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Journal articles on the topic 'Mice Notch genes Mice'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

Broner, Esther Channah, Genia Alpert, Udi Gluschnaider, et al. "AL101 mediated tumor inhibition in notch-altered TNBC PDX models." Journal of Clinical Oncology 37, no. 15_suppl (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 evalua

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2

Kramer, Jan, Ralf Schwanbeck, Horst Pagel, Figen Cakiroglu, Jürgen Rohwedel та 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, № 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), Jag

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3

Wu, Lizi, Ivan Maillard, Makoto Nakamura, Warren S. Pear, and James D. Griffin. "The MAML1 Transcriptional Co-Activator Is Required for the Development of Marginal Zone B Cells." Blood 108, no. 11 (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 form

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4

Hamada, Y., Y. Kadokawa, M. Okabe, M. Ikawa, J. R. Coleman, and Y. Tsujimoto. "Mutation in ankyrin repeats of the mouse Notch2 gene induces early embryonic lethality." Development 126, no. 15 (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, dem

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5

Canalis, Ernesto, Tamar R. Grossman, Michele Carrer, Lauren Schilling, and Jungeun Yu. "Antisense oligonucleotides targeting Notch2 ameliorate the osteopenic phenotype in a mouse model of Hajdu-Cheney syndrome." Journal of Biological Chemistry 295, no. 12 (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 increa

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6

Wang, Qing, Ran Yan, Nancy Pinnell, 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, no. 22 (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 st

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7

Vanorny, Dallas A., Rexxi D. Prasasya, Abha J. Chalpe, Signe M. Kilen, and Kelly E. Mayo. "Notch Signaling Regulates Ovarian Follicle Formation and Coordinates Follicular Growth." Molecular Endocrinology 28, no. 4 (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 in

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8

Ziouti, Fani, Regina Ebert, Maximilian Rummler, et al. "NOTCH Signaling Is Activated through Mechanical Strain in Human Bone Marrow-Derived Mesenchymal Stromal Cells." Stem Cells International 2019 (February 26, 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

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9

Wu, Lizi, Ivan Maillard, Makoto Nakamura, Warren S. Pear, and James D. Griffin. "The transcriptional coactivator Maml1 is required for Notch2-mediated marginal zone B-cell development." Blood 110, no. 10 (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

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10

Luo, B., J. C. Aster, R. P. Hasserjian, F. Kuo, and 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, no. 10 (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

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11

Du, Wei, Jared Sipple, Jonathan Schick, and Qishen Pang. "Enhanced Notch Signaling Skews Hematopoietic Stem Cell Differentiation in Fanconi Anemia Murine Models." Blood 120, no. 21 (2012): 1191. http://dx.doi.org/10.1182/blood.v120.21.1191.1191.

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Abstract Abstract 1191 Objective: Hematopoietic stem cells (HSCs) can either self-renew or differentiate into various types of cells of the blood lineage. Little is known about the signaling pathways that regulate this choice of self-renewal versus differentiation. We studied the effect of altered Notch signaling on HSC differentiation in mouse models of Fanconi anemia (FA), a genetic disorder associated with bone marrow failure and progression to leukemia and other cancers. Methods: The study used a Notch reporter mouse, in which Notch-driven GFP expression acts as a sensor for HSC differenti

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12

Kindler, Thomas, Melanie G. Cornejo, Claudia Scholl та ін. "K-RasG12D–induced T-cell lymphoblastic lymphoma/leukemias harbor Notch1 mutations and are sensitive to γ-secretase inhibitors". Blood 112, № 8 (2008): 3373–82. http://dx.doi.org/10.1182/blood-2008-03-147587.

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Abstract To study the impact of oncogenic K-Ras on T-cell leukemia/lymphoma development and progression, we made use of a conditional K-RasG12D murine knockin model, in which oncogenic K-Ras is expressed from its endogenous promoter. Transplantation of whole bone marrow cells that express oncogenic K-Ras into wild-type recipient mice resulted in a highly penetrant, aggressive T-cell leukemia/lymphoma. The lymphoblasts were composed of a CD4/CD8 double-positive population that aberrantly expressed CD44. Thymi of primary donor mice showed reduced cellularity, and immunophenotypic analysis demons

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13

Kalinichenko, Vladimir V., Galina A. Gusarova, Il-Man Kim, et al. "Foxf1 haploinsufficiency reduces Notch-2 signaling during mouse lung development." American Journal of Physiology-Lung Cellular and Molecular Physiology 286, no. 3 (2004): L521—L530. http://dx.doi.org/10.1152/ajplung.00212.2003.

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The forkhead box (Fox) f1 transcription factor is expressed in the mouse splanchnic (visceral) mesoderm, which contributes to development of the liver, gallbladder, lung, and intestinal tract. Pulmonary hemorrhage and peripheral microvascular defects were found in approximately half of the newborn Foxf1(+/-) mice, which expressed low levels of lung Foxf1 mRNA [low- Foxf1(+/-) mice]. Microvascular development was normal in the surviving newborn high- Foxf1(+/-) mice, which compensated for pulmonary Foxf1 haploinsufficiency and expressed wild-type Foxf1 levels. To identify expression of genes re

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14

Lee, Sung-UK, Min Li, Manami Maeda, et al. "Notch Repression by LRF Is Necessary for the Maintenance of Adult Hematopoietic Stem Cell Pool." Blood 116, no. 21 (2010): 2633. http://dx.doi.org/10.1182/blood.v116.21.2633.2633.

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Abstract Abstract 2633 Among the different stem cells, hematopoietic stem cells (HSCs) are one of the best studied and characterized stem cells. To maintain life-long hematopoiesis in the bone marrow (BM), signals governing the balance between self-renewal and differentiation are tightly regulated in HSC compartment. Notch signals are critical regulators of the lymphoid lineage fate, but their role in adult HSC function in the BM is currently under debate. LRF (Leukemia/Lymphoma Related Factor, also known as Zbtb7a/pokemon) is a transcription factor that acts as a proto-oncogene and plays a ke

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15

Lin, Neng-Yu, Alfiya Distler, Christian Beyer, et al. "Inhibition of Notch1 promotes hedgehog signalling in a HES1-dependent manner in chondrocytes and exacerbates experimental osteoarthritis." Annals of the Rheumatic Diseases 75, no. 11 (2016): 2037–44. http://dx.doi.org/10.1136/annrheumdis-2015-208420.

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ObjectivesNotch ligands and receptors have recently been shown to be differentially expressed in osteoarthritis (OA). We aim to further elucidate the functional role of Notch signalling in OA using Notch1 antisense transgenic (Notch1 AS) mice.MethodsNotch and hedgehog signalling were analysed by real-time PCR and immunohistochemistry. Notch-1 AS mice were employed as a model of impaired Notch signalling in vivo. Experimental OA was induced by destabilisation of the medial meniscus (DMM). The extent of cartilage destruction and osteophyte formation was analysed by safranin-O staining with subse

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16

Jing, Yaxun, Joao Antonio Gimenes, Rahul Mishra, et al. "NOTCH3 contributes to rhinovirus-induced goblet cell hyperplasia in COPD airway epithelial cells." Thorax 74, no. 1 (2018): 18–32. http://dx.doi.org/10.1136/thoraxjnl-2017-210593.

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RationaleGoblet cell hyperplasia (GCH) is one of the cardinal features of chronic obstructive pulmonary disease (COPD) and contributes to airways obstruction. Rhinovirus (RV), which causes acute exacerbations in patients with COPD, also causes prolonged airways obstruction. Previously, we showed that RV enhances mucin gene expression and increases goblet cell number in a COPD mouse model. This study examines whether RV causes sustained GCH in relevant models of COPD.MethodsMucociliary-differentiated COPD and normal airway epithelial cell cultures and mice with normal or COPD phenotype were inf

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17

McCarter, Anna, Ran Yan, Amparo Serna Alarcon, et al. "Ets1 Enhances Context-Dependent Notch1 Activity in T-Cell Leukemia." Blood 132, Supplement 1 (2018): 2595. http://dx.doi.org/10.1182/blood-2018-99-111376.

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Abstract The discovery of NOTCH1 as the most frequently mutated oncogene in T-ALL patients raised hopes for targeted therapy in this cancer. Unfortunately, in clinical trials, the pan-Notch inhibitor GSI caused excessive GI toxicity. Mice treated continuously with GSI die from intestinal stem cell loss and severe intestinal secretory cell metaplasia. Intermittent dosing of GSI is tolerable, but has weak anti-cancer effects. Thus, the challenge has been to find ways to selectively disable Notch in T-ALL. Our idea to meet this challenge stems from work by others showing that Notch cannot activat

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Murta, D., M. Batista, E. Silva, et al. "Differential expression of Notch component and effector genes during ovarian follicle and corpus luteum development during the oestrous cycle." Reproduction, Fertility and Development 27, no. 7 (2015): 1038. http://dx.doi.org/10.1071/rd13399.

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Ovarian dynamics throughout the female oestrous cycle (EC) are characterised by cyclical follicle and corpus luteum (CL) development. These events are tightly regulated, involving extensive cell-to-cell communication. Notch is an evolutionarily well conserved cell-signalling pathway implicated in cell-fate decisions in several tissues. Here, we evaluated the extra-vascular expression patterns of Notch component and effector genes during follicle and CL development throughout the EC. Five mature CD1 female mice were killed at each EC stage. Blood samples were collected for progesterone measurem

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Nichol, Donna, Carrie Shawber, Michael J. Fitch, et al. "Impaired angiogenesis and altered Notch signaling in mice overexpressing endothelial Egfl7." Blood 116, no. 26 (2010): 6133–43. http://dx.doi.org/10.1182/blood-2010-03-274860.

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Abstract Epidermal growth factor-like domain 7 (Egfl7) is important for regulating tubulogenesis in zebrafish, but its role in mammals remains unresolved. We show here that endothelial overexpression of Egfl7 in transgenic mice leads to partial lethality, hemorrhaging, and altered cardiac morphogenesis. These defects are accompanied by abnormal vascular patterning and remodeling in both the embryonic and postnatal vasculature. Egfl7 overexpression in the neonatal retina results in a hyperangiogenic response, and EGFL7 knockdown in human primary endothelial cells suppresses endothelial cell pro

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Al Jaam, Bilal, Katy Heu, Florian Pennarubia, et al. "Reduced Notch signalling leads to postnatal skeletal muscle hypertrophy in Pofut1 cax/cax mice." Open Biology 6, no. 9 (2016): 160211. http://dx.doi.org/10.1098/rsob.160211.

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Postnatal skeletal muscle growth results from the activation of satellite cells and/or an increase in protein synthesis. The Notch signalling pathway maintains satellite cells in a quiescent state, and once activated, sustains their proliferation and commitment towards differentiation. In mammals, POFUT1-mediated O -fucosylation regulates the interactions between NOTCH receptors and ligands of the DELTA/JAGGED family, thus initiating the activation of canonical Notch signalling. Here, we analysed the consequences of downregulated expression of the Pofut1 gene on postnatal muscle growth in muta

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Jundt, Franziska, Rudolf A. Rupec, Bernd Rebholz та ін. "The Notch Ligand Jagged1 Causes a Myeloproliferative Disorder in Mice Lacking IκBα." Blood 106, № 11 (2005): 1226. http://dx.doi.org/10.1182/blood.v106.11.1226.1226.

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Abstract Hematopoiesis occurs in the liver and the bone marrow during murine development. Newborn mice with a ubiquitous deletion of IκBα develop a severe hematological disorder characterized by an increase of granulocyte/erythroid/monocyte/macrophage colony-forming units (CFU-GEMM) and hypergranulopoiesis. Here, we provide evidence that this particular myeloproliferative disturbance is mediated by continuously deregulated perinatal expression of the Notch ligand Jagged1 in IκBα-deficient hepatocytes. Signaling through Notch-family cell surface receptors and their ligands has been shown to be

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Vollrath, Benedikt, Jeffrey Pudney, Sylvia Asa, Philip Leder, and Kevin Fitzgerald. "Isolation of a Murine Homologue of the Drosophila neuralized Gene, a Gene Required for Axonemal Integrity in Spermatozoa and Terminal Maturation of the Mammary Gland." Molecular and Cellular Biology 21, no. 21 (2001): 7481–94. http://dx.doi.org/10.1128/mcb.21.21.7481-7494.2001.

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ABSTRACT The Drosophila neuralized gene shows genetic interactions with Notch, Enhancer of split, and other neurogenic genes and is thought to be involved in cell fate specification in the central nervous system and the mesoderm. In addition, a human homologue of the Drosophila neuralizedgene has been described as a potential tumor suppressor gene in malignant astrocytomas. We have isolated a murine homologue of theDrosophila and human Neuralized genes and, in an effort to understand its physiological function, derived mice with a targeted deletion of this gene. Surprisingly, mice homozygous f

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Pinnell, Nancy, Ran Yan, Hyoje Cho, et al. "Direct Coregulation of Notch1 By Zmiz1 in T-Cell Development and Leukemia." Blood 124, no. 21 (2014): 55. http://dx.doi.org/10.1182/blood.v124.21.55.55.

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Abstract The Notch1 receptor is required throughout normal T-cell development. NOTCH1 is also the most recurrently mutated oncogene in T-ALL, occurring in ~60% of human samples. However, Notch inhibitors cannot be used at full-strength because of intolerable on-target side effects, such as GI toxicity. Another concern is that these inhibitors would reverse the tumor suppressor functions of Notch. Lower doses of Notch inhibitors are better tolerated, but lead to residual Notch signaling. Moreover, collaborating pathways can reinforce these weak signals and drive resistance. Thus, it is importan

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Zhou, Lan, Lebing Wei Li, Quanjian Yan, et al. "Notch-dependent control of myelopoiesis is regulated by fucosylation." Blood 112, no. 2 (2008): 308–19. http://dx.doi.org/10.1182/blood-2007-11-115204.

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Abstract Cell-cell contact–dependent mechanisms that modulate proliferation and/or differentiation in the context of hematopoiesis include mechanisms characteristic of the interactions between members of the Notch family of signal transduction molecules and their ligands. Whereas Notch family members and their ligands clearly modulate T lymphopoietic decisions, evidence for their participation in modulating myelopoiesis is much less clear, and roles for posttranslational control of Notch-dependent signal transduction in myelopoiesis are unexplored. We report here that a myeloproliferative phen

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Wang, Jishi, Yingya Wu, Lila Mei, Yuan Yang, and Lu Shen. "Regulation of Differentiation and Proliferation of Marrow Hematogenesis Stem Cells by Notch1 Signaling System from Patients with Aplastic Anemia and Chronic Myelogenous Leukemia." Blood 108, no. 11 (2006): 4215. http://dx.doi.org/10.1182/blood.v108.11.4215.4215.

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Abstract Notch genes encode evolutionarily conserved transmembrane receptors that regulate cell fate determination. Notch activation promotes proliferation and inhibits differentiation of bone marrow stem cells. Our research was to study the differential expression of Notch1 on bone marrow mononuclear cells (BMMNC) from chronic aplastic anemia (AA) and chronic myelogenous leukemia (CML) patients. We demonstrated that Notch signaling is inactivated in AA patients and activated in CML patients. In CML patients, Notch1 furthers stimulation by its ligand Jagged1, resulting in a strong increase of

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Phelan, James D., Ingrid Saba, Chinavenmeni S. Velu, Tarik Moroy, and H. Leighton Grimes. "Notch Signaling Requires Gfi1 for T Cell Development." Blood 118, no. 21 (2011): 2174. http://dx.doi.org/10.1182/blood.v118.21.2174.2174.

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Abstract Abstract 2174 Growth factor independent-1 (Gfi1) is a zinc finger transcriptional repressor protein originally identified in a rodent model of T-cell leukemia. Gfi1 deficient mice have defects in T cell development and a moderate loss of thymic cellularity. In Drosophila, orthologs of Notch1 and Gfi1 cooperate to specify embryo sensory organ precursors. Given the established requirement for Notch1 in T cell specification and development as well as the functional relationship of Notch and Gfi1 orthologs in Drosophila genetics, we investigated the ability of Gfi1 and Notch to cooperate

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Lee, Sung-UK, Manami Maeda, Nagisa Sakurai, Freddy Radtke, and Takahiro Maeda. "LRF Is Indispensable for Hematopoietic Stem Cell Function Via Blocking Notch1-Mediated T Cell-Instructive Signals in the Bone Marrow Niche." Blood 114, no. 22 (2009): 81. http://dx.doi.org/10.1182/blood.v114.22.81.81.

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Abstract Abstract 81 Hematopoietic stem cells (HSC) have the ability to self-renew and give rise to all hematopoietic lineage cells. Understanding signals that regulate the balance between self-renewal and differentiation of HSCs is an important issue in stem cell biology as well as regenerative medicine. Notch signals are critical regulators of the lymphoid lineage fate, but their role in adult HSC function is currently under debate. We explored the role of the LRF (Leukemia/Lymphoma Related Factor), a Notch repressor (also known as Zbtb7a, pokemon, OCZF and FBI-1) in HSC function, as it play

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Lee, Sung-UK, Manami Maeda, Nagisa Sakurai, Julie Teruya-Feldstein, Freddy Radtke, and Takahiro Maeda. "LRF Regulates Self-Renewal of Hematopoietic Stem Cells by Blocking Notch1-Mediated T Cell Differentiation." Blood 112, no. 11 (2008): 75. http://dx.doi.org/10.1182/blood.v112.11.75.75.

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Abstract The proto-oncogene LRF, encoded by the Zbtb7a gene, is a transcriptional repressor that belongs to the POK (POZ/BTB and KrŸppel) protein family. Along with its oncogenic property, recent evidence has shown that POK proteins play distinct roles in hematopoiesis and immune system development. Conditional inactivation of the LRF gene in mouse hematopoietic stem cells (HSCs) results in the development of CD4/8 double positive (DP) T cells in bone marrow (BM) at the expense of B cell development (Maeda et al. Science 2007). While LRF acts as a master regulator of B versus T lymphoid linea

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Svensson, Per, Ingela Bergqvist, Stefan Norlin, and Helena Edlund. "MFng Is Dispensable for Mouse Pancreas Development and Function." Molecular and Cellular Biology 29, no. 8 (2009): 2129–38. http://dx.doi.org/10.1128/mcb.01644-08.

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ABSTRACT Notch signaling regulates pancreatic cell differentiation, and mutations of various Notch signaling components result in perturbed pancreas development. Members of the Fringe family of β1,3-N-acetylglucosaminyltransferases, Manic Fringe (MFng), Lunatic Fringe (LFng), and Radical Fringe (RFng), modulate Notch signaling, and MFng has been suggested to regulate pancreatic endocrine cell differentiation. We have characterized the expression of the three mouse Fringe genes in the developing mouse pancreas between embryonic days 9 and 14 and show that the expression of MFng colocalized with

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Zubeldía-Brenner, Lautaro, Catalina De Winne, Sofía Perrone, et al. "Inhibition of Notch signaling attenuates pituitary adenoma growth in Nude mice." Endocrine-Related Cancer 26, no. 1 (2019): 13–29. http://dx.doi.org/10.1530/erc-18-0337.

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Preclinical and clinical studies support that Notch signaling may play an important oncogenic role in cancer, but there is scarce information for pituitary tumors. We therefore undertook a functional study to evaluate Notch participation in pituitary adenoma growth. Tumors generated in Nude mice by subcutaneous GH3 somatolactotrope cell injection were treated in vivo with DAPT, a γ-secretase inhibitor, thus inactivating Notch signaling. This treatment led to pituitary tumor reduction, lower prolactin and GH tumor content and a decrease in angiogenesis. Furthermore, in silico transcriptomic and

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Loganathan, Sampath K., Krista Schleicher, Ahmad Malik, et al. "Rare driver mutations in head and neck squamous cell carcinomas converge on NOTCH signaling." Science 367, no. 6483 (2020): 1264–69. http://dx.doi.org/10.1126/science.aax0902.

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In most human cancers, only a few genes are mutated at high frequencies; most are mutated at low frequencies. The functional consequences of these recurrent but infrequent “long tail” mutations are often unknown. We focused on 484 long tail genes in head and neck squamous cell carcinoma (HNSCC) and used in vivo CRISPR to screen for genes that, upon mutation, trigger tumor development in mice. Of the 15 tumor-suppressor genes identified, ADAM10 and AJUBA suppressed HNSCC in a haploinsufficient manner by promoting NOTCH receptor signaling. ADAM10 and AJUBA mutations or monoallelic loss occur in

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De Decker, Matthias, Marieke Lavaert, Juliette Roels, et al. "HES1 and HES4 have non-redundant roles downstream of Notch during early human T-cell development." Haematologica 106, no. 1 (2020): 130–41. http://dx.doi.org/10.3324/haematol.2019.226126.

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In both mouse and human, Notch1 activation is the main initial driver to induce T-cell development in hematopoietic progenitor cells. The initiation of this developmental process coincides with Notch1-dependent repression of differentiation towards other hematopoietic lineages. Although well described in mice, the role of the individual Notch1 target genes during these hematopoietic developmental choices is still unclear in human, particularly for HES4 since no orthologous gene is present in the mouse. Here, we investigated the functional capacity of the Notch1 target genes HES1 and HES4 to mo

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Ungerbäck, Jonas, Josefine Åhsberg, Tobias Strid, Rajesh Somasundaram, and Mikael Sigvardsson. "Combined heterozygous loss of Ebf1 and Pax5 allows for T-lineage conversion of B cell progenitors." Journal of Experimental Medicine 212, no. 7 (2015): 1109–23. http://dx.doi.org/10.1084/jem.20132100.

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To investigate how transcription factor levels impact B-lymphocyte development, we generated mice carrying transheterozygous mutations in the Pax5 and Ebf1 genes. Whereas combined reduction of Pax5 and Ebf1 had minimal impact on the development of the earliest CD19+ progenitors, these cells displayed an increased T cell potential in vivo and in vitro. The alteration in lineage fate depended on a Notch1-mediated conversion process, whereas no signs of de-differentiation could be detected. The differences in functional response to Notch signaling in Wt and Pax5+/−Ebf1+/− pro–B cells were reflect

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Luo, Xiaodan, Pengfei Qin, Chunyan Wang, Zhenqian Huang, and Huo Tan. "Notch Is a Novel Critical Signaling Pathway Regulating Responses of T Cell and Antigen Presenting Cells in Multiple Murine aGVHD Models." Blood 126, no. 23 (2015): 5418. http://dx.doi.org/10.1182/blood.v126.23.5418.5418.

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Abstract Introduction: Acute graft-versus-host disease (aGVHD) is a potentially life-threatening complication mediated by both host-derived antigen presenting cells (APCs) and donor T cells after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Despite prophylaxis and treatments, aGVHD stell occurs in many allo-HSCT patients. The role of Notch1 signal inhibition becomes more and more important in aGVHD study. This study is to investigate the role of Notch1 inhibition by γ-secretase inhibitor DAPT in murine aGVHD model. Methods: We established a C57BL/6 BALB/c murine aGVHD model.

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Anderson, Leah J., and Richard Longnecker. "Epstein-Barr virus latent membrane protein 2A exploits Notch1 to alter B-cell identity in vivo." Blood 113, no. 1 (2009): 108–16. http://dx.doi.org/10.1182/blood-2008-06-160937.

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Abstract Expression of latent membrane protein 2 (LMP2A) during B-cell development leads to global alterations in gene transcription similar to those seen in Hodgkin Reed-Sternberg cells of Hodgkin lymphoma (HL). Along with the consistent detection of LMP2A in Epstein-Barr virus–associated HL, this implicates a role for LMP2A in the pathogenesis of HL. We have shown that LMP2A constitutively activates the Notch1 pathway to autoregulate the LMP2A promoter. To determine whether constitutive activation of the Notch pathway is important for LMP2A-mediated alterations in B-cell development in vivo,

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Feldman, Brian J., Tracy Hampton, and Michael L. Cleary. "A carboxy-terminal deletion mutant of Notch1accelerates lymphoid oncogenesis in E2A-PBX1transgenic mice." Blood 96, no. 5 (2000): 1906–13. http://dx.doi.org/10.1182/blood.v96.5.1906.

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Abstract PBX1 is a proto-oncogene that plays important roles in pattern formation during development. It was discovered as a fusion with the E2A gene after chromosomal translocations in a subset of acute leukemias. The resulting E2a-Pbx1 chimeric proteins display potent oncogenic properties that appear to require dimerization with Hox DNA binding partners. To define molecular pathways that may be impacted by E2a-Pbx1, a genetic screen consisting of neonatal retroviral infection was used to identify genes that accelerate development of T-cell tumors in E2A-PBX1 transgenic mice. Retroviral inser

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Feldman, Brian J., Tracy Hampton, and Michael L. Cleary. "A carboxy-terminal deletion mutant of Notch1accelerates lymphoid oncogenesis in E2A-PBX1transgenic mice." Blood 96, no. 5 (2000): 1906–13. http://dx.doi.org/10.1182/blood.v96.5.1906.h8001906_1906_1913.

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PBX1 is a proto-oncogene that plays important roles in pattern formation during development. It was discovered as a fusion with the E2A gene after chromosomal translocations in a subset of acute leukemias. The resulting E2a-Pbx1 chimeric proteins display potent oncogenic properties that appear to require dimerization with Hox DNA binding partners. To define molecular pathways that may be impacted by E2a-Pbx1, a genetic screen consisting of neonatal retroviral infection was used to identify genes that accelerate development of T-cell tumors in E2A-PBX1 transgenic mice. Retroviral insertions in

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Filipović, M., A. Šućur, D. Flegar, et al. "POS0042 NOTCH 1 INHIBITION INCREASES OSTEOCLAST PROGENITOR ACTIVITY IN THE MOUSE MODEL OF RHEUMATOID ARTHRITIS." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 226.3–226. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2601.

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Background:Osteoclasts mediate periarticular and systemic bone loss in rheumatoid arthritis (RA). Osteoclast progenitor cells (OCPs) derived from the myeloid lineage are susceptible to regulation through Notch signaling. Murine bone marrow and splenic OCPs, identified as CD45+Ly6G-CD3-B220-NK1.1-CD11blo/+CD115+CCR2+ cells, are specifically increased in arthritis. We previously identified an increased frequency of OCPs expressing Notch receptors in arthritic mice.Objectives:Several studies suggested that Notch signaling modulation affects the course of experimental arthritis. We aimed to determ

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Fragoso, Ana Rita, Tin Mao, Song Wang, et al. "Essential Role for Mir-181a1/b1 In T-Cell Acute Lymphoblastic Leukemia." Blood 116, no. 21 (2010): 470. http://dx.doi.org/10.1182/blood.v116.21.470.470.

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Abstract Abstract 470 MiRNA-mediated gene regulation represents a fundamental layer of post-transcriptional control of gene expression with diverse functional roles in normal development and tumorigenesis. Whereas some studies have shown that over-expression of miRNA genes may contribute to cancer development and progression, it is yet to be rigorously tested by the loss-of-function genetic approaches whether miRNA genes are required for cancer development and maintenance in mice. Here we show that mir-181a1/b1 coordinates Notch and pre-TCR signals during normal thymocyte differentiation and p

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Myllymäki, Mikko, Jenni Määttä, Elitsa Dimova, et al. "Extramedullary Erythropoiesis in Spleen of HIF Prolyl 4-Hydroxylase-2 Deficient Mice Is Mediated By Notch Signaling Downregulation." Blood 128, no. 22 (2016): 2656. http://dx.doi.org/10.1182/blood.v128.22.2656.2656.

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Abstract Erythrocytosis, an increase in absolute red cell mass, is mainly driven by erythropoietin, while hypoxia-inducible factor (HIF) regulates the expression of a number of genes involved in it, including erythropoietin. Mutations in HIF prolyl 4-hydroxylase 2 (HIF-P4H-2/PHD2/EGLN1), the major regulator of the stability of HIFα subunits, are found in familiar erythrocytosis, and large-spectrum conditional inactivation of HIF-P4H-2 in mice leads to severe erythrocytosis and premature death. Although bone marrow is the primary site for erythropoiesis, spleen retains a capability for extramed

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Koizumi, K. i., M. Nakajima, S. Yuasa, et al. "The role of presenilin 1 during somite segmentation." Development 128, no. 8 (2001): 1391–402. http://dx.doi.org/10.1242/dev.128.8.1391.

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The Notch signalling pathway plays essential roles during the specification of the rostral and caudal somite halves and subsequent segmentation of the paraxial mesoderm. We have re-investigated the role of presenilin 1 (Ps1; encoded by Psen1) during segmentation using newly generated alleles of the Psen1 mutation. In Psen1-deficient mice, proteolytic activation of Notch1 was significantly affected and the expression of several genes involved in the Notch signalling pathway was altered, including Δ-like3, Hes5, lunatic fringe (Lfng) and Mesp2. Thus, Ps1-dependent activation of the Notch pathway

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Crcareva, Aleksandra, Toshiki Saito, Keiki Kumano, Mamiko Sakata-Yanagimoto, Hisamaru Hirai, and Shigeu Chiba. "Notch2 Regulates Macrophage-Related Genes in Marginal Zone B Cells." Blood 104, no. 11 (2004): 4197. http://dx.doi.org/10.1182/blood.v104.11.4197.4197.

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Abstract [Background] While Notch1 plays critical roles in early T cell development, Notch2 is indispensable for B cell development. Conditional inactivation of Notch2 in the hematopoietic compartment leads to loss of the marginal zone B (MZB) cells and defect in the particular fraction of follicular B (FOB) cells characterized as T2 B cells. Because of their position bordering the marginal sinuses and red pulp in the spleen, MZB cells are amongst the first cells that come in contact with blood-borne substances and thus thought to have critical roles in the defense against bacterial pathogens

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del Toro, Raquel, Claudia Prahst, Thomas Mathivet, et al. "Identification and functional analysis of endothelial tip cell–enriched genes." Blood 116, no. 19 (2010): 4025–33. http://dx.doi.org/10.1182/blood-2010-02-270819.

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Abstract Sprouting of developing blood vessels is mediated by specialized motile endothelial cells localized at the tips of growing capillaries. Following behind the tip cells, endothelial stalk cells form the capillary lumen and proliferate. Expression of the Notch ligand Delta-like-4 (Dll4) in tip cells suppresses tip cell fate in neighboring stalk cells via Notch signaling. In DLL4+/− mouse mutants, most retinal endothelial cells display morphologic features of tip cells. We hypothesized that these mouse mutants could be used to isolate tip cells and so to determine their genetic repertoire

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Hong, S. N., J. H. Song, G. Seong, et al. "P097 Depletion of delta-like ligand 4 (Dll4) contributes to the alteration of secretory progenitor differentiation in SAMP1/YitFc mice with Crohn’s disease-like ileitis." Journal of Crohn's and Colitis 14, Supplement_1 (2020): S184. http://dx.doi.org/10.1093/ecco-jcc/jjz203.226.

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Abstract Background When the intestinal epithelium would be exposed to harmful substances, mucosal damage can be occurred and followed by epithelial restoration with regenerative epithelium derived from intestinal stem cells (ISCs). Crohn’s disease (CD) is characterised by chronic mucosal damage and ulceration predominantly involved in the ileum. Thus, we hypothesised that epithelial regeneration in CD might be impaired due to the dysfunction of ileal ISCs or its niche. Methods SAMP1/YitFcsI (SAMP1) mice are recombinant-inbred mice that spontaneously develop ileitis resembling human CD. Altera

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Zhang, Honglai, Tao Xu, Claire Peabody, et al. "CSIG-20. L3MBTL3 SUPPRESSES MEDULLOBLASTOMA TUMORIGENESIS THROUGH MODULATION OF THE NOTCH/RBPJ SIGNALING PATHWAY." Neuro-Oncology 22, Supplement_2 (2020): ii32. http://dx.doi.org/10.1093/neuonc/noaa215.132.

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Abstract The NOTCH/RBPJ pathway governs cell proliferation in many biological contexts, including SHH and Group#3medulloblastoma (MB) tumorigenesis. Using our proteomic platform, we discovered an interaction between RBPJ, a key co-factor of NOTCH for the modulation of the NOTCH/RBPJ signaling pathway, and L3MBTL3, a methyllysine reader. L3MBTL3 is recruited by RBPJ on chromatin at the enhancers of NOTCH/RBPJ target genes to repress their expression. Deletions of the L3MBTL3 locus are observed in patients with WNT and Group#3 MB and expression of L3MBTL3 in the SHH MB-derived cell DAOY inhibits

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Sharma, Madhulika, Sireesha Yerrathota, Mackenzie M. Thornton, and Sumedha Gunewardena. "Transcriptomic data showing differentially expressed genes between Notch3 and Notch4 deleted mice." Data in Brief 35 (April 2021): 106873. http://dx.doi.org/10.1016/j.dib.2021.106873.

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García-Domínguez, Daniel J., Dominique Morello, Elsa Cisneros, Dimitris L. Kontoyiannis, and José M. Frade. "Stabilization of Dll1 mRNA by Elavl1/HuR in neuroepithelial cells undergoing mitosis." Molecular Biology of the Cell 22, no. 8 (2011): 1227–39. http://dx.doi.org/10.1091/mbc.e10-10-0808.

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In the vertebrate neuroepithelium, the decision to differentiate is made by neural precursors soon after mitosis, when they are apically located. This process is controlled by lateral inhibitory signals triggered by the Delta/Notch pathway. During mitosis, the capacity of neural precursors to express the neurogenic genes Dll1 and Notch1 is maximal due to mRNA stabilization, but the mechanism controlling this process remains unknown. Here we show that Elav-like (Elavl1)/HuR becomes enriched in the cytoplasm of neuroepithelial cells undergoing mitosis and that this ribonucleoprotein interacts wi

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48

Gong, Zhijuan, Qingwen Ma, Xujun Wang, et al. "A Herpes Simplex Virus Thymidine Kinase-Induced Mouse Model of Hepatocellular Carcinoma Associated with Up-Regulated Immune-Inflammatory-Related Signals." Genes 9, no. 8 (2018): 380. http://dx.doi.org/10.3390/genes9080380.

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Inflammation and fibrosis in human liver are often precursors to hepatocellular carcinoma (HCC), yet none of them is easily modeled in animals. We previously generated transgenic mice with hepatocyte-specific expressed herpes simplex virus thymidine kinase (HSV-tk). These mice would develop hepatitis with the administration of ganciclovir (GCV)(Zhang, 2005 #1). However, our HSV-tk transgenic mice developed hepatitis and HCC tumor as early as six months of age even without GCV administration. We analyzed the transcriptome of the HSV-tk HCC tumor and hepatitis tissue using microarray analysis to

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Tu, Xiaolin, Jesus Delgado-Calle, Keith W. Condon та ін. "Osteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone". Proceedings of the National Academy of Sciences 112, № 5 (2015): E478—E486. http://dx.doi.org/10.1073/pnas.1409857112.

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Osteocytes, >90% of the cells in bone, lie embedded within the mineralized matrix and coordinate osteoclast and osteoblast activity on bone surfaces by mechanisms still unclear. Bone anabolic stimuli activate Wnt signaling, and human mutations of components along this pathway underscore its crucial role in bone accrual and maintenance. However, the cell responsible for orchestrating Wnt anabolic actions has remained elusive. We show herein that activation of canonical Wnt signaling exclusively in osteocytes [dominant active (da)βcatOt mice] induces bone anabolism and triggers Notch signalin

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Xu, Dehui, Jinsong Hu, Elke De Bruyne, et al. "Involvement of Dll1/Notch Interaction In MM Drug Resistance, Clonogenic Growth and In Vivo Engraftment." Blood 116, no. 21 (2010): 2966. http://dx.doi.org/10.1182/blood.v116.21.2966.2966.

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Abstract Abstract 2966 The great challenges in multiple myeloma (MM) treatment are to overcome drug resistance and to prevent relapse. The bone marrow (BM) microenvironment plays a critical role in MM cell growth and survival. The Notch pathway was found to be activated in MM. In this study we aimed at investigating the role of Dll1/Notch interaction in MM clonogenic growth and in vivo engraftment, as well as the role of Notch pathway in BM-induced drug resistance. Dll1 is a Notch ligand expressed in BM stromal cells. Cocultures were performed using murine 5T33MM cells with Dll1 ligand or MS5.

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