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Literatura académica sobre el tema "Mice Notch genes Mice"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 12 de febrero de 2022

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Artículos de revistas sobre el tema "Mice Notch genes Mice"

1

Broner, Esther Channah, Genia Alpert, Udi Gluschnaider, Adi Mondshine, Oz Solomon, Ido Sloma, Rami Rauch, Evgeny Izumchenko, Jon Christopher Aster y Matti Davis. "AL101 mediated tumor inhibition in notch-altered TNBC PDX models." Journal of Clinical Oncology 37, n.º 15_suppl (20 de mayo de 2019): 1064. http://dx.doi.org/10.1200/jco.2019.37.15_suppl.1064.

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1064 Background: The Notch pathway is activated during mammary gland development and has been implicated as a key driver in breast cancer. There is an urgent need to identify new therapeutic strategies for triple-negative breast cancer (TNBC), a sub-type associated with poor prognosis and no available targeted therapies. Notch gain of function (GOF) genetic alterations are potential tumor drivers found in ~10% of TNBC. This motivated the development of Notch inhibitors, including AL101 a pan-Notch, gamma secretase inhibitor (J Clin Oncol 36, 2018 abstract 2515). AL101 is currently being evaluated in Adenoid Cystic Carcinoma patients with activating Notch mutations (NCT03691207, ACCURACY trial). Here, we aim to test the activity of AL101 in TNBC patient derived xenograft (PDX) models with Notch activating genetic alterations. Methods: Gene expression cluster analysis was performed for 38 TNBC PDX tumors using a list of 21 Notch target genes. Seven tumors, bearing a “Notch-on” signature, were enriched with mutated/fusion (M/F) Notch genes and clustered separately from all other tumors. Of 9 models selected for study, 4 had a Notch-on signature and were expected to respond to AL101. Tumors were implanted into female athymic nude mice. Once tumors reached an average size of 150-300 mm3, mice (n = 5/group) were randomized to Vehicle or AL101 treatment arms (3 mg/kg, PO, 4on/3off) until tumors reached 1500 mm3 or day 60. Results: As measured by tumor growth inhibition (TGI), AL101 was more potent in tumors with a putative Notch-on signature. Within these 4 models, M/F genes were present in Notch1-NRR GOF (103% TGI p = 0.0004); Notch2-fusion (62%TGI p = 0.036); Notch3-fusion (75% TGI p = 0.032); or Notch4-fusion (147% TGI p < 0.00001). Tumors lacking the Notch signature did not respond significantly to AL101: WT Notch (43% TGI p = 0.0104; 64% TGI p = 0.13); Notch1 with a predicted loss of function mutation (12% TGI p = 0.53), Notch1 Variant of Unknown Significance (VUS) (30% TGI p = 0.44), Notch2 VUS (41% TGI p = 0.44). Conclusions: We demonstrate that in TNBC PDX models, the presence of a Notch-on signature and Notch GOF mutations/fusions correlates with potent response to AL101. These data support the clinical development of AL101 as a targeted therapy for TNBC with Notch GOF alterations.
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Kramer, Jan, Ralf Schwanbeck, Horst Pagel, Figen Cakiroglu, Jürgen Rohwedel y Ursula Just. "Inhibition of Notch Signaling Ameliorates Acute Kidney Failure and Downregulates Platelet-Derived Growth Factor Receptor β in the Mouse Model". Cells Tissues Organs 201, n.º 2 (2016): 109–17. http://dx.doi.org/10.1159/000442463.

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Ischemic acute kidney injury (AKI) is associated with high morbidity and frequent complications. Repeated episodes of AKI may lead to end-stage renal failure. The pathobiology of regeneration in AKI is not well understood and there is no effective clinical therapy that improves regeneration. The Notch signaling pathway plays an essential role in kidney development and has been implicated in tissue repair in the adult kidney. Here, we found that kidneys after experimental AKI in mice showed increased expression of Notch receptors, specifically Notch1-3, of the Notch ligands Jagged-1 (Jag1), Jag2 and Delta-like-4 (Dll4) and of the Notch target genes Hes1, Hey2, HeyL, Sox9 and platelet-derived growth factor receptor β (Pdgfrb). Treatment of ischemic mice with the γ-secretase inhibitor DBZ blocked Notch signaling and specifically downregulated the expression of Notch3 and the Notch target genes Hes1, Hey2, HeyL and Pdgfrb. After DBZ treatment, the mice developed less interstitial edema and displayed altered interstitial inflammation patterns. Furthermore, serum urea and creatinine levels were significantly decreased from 6 h onwards when compared to control mice treated with DMSO only. Our data are consistent with an amelioration of the severity of kidney injury by blocking Notch activation following AKI, and suggest an involvement of Notch-regulated Pdgfrb in AKI pathogenesis.
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Wu, Lizi, Ivan Maillard, Makoto Nakamura, Warren S. Pear y James D. Griffin. "The MAML1 Transcriptional Co-Activator Is Required for the Development of Marginal Zone B Cells." Blood 108, n.º 11 (16 de noviembre de 2006): 777. http://dx.doi.org/10.1182/blood.v108.11.777.777.

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Abstract Notch1 and Notch2 receptor-mediated signaling appear to have important and unique roles in lymphoid lineage commitment. Notch1 is required for T cell development, while Notch2 is essential for marginal zone B cell development. This specificity is not completely explained by differential expression patterns of Notch1 and 2 or Notch ligands, suggesting that there are other genes that contribute to specifying Notch receptor functions. We have previously shown that the MAML family of transcriptional co-activators is essential for Notch-induced transcriptional events, and functions by forming ternary complexes with Notch and the transcription factor CSL in the nucleus. This MAML family currently consists of three members, MAML1-3, all of which can function as co-activators for Notch receptors in vitro . In this study, we investigated the possibility that MAML1 co-activator contributes to determining Notch receptor function by generating mice deficient in the Maml1 gene. Maml1 -deficient mice fail to thrive and die within 10 days of birth. The morphology of marrow, nodes, and spleen was grossly intact. The ability of Maml1-deficient stem cells to generate different T and B lineages of lymphoid cells was determined by transplanting fetal liver cells isolated from E14.5 embryos into lethally irradiated wild-type recipient mice and analyzing donor-derived lymphoid cells 12 weeks post-transplantation. We found that the deletion of Maml1 results in complete loss of marginal zone B cell lineage (MZB, defined by B220+CD21hiCD23lo). Moreover, the number of MZB cells was reduced to about 50% in Maml1 -heterozygous fetal liver chimeras as compared to wild type controls. However, T cell development was largely unaffected, with only a modest but significant increase in the number of γδ T cells (about 2 fold) in both the thymus and the spleen. Therefore, these results suggest the unexpected finding that targeted deletion of Maml1 in hematopoietic cells is similar to the targeted deletion of either Notch2 or the Notch ligand, Delta-like 1 (Dll1) resulting in the loss of marginal zone B cells and minimal effects on T cell development. Moreover, the number of marginal zone B cells is correlated with Maml1 gene dosage, indicating haploinsufficiency. These data suggest that the Notch ligand Dll1 activates Notch2 signaling resulting in a Notch2/MAML1/CSL complex that is essential for marginal zone B cell development. Further studies with respect to relative expression levels of various MAML genes and interactions of MAML co-activators and Notch receptors may shed additional light into understanding how different Notch receptors regulate cell fate decisions in hematopoiesis.
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Hamada, Y., Y. Kadokawa, M. Okabe, M. Ikawa, J. R. Coleman y Y. Tsujimoto. "Mutation in ankyrin repeats of the mouse Notch2 gene induces early embryonic lethality". Development 126, n.º 15 (1 de agosto de 1999): 3415–24. http://dx.doi.org/10.1242/dev.126.15.3415.

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Notch family genes encode transmembrane proteins involved in cell-fate determination. Using gene targeting procedures, we disrupted the mouse Notch2 gene by replacing all but one of the ankyrin repeat sequences in the cytoplasmic domain with the E. coli (beta)-galactosidase gene. The mutant Notch2 gene encodes a 380 kDa Notch2-(beta)-gal fusion protein with (beta)-galactosidase activity. Notch2 homozygous mutant mice die prior to embryonic day 11.5, whereas heterozygotes show no apparent abnormalities and are fully viable. Analysis of Notch2 expression patterns, revealed by X-gal staining, demonstrated that the Notch2 gene is expressed in a wide variety of tissues including neuroepithelia, somites, optic vesicles, otic vesicles, and branchial arches, but not heart. Histological studies, including in situ nick end labeling procedures, showed earlier onset and higher incidence of apoptosis in homozygous mutant mice than in heterozygotes or wild type mice. Dying cells were particularly evident in neural tissues, where they were seen as early as embryonic day 9.5 in Notch2-deficient mice. Cells from Notch2 mutant mice attach and grow normally in culture, demonstrating that Notch2 deficiency does not interfere with cell proliferation and that expression of the Notch2-(beta)-gal fusion protein is not toxic per se. In contrast to Notch1-deficient mice, Notch2 mutant mice did not show disorganized somitogenesis, nor did they fail to properly regulate the expression of neurogenic genes such as Hes-5 or Mash1. In situ hybridization studies show no indication of altered Notch1 expression patterns in Notch2 mutant mice. The results indicate that Notch2 plays an essential role in postimplantation development in mice, probably in some aspect of cell specification and/or differentiation, and that the ankyrin repeats are indispensable for its function.
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Canalis, Ernesto, Tamar R. Grossman, Michele Carrer, Lauren Schilling y Jungeun Yu. "Antisense oligonucleotides targeting Notch2 ameliorate the osteopenic phenotype in a mouse model of Hajdu-Cheney syndrome". Journal of Biological Chemistry 295, n.º 12 (28 de enero de 2020): 3952–64. http://dx.doi.org/10.1074/jbc.ra119.011440.

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Notch receptors play critical roles in cell-fate decisions and in the regulation of skeletal development and bone remodeling. Gain–of–function NOTCH2 mutations can cause Hajdu-Cheney syndrome, an untreatable disease characterized by osteoporosis and fractures, craniofacial developmental abnormalities, and acro-osteolysis. We have previously created a mouse model harboring a point 6955C→T mutation in the Notch2 locus upstream of the PEST domain, and we termed this model Notch2tm1.1Ecan. Heterozygous Notch2tm1.1Ecan mutant mice exhibit severe cancellous and cortical bone osteopenia due to increased bone resorption. In this work, we demonstrate that the subcutaneous administration of Notch2 antisense oligonucleotides (ASO) down-regulates Notch2 and the Notch target genes Hes-related family basic helix–loop–helix transcription factor with YRPW motif 1 (Hey1), Hey2, and HeyL in skeletal tissue from Notch2tm1.1Ecan mice. Results of microcomputed tomography experiments indicated that the administration of Notch2 ASOs ameliorates the cancellous osteopenia of Notch2tm1.1Ecan mice, and bone histomorphometry analysis revealed decreased osteoclast numbers in Notch2 ASO-treated Notch2tm1.1Ecan mice. Notch2 ASOs decreased the induction of mRNA levels of TNF superfamily member 11 (Tnfsf11, encoding the osteoclastogenic protein RANKL) in cultured osteoblasts and osteocytes from Notch2tm1.1Ecan mice. Bone marrow-derived macrophage cultures from the Notch2tm1.1Ecan mice displayed enhanced osteoclastogenesis, which was suppressed by Notch2 ASOs. In conclusion, Notch2tm1.1Ecan mice exhibit cancellous bone osteopenia that can be ameliorated by systemic administration of Notch2 ASOs.
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Wang, Qing, Ran Yan, Nancy Pinnell, Yiran Liu, Amparo Serna Alarcon, Jason Qin, Yitong Chen et al. "The Direct Notch1 Cofactor Zmiz1 Differentially Regulates Notch1 Signals in a Stage-Specific Manner to Preserve Early T-Cell Precursors and Expand Committed T Cells". Blood 128, n.º 22 (2 de diciembre de 2016): 426. http://dx.doi.org/10.1182/blood.v128.22.426.426.

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Abstract When stem cells first enter the thymus and become early T-cell precursor (ETP) cells, they are exposed to high levels of Notch1 ligand. Notch1 signal strength must be tightly regulated because on one hand, excessive Notch1 signals drive premature T-cell commitment, resulting in loss of ETP cells and alternative cell fates. On the other hand, complete loss of Notch1 signals impairs ETP proliferation, also resulting in loss of ETP cells. Thus, keeping Notch signals finely balanced in ETP cells preserves "stemness". However, after ETP cells commit to the T-cell lineage by the DN3 cell stage, Notch1 signals ramp up dramatically to drive proliferation. It is unclear how Notch1 signals are initially restrained and then amplified. We previously showed that the PIAS-like coregulator Zmiz1 is a direct, context-dependent cofactor of Notch1 in T-cell leukemia. In contrast to drosophila Zmiz1, mammalian Zmiz1 evolved a tetratricopeptide repeat (TPR) domain that binds directly to Notch1 and selectively induces oncogenic target genes such as Myc through its transactivation domain (TAD). To understand the role of Zmiz1 in T-cell development, we bred conditional Zmiz1 and Notch1 knockout mice to Cre strains that delete floxed genes in hematopoietic cells (VavCre/MxCre), in early T cells (LckCre), and in late T-cells (CD4Cre). Like deletion of Notch1, deletion of Zmiz1 caused an early defect at the ETP stage and a late defect at the DN3 stage. The defect with Zmiz1 deletion was less severe than with Notch1 deletion (~4-fold reduction for Zmiz1 deletion versus ~8-fold reduction for Notch1 deletion). Unexpectedly, the ETP defect in Zmiz1-deficient mice partially phenocopied excessive Notch1 activation with increased differentiation to DN2 cells and loss of ETP cells and alternative cell fates (myeloid and NK). To confirm this effect, we plated Zmiz1-deficient hematopoietic stem and progenitor cells (HSPCs) directly on OP9-DL stromal cells. Accordingly, these cultures recapitulated the in vivo phenotype, including suppression of myeloid cells. Reducing Notch signals slightly with modest doses of Notch inhibitors restored myeloid differentiation. In contrast to the ETP defect, the DN3 defect resembled Notch1 loss-of function. Accordingly, overexpression of activated Notch1 or a fusion protein containing only the Notch-interacting domain (TPR) and the TAD was sufficient to rescue the DN3 block. To determine mechanism, we performed RNA-Seq in sorted ETP and DN3 cells from Zmiz1-deficient mice and mice treated with the anti-NRR Notch1 antibody. Zmiz1 coregulated ~16% of Notch1 target genes in ETP cells and ~24% in DN3 cells. In ETP cells, Zmiz1 primarily acted as a repressor of Notch1 target genes. Enrichment analyses showed that Notch1 promoted changes associated with T-lineage commitment, such as induction of Dtx1, Notch3, and Ptcra. In contrast, Zmiz1 reversed these changes. Although generally antagonistic with each other, Zmiz1 and Notch1 concordantly activated a minority of target genes important for proliferation, such as Myc. Upon differentiation to the DN3 cell stage, Zmiz1 switched from primarily a repressor of Notch1 target genes to primarily an activator, inducing Myc and Wnt pathway genes. Accordingly, overexpression of Myc in Zmiz1-deficient DN3 cells was sufficient to rescue the DN3 block in OP9-DL culture. To determine whether Zmiz1 needed to bind Notch1 in order activate or repress Notch1 target genes, we used HSQC NMR to identify amino acids in the TPR that were required for Notch1 binding. Two amino acids, R14 and E34, were confirmed by reporter and co-IP assays to be critical for the Zmiz1-Notch1 interaction. The Zmiz1(R14A+E34A) mutant, which was incapable of binding Notch1, failed to induce Myc. In contrast, this mutant retained full ability to repress Notch target genes associated with T-cell commitment. These data suggest that in ETP cells, Zmiz1 preferentially restrains Notch1 T-cell commitment genes. However, after T-lineage commitment, Zmiz1 switches primarily into a Notch1-interaction mode that preferentially promotes Notch1 signals. It has been puzzling how Notch1 can drive seemingly conflicting biological processes of self-renewal and commitment. Zmiz1 appears to be one solution that evolved to differentially regulate Notch1 signals at a given Notch dosage strength in order to preserve ETP "stemness" while at the same time expanding committed T cells. Disclosures No relevant conflicts of interest to declare.
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Vanorny, Dallas A., Rexxi D. Prasasya, Abha J. Chalpe, Signe M. Kilen y Kelly E. Mayo. "Notch Signaling Regulates Ovarian Follicle Formation and Coordinates Follicular Growth". Molecular Endocrinology 28, n.º 4 (1 de abril de 2014): 499–511. http://dx.doi.org/10.1210/me.2013-1288.

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Abstract Ovarian follicles form through a process in which somatic pregranulosa cells encapsulate individual germ cells from germ cell syncytia. Complementary expression of the Notch ligand, Jagged1, in germ cells and the Notch receptor, Notch2, in pregranulosa cells suggests a role for Notch signaling in mediating cellular interactions during follicle assembly. Using a Notch reporter mouse, we demonstrate that Notch signaling is active within somatic cells of the embryonic ovary, and these cells undergo dramatic reorganization during follicle histogenesis. This coincides with a significant increase in the expression of the ligands, Jagged1 and Jagged2; the receptor, Notch2; and the target genes, Hes1 and Hey2. Histological examination of ovaries from mice with conditional deletion of Jagged1 within germ cells (J1 knockout [J1KO]) or Notch2 within granulosa cells (N2 knockout [N2KO]) reveals changes in follicle dynamics, including perturbations in the primordial follicle pool and antral follicle development. J1KO and N2KO ovaries also contain multi-oocytic follicles, which represent a failure to resolve germ cell syncytia, and follicles with enlarged oocytes but lacking somatic cell growth, signifying a potential role of Notch signaling in follicle activation and the coordination of follicle development. We also observed decreased cell proliferation and increased apoptosis in the somatic cells of both conditional knockout lines. As a consequence of these defects, J1KO female mice are subfertile; however, N2KO female mice remain fertile. This study demonstrates important functions for Jagged1 and Notch2 in the resolution of germ cell syncytia and the coordination of somatic and germ cell growth within follicles of the mouse ovary.
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Ziouti, Fani, Regina Ebert, Maximilian Rummler, Melanie Krug, Sigrid Müller-Deubert, Martin Lüdemann, Franz Jakob, Bettina M. Willie y Franziska Jundt. "NOTCH Signaling Is Activated through Mechanical Strain in Human Bone Marrow-Derived Mesenchymal Stromal Cells". Stem Cells International 2019 (26 de febrero de 2019): 1–13. http://dx.doi.org/10.1155/2019/5150634.

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Skeletal development and remodeling of adult bone are critically controlled by activated NOTCH signaling in genetically modified mice. It is yet unclear whether NOTCH signaling is activated by mechanical strain sensed by bone cells. We found that expression of specific NOTCH target genes is induced after in vivo tibial mechanical loading in wild-type mice. We further applied mechanical strain through cyclic stretching in human bone marrow-derived mesenchymal stromal cells (BMSCs) in vitro by using a bioreactor system and detected upregulation of NOTCH target gene expression. Inhibition of the NOTCH pathway in primary BMSCs as well as telomerase-immortalized human BMSCs (hMSC-TERT) through the gamma-secretase inhibitor GSI XII blocked mechanotransduction and modulated actin cytoskeleton organization. Short-hairpin RNA gene silencing identified NOTCH2 as the key receptor mediating NOTCH effects on hMSC-TERT cells. Our data indicate a functional link between NOTCH activation and mechanotransduction in human BMSCs. We suggest that NOTCH signaling is an important contributor to molecular mechanisms that mediate the bone formation response to mechanical strain.
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Wu, Lizi, Ivan Maillard, Makoto Nakamura, Warren S. Pear y James D. Griffin. "The transcriptional coactivator Maml1 is required for Notch2-mediated marginal zone B-cell development". Blood 110, n.º 10 (15 de noviembre de 2007): 3618–23. http://dx.doi.org/10.1182/blood-2007-06-097030.

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Abstract Signaling mediated by various Notch receptors and their ligands regulates diverse biological processes, including lymphoid cell fate decisions. Notch1 is required during T-cell development, while Notch2 and the Notch ligand Delta-like1 control marginal zone B (MZB) cell development. We previously determined that Mastermind-like (MAML) transcriptional coactivators are required for Notchinduced transcription by forming ternary nuclear complexes with Notch and the transcription factor CSL. The 3 MAML family members (MAML1-MAML3) are collectively essential for Notch activity in vivo, but whether individual MAMLs contribute to the specificity of Notch functions is unknown. Here, we addressed this question by studying lymphopoiesis in the absence of the Maml1 gene. Since Maml1−/− mice suffered perinatal lethality, hematopoietic chimeras were generated with Maml1−/−, Maml1+/−, or wild-type fetal liver progenitors. Maml1 deficiency minimally affected T-cell development, but was required for the development of MZB cells, similar to the phenotype of Notch2 deficiency. Moreover, the number of MZB cells correlated with Maml1 gene dosage. Since all 3 Maml genes were expressed in MZB cells and their precursors, these results suggest that Maml1 is specifically required for Notch2 signaling in MZB cells.
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Luo, B., J. C. Aster, R. P. Hasserjian, F. Kuo y J. Sklar. "Isolation and functional analysis of a cDNA for human Jagged2, a gene encoding a ligand for the Notch1 receptor." Molecular and Cellular Biology 17, n.º 10 (octubre de 1997): 6057–67. http://dx.doi.org/10.1128/mcb.17.10.6057.

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Signaling through Notch receptors has been implicated in the control of cellular differentiation in animals ranging from nematodes to humans. Starting from a human expressed sequence tag-containing sequence resembling that of Serrate, the gene for a ligand of Drosophila melanogaster Notch, we assembled a full-length cDNA, now called human Jagged2, from overlapping cDNA clones. The full-length cDNA encodes a polypeptide having extensive sequence homology to Serrate (40.6% identity and 58.7% similarity) and even greater homology to several putative mammalian Notch ligands that have subsequently been described. When in situ hybridization was performed, expression of the murine Jagged2 homolog was found to be highest in fetal thymus, epidermis, foregut, dorsal root ganglia, and inner ear. In Northern blot analysis of RNA from tissues of 2-week-old mice, the 5.0-kb Jagged2 transcript was most abundant in heart, lung, thymus, skeletal muscle, brain, and testis. Immunohistochemistry revealed coexpression of Jagged2 and Notch1 within thymus and other fetal murine tissues, consistent with interaction of the two proteins in vivo. Coculture of fibroblasts expressing human Jagged2 with murine C2C12 myoblasts inhibited myogenic differentiation, accompanied by increased Notch1 and the appearance of a novel 115-kDa Notch1 fragment. Exposure of C2C12 cells to Jagged2 led to increased amounts of Notch mRNA as well as mRNAs for a second Notch receptor, Notch3, and a second Notch ligand, Jagged1. Constitutively active forms of Notchl in C2C12 cells also induced increased levels of the same set of mRNAs, suggesting positive feedback control of these genes initiated by binding of Jagged2 to Notch1. This feedback control may function in vivo to coordinate differentiation across certain groups of progenitor cells adopting identical cell fates.
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Tesis sobre el tema "Mice Notch genes Mice"

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Ruivenkamp, Claudia Antoinette Laetitia. "Colon cancer susceptibility genes in mice and humans". [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/67685.

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Jakt, Lars Martin. "Isolation of mouse Hoxb-3 protein binding sequences : a whole genome approach /". Thesis, Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21185505.

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Rigby, Robert James. "The identification of lupus susceptibility genes in New Zealand mice". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429877.

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Randhawa, J. S. "Molecular characterisation of the pneumonia virus of mice glycoprotein genes". Thesis, University of Warwick, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387336.

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Boukouvala, Sotiria. "Expression of the genes for arylamine N-acetyltransferases in mice". Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:ed864a10-2cb9-4ebe-8a2c-934d707c5a0d.

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Freland, Sofia. "Lymphoid development and function in MHC class I deficient mice /". Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3714-1/.

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Keshavarz, Maryam [Verfasser]. "Analysis of candidate genes for behavioral differences in mice / Maryam Keshavarz". Kiel : Universitätsbibliothek Kiel, 2019. http://d-nb.info/1187242616/34.

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Faulkes, David Julian. "The analysis of human serum amyloid A genes using transgenic mice". Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287010.

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Scherer, Christina Ann. "An in vitro screen to isolate developmentally regulated genes in mice". Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/32638.

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Dershem, Victoria Lynne. "The Expression of Dopamine-Related Genes and Behavioral Performance in Mice". Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1484217370390211.

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Libros sobre el tema "Mice Notch genes Mice"

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Ormestad, Mattias. FoxF genes in embryonic development. Göteborg: Department of Cell and Molecular Biology, Göteborg University, 2006.

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Haddad, George E. Expression of HLA class II genes in transgenic mice. Ottawa: National Library of Canada, 1994.

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Randhawa, J. S. Molecular characterisation of the pneumonia virus of mice glycoprotein genes. [s.l.]: typescript, 1993.

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Tsang, Michael Wai Kok. Characterisation of structure and function of mouse dishevelled genes. Dublin: University College Dublin, 1996.

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Howard, Lorraine Tamar. The construction and characterization of hypoxia responsive reporter genes for use in transgenic mice. Ottawa: National Library of Canada, 2001.

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Barr, John Nicholas. Expression of the nucleoprotein and phosphoprotein genes of pneumonia virus of mice and specific interactions ofthe gene products. [s.l.]: typescript, 1993.

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Thomas, David Peter. Studies on tumourigenesis in transgenic mice expressing the early region genes of human papillomavirus type 16 (HPV-16). Birmingham: University of Birmingham, 1996.

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E, Davies K. y Tilghman Shirley M, eds. Genes and phenotypes. Plainview, N.Y: Cold Spring Harbor Laboratory Press, 1991.

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(Foreword), Thomas R. Cech y Maya Pines (Introduction), eds. Genes We Share With Yeast, Flies, Worms and Mice: New Clues to Human Health and Disease. Diane Pub Co, 2003.

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Maya, Pines y Howard Hughes Medical Institute, eds. The genes we share with yeast, flies, worms, and mice: New clues to human health and disease. Chevy Chase, Md: Howard Hughes Medical Institute, 2001.

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Capítulos de libros sobre el tema "Mice Notch genes Mice"

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Aiba, Atsu y Motoya Katsuki. "Mutant Mice Lacking Dopamine Receptor Genes". En Catecholamine Research, 165–66. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4757-3538-3_37.

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Kono, D. H. y A. N. Theofilopoulos. "Genetic Susceptibility to Spontaneous Lupus in Mice". En Genes and Genetics of Autoimmunity, 72–98. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000060497.

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Kohda, Takashi, Fumitoshi Ishino y Atsuo Ogura. "Expression of Imprinted Genes in Cloned Mice". En Methods in Molecular Biology, 237–46. Totowa, NJ: Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59745-154-3_16.

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Lovell-Badge, Robin, Clare Canning y Ryohei Sekido. "Sex-Determining Genes in Mice: Building Pathways". En The Genetics and Biology of Sex Determination, 4–22. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868732.ch2.

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Jami, J. y R. Pictet. "Expression of Foreign Genes in Transgenic Mice". En Future Aspects in Human In Vitro Fertilization, 180–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71412-2_26.

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Kawade, Yoshimi, Masahide Asano, Hitoshi Nagashima y Yoichiro Iwakura. "Transgenic Mice Carrying Exogenous Mouse Interferon Genes". En The Biology of the Interferon System 1986, 305–11. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3543-3_43.

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Wilder, R. L., E. F. Remmers, Y. Kawahito, P. S. Gulko, G. W. Cannon y M. M. Griffiths. "Genetic Factors Regulating Experimental Arthritis in Mice and Rats". En Genes and Genetics of Autoimmunity, 121–65. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000060492.

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Storb, U., P. Engler, E. Klotz, A. Weng, D. Haasch, C. Pinkert, L. Doglio, M. Glymour y R. Brinster. "Rearrangement and Expression of Immunoglobulin Genes in Transgenic Mice". En Current Topics in Microbiology and Immunology, 137–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77633-5_16.

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Kozak, C. A. y R. R. O’Neill. "Xenotropic and MCF Related Retroviral Genes in Wild Mice". En The Wild Mouse in Immunology, 349–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71304-0_42.

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Levine, Arnold J. "Expression of SV40 Early Region Genes in Transgenic Mice". En Concepts in Viral Pathogenesis III, 158–63. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4613-8890-6_18.

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Actas de conferencias sobre el tema "Mice Notch genes Mice"

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Estrella, A. M., E. Dobrinskikh, C. E. Hennessy, I. V. Yang y D. A. Schwartz. "Muc5b and Other Genes Predispose Mice to Lung Fibrosis". En American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2159.

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Trivedi, S., J. Ciencewicki, HY Cho, K. Horvath, I. Jaspers y SR Kleeberger. "Expression of Notch and Its Ligands in Mice Exposed to Ozone." En American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2572.

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Yongbin, Chen, Zhang Liyan y Guo Guozhen. "Effect of EMP on mice polydactylia and related genes expression (Gli3, Shh and Fgf4) during the development of mice limbs". En 2006 4th Asia-Pacific Conference on Environmental Electromagnetics. IEEE, 2006. http://dx.doi.org/10.1109/ceem.2006.257966.

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Turner, Charles H. y Alexander G. Robling. "Genetic Effects on Skeletal Mechanosensitivity in Mice". En ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32596.

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The accumulation of bone mass during growth can be enhanced by environmental factors such as mechanical loading (exercise) or calcium intake, but 60–70% of the variance in adult bone mineral density (BMD) is explained by heredity. Consequently, understanding the signaling pathways targeted by the genes governing bone accumulation holds perhaps the greatest potential in reducing fracture incidence later in life. Rodent models are particularly useful for studying the genetics of skeletal traits. Of the available inbred mouse strains, three in particular have been studied extensively in skeletal genetics: C57BL/6, DBA/2, and C3H/He. The C57BL/6 strain is characterized by low BMD and large total cross-sectional area (CSA) in the midshaft femur; the C3H/He strain exhibits very high femoral BMD and a smaller femoral CSA than the C57BL/6 mice; and DBA/2 mice have moderately high femoral BMD and a very small midshaft femur CSA. Mechanical loading of the skeleton during growth can substantially enhance periosteal bone apposition, and ultimately produce a diaphyseal cross section with enlarged area. Therefore we hypothesized that the mouse strain with greater femoral cross-sectional area (C57BL/6) might have a genetic predisposition for greater mechanosensitivity than mice with smaller cross sections (C3H/He and DBA/2).
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Evert, K., Y. Qiao, J. Wang, E. Karagoz, X. Song, M. Xu, L. Che et al. "Loss of Axin1 induced hepatocarcinogenesis requires intact β-Catenin but not Notch cascade in mice". En 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677207.

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Hall, R., M. Krawczyk, S. Weber, M. Milkiewicz, P. Milkiewicz y F. Lammert. "Genes involved in hepatic cholesterol homeostasis identified as modifiers of cholestasis in Abcb4 deficient mice". En 36. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3402110.

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Leikauf, George D., Hannah Pope-Varsalona, Vincent J. Concel, Pengyuan Liu, Kiflai Bein, Kelly A. Brant, Richard A. Dopico, Jr. et al. "Candidate Susceptibility Genes Identified By Genomewide Analysis Of Chloride-induced Acute Lung Injury In Mice". En American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5370.

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Chen, Richard, Daniel Nemeth, Jason Mora, Mohan Muvvala, Derek Wu y Yuri Griko. "Changes in Differential Expression of Genes in Normal and Metabolically Suppressed Mice in Response to Radiation". En 2018 40th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2018. http://dx.doi.org/10.1109/embc.2018.8513624.

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El-fadl, Rihab, Nasser Rizk, Amena Fadel y Abdelrahman El Gamal. "The Profile of Hepatic Gene Expression of Glucose Metabolism in Mice on High Fat Diet". En Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0213.

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Obesity is a growing problem worldwide, and recent data indicated that 20% of the populations would be obese. Obesity arises as a multifactorial disease caused by inherited traits that interact with lifestyle factors such as diet and physical activity. The liver plays an essential role in the gluco-regulation via regulating glucose, lipid and protein metabolism. The process of glucose metabolism is controlled by a range of molecular mechanisms and genes which affect the metabolism of the liver during intake of high fat diet (HFD). The objective of this research is to investigate the profile of hepatic gene expression of glucose metabolism in mice on HFD treated with leptin (5 mg/kg BW Ip injection). Ten wild type CD1 mice fed on HFD is used for this study, where groups are control (vehicle - leptin) and test group (vehicle + leptin). Body weight (BW) was measured, and blood chemistry, insulin and leptin were measured at the end of the experiments. Total RNA was isolated from the liver tissue, and RTPCR profiler array technology was used to evaluate the mRNA expression of 84 essential genes of hepatic glucose metabolism. The data of the BW and blood chemistry are not significantly different between the two groups. Leptin treatment enhanced the metabolic pathways and the candidate genes of the different metabolic pathway; glycogen metabolism such as Gys1, Gys2 and Pygm, pentose phosphate shunt such as Rpia and suppressed the glycolysis such as Aldob, and TCA cycle such as Mdh1b. In conclusion, this study has shown that leptin could affect the profile of the hepatic mouse genes of glucose metabolism in the early stages of HFD to induce obesity
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Duarte, Antonio, Marina Badenes, Alexandre Trindade, Ren Liu y Parkash S. Gill. "Abstract LB-285: Blocking Dll4/Notch signaling inhibits development of chronic colitis-associated colorectal cancer in mice". En Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-lb-285.

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Informes sobre el tema "Mice Notch genes Mice"

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Connolly, Denise C. Modeling Human Epithelial Ovarian Cancer in Mice by Alteration of Expression of the BRCA1 and/or p53 Genes. Fort Belvoir, VA: Defense Technical Information Center, febrero de 2008. http://dx.doi.org/10.21236/ada485053.

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Connolly, Denise C. Modeling Human Epithelial Ovarian Cancer in Mice by Alteration of Expression of the BRCA1 and/or P53 Genes. Fort Belvoir, VA: Defense Technical Information Center, febrero de 2005. http://dx.doi.org/10.21236/ada436423.

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Blackburn, Anneke C. y Joseph Jerry. Development of Spontaneous Mammary Tumors in BALB/c-p53+-Mice: Detection of Early Genetic Alterations and the Mapping of BALB/c Susceptibility Genes. Fort Belvoir, VA: Defense Technical Information Center, julio de 2002. http://dx.doi.org/10.21236/ada410279.

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Smith, Sallie y Joseph Jerry. Development of Spontaneous Mammary Tumors in BALB/c-p53+/-Mice: Detection of Early Genetic Alterations and the Mapping of BALB/c Susceptibility Genes. Fort Belvoir, VA: Defense Technical Information Center, enero de 2004. http://dx.doi.org/10.21236/ada424523.

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