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Notch activates cell differentiation. 1000 / 1594
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"This Notch mediated increase in cardiac differentiation resulted in an 8-fold increase in cardiac differentiation efficiency (XREF_FIG G), as every KDR+ progenitor cell plated on an oriented Jagged-1 surface generated roughly two TNNT2+ cardiomyocytes, whereas control surfaces required more than four KDR+ progenitors to generate a single TNNT2+ cardiomyocyte."
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"In contrast to the tumor promoting function commonly attributed to this pathway in mammalian cells, our prior work demonstrated that Notch signaling contributed in suppression of mouse and human keratinocyte tumor development, by essentially affecting global control of gene expression and differentiation [XREF_BIBR, XREF_BIBR, XREF_BIBR]."
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"This differentiation pattern is reminiscent of defective Notch signaling, which is known to cause the lens progenitor cells to undergo premature differentiation before reaching the lens equator, resulting in an anteriorly shift of the transitional zone (Jia et al., 2007; Le et al., 2009; Li et al., 2019; Rowan et al., 2008; Saravanamuthu et al., 2012)."
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"Finally, an exciting possibility for future studies is that the concomitant pharmacological up-regulation of the p53 and Notch pathways, known to induce senescence and/or differentiation, may be of clinical significance in reducing the risk of cutaneous SCCs in patients under treatment with calcineurin inhibitors and related predisposing conditions."
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"Some findings suggest that activation of Notch signaling can contribute to neuronal death, generation and activation of microglial cells and astrocytes, inhibition of neurite growth [9-11], more dendritic branching [12], differentiation of oligodendrocyte progenitors and demyelination in both the peripheral nervous system [13] and the CNS (central nervous system) [14]."
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"For example, Hh ligands released by apoptotic hepatocytes can act on surrounding LPC and hepatic stellate cells (the key cell involved in scar tissue accumulation) to promote liver repair, while Wnt and Notch signals within the microenvironment could modulate LPC differentiation into either hepatocytes or cholangiocytes, respectively."
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"Using the lineage tracing technique in mice carrying a conditional dominant negative mutant of Maml1 (a transcriptional coactivator for NOTCH), Alcolea et al found that NOTCH inhibition prevented differentiation of mutant progenitor cells and promoted differentiation of neighboring wild-type progenitor cells in mouse esophagus."
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"Loss of Notch signalling in zebrafish causes excessive differentiation of endocrine cells in the intrapancreatic duct, whereas ectopic activation of the Notch pathway inhibits both acinar cell differentiation and maintenance of beta-cell differentiation in embryonic zebrafish XREF_BIBR XREF_BIBR."
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"Consistent with this view, BBS2 loss consistently showed sustained or elevated Notch reporter activity and K10 expression in our studies, whereas depletion of other ciliary or cilia related proteins consistently suppressed Notch signaling and K10 mediated differentiation in cultured keratinocytes."
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"It is clear from the differences observed that carefully designed studies, preferably conducted in vivo, are needed to clarify the role of Notch signaling in this context.Ross and colleagues (2004) indicated that Notch signaling can either potentiate or inhibit 3T3-L1 preadipocyte differentiation [152]."
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"The authors concluded that sustained Notch activation induces a failed or incomplete differentiation of epithelial cells promoting proliferation and growth factor production that resulted in a vicious cycle that perpetuated inflammation and proliferation eventually leading to interstitial fibrosis."
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"Similarly, we have also demonstrated that expression of the Hairy-Enhancer-of-Split (Hes) genes Hes1 and Hes5, which are key regulators of Notch signaling induced stem cell self-renewal, are upregulated in Nfia and Nfib null mice, suggesting that NFIs may repress elements of the Notch pathway associated with self-renewal, while simultaneously co-operating with the JAK and STAT element of the Notch pathway that promotes glial differentiation (XREF_FIG)."
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"This finding is consistent with prior evidence indicating that in squamous cells (as opposed to other cell types), NOTCH1 signaling is growth-repressive For example, functional studies have shown that NOTCH genes suppress proliferation and promote differentiation of keratinocytes, the cell type that populates the normal keratinizing squamous epithelial lining."
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"Specifically, CCN2/CTGF is expressed in the early notochord of zebrafish, and when the gene is knocked down, the notochord fails to form correctly.4445Transcription factors (e.g., Foxa2, T, Noto, SOX5/-6, and Jun) as well as Notch and Wnt/β-catenin signaling pathways support the formation, development, and differentiation of the notochord and NP."
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"The Notch signalling pathway also promotes astrocyte differentiation XREF_BIBR XREF_BIBR but we found that forced activation of this pathway or of the STAT pathway by expression of the intracellular form of Notch1 (NICD) or an activated form of STAT3 (STAT3-C), respectively, also did not increase the abundance of Zbtb20 mRNA in NPCs (XREF_FIG)."
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"A specific gene product induced by HDAC inhibition, Delta and Notch like epidermal growth factor related receptor (DNER), inhibited the growth of GBM derived neurospheres, induced their differentiation in vivo and in vitro, and inhibited their engraftment and growth as tumor xenografts."
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"Although TAPI-1 had a less pronounced effect on promoting differentiation of myosin VIIa immunoreactivity than DAPT, these results are consistent with the interpretation that inactivation of notch signaling promotes new hair cell differentiation in the adult mouse utricle following damage."
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"To identify the hematopoietic specific ligands that may trigger Notch induced T FH cell differentiation, we made use of Mx-Cre mice and generated BM chimeras transplanting CD45.2 + BM cells from poly I-C-induced DL1 Delta and DeltaMx, DL4 Delta and DeltaMx, DL1 and DL4 Delta and DeltaMx, J1 Delta and DeltaMx, J2 Delta and DeltaMx, and J1/J2 Delta and DeltaMx mice into lethally irradiated CD45.1 + wild-type mice."
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"Our demonstration that naringin promotes osteogenic differentiation of BMSCs via enhancing Notch signal pathway activation is consistent with a previous study showing that Notch family members positively regulate the differentiation of osteoblasts, and that Notch could be an interesting target molecule for the treatment of osteoporosis [XREF_BIBR]."
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"Taken together, TMEM16A/F are important for exocytosis, mucus secretion and formation of extracellular vesicles (exosomes or ectosomes) but the present data do no not support a functional role of TMEM16A/F in Notch-mediated differentiation of BCi-NS1.1 cells towards a secretory epithelium."
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"Together, these observations suggest the molecular mechanisms that the Wnt-related pathway could maintain the self-renewal of CVSCs (Clevers et al. 2014; Farin et al. 2012) and the Notch-related pathway induced cell maturation, especially epithelium differentiation (VanDussen et al. 2012; Noah and Shroyer 2013)."
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"This review systematically discusses that polysaccharides can directly or indirectly activate macrophages, dendritic cells, natural killer cells etc., binding to their surface receptors, inducing PI3K and Akt, mitogen activated protein kinase, Notch and other pathways, promote their proliferation and differentiation, increasing the secretion of cytokines, and improve the state of immune suppression."
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"It is tempting to speculate that such a GATA3 repressive mechanism onto the Notch pathway may be defective in early T-cell precursor acute lymphoblastic leukaemia (ETP-ALL) cases that are associated with GATA3 mutations XREF_BIBR as these may lead to aberrant Notch activation and inhibition of further T-lineage differentiation."
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"The negative role of physiological Notch signaling in osteoblast differentiation uncovered in mice is congruent with the clinical findings that Notch1 haploinsufficiency causes ectopic osteoblast differentiation and calcification in the aortic valves XREF_BIBR, XREF_BIBR, whereas Notch2 stabilizing mutations are responsible for the Hadju-Cheney syndrome, a disorder of severe and progressive bone loss XREF_BIBR, XREF_BIBR."
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"Mukuherjee et al. [XREF_BIBR] found that the Notch ligand Dll4 promoted T-cell differentiation through increased expression of IL-17 and RORgamma T. Schaller et al. [XREF_BIBR] also found that Dll4 expression on bone marrow derived dendritic cells (DCs) increased significantly after infection of mice with respiratory syncytial virus, accompanied by increased secretion of Th2 cytokines and reduced production of INF-gamma."
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"Apart from playing an essential role in cancer cells, Notch, Hedgehog, and Wnt signaling pathways have prominent roles in modifying tumor microenvironment, which has been implicated in providing chemo-resistance.The Notch signaling can induce the differentiation of the neighboring cancer cells, which can adopt different cell fate, thus creating a heterogeneous population."
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"It was elucidated 16 that survival, differentiation and neurogenesis of htNSCs were mechanistically mediated by IKKbeta and NF-kappaB-controlled apoptosis and Notch signaling, thus further reinforcing the role of inflammatory machinery in neurogenesis, neuroplasticity and the structural remodeling of the brain."
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"Notch pathway plays a complex role depending on cellular contexts : promotes stem cell maintenance or induces terminal differentiation in potential cancer initiating cells; acts as an oncogene in lymphocytes and mammary tissue or plays a growth-suppressive role in leukemia, liver, skin, and head and neck cancer."
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"The role of Notch signaling in the proliferation and differentiation of osteoblasts isolated from calvarial was examined in vitro by EdU incorporation assays and real-time quantitative reverse transcription polymerase chain reaction after activating and inhibiting Notch signaling."
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"Regarding conserved stroma-defined signals, we and others have shown that ectopic expression of human NOTCH ligands such as DLL1 and DLL4 into murine OP9 stroma cells enhanced the efficiency of differentiation into the NK cell lineage (34, 59, 63) and, as recently shown, similarly into the ILC lineage (33)."
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"Inhibition of Notch signaling using Numb or dominant negative form of Su (H) resulted in a luminal differentiation, while forced activation of Notch signaling promoted the specification of immature glandular cells, but prevented the subsequent differentiation and the invagination of the glands."
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"Since Notch activation is thus sufficient to induce differentiation of Esg progenitors into ECs even in the absence of Klu, we conclude that induction of Klu by Notch in EBs is important to prevent specification of EBs into EE progenitors, but is not essential for other steps in EC differentiation.Altogether, our results indicate that the Notch-mediated induction of Klu in EBs is required to restrict lineage commitment of EBs to the EC fate."
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"Using mice genetically engineered to inducibly knock in or knock out Notch signaling in postnatal NSPCs, Breunig et al. [XREF_BIBR] recently demonstrated that loss of Notch signaling depleted the progenitor pool and skewed differentiation toward the neuronal lineage, while over activation of Notch signaling decreased cell cycle exit and increased the size of the progenitor pool."
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"As Notch signaling promotes progenitor cell identity at the expense of differentiated cell phenotypes, we test whether genetic activation of Notch could rescue the Eya1 (-/-) lung phenotype, which is characterized by loss of epithelial progenitors, increased epithelial differentiation but reduced branching."
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"Notch signaling has been shown to influence phenotypic properties of smooth muscle cells, but reports are discrepant, leading to the proposition that NOTCH itself may promote smooth muscle differentiation and that this in turn is antagonized by target genes that are themselves transcription factors 33."
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"Next, to determine whether extended Notch activity caused the E/A switch and cell differentiation defects by suppressing Ttk69 up-regulation, we co-overexpressed NICD and Ttk69 in follicle cells and found that one copy of UAS-ttk69, ttk 1e11 could restore Ttk69 to wild-type or higher levels in the presence of NICD (XREF_FIG, compare C ' with A)."
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"They showed that Dll1 and Dll4 were selectively expressed in goblet cells within the human colonic epithelium and knockdown of Dll1 abrogated the Hath1 and MUC2 gene expression under activation of the goblet cell genes by a Notch signal inhibitor, suggesting the Notch ligand triggers the goblet cell differentiation through Atoh1 activation."
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"In addition, both old and new work has shown that keratinocytes harbouring NOTCH loss-of-function mutations that lead to defective keratinocyte differentiation and loss of squamous epithelial barrier function may act as a tumour promoting stimulus for initiated cells harbouring RAS pathway mutations by activating a wound response in the tumour mesenchyme."
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"Finally, in mice fed a CDE diet, expression of the Notch ligand Jagged-1 promoted Notch signaling and biliary differentiation in LPCs, whereas macrophage derived Wnt3a induced canonical Wnt and beta-catenin signaling in LPCs and promoted their differentiation to hepatocytes (XREF_FIG)."
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"The need for proper activation of the Akt-mTOR and Notch signaling pathways for SLEC differentiation raises the possibility that Notch signaling promotes SLEC differentiation via the induction of the common effector HES1, which then represses Pten transcription allowing for proper activation of the Akt signaling pathway."
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"Therefore, Huang et al. showed that Wnt3a, Retinoic acid, BMP as well as TGF- and Notch signaling pathway inhibitors should be added to the R-spondin culture system to activate the Wnt signaling pathway and promote the differentiation of the progenitor cells to provide a long term culture of human pluripotent stem cell- and patient derived pancreatic cancer organoids [XREF_BIBR]."
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"In this study, we have investigated how Notch signaling contributes to esophageal epithelial homeostasis in vitro and in vivo to find that N1 can trigger a robust induction and activation of N3 as a unique target for canonical CSL dependent transcription at the onset of squamous differentiation, and that a novel functional interplay between ICN1 and ICN3 has a critical role in transcriptional activation of cellular components essential in terminal differentiation."
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"Broad ranging examples of Notch pathway activity have been described in bilaterians, and recent studies in the Cnidaria have implicated Notch signaling in the differentiation of the interstitial cell lineage and boundary formation in the hydrozoan Hydra, and in nervous system development of the anthozoan Nematostella vectensis [XREF_BIBR - XREF_BIBR]."
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"The authors concluded that sustained Notch activation induces a failed differentiation in epithelial cells and that incomplete epithelial cell differentiation along with prolonged proliferation and growth factor production results in a vicious circle, activating other pathways and mechanisms, which in turn perpetuate the process and eventually lead to CKD and TIF development."
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"Previous studies have shown that Notch activates smooth muscle differentiation markers XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR; accordingly, we detected upregulation of key mature smooth muscle transcripts encoding SM22, SMA, SM-MHC, and calponin in A7R5 cell lines cocultured with Jagged expressing cells (XREF_FIG)."
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"Notch signaling, which promotes keratinocyte differentiation, is upregulated in embryonic keratinocyte and epidermis, and elevated caspase 3 expression, which we identify as a transcriptional Notch1 target, accounts in part for the high commitment of embryonic keratinocytes to terminal differentiation."
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"We separated Hes1-high and Hes1-low ES cells by the Venus fluorescence and found that Hes1-high ES cells tended to differentiate into the mesodermal fate rather than the neural fate, although past investigation has shown that activation of Notch signaling promotes neural differentiation."
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"It has been documented that Notch signaling promoted goblet cells differentiation and mucin production, and inhibited the differentiation of ciliated cells in both developmental and mature lung epithelia (Guseh et al, 2009; Tsao et al, 2009; Rock et al, 2011; Whitsett & Kalinichenko, 2011; Gomi et al, 2015; Yao et al, 2018)."
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"Cells with Notch activation and loss of neuroendocrine differentiation were resistant to the standard chemotherapy regimen used to treat SCLC; this subpopulation also secreted factors that promoted proliferation in neighbouring cells that maintained neuroendocrine differentiation."
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"It has been shown that hypoxia controls transcription of Notch targets in neuroendocrine differentiation of human CaP cells [XREF_BIBR]; this implies the possibility of Notch signaling in hypoxia mediated control of DLG7 expression in CaP and its role in the manifestation of tumor aggressiveness."
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"In neural stem cells, targets of Notch signalling work together to prevent terminal differentiation and preserve a pool of stem cells [XREF_BIBR, XREF_BIBR]; Notch1 also promotes radial glia like identity and negatively regulates cell cycle exit and neuronal differentiation in GFAP-NSCs in the postnatal brain [XREF_BIBR]."
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"The NOTCH gene signaling molecules have been shown to be present in human mesenchymal stem cells in human cartilage, and the JAG1 ligand expression increases rapidly in early NOTCH driven cell differentiation, which supports the role of JAG1 as a key ligand in the activation of NOTCH signaling and the effective catalyst of bone marrow mesenchymal stem cell differentiation to chondrocytes [XREF_BIBR, XREF_BIBR]."
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"In the analysis of liver progenitor differentiation, a cell microarray based approach showed that the Notch ligands Jagged-1, Delta like 1, and Delta like 4 each can induce an increase in biliary differentiation, and this occurs in the absence of any additional exogenous differentiation inducing factors."
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"Notch signalling promotes a range of cell differentiation programs including neuronal and vascular fates XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR, and it is reported to be essential in three aspects of haematopoietic cell differentiation : maintenance of HSCs XREF_BIBR, XREF_BIBR, initiation of the T cell lineage XREF_BIBR, XREF_BIBR, XREF_BIBR, and maturation of CD4 and CD8 thymocytes XREF_BIBR, XREF_BIBR."
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"The Hidalgo lab demonstrated that the glial regenerative response to CNS injury in Drosophila depends on a gene network involving the genes Notch and prospero (pros), whereby Notch promotes glial proliferation and Pros glial differentiation (Griffiths and Hidalgo, 2004; Griffiths et al., 2007; Kato et al., 2011)."
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"In conclusion, activation of Notch promotes osteogenic differentiation in a tissue specific dose dependent manner; both NICD and Jag1 are able to increase osteogenic potential but at moderate doses only and a high dosage of Notch activation is detrimental to osteogenic differentiation."
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"These genetic variations result in a dysfunction of the g-secretase activity that induces alterations in Notch signalling; alterations of Notch signalling can induce a failure in the regulation of keratinocytes functions, in particular in keratinocytes proliferation and differentiation [103]."
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"Two mechanisms are possible : Notch inhibition might directly up-regulate hepatocyte differentiation via HGF (hepatocyte growth factor) and HNF (hepatocyte nuclear factor)-4alpha or might impair cholangiocyte differentiation thereby indirectly rendering hepatocyte differentiation as the dominant state."
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"Based on the findings that the Notch signaling contributes not only to cellular differentiation but also to proliferation of immature cells of the intestine [XREF_BIBR, XREF_BIBR], our data showing dynamic changes in CCN3 expression in the middle colon during tissue regeneration, i.e. the significant decrease in the acute phase of colitis and increase in the regenerative phase, may represent the hyperactive and hypoactive states of Notch signaling during tissue repair in this colonic region (XREF_FIG A)."
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"In addition to defining the role for Notch signaling in normal stratified squamous epithelial differentiation and dysregulated Notch signaling in conditions of basal cell hyperplasia, 3D organoids have been instrumental in elucidating mechanisms of epithelial stress responses in the setting of toxic and carcinogenic exposures, such as alcohol."
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"The growth advantages provided by GFP high cells were not affected by Notch inhibition in co-culture assays (XREF_FIG), indicating that the tumor promoting effects of non NE tumor cells are due to the differentiation state triggered by Notch activity, and not to ongoing Notch signaling."
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"These observations suggest that Notch signaling simultaneously exerts dual opposing effects on SGs from two different stem cell niches : Whereas Notch directly promotes sebocyte differentiation from SG stem cells, this pathway also indirectly suppresses these glands from outside the SG stem compartment, likely from the IFE."
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"During early pancreatic development, distinct levels of Notch signaling at two different transition stages trigger the proliferation and differentiation of progenitors; strict control of the time and dosage of the Notch signaling components is necessary for proper organ homeostasis."
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"Given the importance of the Notch and Wnt pathways in mediating lung proliferation and differentiation and their contribution to recovery from IAV, we next investigated if the circadian clock was relevant to this process.To determine whether clock-gated lung repair is associated with selective deficiencies in the cellular composition of the lung epithelium, we stained the lungs for AT1 and AT2 markers from C57bl6J 30 day post IAV recovery model explained in Fig 1A."
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"Given the recent findings that increased Notch activity caused rapid proliferation of premature exhaustion of bona fide HSPCs and increased lymphoid differentiation, it is conceivable that jagged-2 expression on ECs curbs the expression of Hes1 on HSPCs to ensure proper balance of downstream Notch targets in HSPCs and maintains HSPC self-renewal and differentiation."
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"DAPT treatment induced Notch signaling inhibition, as demonstrated by the decrease in Hes1 mRNA levels (data not shown), but the expression of the podocyte marker nephrin was unaffected, thus demonstrating that downregulation of the Notch pathway was not sufficient to induce the differentiation of renal progenitors."
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"When DNMAML1 was repressed by doxycycline in the Tet-Off system, Notch functions and squamous differentiation were restored in both monolayer and 3D cultures (XREF_FIG, and XREF_SUPPLEMENTARY), consistent with Notch mediated direct transcriptional regulation of squamous differentiation."
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"Respective animals display increased numbers of proliferating cells while levels of the Notch target gene hairy enhancer of split 1 (hes1), a differentiation factor directing cells towards the enterocyte fate, and vascular endothelial growth factor (VEGF), which is important for epithelial cell restitution, were reduced."
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"Studies in flies, where Notch promotes differentiation and regulates cell fate decision of ISC daughter cells, have already shed new light on these processes, providing new insight also into the regulation of mammalian stem cell systems : Notch signaling was recently shown to regulate cell-fate decisions in the regenerating airway epithelium in a manner reminiscent of the Drosophila ISC lineage."
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"Lack of CD27 expression, which is thought to mark emerging alphabeta and gammadelta T cells in the adult, on fetal DN3 cells already points to distinct mechanisms in these processes, and previous identification of progenitor cells that are negative for TCRbeta or gammadelta among fetal DN4 population may suggest that the Notch signal alone can be sufficient to drive further differentiation."
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"As reported by Vaughan in their study, persistent Notch signaling prevented Krt5 cells from differentiating into alveolar cell types and led to the formation of honeycomb cysts in the lung, while removal of Notch signaling promoted Krt5 cell differentiation into alveolar type II cells [35]."
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"Together, these data highlight (i) the importance of Notch signalling downstream of BRCA1 and suggest an interdependence between Notch and estrogen signalling to maintain the luminal phenotype and (ii) how inhibition of Notch signalling may lead the disruption of normal mammary differentiation leading to the emergence of more aggressive basal like cancer subtypes."
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"While a direct role for Notch in the regulation of medial MVSCs has not yet been fully investigated, a putative role is strongly implicated as activation of Notch signalling in MVSCs directs their differentiation into mature SMCs when cocultured with OP9-Delta1 Notch ligand presenting feeder cells [XREF_BIBR]."
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"To further define the capacity of Notch ligands to modulate development of human NK cells, we determined the differential ability of the 5 different Notch ligands found in vertebrates to induce NK cell differentiation and expansion from CD34+ HPCs isolated from umbilical cord blood (UCB)."
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"The three leading hypotheses on the pathogenesis of IH are (1) local hypoxemia leading to hypoxia-inducible factor 1 alpha (HIF-1α)-induced proliferation
, (2) embolization of placental cells
, and (3) vasculogenesis/angiogenesis driven by hypoxemia-induced differentiation of mesenchymal stem cells into endothelial cells and Notch-mediated differentiation of mesenchymal stem cells into proangiogenic pericytes
."
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"The mutations in the Wnt, Notch, and Ras-ERK signaling pathways exemplified by C. elegans strains are already established to promote carcinogenesis in humans since these pathways control different aspects of cell proliferation, cell differentiation, cell cycle progression, cell fate and cell death [6], [7], [8]."
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"Signalling strength is a major regulatory factor of Notch mediated differentiation in human alpha/beta or gamma and delta T cells XREF_BIBR, endothelial cell fate determination XREF_BIBR and of patterning in inner ear development XREF_BIBR, in which Notch signalling strength is determined by competition between DLL1 and JAG1 ligands in adjacent cells."
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"It has been proposed that Notch ligands promote the differentiation of satellite glial cells that envelop neuronal cell bodies whereas Neuregulin likely functions to facilitate proliferation and differentiation of glial cells associated with myelinated nerves such as Schwann cells."
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"XREF_BIBR Considering the known role of Notch signaling in T-cell lineage differentiation in mice and human subjects, XREF_BIBR we have implemented a feeder cell-free culture system based on the immobilized Notch ligand delta like (DL) 4 in combination with a specific set of cytokines."
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"Furthermore, an unbiased approach to eliminate all functional Notch ligands using conditional deletion of the E3 ubiquitin ligase Mind bomb1 (Mib1) in dendritic cells, B cells, T cells and FDC shows that the source of Notch ligands driving Tfh cell differentiation can be distinct from the cells presenting or harboring cognate antigen during a prototypical type-2 immune response."
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"In accordance with others XREF_BIBR XREF_BIBR, we also found the activation of Notch pathway in TGFbeta activated HSCs and showed that pharmacological inhibition of Notch signaling pathway using Avagacestat attenuated HSCs activation, collagen deposition and their contractility suggesting the crucial role of Notch pathway in the differentiation and activation of HSCs."
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"10 In human , however , Notch signaling then needs to be reduced for efficient differentiation towards committed thymocytes ,11 while in mouse high Notch activity is maintained.12 Thereafter , Notch also differentially modulates the differentiation towards T-cell receptor ( TCR ) - and TCR-T-cells in mouse versus human.13-15 Activation of Notch1 results in the expression of many different target genes whose individual roles in controlling hematopoietic lineage decisions are still unclear ."
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"One individual with Alagille syndrome, an autosomal dominant disorder associated with Jag1 gene, was reported as having aortic calcification [XREF_BIBR], These in vivo findings suggest an inhibitory effect, however, in vitro studies show stimulatory effects of Notch signaling in osteoblastic differentiation of VSMC, osteoblasts and multipotent mesenchymal cells [XREF_BIBR - XREF_BIBR]."
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"An essential role for Notch signaling in arterial differentiation and vascular remodeling has been demonstrated by genetic studies of mice with targeted mutations in either Notch (Notch1 -/-, and Notch1 -/-; Notch4 -/-), or Notch ligands (Jagged1 -/- and Dll4 -/+ or Dll4 -/-), reviewed in Shawber et al. [XREF_BIBR]."
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"It is worth noting that although the Notch signaling promotes the differentiation of monocyte into TAMs, the Notch signaling can promote the pro inflammatory polarization of differentiated TAMs toward M1, which suggests that targeting to enhance the expression of RBP-J of TAMs and enhancing Notch signaling to promote the M1 polarization of TAMs may have potential for tumor treatment."
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"Previously published work demonstrated a role for Notch signaling in aRMS tumorigenesis, as the Notch target Hes1 was found to allow evasion of differentiation and promote proliferation in the RhJT aRMS cell line, and Notch inhibition reduced both eRMS and aRMS invasiveness in vitro."
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"This apparent discordance between infrequent NOTCH1 mutations per se and a still defective Notch pathway through other gene mutations in 32% of OTSCC patients highlights the importance of deregulating the Notch driven epithelial cell differentiation program in OTSCC through a range of convergent targets."
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"The Notch signaling pathway, activated by ligand binding, can switch the conversion of the cell cycle, regulate cell apoptosis and fate, affect the nervous system formation and morphogenesis, and contribute to the differentiation and development of the nervous system [XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR XREF_BIBR]."
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"These data suggest an important role of JAG1-mediated Notch signaling in the induction of anti-tumor T-cell responses.We also assessed whether the engineered Notch ligand DLL1 and JAG1 constructs modulate the differentiation of memory T-cells in vitro in a T:DC stimulation co-culture."
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"In considering the importance of Notch in IEC differentiation, the observed elevated cell proliferation after bowel resection may result from activated Wnt-beta-catenin signaling, while Notch signaling is activated to enhance cell differentiation of the rapidly expanding number of cell progenitors."
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"To address the thymocyte-autonomous nature of the developmental block observed in vivo, we performed experiments on cultured T cells by sorting Sca-1 + fetal liver haematopoietic stem and progenitor cells on OP9 stromal cells expressing the Notch ligand Delta-1 (OP9-DL1), which allows in vitro differentiation of T cells up to the DP stage."
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"This hypothesis is supported by a recent study showing that Notch signaling modulates PSCs in a cellular context dependent manner, and that Notch signaling inhibits proliferation and promotes epithelial differentiation in basal cells but promotes proliferation in luminal cells 46."
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"The influence of Notch signaling in differentiation and development can not be overstated as Notch regulates fate decisions in cell types of all four major tissues : epithelium, muscle, connective (specifically hematopoietic cells and bone in this group), and nervous tissue [XREF_BIBR]."
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"Evidence supports that Notch signaling promotes differentiation of naïve CD8 T cells into cytotoxic and memory T lymphocytes by upregulating the transcription factor Eomesodermin responsible for regulating expression of effector molecules IFNγ, granzymes, and perforins (Biktasova et al., 2015; Palaga et al., 2003; Radtke et al., 2010; Sauma et al., 2012; Thounaojam et al., 2015; Tsukumo and Yasutomo, 2004)."
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"In T-ALL, a vital role in Notch driven thymocyte differentiation and leukemia has been assigned to mTOR complex 2, suggesting a potential role of mTOR C2 inhibition in undifferentiated T-ALL [XREF_BIBR, XREF_BIBR]; however, activation of the PI3K axis is a common feature among T-ALL independent of differentiation stage."
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"In lung fibrosis, characterized by fibroblast proliferation leading to excess extracellular matrix deposition (collagen and glycosaminoglycans) and tissue remodeling occurring frequently 6-9months after radiation treatment, GSI prevents NOTCH and JAGGED1 induced myofibroblast differentiation in response to frizzled class receptor 1 (FZZ1) by decreasing the expression of alpha-smooth muscle actin (alpha-SMA)."
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"The juxtacrine case could model lateral induction through Notch signalling, which is known to be involved in regulating differentiation and has been found to stimulate the differentiation of embryonic stem cells (ESCs) into neurons [XREF_BIBR] and epithelial stem cells into the functioning cells of the intestinal crypt [XREF_BIBR]."
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"Notch inhibition shortly after influenza injury (5 days post-infection) significantly attenuates Krt5 + expansion, while Notch inhibition both in vitro and at later time points in vivo (31 days post-infection) increases the differentiation of Krt5 + cells into SPC + AT2s, again demonstrating that some plasticity toward alveolar cell types is present in these cells (Vaughan et al., 2015)."
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"The upregulation of RhoA could also be observed, which further contributed to the activation of the Ras pathway.14, 15 A number of other studies have confirmed that changes in the Ras/Mek pathway affect the Notch pathway and that activation of the Notch pathway promotes arterial differentiation and inhibits the expression of vein‐related marker proteins."
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"For example, Notch induces the differentiation of angioblasts into ECs during early vascular development but regulates the arterial and venous specification of ECs at a later stage XREF_BIBR, and while VEGF-A activates Notch in ECs, the downstream effects of this interaction include declines in VEGFR2 levels and, consequently, an impaired response to VEGF XREF_BIBR."
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"For example, gammaSec inhibition did not block all Notch functioning in cancer cells, Rbpjkappa knockout mice showed that non canonical Notch-4 signaling is involved in mammary gland tumorigenesis, and numerous studies have shown Th cell differentiation to be driven by Notch signaling, but independent of Rbpjkappa."
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"However, previous reports demonstrated that Notch activation promotes osteogenic differentiation in various cell types, including human periodontal ligament stem cells, stem cells isolated from human exfoliated deciduous teeth (SHEDs), and human bone marrow mesenchymal stem cells (hBMSCs) XREF_BIBR - XREF_BIBR."
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"On the contrary, Pasut and co-workers demonstrated that, subsequent to the deletion of the transcription factor PAX7 (Paired Box 7) and following acute muscle injury, NOTCH signaling promoted the differentiation of satellite cells into brown adipocytes rather than into a skeletal muscle cell phenotype ."
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"XREF_BIBR This contrasts with adult hematopoiesis, where Notch activation has been shown to inhibit myelopoiesis and promote lymphoid differentiation, and previous studies have employed stroma that constitutively express Dll1 to generate T-cells from hESC derived hematopoietic progenitors."
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"Notch signaling was previously shown to be required for in vitro differentiation from CLPs into nuocytes and a recent study demonstrated that high levels of Notch signaling trigger ILC2 differentiation from human uncommitted thymic progenitor cells, and lower levels trigger a T cell program of differentiation [XREF_BIBR, XREF_BIBR]."
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"Using either an anti-c-kit monoclonal antibody or Gleevec, a pharmacological inhibitor of c-kit signaling, we show that the Notch induced T cell differentiation of either Pax5 deficient progenitor B cells, or the equivalent cell from the bone marrow of normal mice, is strictly dependent on c-kit signaling, whereas the differentiation of normal progenitors into the B cell lineage is not."
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"Taken together, this work demonstrates for the first time that OP9-DL1 cells provide a unique microenvironment for conferring pMHC-I-restricted TCR specific signals to immature DP cells to enable effective positive and negative selection, and revealing a requirement for Notch signaling in CD8 lineage commitment and differentiation in vitro."
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"During Drosophila oogenesis, Notch activity is required first to specify particular follicle cell fates, then to promote the differentiation of all follicle cell types, to promote border cell migration, and then to form dorsal appendages, raising the question as to how Notch activity is spatially and temporally regulated."
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"Indeed, we show that although elevated Notch activity promotes MZ B cell maturation while diminishing FO B cell development, expression of ET2 or E2A M/M led to reduced accumulation of MZ B cells to a varying degree, suggesting that ET2 and E2A M/M can oppose the effects of Notch signaling and the mechanism whereby Notch supports MZ B cell differentiation at least in part includes down-regulation of E protein function."
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"We demonstrated that genetically modified iPSCs with Ag specific T cell receptor (TCR) and the transcriptional factor FoxP3, followed by differentiation driven by Notch signaling can enable iPSCs to pass hematopoietic and T lineage differentiation checkpoints, resulting in the development of Ag specific CD4 + T regs."
reach
"The NRG1 and Notch pathways are known to suppress the generation of fibroblast-like cells and contribute to SC differentiation (reviewed in Jessen and Mirsky, 2005), and recent evidence from zebrafish studies has shown that the Wnt/β-catenin pathway governs the decision between melanocyte and SC fates for SCPs (Colombo et al., 2022)."
reach
"We find differential gene expression for the Nodal and Activin, fibroblast growth factor (FGF), Wnt, and Hedgehog (Hh) signaling pathways in the H1T line, which implicates each of these molecules in maintaining the undifferentiated state, whereas the bone morphogenic protein (BMP) and Notch pathways could promote hESCs differentiation."