many factors have been reported to affect this process. We have used cultured primary mammary epithelial organoids and mammary epithelial cell lines in three-dimensional collagen gels to elucidate which growth factors, matrix metalloproteinases (MMPs) and mammary morphogens interact in branching morphogenesis. Branching stimulated by stromal fibroblasts, epidermal growth factor, fibroblast growth factor 7, fibroblast growth factor 2 and hepatocyte growth factor was strongly reduced by inhibitors of MMPs, indicating the requirement of MMPs for three-dimensional growth involved in morphogenesis. Recombinant stromelysin 1/MMP3 alone was sufficient to drive branching in the absence of growth factors in the organoids. Plasmin also stimulated branching; however, plasmin-dependent branching was abolished by both inhibitors of plasmin and MMPs, suggesting that plasmin activates MMPs. To differentiate between signals for proliferation and morphogenesis, we used a cloned mammary epithelial cell line that lacks epimorphin, an essential mammary morphogen. Both epimorphin and MMPs were required for morphogenesis, but neither was required for epithelial cell proliferation. These results provide direct evidence for a crucial role of MMPs in branching in mammary epithelium and suggest that, in addition to epimorphin, MMP activity is a minimum requirement for branching morphogenesis in the mammary gland.
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2

Sakurai, H., and S. K. Nigam. "Transforming growth factor-beta selectively inhibits branching morphogenesis but not tubulogenesis." American Journal of Physiology-Renal Physiology 272, no. 1 (January 1, 1997): F139—F146. http://dx.doi.org/10.1152/ajprenal.1997.272.1.f139.

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When cultured in type I collagen gels, two kidney-derived cell lines, Madin-Darby canine kidney (MDCK) cells and murine inner medullary collecting duct (mIMCD3) cells, from branching tubular structures in the presence of Swiss 3T3 conditioned medium, in which hepatocyte growth factor (HGF) is the major branching tubule inducing factor. However, upon incubation with transforming growth factor-beta (TGF-beta) in the presence of 3T3 conditioned medium, MDCK tubulogenesis and branching was markedly inhibited. In contrast, mIMCD3 cells, which are much less susceptible to growth and tubulogenesis inhibition by TGF-beta, formed long straight tubulelike structures in presence of TGF-beta, suggesting a dissociation between tubulogenesis and branching morphogenesis. Interestingly, those long tubules that did branch often superficially resembled the early branching ureteric bud in embryonic kidneys. Quantitation of branching events revealed a selective branch-inhibiting effect of TGF-beta on mIMCD3 cells at concentrations between 0.02 and 2 ng/ml. There was no qualitative or quantitative difference among TGF-beta 1, -beta 2, and -beta 3 on inhibition of branching events, suggesting existence of potentially redundant mechanisms for modulating branching morphogenesis. Concentrations of TGF-beta that resulted in long nonbranching tubules also altered the profile of extracellular matrix-degrading proteases and their inhibitors expressed by developing tubules. Ratios of urokinase type plasminogen activator (u-PA) to plasminogen activator inhibitor (PAI-l) and matrix metalloprotease (MMP)-1 to tissue inhibitor of metalloprotease (TIMP)-1 were both markedly decreased. In addition, apart from a direct effect on epithelial cell branching morphogenesis, TGF-beta downregulated the expression of HGF mRNA in Swiss 3T3 cells. Thus TGF-beta exerts at least three distinct effects relevant to tubulogenesis and branching morphogenesis inhibition of branching morphogenesis alone (mIMCD3 cells), inhibition of both tubulogenesis and branching morphogenesis (MDCK cells), and inhibition of the expression of growth factor which induce tubulogenesis and branching morphogenesis (3T3 cells). In the context of epithelial tissue development, which requires tightly regulated branching tubulogenesis of epithelial cells, the data suggest a model where branching patterns are regulated by a precise temporal and spatial balance between branching morphogens such as HGF and inhibitory morphogens such as members of the TGF-beta superfamily [e.g., TGF-beta isoforms, certain bone morphogenetic proteins].
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3

BERG, THOMAS. "Branching direction in recursive structures." English Language and Linguistics 16, no. 3 (October 22, 2012): 385–401. http://dx.doi.org/10.1017/s1360674312000160.

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English makes regular use of a number of recursive structures spanning the syntax–lexicon continuum. While NPs with recursive relative clauses occupy the syntactic end, nominal compounds are located at the lexical end. In between these extremes we find NPs with recursive periphrastic genitives (towards the syntactic end) and NPs with recursive Saxon genitives (towards the lexical end). This study presents a comparative analysis of the branching direction preferences in these recursive structures. The empirical focus is on double of-genitives, which exhibit an overwhelming predilection for right-branching. This contrasts sharply with the double Saxon genitives, which gravitate towards left-branching. The branching direction decision is argued to be under the sway of several distinct factors: a syntactic factor controlling the alternative between leftward and rightward expansion; a lexical factor regulating the idiomatization of a given pair of elements; and a processing factor geared towards preventing garden path effects. Furthermore, branching direction is determined by listeners’ desire to minimize constituent recognition domains. Taken together, these factors are held accountable for the varying branching direction biases found in the different types of NP.
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4

Sakurai, Hiroyuki, Kevin T. Bush, and Sanjay K. Nigam. "Identification of pleiotrophin as a mesenchymal factor involved in ureteric bud branching morphogenesis." Development 128, no. 17 (September 1, 2001): 3283–93. http://dx.doi.org/10.1242/dev.128.17.3283.

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Branching morphogenesis is central to epithelial organogenesis. In the developing kidney, the epithelial ureteric bud invades the metanephric mesenchyme, which directs the ureteric bud to undergo repeated branching. A soluble factor(s) in the conditioned medium of a metanephric mesenchyme cell line is essential for multiple branching morphogenesis of the isolated ureteric bud. The identity of this factor had proved elusive, but it appeared distinct from factors such as HGF and EGF receptor ligands that have been previously implicated in branching morphogenesis of mature epithelial cell lines. Using sequential column chromatography, we have now purified to apparent homogeneity an 18 kDa protein, pleiotrophin, from the conditioned medium of a metanephric mesenchyme cell line that induces isolated ureteric bud branching morphogenesis in the presence of glial cell-derived neurotrophic factor. Pleiotrophin alone was also found to induce the formation of branching tubules in an immortalized ureteric bud cell line cultured three-dimensionally in an extracellular matrix gel. Consistent with an important role in ureteric bud morphogenesis during kidney development, pleiotrophin was found to localize to the basement membrane of the developing ureteric bud in the embryonic kidney. We suggest that pleiotrophin could act as a key mesenchymally derived factor regulating branching morphogenesis of the ureteric bud and perhaps other embryonic epithelial structures.
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5

Ohmichi, H., U. Koshimizu, K. Matsumoto, and T. Nakamura. "Hepatocyte growth factor (HGF) acts as a mesenchyme-derived morphogenic factor during fetal lung development." Development 125, no. 7 (April 1, 1998): 1315–24. http://dx.doi.org/10.1242/dev.125.7.1315.

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Mesenchymal-epithelial tissue interactions are important for development of various organs, and in many cases, soluble signaling molecules may be involved in this interaction. Hepatocyte growth factor (HGF) is a mesenchyme-derived factor which has mitogenic, motogenic and morphogenic activities on various types of epithelial cells and is considered to be a possible mediator of epithelial-mesenchymal interaction during organogenesis and organ regeneration. In this study, we examined the role of HGF during lung development. In situ hybridization analysis showed HGF and the c-met/HGF receptor gene to be respectively expressed in mesenchyme and epithelium in the developing lung. In organ cultures, exogenously added HGF apparently stimulated branching morphogenesis of the fetal lung. In contrast, HGF translation arrest or neutralization assays resulted in clear inhibition of epithelial branching. These results suggest that HGF is a putative candidate for a mesenchyme-derived morphogen regulating lung organogenesis. We also found that HGF is involved in epithelial branching, in collaboration with fibroblast growth factor (FGF) family molecule(s). In mesenchyme-free culture, HGF alone did not induce epithelial morphogenesis, however, addition of both HGF and acidic FGF (aFGF) or keratinocyte growth factor (KGF), ligands for the KGF receptor, induced epithelial branching more extensively than that was observed in explants treated with aFGF or KGF alone. In addition, the simultaneous inhibition of HGF- and FGF-mediated signaling using neutralizing antibody and antisense oligo-DNA resulted in drastic impairment of epithelial growth and branching. Possible interactions between HGF and FGFs or other growth factors in lung development is given consideration.
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6

Motokawa, Tomonori, Takahiro Miwa, Mayu Mochizuki, Minako Toritsuka, Aya Sakata, and Masaaki Ito. "Adrenomedullin: A novel melanocyte dendrite branching factor." Journal of Dermatological Science 79, no. 3 (September 2015): 307–10. http://dx.doi.org/10.1016/j.jdermsci.2015.06.001.

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7

Wescott, Melanie P., Meritxell Rovira, Maximilian Reichert, Johannes von Burstin, Anna Means, Steven D. Leach, and Anil K. Rustgi. "Pancreatic Ductal Morphogenesis and the Pdx1 Homeodomain Transcription Factor." Molecular Biology of the Cell 20, no. 22 (November 15, 2009): 4838–44. http://dx.doi.org/10.1091/mbc.e09-03-0203.

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Embryonic development of the pancreas is marked by an early phase of dramatic morphogenesis, in which pluripotent progenitor cells of the developing pancreatic epithelium give rise to the full array of mature exocrine and endocrine cell types. The genetic determinants of acinar and islet cell lineages are somewhat well defined; however, the molecular mechanisms directing ductal formation and differentiation remain to be elucidated. The complex ductal architecture of the pancreas is established by a reiterative program of progenitor cell expansion and migration known as branching morphogenesis, or tubulogenesis, which proceeds in mouse development concomitantly with peak Pdx1 transcription factor expression. We therefore evaluated Pdx1 expression with respect to lineage-specific markers in embryonic sections of the pancreas spanning this critical period of duct formation and discovered an unexpected population of nonislet Pdx1-positive cells displaying physical traits of branching. We then established a 3D cell culture model of branching morphogenesis using primary pancreatic duct cells and identified a transient surge of Pdx1 expression exclusive to branching cells. From these observations we propose that Pdx1 might be involved temporally in a program of gene expression sufficient to facilitate the biochemical and morphological changes necessary for branching morphogenesis.
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8

Sakurai, H., T. Tsukamoto, C. A. Kjelsberg, L. G. Cantley, and S. K. Nigam. "EGF receptor ligands are a large fraction of in vitro branching morphogens secreted by embryonic kidney." American Journal of Physiology-Renal Physiology 273, no. 3 (September 1, 1997): F463—F472. http://dx.doi.org/10.1152/ajprenal.1997.273.3.f463.

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Much attention has recently focused upon hepatocyte growth factor (HGF) as a potential regulator of epithelial branching morphogenesis. However, since neither the HGF nor c-met "knockout" mice show abnormal kidney branching morphogenesis, we sought to analyze the relative importance of HGF in in vitro branching morphogenesis compared with other factors secreted by the embryonic kidney. Exploiting an assay that employs kidney epithelial cells (murine inner medullary collecting duct, mIMCD3) seeded in collagen cocultured with the embryonic kidney, we found that a tyrosine kinase inhibitor that is highly specific for the epidermal growth factor (EGF) receptor (EGFR), tyrphostin AG1478, inhibited mIMCD3 cell process formation (an early step in branching tubulogenesis) by 40%, whereas high concentrations of neutralizing anti-HGF antibodies had a lesser effect (20% inhibition), suggesting that EGFR ligands account for a larger fraction of branching morphogens secreted by the embryonic kidney than HGF. In addition, when an embryonic epithelial cell line derived from c-met (-/-) mice was cocultured with the embryonic kidney, these c-met (-/-) cells underwent process formation. EGFR ligands but not HGF were able to induce branching tubulogenesis in these cells. All EGFR ligands tested, including EGF, transforming growth factor-alpha, heparin-binding EGF, betacellulin, and amphiregulin, induced mIMCD3 cell tubulogenesis. EGFR ligands caused upregulation of urokinase, urokinase receptor, and matrix metalloprotease-1, and tubulogenesis could be inhibited by the metalloprotease inhibitor 1,10-phenanthroline. Our results support the notion that multiple parallel and potentially redundant growth factor-dependent pathways regulate branching tubulogenesis.
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9

RAGGI, MAURO. "TESTS OF CHPT WITH ${\rm K}_{{\rm e}4}^{+-}$ AND ${\rm K}_{{\rm e}4}^{00}$ DECAYS AT THE NA48/2 EXPERIMENT AT CERN." International Journal of Modern Physics: Conference Series 35 (January 2014): 1460458. http://dx.doi.org/10.1142/s201019451460458x.

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The NA48/2 experiment has collected the largest samples to date of semi-leptonic charged kaon decays in the [Formula: see text] (K± → π+π-e±ν) and [Formula: see text] (K± → π0π0e±ν) modes. From 1.1 million [Formula: see text] decays, form factors in the S- and P-wave have been extensively studied. Branching ratio and form factors have been measured at unprecedented precision. From ~ 66000 [Formula: see text] decays, preliminary values of the Branching ratio and form factor have been obtained at a percent level precision. The comparison of Branching ratio and form factor values in both Ke4 modes sheds new light on isospin symmetry breaking effects. Form factor measurements are major inputs to the study of low energy QCD and are powerful tests of Chiral Perturbation Theory predictions.
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10

Sicouri, Lara, Federica Pisati, Salvatore Pece, Francesco Blasi, and Elena Longobardi. "Prep1 (pKnox1) transcription factor contributes to pubertal mammary gland branching morphogenesis." International Journal of Developmental Biology 62, no. 11-12 (2018): 827–36. http://dx.doi.org/10.1387/ijdb.180278fb.

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Prep1 (pKnox1) is a homeodomain transcription factor essential for in utero and post-natal development and an oncosuppressor gene in human and adult mice. We have analyzed its role in the development of the mouse mammary gland. We used Prep1i/i hypomorphic and Prep1F/F-Ker5CRE crosses to analyze the role of Prep1 in vivo in adult mouse mammary gland development. We also cultured mammary gland stem/progenitor cells in mammospheres to perform biochemical studies. Prep1 was expressed in mammary gland progenitors and fully differentiated mammary gland cells. Using different Prep1-deficient mouse models we show that in vivo Prep1 contributes to mammary gland branching since the branching efficiency of the mammary gland in Prep1-deleted or Prep1 hypomorphic mice was largely reduced. In-vitro, Prep1 sustained functions of the mammary stem/progenitor compartment. Prep1-deficient mammary stem/progenitor cells showed reduced ability to form mammospheres; they were not able to branch in a 3D assay, and exhibited reduced expression of Snail1, Snail2 and vimentin. The branching phenotype associated with increased Tp53-dependent apoptosis and inability to properly activate signals involved in branching morphogenesis. Finally, Prep1 formed complexes with Snail2, a transcription factor essential in branching morphogenesis, and its absence destabilizes and promotes Snail2 proteasome-mediated degradation. We conclude that Prep1 is required for normal adult mammary gland development, in particular at its branching morphogenesis step. By binding Snail2, Prep1 protects it from the proteasomal degradation.
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11

Post, M., P. Souza, J. Liu, I. Tseu, J. Wang, M. Kuliszewski, and A. K. Tanswell. "Keratinocyte growth factor and its receptor are involved in regulating early lung branching." Development 122, no. 10 (October 1, 1996): 3107–15. http://dx.doi.org/10.1242/dev.122.10.3107.

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Lung branching morphogenesis depends on mesenchymal-epithelial tissue interactions. Keratinocyte growth factor (KGF) has been implicated to be a regulator of these tissue interactions. In the present study, we investigated the role of KGF in early rat lung organogenesis. Reverse transcriptase-polymerase chain reaction analysis revealed KGF mRNA expression in the mesenchymal component of the 13-day embryonic lung, while message for KGF receptor (KGFR) was expressed in the epithelium, confirming the paracrine nature of KGF/KGFR axis. Antisense KGF oligonucleotides inhibited DNA synthesis of embryonic lung explants. This inhibitory effect of antisense KGF was partially reversed by the addition of exogenous KGF. Recombinant KGF was mitogenic for 13-day isolated embryonic lung epithelial cells. Medium conditioned by 13-day lung mesenchymal cells also stimulated DNA synthesis of 13-day embryonic lung epithelial cells. This stimulatory effect was partially abrogated by a neutralizing KGF antibody. The number of terminal buds of lung explants cultured in the presence of antisense KGF oligonucleotides was significantly reduced compared to control explants. Exogenous KGF partially abrogated the inhibitory effect of antisense KGF on early lung branching. Sense or scrambled KGF oligonucleotides had no inhibitory effect on lung growth and branching. Addition of neutralizing KGF antibodies to the explants also reduced the degree of branching, while non-immune IgG and neutralizing acidic FGF antibodies had no effect. Explants incubated with antisense oligonucleotides targeted to the initiation site of translation of both the splice variants of the fibroblast growth factor receptor-2 (FGFR2) gene, KGFR and bek, exhibited a similar reduction in lung branching as observed with antisense KGF oligonucleotides. Antisense KGFR-specific oligonucleotides dramatically inhibited lung branching, while exposure of explants to antisense bek-specific oligonucleotides resulted in reduced branching albeit to a lesser degree than that observed with antisense KGFR-specific oligonucleotides. Neither sense nor scrambled KGFR-specific oligonucleotides had any effect on early lung branching. These results suggest that the KGF/KGFR system has a critical role in early lung organogenesis.
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12

Berdichevsky, F., D. Alford, B. D'Souza, and J. Taylor-Papadimitriou. "Branching morphogenesis of human mammary epithelial cells in collagen gels." Journal of Cell Science 107, no. 12 (December 1, 1994): 3557–68. http://dx.doi.org/10.1242/jcs.107.12.3557.

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To study the morphogenesis of human epithelial cells in vitro we have used a three-dimensional collagen matrix and a newly developed mammary epithelial cell line, 1–7 HB2. In standard medium 1–7 HB2 cells formed compact balls/spheres inside collagen type I gels, while cocultivation with various fibroblast cell lines or growth in fibroblast-conditioned media resulted in the appearance of branching structures. At least two different soluble factors secreted by fibroblasts were found to be implicated in the branching morphogenesis. Firstly, hepatocyte growth factor/scatter factor could induce branching in a concentration-dependent manner. Moreover, a polyclonal serum against hepatocyte growth factor/scatter factor completely inhibited the branching morphogenesis induced by medium conditioned by MRC-5 fibroblast cells. In contrast, a morphogenetic activity secreted by human foreskin fibroblasts was identified that appears to be different from hepatocyte growth factor/scatter factor and from a number of other well-characterized growth factors or cytokines. This model system has been used to examine the role of integrins in mammary morphogenesis. The expression of the alpha 2 beta 1, alpha 3 beta 1 and alpha 6 beta 4 integrins was decreased when cells were plated on collagen gels. The addition of specific blocking monoclonal antibodies directed to the alpha 2- and beta 1-integrin subunits to growth media impaired cell-cell interactions and interfered with the formation of compact structures inside collagen gels, suggesting that the alpha 2 beta 1 integrin can control intercellular adhesion in mammary morphogenesis. In contrast one of the blocking monoclonal antibodies against the alpha 3-integrin subunit (P1B5) mimicked the effect of soluble ‘morphogens’. Our results suggest that the modulation of alpha 3 beta 1 activity may represent an important event in the induction of branching morphogenesis of human mammary epithelial cells.
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13

Warburton, David, Carol Wuenschell, Guillermo Flores-Delgado, and Kathryn Anderson. "Commitment and differentiation of lung cell lineages." Biochemistry and Cell Biology 76, no. 6 (December 1, 1998): 971–95. http://dx.doi.org/10.1139/o98-104.

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To form a large diffusible interface capable of conducting respiratory gases to and from the circulation, the lung must undergo extensive cell proliferation, branching morphogenesis, and alveolar saccule formation, to generate sufficient surface area. In addition, the cells must differentiate into at least 40 distinct lung cell lineages. Specific transcriptional factors, peptide growth factor receptor-mediated signaling pathways, extracelluar matrix components, and integrin-signaling pathways interact to direct lung morphogenesis and lung cell lineage differentiation. Branching mutants of the respiratory tracheae in Drosophila have identified several functionally conserved genes in the fibroblast growth factor signaling pathway that also regulate pulmonary organogenesis in mice and probably also in man. Key transcriptional factors including Nkx2.1, hepatocyte nuclear factor family forkhead homologues, GATA family zinc finger factors, pou and homeodomain proteins, as well as basic helix-loop-helix factors, serve as master genes to integrate the developmental genetic instruction of lung morphogenesis and cell lineage determination. Key words: lung branching morphogenesis, lung cell proliferation, lung cell differentiation, alveolization, master genes, peptide growth factor signaling, extracellular matrix signaling, mesenchyme induction, alveolar epithelial cells, pulmonary neuroendocrine cells, stem cells, retinoic acid.
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14

Stuart, R. O., E. J. Barros, E. Ribeiro, and S. K. Nigam. "Epithelial tubulogenesis through branching morphogenesis: relevance to collecting system development." Journal of the American Society of Nephrology 6, no. 4 (October 1995): 1151–59. http://dx.doi.org/10.1681/asn.v641151.

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Branching tubulogenesis of the ureteric bud, which gives rise to the urinary collecting system, is of considerable clinical interest because this process plays a major role in determining nephron number in the kidney. Data from in vitro model systems, including organ culture of the embryonic kidney and renal epithelial cells cultured in three-dimensional collagen matrices, indicate that growth factors, extracellular matrix composition, matrix-remodeling proteinases, and integrin expression are important factors in tubulogenesis and branching in the renal epithelium. One possibility is that gradients of soluble factors in the interstitial milieu of the embryonic kidney regulate the directionality of tubulogenesis and the degree of branching. Growth factors that enhance branching also appear to up-regulate matrix-remodeling extracellular proteinases. Redundancy in the ability of growth factors to induce tubulogenesis and branching may explain the apparent lack of a renal phenotype observed in targeted growth factor gene deletion experiments in mice. At the same time, differential effects in the efficiency of growth factors in inducing branching and/or changes in local matrix composition may be important in regulating the degree of arborization of the developing collecting system.
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15

Sameljuk, A. V., A. D. Vasilev, and S. A. Firstov. "Temperature dependences of the branching stress intensity factor and the branching crack length in chromium 0.5La2O3." International Journal of Refractory Metals and Hard Materials 15, no. 4 (January 1997): 215–18. http://dx.doi.org/10.1016/s0263-4368(97)00001-2.

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16

Maihöfer, Christian, and Kurt Rothermel. "Optimal branching factor for tree-based reliable multicast protocols." Computer Communications 25, no. 11-12 (July 2002): 1018–27. http://dx.doi.org/10.1016/s0140-3664(02)00016-6.

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17

Exner, Vivien, Wilhelm Gruissem, and Lars Hennig. "Control of trichome branching by Chromatin Assembly Factor-1." BMC Plant Biology 8, no. 1 (2008): 54. http://dx.doi.org/10.1186/1471-2229-8-54.

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18

Zou, Hong-Feng, Yu-Qin Zhang, Wei Wei, Hao-Wei Chen, Qing-Xin Song, Yun-Feng Liu, Ming-Yu Zhao, et al. "The transcription factor AtDOF4.2 regulates shoot branching and seed coat formation in Arabidopsis." Biochemical Journal 449, no. 2 (December 14, 2012): 373–88. http://dx.doi.org/10.1042/bj20110060.

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Plant-specific DOF (DNA-binding with one finger)-type transcription factors regulate various biological processes. In the present study we characterized a silique-abundant gene AtDOF (Arabidopsis thaliana DOF) 4.2 for its functions in Arabidopsis. AtDOF4.2 is localized in the nuclear region and has transcriptional activation activity in both yeast and plant protoplast assays. The T-M-D motif in AtDOF4.2 is essential for its activation. AtDOF4.2-overexpressing plants exhibit an increased branching phenotype and mutation of the T-M-D motif in AtDOF4.2 significantly reduces branching in transgenic plants. AtDOF4.2 may achieve this function through the up-regulation of three branching-related genes, AtSTM (A. thaliana SHOOT MERISTEMLESS), AtTFL1 (A. thaliana TERMINAL FLOWER1) and AtCYP83B1 (A. thaliana CYTOCHROME P450 83B1). The seeds of an AtDOF4.2-overexpressing plant show a collapse-like morphology in the epidermal cells of the seed coat. The mucilage contents and the concentration and composition of mucilage monosaccharides are significantly changed in the seed coat of transgenic plants. AtDOF4.2 may exert its effects on the seed epidermis through the direct binding and activation of the cell wall loosening-related gene AtEXPA9 (A. thaliana EXPANSIN-A9). The dof4.2 mutant did not exhibit changes in branching or its seed coat; however, the silique length and seed yield were increased. AtDOF4.4, which is a close homologue of AtDOF4.2, also promotes shoot branching and affects silique size and seed yield. Manipulation of these genes should have a practical use in the improvement of agronomic traits in important crops.
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19

Ito, Akihiro. "Japanese EFL Learners' Processing in English Relativization." ITL - International Journal of Applied Linguistics 133-134 (January 1, 2001): 325–45. http://dx.doi.org/10.1075/itl.133-134.07ito.

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Abstract The purpose of the present study is to investigate the effects of branching type (Factor 1) and grammatical function of noun phrase (NP) (factor 2) of English relative clauses on interlanguage performance among Japanese learners of English as a foreign language (EFL). The sentence combining test was administered to Japanese learners of English. Results indicated that both of the two factors significantly determine the difficulty of English relative clauses. Left-branching (center-embedded) relative clauses have a tendency to be more difficult than right-branching ones. Moreover, it is implied that subject-relative clauses are answered more accurately than object-relative clauses. These findings suggested that branching type and grammatical function of the noun phrase are complimentary determine the difficulty level of English relative clauses. The results implied the validity of KAWAUCHl's (1988) hypothesis that the difficulty order of relative clauses is as follows : OS > 00 > SS > SO. The results are also discussed with the recent theoretical frameworks in psycholinguistic research. The limitation of the present investigation and the directions of the further research are also discussed.
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20

van Tuyl, Minke, Jason Liu, Jinxia Wang, Maciek Kuliszewski, Dick Tibboel, and Martin Post. "Role of oxygen and vascular development in epithelial branching morphogenesis of the developing mouse lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 288, no. 1 (January 2005): L167—L178. http://dx.doi.org/10.1152/ajplung.00185.2004.

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Recent investigations have suggested an active role for endothelial cells in organ development, including the lung. Herein, we investigated some of the molecular mechanisms underlying normal pulmonary vascular development and their influence on epithelial branching morphogenesis. Because the lung in utero develops in a relative hypoxic environment, we first investigated the influence of low oxygen on epithelial and vascular branching morphogenesis. Two transgenic mouse models, the C101-LacZ (epithelial-LacZ marker) and the Tie2-LacZ (endothelial-LacZ marker), were used. At embryonic day 11.5, primitive lung buds were dissected and cultured at either 20 or 3% oxygen. At 24-h intervals, epithelial and endothelial LacZ gene expression was visualized by X-galactosidase staining. The rate of branching of both tissue elements was increased in explants cultured at 3% oxygen compared with 20% oxygen. Low oxygen increased expression of VEGF, but not that of the VEGF receptor (Flk-1). Expression of two crucial epithelial branching factors, fibroblast growth factor-10 and bone morphogenetic protein-4, were not affected by low oxygen. Epithelial differentiation was maintained at low oxygen as shown by surfactant protein C in situ hybridization. To explore epithelial-vascular interactions, we inhibited vascular development with antisense oligonucleotides targeted against either hypoxia inducible factor-1α or VEGF. Epithelial branching morphogenesis in vitro was dramatically abrogated when pulmonary vascular development was inhibited. Collectively, the in vitro data show that a low-oxygen environment enhances branching of both distal lung epithelium and vascular tissue and that pulmonary vascular development appears to be rate limiting for epithelial branching morphogenesis.
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21

Ontañón, Santiago. "Combinatorial Multi-armed Bandits for Real-Time Strategy Games." Journal of Artificial Intelligence Research 58 (March 29, 2017): 665–702. http://dx.doi.org/10.1613/jair.5398.

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Games with large branching factors pose a significant challenge for game tree search algorithms. In this paper, we address this problem with a sampling strategy for Monte Carlo Tree Search (MCTS) algorithms called "naive sampling", based on a variant of the Multi-armed Bandit problem called "Combinatorial Multi-armed Bandits" (CMAB). We analyze the theoretical properties of several variants of naive sampling, and empirically compare it against the other existing strategies in the literature for CMABs. We then evaluate these strategies in the context of real-time strategy (RTS) games, a genre of computer games characterized by their very large branching factors. Our results show that as the branching factor grows, naive sampling outperforms the other sampling strategies.
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22

Hirai, Yohei, André Lochter, Sybille Galosy, Shogo Koshida, Shinichiro Niwa, and Mina J. Bissell. "Epimorphin Functions as a Key Morphoregulator for Mammary Epithelial Cells." Journal of Cell Biology 140, no. 1 (January 12, 1998): 159–69. http://dx.doi.org/10.1083/jcb.140.1.159.

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Hepatocyte growth factor (HGF) and EGF have been reported to promote branching morphogenesis of mammary epithelial cells. We now show that it is epimorphin that is primarily responsible for this phenomenon. In vivo, epimorphin was detected in the stromal compartment but not in lumenal epithelial cells of the mammary gland; in culture, however, a subpopulation of mammary epithelial cells produced significant amounts of epimorphin. When epimorphin-expressing epithelial cell clones were cultured in collagen gels they displayed branching morphogenesis in the presence of HGF, EGF, keratinocyte growth factor, or fibroblast growth factor, a process that was inhibited by anti-epimorphin but not anti-HGF antibodies. The branch length, however, was roughly proportional to the ability of the factors to induce growth. Accordingly, epimorphin-negative epithelial cells simply grew in a cluster in response to the growth factors and failed to branch. When recombinant epimorphin was added to these collagen gels, epimorphin-negative cells underwent branching morphogenesis. The mode of action of epimorphin on morphogenesis of the gland, however, was dependent on how it was presented to the mammary cells. If epimorphin was overexpressed in epimorphin-negative epithelial cells under regulation of an inducible promoter or was allowed to coat the surface of each epithelial cell in a nonpolar fashion, the cells formed globular, alveoli-like structures with a large central lumen instead of branching ducts. This process was enhanced also by addition of HGF, EGF, or other growth factors and was inhibited by epimorphin antibodies. These results suggest that epimorphin is the primary morphogen in the mammary gland but that growth factors are necessary to achieve the appropriate cell numbers for the resulting morphogenesis to be visualized.
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Nogawa, H., and Y. Takahashi. "Substitution for mesenchyme by basement-membrane-like substratum and epidermal growth factor in inducing branching morphogenesis of mouse salivary epithelium." Development 112, no. 3 (July 1, 1991): 855–61. http://dx.doi.org/10.1242/dev.112.3.855.

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Mouse salivary epithelium cannot undergo branching morphogenesis in the absence of the surrounding mesenchyme. To clarify the nature of the mesenchymal influence on the epithelium, we have investigated the culture conditions in which the epithelium could normally branch in the absence of mesenchymal cells. Combination of basement-membrane-like substratum (Matrigel) and epidermal growth factor (EGF) could substitute for the mesenchyme, the epithelium showing typical branching morphogenesis. Transforming growth factor alpha had the same effect as EGF. Matrigel plus basic fibroblast growth factor or transforming growth factor beta 1 and collagen gel plus EGF were not sufficient to support the branching of the epithelium. These results clearly reveal that the role of mesenchyme in salivary morphogenesis is both to provide the epithelium with an appropriate substratum and to accelerate growth of the epithelium.
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Wiesen, J. F., P. Young, Z. Werb, and G. R. Cunha. "Signaling through the stromal epidermal growth factor receptor is necessary for mammary ductal development." Development 126, no. 2 (January 15, 1999): 335–44. http://dx.doi.org/10.1242/dev.126.2.335.

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Stromal-epithelial interactions are critical in determining patterns of growth, development and ductal morphogenesis in the mammary gland, and their perturbations are significant components of tumorigenesis. Growth factors such as epidermal growth factor (EGF) contribute to these reciprocal stromal-epithelial interactions. To determine the role of signaling through the EGF receptor (EGFR) in mammary ductal growth and branching, we used mice with a targeted null mutation in the Egfr. Because Egfr−/− mice die perinatally, transplantation methods were used to study these processes. When we transplanted neonatal mammary glands under the renal capsule of immuno-compromised female mice, we found that EGFR is essential for mammary ductal growth and branching morphogenesis, but not for mammary lobulo-alveolar development. Ductal growth and development was normal in transplants of mammary epithelium from Egfr−/− mice into wild-type (WT) gland-free fat pads and in tissue recombinants prepared with WT stroma, irrespective of the source of epithelium (StromaWT/Epi−/−, StromaWT/EpiWT). However, ductal growth and branching was impaired in tissue recombinants prepared with Egfr−/− stroma (Stroma−/−/EpiWT, Stroma−/−/Epi−/−). Thus, for ductal morphogenesis, signaling through the EGFR is required only in the stromal component, the mammary fat pad. These data indicate that the EGFR pathway plays a key role in the stromal-epithelial interactions required for mammary ductal growth and branching morphogenesis. In contrast, signaling through the EGFR is not essential for lobulo-alveolar development. Stimulation of lobulo-alveolar development in the mammary gland grafts by inclusion of a pituitary isograft under the renal capsule as a source of prolactin resulted in normal alveolar development in both Egfr−/− and wild-type transplants. Through the use of tissue recombinants and transplantation, we have gained new insights into the nature of stromal-epithelial interactions in the mammary gland, and how they regulate ductal growth and branching morphogenesis.
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Yuan, Cunquan, Jingtian Shi, and Liangjun Zhao. "The CmbZIP1 transcription factor of chrysanthemum negatively regulates shoot branching." Plant Physiology and Biochemistry 151 (June 2020): 69–76. http://dx.doi.org/10.1016/j.plaphy.2020.03.013.

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Tirziu, Daniela, Irina M. Jaba, Pengchun Yu, Bruno Larrivée, Brian G. Coon, Brunella Cristofaro, Zhen W. Zhuang, et al. "Endothelial Nuclear Factor-κB–Dependent Regulation of Arteriogenesis and Branching." Circulation 126, no. 22 (November 27, 2012): 2589–600. http://dx.doi.org/10.1161/circulationaha.112.119321.

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Marchione, Robb, Nancy Kim, and Robert S. Kirsner. "Epidermal Growth Factor Receptor Regulates Skin Nerve Outgrowth and Branching." Journal of Investigative Dermatology 129, no. 3 (March 2009): 524. http://dx.doi.org/10.1038/jid.2008.462.

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Basnet, Nirakar, Hana Nedozralova, Alvaro H. Crevenna, Satish Bodakuntla, Thomas Schlichthaerle, Michael Taschner, Giovanni Cardone, et al. "Direct induction of microtubule branching by microtubule nucleation factor SSNA1." Nature Cell Biology 20, no. 10 (September 24, 2018): 1172–80. http://dx.doi.org/10.1038/s41556-018-0199-8.

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Tsuji, Kenji, Shinji Kitamura, and Hirofumi Makino. "Hypoxia-inducible factor 1α regulates branching morphogenesis during kidney development." Biochemical and Biophysical Research Communications 447, no. 1 (April 2014): 108–14. http://dx.doi.org/10.1016/j.bbrc.2014.03.111.

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30

Nigam, Sanjay K., and Kevin T. Bush. "Growth factor–heparan sulfate “switches” regulating stages of branching morphogenesis." Pediatric Nephrology 29, no. 4 (February 2, 2014): 727–35. http://dx.doi.org/10.1007/s00467-013-2725-z.

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31

Yang, Y., E. Spitzer, D. Meyer, M. Sachs, C. Niemann, G. Hartmann, K. M. Weidner, C. Birchmeier, and W. Birchmeier. "Sequential requirement of hepatocyte growth factor and neuregulin in the morphogenesis and differentiation of the mammary gland." Journal of Cell Biology 131, no. 1 (October 1, 1995): 215–26. http://dx.doi.org/10.1083/jcb.131.1.215.

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We have examined the role of two mesenchymal ligands of epithelial tyrosine kinase receptors in mouse mammary gland morphogenesis. In organ cultures of mammary glands, hepatocyte growth factor (HGF, scatter factor) promoted branching of the ductal trees but inhibited the production of secretory proteins. Neuregulin (NRG, neu differentiation factor) stimulated lobulo-alveolar budding and the production of milk proteins. These functional effects are paralleled by the expression of the two factors in vivo: HGF is produced in mesenchymal cells during ductal branching in the virgin animal; NRG is expressed in the mesenchyme during lobulo-alveolar development at pregnancy. The receptors of HGF and NRG (c-met, c-erbB3, and c-erbB4), which are expressed in the epithelial cells, are not regulated. In organ culture, branching morphogenesis and lobulo-alveolar differentiation of the mammary gland could be abolished by blocking expression of endogenous HGF and NRG by the respective antisense oligonucleotides; in antisense oligonucleotide-treated glands, morphogenesis could again be induced by the addition of recombinant HGF and NRG. We thus show that two major postnatal morphogenic periods of mammary gland development are dependent on sequential mesenchymal-epithelial interactions mediated by HGF and NRG.
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Popsueva, Anna, Dmitry Poteryaev, Elena Arighi, Xiaojuan Meng, Alexandre Angers-Loustau, David Kaplan, Mart Saarma, and Hannu Sariola. "GDNF promotes tubulogenesis of GFRα1-expressing MDCK cells by Src-mediated phosphorylation of Met receptor tyrosine kinase." Journal of Cell Biology 161, no. 1 (April 7, 2003): 119–29. http://dx.doi.org/10.1083/jcb.200212174.

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Glial cell line–derived neurotrophic factor (GDNF) and hepatocyte growth factor (HGF) are multifunctional signaling molecules in embryogenesis. HGF binds to and activates Met receptor tyrosine kinase. The signaling receptor complex for GDNF typically includes both GDNF family receptor α1 (GFRα1) and Ret receptor tyrosine kinase. GDNF can also signal independently of Ret via GFRα1, although the mechanism has remained unclear. We now show that GDNF partially restores ureteric branching morphogenesis in ret-deficient mice with severe renal hypodysplasia. The mechanism of Ret-independent effect of GDNF was therefore studied by the MDCK cell model. In MDCK cells expressing GFRα1 but no Ret, GDNF stimulates branching but not chemotactic migration, whereas both branching and chemotaxis are promoted by GDNF in the cells coexpressing Ret and GFRα1, mimicking HGF/Met responses in wild-type MDCK cells. Indeed, GDNF induces Met phosphorylation in several ret-deficient/GFRα1-positive and GFRα1/Ret-coexpressing cell lines. However, GDNF does not immunoprecipite Met, making a direct interaction between GDNF and Met highly improbable. Met activation is mediated by Src family kinases. The GDNF-induced branching of MDCK cells requires Src activation, whereas the HGF-induced branching does not. Our data show a mechanism for the GDNF-induced branching morphogenesis in non-Ret signaling.
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Joseph, Heather, Agnieszka E. Gorska, Philip Sohn, Harold L. Moses, and Rosa Serra. "Overexpression of a Kinase-deficient Transforming Growth Factor-β Type II Receptor in Mouse Mammary Stroma Results in Increased Epithelial Branching." Molecular Biology of the Cell 10, no. 4 (April 1999): 1221–34. http://dx.doi.org/10.1091/mbc.10.4.1221.

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Members of the transforming growth factor-β (TGF-β) superfamily signal through heteromeric type I and type II serine/threonine kinase receptors. Transgenic mice that overexpress a dominant-negative mutation of the TGF-β type II receptor (DNIIR) under the control of a metallothionein-derived promoter (MT-DNIIR) were used to determine the role of endogenous TGF-βs in the developing mammary gland. The expression of the dominant-negative receptor was induced with zinc and was primarily localized to the stroma underlying the ductal epithelium in the mammary glands of virgin transgenic mice from two separate mouse lines. In MT-DNIIR virgin females treated with zinc, there was an increase in lateral branching of the ductal epithelium. We tested the hypothesis that expression of the dominant-negative receptor may alter expression of genes that are expressed in the stroma and regulated by TGF-βs, potentially resulting in the increased lateral branching seen in the MT-DNIIR mammary glands. The expression of hepatocyte growth factor mRNA was increased in mammary glands from transgenic animals relative to the wild-type controls, suggesting that this factor may play a role in TGF-β-mediated regulation of lateral branching. Loss of responsiveness to TGF-βs in the mammary stroma resulted in increased branching in mammary epithelium, suggesting that TGF-βs play an important role in the stromal–epithelial interactions required for branching morphogenesis.
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34

Ide, Shintaro, Gal Finer, Yoshiro Maezawa, Tuncer Onay, Tomokazu Souma, Rizaldy Scott, Kana Ide, et al. "Transcription Factor 21 Is Required for Branching Morphogenesis and Regulates the Gdnf-Axis in Kidney Development." Journal of the American Society of Nephrology 29, no. 12 (October 30, 2018): 2795–808. http://dx.doi.org/10.1681/asn.2017121278.

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BackgroundThe mammalian kidney develops through reciprocal inductive signals between the metanephric mesenchyme and ureteric bud. Transcription factor 21 (Tcf21) is highly expressed in the metanephric mesenchyme, including Six2-expressing cap mesenchyme and Foxd1-expressing stromal mesenchyme. Tcf21 knockout mice die in the perinatal period from severe renal hypodysplasia. In humans, Tcf21 mRNA levels are reduced in renal tissue from human fetuses with renal dysplasia. The molecular mechanisms underlying these renal defects are not yet known.MethodsUsing a variety of techniques to assess kidney development and gene expression, we compared the phenotypes of wild-type mice, mice with germline deletion of the Tcf21 gene, mice with stromal mesenchyme–specific Tcf21 deletion, and mice with cap mesenchyme–specific Tcf21 deletion.ResultsGermline deletion of Tcf21 leads to impaired ureteric bud branching and is accompanied by downregulated expression of Gdnf-Ret-Wnt11, a key pathway required for branching morphogenesis. Selective removal of Tcf21 from the renal stroma is also associated with attenuation of the Gdnf signaling axis and leads to a defect in ureteric bud branching, a paucity of collecting ducts, and a defect in urine concentration capacity. In contrast, deletion of Tcf21 from the cap mesenchyme leads to abnormal glomerulogenesis and massive proteinuria, but no downregulation of Gdnf-Ret-Wnt11 or obvious defect in branching.ConclusionsOur findings indicate that Tcf21 has distinct roles in the cap mesenchyme and stromal mesenchyme compartments during kidney development and suggest that Tcf21 regulates key molecular pathways required for branching morphogenesis.
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Shim, Sangrea, Jungmin Ha, Moon Young Kim, Man Soo Choi, Sung-Taeg Kang, Soon-Chun Jeong, Jung-Kyung Moon, and Suk-Ha Lee. "GmBRC1 is a Candidate Gene for Branching in Soybean (Glycine max (L.) Merrill)." International Journal of Molecular Sciences 20, no. 1 (January 1, 2019): 135. http://dx.doi.org/10.3390/ijms20010135.

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Branch number is one of the main factors affecting the yield of soybean (Glycine max (L.)). In this study, we conducted a genome-wide association study combined with linkage analysis for the identification of a candidate gene controlling soybean branching. Five quantitative trait nucleotides (QTNs) were associated with branch numbers in a soybean core collection. Among these QTNs, a linkage disequilibrium (LD) block qtnBR6-1 spanning 20 genes was found to overlap a previously identified major quantitative trait locus qBR6-1. To validate and narrow down qtnBR6-1, we developed a set of near-isogenic lines (NILs) harboring high-branching (HB) and low-branching (LB) alleles of qBR6-1, with 99.96% isogenicity and different branch numbers. A cluster of single nucleotide polymorphisms (SNPs) segregating between NIL-HB and NIL-LB was located within the qtnBR6-1 LD block. Among the five genes showing differential expression between NIL-HB and NIL-LB, BRANCHED1 (BRC1; Glyma.06G210600) was down-regulated in the shoot apex of NIL-HB, and one missense mutation and two SNPs upstream of BRC1 were associated with branch numbers in 59 additional soybean accessions. BRC1 encodes TEOSINTE-BRANCHED1/CYCLOIDEA/PROLIFERATING CELL FACTORS 1 and 2 transcription factor and functions as a regulatory repressor of branching. On the basis of these results, we propose BRC1 as a candidate gene for branching in soybean.
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36

Carrillo-Mendoza, Omar, José X. Chaparro, and Jeffrey Williamson. "Branching and Blind Node Incidence in Interspecific Backcross Families of Peach." HortScience 48, no. 9 (September 2013): 1119–24. http://dx.doi.org/10.21273/hortsci.48.9.1119.

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Tree size and branching control has gained importance as labor and pruning costs have increased. In addition, the occurrence of blind nodes is a critical factor that affects peach tree architecture and productivity in subtropical climates. Seven backcross families segregating for branching and blind nodes were developed using ‘Flordaguard’ peach × P. kansuensis or ‘Tardy Nonpareil’ almond F1s backcrossed to ‘AP00-30WBS’, ‘UFSharp’, or ‘UF97-47’ peach selections and evaluated for branching index and blind node frequency during the winters of 2010 and 2011. P. kansuensis backcrosses presented increased branching and lower blind node incidence, whereas almond backcrosses presented less branching and higher blind node incidence, resembling the P. kansuensis and almond F1 parents, respectively. There was also broad variability for branching and blind nodes within the P. kansuensis and ‘Tardy Nonpareil’ almond backcross families influenced by the peach parents that were used to generate the backcross populations. The moderate heritability and year-to-year correlation for these traits indicate that they are affected by the environment, but selection for reduced branching and lower blind node incidence is feasible.
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37

Yaghini, Nazila, and Piet D. Iedema. "Branching determination from radius of gyration contraction factor in radical polymerization." Polymer 59 (February 2015): 166–79. http://dx.doi.org/10.1016/j.polymer.2014.12.070.

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38

Orosa-Puente, Beatriz, Nicola Leftley, Daniel von Wangenheim, Jason Banda, Anjil K. Srivastava, Kristine Hill, Jekaterina Truskina, et al. "Root branching toward water involves posttranslational modification of transcription factor ARF7." Science 362, no. 6421 (December 20, 2018): 1407–10. http://dx.doi.org/10.1126/science.aau3956.

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Plants adapt to heterogeneous soil conditions by altering their root architecture. For example, roots branch when in contact with water by using the hydropatterning response. We report that hydropatterning is dependent on auxin response factor ARF7. This transcription factor induces asymmetric expression of its target gene LBD16 in lateral root founder cells. This differential expression pattern is regulated by posttranslational modification of ARF7 with the small ubiquitin-like modifier (SUMO) protein. SUMOylation negatively regulates ARF7 DNA binding activity. ARF7 SUMOylation is required to recruit the Aux/IAA (indole-3-acetic acid) repressor protein IAA3. Blocking ARF7 SUMOylation disrupts IAA3 recruitment and hydropatterning. We conclude that SUMO-dependent regulation of auxin response controls root branching pattern in response to water availability.
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39

Carmeliet, P. "Fibroblast Growth Factor-1 Stimulates Branching and Survival of Myocardial Arteries." Circulation Research 87, no. 3 (August 4, 2000): 176–78. http://dx.doi.org/10.1161/01.res.87.3.176.

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40

Haktanır, Tefaruk, and Mehmet Ardıçlıoğlu. "Numerical modeling of Darcy–Weisbach friction factor and branching pipes problem." Advances in Engineering Software 35, no. 12 (December 2004): 773–79. http://dx.doi.org/10.1016/j.advengsoft.2004.07.005.

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41

Cantley, L. G., E. J. Barros, M. Gandhi, M. Rauchman, and S. K. Nigam. "Regulation of mitogenesis, motogenesis, and tubulogenesis by hepatocyte growth factor in renal collecting duct cells." American Journal of Physiology-Renal Physiology 267, no. 2 (August 1, 1994): F271—F280. http://dx.doi.org/10.1152/ajprenal.1994.267.2.f271.

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Hepatocyte growth factor (HGF) has been implicated in branching tubulogenesis of the developing kidney and in response to renal injury. We therefore examined the effects of response to renal injury. We therefore examined the effects of HGF on a recently described murine inner medullary collecting duct epithelial cell line (mIMCD-3 cells) in comparison with Madin-Darby canine kidney (MDCK) cells. HGF induced mitosis, scattering, and tubulogenesis in both mIMCD-3 cells and MDCK cells. However, mIMCD-3 cells underwent branching tubulogenesis under matrix conditions that did not support these morphogenetic changes in MDCK cells, suggesting substantial differences in regulation of tubulogenesis in these two cell types. In quiescent mIMCD-3 cells, the high-affinity receptor for HGF, c-met, was expressed in a nonphosphorylated state. After stimulation with HGF, there was a > 10-fold increase in receptor tyrosine phosphorylation and selective association with at least two intracellular proteins, including the phosphatidylinositol-3-kinase. Thus mIMCD-3 cells, which undergo HGF-dependent mitosis, scattering, and branching tubulogenesis, express the c-met receptor in a highly regulated state and therefore should make an excellent model for examining the mechanisms of HGF-dependent tubulogenesis in the renal collecting duct.
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Qiang, Liang, Wenqian Yu, Mei Liu, Joanna M. Solowska, and Peter W. Baas. "Basic Fibroblast Growth Factor Elicits Formation of Interstitial Axonal Branches via Enhanced Severing of Microtubules." Molecular Biology of the Cell 21, no. 2 (January 15, 2010): 334–44. http://dx.doi.org/10.1091/mbc.e09-09-0834.

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The formation of interstitial axonal branches involves the severing of microtubules at sites where new branches form. Here we wished to ascertain whether basic fibroblast growth factor (bFGF) enhances axonal branching through alterations in proteins involved in the severing of microtubules. We found that treatment of cultured hippocampal neurons with bFGF heightens expression of both katanin and spastin, which are proteins that sever microtubules in the axon. In addition, treatment with bFGF enhances phosphorylation of tau at sites expected to cause it to dissociate from microtubules. This is important because tau regulates the access of katanin to the microtubule. In live-cell imaging experiments, axons of neurons treated with bFGF displayed greater numbers of dynamic free ends of microtubules, as well as greater numbers of short mobile microtubules. Entirely similar enhancement of axonal branching, short microtubule transport, and frequency of microtubule ends was observed when spastin was overexpressed in the neurons. Depletion of either katanin or spastin with siRNA diminished but did not eliminate the enhancement in branching elicited by bFGF. Collectively, these results indicate that bFGF enhances axonal branch formation by augmenting the severing of microtubules through both a spastin-based mode and a katanin-based mode.
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Brantley, Dana M., Chih-Li Chen, Rebecca S. Muraoka, Paul B. Bushdid, Jonathan L. Bradberry, Frances Kittrell, Daniel Medina, Lynn M. Matrisian, Lawrence D. Kerr, and Fiona E. Yull. "Nuclear Factor-κB (NF-κB) Regulates Proliferation and Branching in Mouse Mammary Epithelium." Molecular Biology of the Cell 12, no. 5 (May 2001): 1445–55. http://dx.doi.org/10.1091/mbc.12.5.1445.

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The nuclear factor-κB (NF-κB) family of transcription factors has been shown to regulate proliferation in several cell types. Although recent studies have demonstrated aberrant expression or activity of NF-κB in human breast cancer cell lines and tumors, little is known regarding the precise role of NF-κB in normal proliferation and development of the mammary epithelium. We investigated the function of NF-κB during murine early postnatal mammary gland development by observing the consequences of increased NF-κB activity in mouse mammary epithelium lacking the gene encoding IκBα, a major inhibitor of NF-κB. Mammary tissue containing epithelium from inhibitor κBα (IκBα)-deficient female donors was transplanted into the gland-free mammary stroma of wild-type mice, resulting in an increase in lateral ductal branching and pervasive intraductal hyperplasia. A two- to threefold increase in epithelial cell number was observed in IκBα-deficient epithelium compared with controls. Epithelial cell proliferation was strikingly increased in IκBα-deficient epithelium, and no alteration in apoptosis was detected. The extracellular matrix adjacent to IκBα-deficient epithelium was reduced. Consistent with in vivo data, a fourfold increase in epithelial branching was also observed in purified IκBα-deficient primary epithelial cells in three-dimensional culture. These data demonstrate that NF-κB positively regulates mammary epithelial proliferation, branching, and functions in maintenance of normal epithelial architecture during early postnatal development.
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Golubtsov, G. B., and R. S. Chalov. "COMPARATIVE HYDRO-MORPHOLOGICAL ANALYSIS OF THE ISLANDS OF DIFFERENTLY BRANCHED UPPER OB AND MIDDLE LENA RIVER CHANNELS." Bulletin of Udmurt University. Series Biology. Earth Sciences 30, no. 2 (July 30, 2020): 164–74. http://dx.doi.org/10.35634/2412-9518-2020-30-2-164-174.

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This article is devoted to the formation conditions and morphometric features of the river islands. Also it considers the rate of branching of the Upper Ob and Middle Lena river channels. They are the largest rivers, but the Middle Lena River is bigger than the Upper Ob River by 6.15 times of total runoff and 2.5 times of width. However, both of them have unstable or weakly stable channels, characterized by parallel-sleeve, alternating, one-sided and single branchings, formed by numerous islands. Their comparison makes it possible to establish the dependence of the conditions of islands formation, their parameters (length - L , width - B , shape - L / B ), types and number on the indicators of stability, total runoff, branching types and location in the channel (active or peripheral part). These correlations based on hydro-morphological analysis show that the shape of islands L / B and the branching rate of the channel - n / x depend on the degree of stability. It is a common feature of all branching types and stages of island evolution (elementary, small, large islands and island massifs). Uniform dependencies of island parameters on river bed stability for both rivers, despite their large-scale distortions, were obtained by taking into account the connection of channel width ( b ) with its runoff ( Q ) by introducing a correction factor of 2.5 for the river size. Also the formation conditions of elongated islands ( L / B > 5), were determined. Their shape does not correspond to the optimal ratio L / B = 3...4. The revealed patterns give an opportunity to clarify the previously proposed classification of the islands.
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Samakovlis, C., N. Hacohen, G. Manning, D. C. Sutherland, K. Guillemin, and M. A. Krasnow. "Development of the Drosophila tracheal system occurs by a series of morphologically distinct but genetically coupled branching events." Development 122, no. 5 (May 1, 1996): 1395–407. http://dx.doi.org/10.1242/dev.122.5.1395.

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The tracheal (respiratory) system of Drosophila melanogaster is a branched network of epithelial tubes that ramifies throughout the body and transports oxygen to the tissues. It forms by a series of sequential branching events in each hemisegment from T2 to A8. Here we present a cellular and initial genetic analysis of the branching process. We show that although branching is sequential it is not iterative. The three levels of branching that we distinguish involve different cellular mechanisms of tube formation. Primary branches are multicellular tubes that arise by cell migration and intercalation; secondary branches are unicellular tubes formed by individual tracheal cells; terminal branches are subcellular tubes formed within long cytoplasmic extensions. Each level of branching is accompanied by expression of a different set of enhancer trap markers. These sets of markers are sequentially activated in progressively restricted domains and ultimately individual tracheal cells that are actively forming new branches. A clonal analysis demonstrates that branching fates are not assigned to tracheal cells until after cell division ceases and branching begins. We further show that the breathless FGF receptor, a tracheal gene required for primary branching, is also required to activate expression of markers involved in secondary branching and that the pointed ETS-domain transcription factor is required for secondary branching and also to activate expression of terminal branch markers. The combined morphological, marker expression and genetic data support a model in which successive branching events are mechanistically and genetically distinct but coupled through the action of a tracheal gene regulatory hierarchy.
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TAKEMURA, TSUKASA, SATOSHI HINO, HIROAKI KUWAJIMA, HIDEHIKO YANAGIDA, MITSURU OKADA, MICHIO NAGATA, SEI SASAKI, JONATHAN BARASCH, RAYMOND C. HARRIS, and KAZUO YOSHIOKA. "Induction of Collecting Duct MorphogenesisIn Vitroby Heparin-Binding Epidermal Growth Factor-Like Growth Factor." Journal of the American Society of Nephrology 12, no. 5 (May 2001): 964–72. http://dx.doi.org/10.1681/asn.v125964.

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Abstract. Heparin-binding epidermal growth factor-like growth factor (HB-EGF), a member of the epidermal growth factor family of growth factors, is synthesized as a membrane-an-chored precursor (proHB-EGF) that is capable of stimulating adjacent cells in a juxtacrine manner. ProHB-EGF is cleaved in a protein kinase C-dependent process, to yield the soluble form. It was observed that HB-EGF acts as a morphogen for the collecting duct system in developing kidneys. HB-EGF protein was expressed in the ureteric bud of embryonic kidneys. Cultured mouse ureteric bud cells (UBC) produced HB-EGF via protein kinase C activation. After stimulation with phorbol ester (12-O-tetradecanoylphorbol-13-acetate) or recombinant soluble HB-EGF, UBC cultured in three-dimensional collagen gels formed short tubules with varied abundant branches. When proHB-EGF-transfected UBC were stimulated with 12-O-tetradecanoylphorbol-13-acetate and cultured in collagen gels, they exhibited linear growth, forming long tubular structures with few branches at the time of appearance of proHB-EGF on the cell surface. The structures exhibited a strong resemblance to the early branching ureteric bud of embryonic kidneys. When UBC were cultured in the presence of transforming growth factor-β and soluble HB-EGF, they formed long tubules and few branches, similar to the structures observed in proHB-EGF-transfected UBC. These cells exhibited apical-basolateral polarization and expression of the water channel aquaporin-2. These findings indicate that soluble HB-EGF and proHB-EGF induce branching tubulogenesis in UBC in different ways. Juxtacrine activation by proHB-EGF or the synergic action of soluble HB-EGF with transforming growth factor-β is important for well balanced morphogenesis of the collecting duct system.
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Koochekpour, Shahriar, Michael Jeffers, Paul H. Wang, Changning Gong, Gregory A. Taylor, Lisa M. Roessler, Robert Stearman, et al. "The von Hippel-Lindau Tumor Suppressor Gene Inhibits Hepatocyte Growth Factor/Scatter Factor-Induced Invasion and Branching Morphogenesis in Renal Carcinoma Cells." Molecular and Cellular Biology 19, no. 9 (September 1, 1999): 5902–12. http://dx.doi.org/10.1128/mcb.19.9.5902.

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ABSTRACT Loss of function in the von Hippel-Lindau (VHL) tumor suppressor gene occurs in familial and most sporadic renal cell carcinomas (RCCs). VHL has been linked to the regulation of cell cycle cessation (G0) and to control of expression of various mRNAs such as for vascular endothelial growth factor. RCC cells express the Met receptor tyrosine kinase, and Met mediates invasion and branching morphogenesis in many cell types in response to hepatocyte growth factor/scatter factor (HGF/SF). We examined the HGF/SF responsiveness of RCC cells containing endogenous mutated (mut) forms of the VHL protein (VHL-negative RCC) with that of isogenic cells expressing exogenous wild-type (wt) VHL (VHL-positive RCC). We found that VHL-negative 786-0 and UOK-101 RCC cells were highly invasive through growth factor-reduced (GFR) Matrigel-coated filters and exhibited an extensive branching morphogenesis phenotype in response to HGF/SF in the three-dimensional (3D) GFR Matrigel cultures. In contrast, the phenotypes of A498 VHL-negative RCC cells were weaker, and isogenic RCC cells ectopically expressing wt VHL did not respond at all. We found that all VHL-negative RCC cells expressed reduced levels of tissue inhibitor of metalloproteinase 2 (TIMP-2) relative to the wt VHL-positive cells, implicating VHL in the regulation of this molecule. However, consistent with the more invasive phenotype of the 786-0 and UOK-101 VHL-negative RCC cells, the levels of TIMP-1 and TIMP-2 were reduced and levels of the matrix metalloproteinases 2 and 9 were elevated compared to the noninvasive VHL-positive RCC cells. Moreover, recombinant TIMPs completely blocked HGF/SF-mediated branching morphogenesis, while neutralizing antibodies to the TIMPs stimulated HGF/SF-mediated invasion in vitro. Thus, the loss of the VHL tumor suppressor gene is central to changes that control tissue invasiveness, and a more invasive phenotype requires additional genetic changes seen in some but not all RCC lines. These studies also demonstrate a synergy between the loss of VHL function and Met signaling.
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48

Koledova, Zuzana, Xiaohong Zhang, Charles Streuli, Robert B. Clarke, Ophir D. Klein, Zena Werb, and Pengfei Lu. "SPRY1 regulates mammary epithelial morphogenesis by modulating EGFR-dependent stromal paracrine signaling and ECM remodeling." Proceedings of the National Academy of Sciences 113, no. 39 (September 12, 2016): E5731—E5740. http://dx.doi.org/10.1073/pnas.1611532113.

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The role of the local microenvironment in influencing cell behavior is central to both normal development and cancer formation. Here, we show that sprouty 1 (SPRY1) modulates the microenvironment to enable proper mammary branching morphogenesis. This process occurs through negative regulation of epidermal growth factor receptor (EGFR) signaling in mammary stroma. Loss of SPRY1 resulted in up-regulation of EGFR–extracellular signal–regulated kinase (ERK) signaling in response to amphiregulin and transforming growth factor alpha stimulation. Consequently, stromal paracrine signaling and ECM remodeling is augmented, leading to increased epithelial branching in the mutant gland. By contrast, down-regulation of EGFR–ERK signaling due to gain of Sprouty function in the stroma led to stunted epithelial branching. Taken together, our results show that modulation of stromal paracrine signaling and ECM remodeling by SPRY1 regulates mammary epithelial morphogenesis during postnatal development.
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49

Groenman, Freek A., Martin Rutter, Jinxia Wang, Isabella Caniggia, Dick Tibboel, and Martin Post. "Effect of chemical stabilizers of hypoxia-inducible factors on early lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 293, no. 3 (September 2007): L557—L567. http://dx.doi.org/10.1152/ajplung.00486.2006.

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Low oxygen stimulates pulmonary vascular development and airway branching and involves hypoxia-inducible factor (HIF). HIF is stable and initiates expression of angiogenic factors under hypoxia, whereas normoxia triggers hydroxylation of the HIF-1α subunit by prolyl hydroxylases (PHDs) and subsequent degradation. Herein, we investigated whether chemical stabilization of HIF-1α under normoxic (20% O2) conditions would stimulate vascular growth and branching morphogenesis in early lung explants. Tie2-LacZ (endothelial LacZ marker) mice were used for visualization of the vasculature. Embryonic day 11.5 (E11.5) lung buds were dissected and cultured in 20% O2 in the absence or presence of cobalt chloride (CoCl2, a hypoxia mimetic), dimethyloxalylglycine (DMOG; a nonspecific inhibitor of PHDs), or desferrioxamine (DFO; an iron chelator). Vascularization was assessed by X-gal staining, and terminal buds were counted. The fine vascular network surrounding the developing lung buds seen in control explants disappeared in CoCl2- and DFO-treated explants. Also, epithelial branching was reduced in the explants treated with CoCl2 and DFO. In contrast, DMOG inhibited branching but stimulated vascularization. Both DFO and DMOG increased nuclear HIF-1α protein levels, whereas CoCl2 had no effect. Since HIF-1α induces VEGF expression, the effect of SU-5416, a potent VEGF receptor (VEGFR) blocker, on early lung development was also investigated. Inhibition of VEGFR2 signaling in explants maintained under hypoxic (2% O2) conditions completely abolished vascularization and slightly decreased epithelial branching. Taken together, the data suggest that DMOG stabilization of HIF-1α during early development leads to a hypervascular lung and that airway branching proceeds without the vasculature, albeit at a slower rate.
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50

Ruan, Weifeng, Marie E. Monaco, and David L. Kleinberg. "Progesterone Stimulates Mammary Gland Ductal Morphogenesis by Synergizing with and Enhancing Insulin-Like Growth Factor-I Action." Endocrinology 146, no. 3 (March 1, 2005): 1170–78. http://dx.doi.org/10.1210/en.2004-1360.

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Progestins have been implicated in breast cancer development, yet a role for progesterone (Pg) in ductal morphogenesis (DM) has not been established. To determine whether Pg could cause DM, we compared relative effects of Pg, estradiol (E2) and IGF-I on anatomical and molecular biological parameters of IGF-I-related DM in oophorectomized female IGF-I(−/−) mice. Pg had little independent effect on mammary development, but together with IGF-I, in the absence of E2, Pg stimulated an extensive network of branching ducts, occupying 92% of the gland vs. 28.3% with IGF-I alone, resembling pubertal development (P < 0.002). Its major effect was on enhancing duct length and branching (P < 0.002). Additionally, Pg enhanced phosphorylation of IRS-1, increased cell division, and increased the antiapoptotic effect of IGF-I. Pg action was inhibited by RU486 (P < 0.01). E2 also stimulated DM by enhancing IGF-I action but had a greater effect on terminal end bud formation and side branching (P < 0.002). In contrast to previous findings, long-term exposure to E2 alone, without IGF-I, caused formation of ducts and side branches, a novel finding. Both IGF-I and E2 were found necessary for Pg-induced alveolar development. In conclusion, Pg, through Pg receptor can enhance IGF-I action in DM, and E2 acts through a similar mechanism; E2 alone caused formation of ducts and side branches; there were differences in the actions of Pg and E2, the former largely affecting duct formation and extension, and the latter side branching; and both IGF-I and E2 were necessary for Pg to form mature alveoli.
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