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Notch activates cell differentiation. 1000 / 2259
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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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"NOTCH blockade, however, suppressed the differentiation of monocyte-derived tumor-associated macrophages (TAMs), but promoted the proliferation of Kupffer cell-like TAMs in hepatocellular carcinoma and hepatic metastasis of colorectal cancer by upregulating Wnt/β-catenin signaling [70]."
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"Additionally, there are other ways to increase and restore the Th1/Th2 balance in patients with tuberculosis by blocking Notch signaling using N-[N-(3, 5-difluorophenacetyl)-l-alanyl]-s-phenylglycinet-butyl ester.15In contrast, another study showed that Notch signaling inhibits Th2 polarization, enhances Th1 cell differentiation, and increases the Th1/Th2 balance in mice, and this inhibits or reduces food allergy in mice."
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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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"However, Notch signaling in different tissues can drive either terminal differentiation or cellular proliferation, making this subject complex, especially in the context of a viral infection that co-express other viral early gene products in a temporally and spatially controlled manner."
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"Our previous studies confirmed that the activation of Notch signaling promotes the differentiation of HSCs into biliary epithelial cells (BECs) and the progression of rat CLF induced by bile duct ligation (BDL), whereas blocking Notch signaling inhibits this pathological process [12]."
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"Another interesting study [XREF_BIBR] showed that the differentiation of tumor stem like cells into endothelial cells might be mediated initially by the Notch pathway for the differentiation in endothelial progenitor cells and subsequently by the vascular-endothelium-growth-factor- (VEGF-) signaling pathway, selectively affecting the differentiation of endothelial progenitors to tumor derived endothelial cells."
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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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"Zender et al. developed a transgenic murine model with constitutive Notch overexpression in albumin expressing cells (Notch1C : AlbCre) to demonstrate that aberrant Notch activity in hepatic progenitor cells promotes differentiation of these cells towards a biliary lineage, contributing to malignant transformation [XREF_BIBR]."
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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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"Notch regulation of Ascl1 was also demonstrated in a genetic mouse model of Notch activation, as well as Notch-manipulated antral organoid cultures, thus suggesting that ASCL1 is a key downstream Notch pathway effector promoting endocrine cell differentiation in the gastric epithelium."
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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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"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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"Notch signaling is thought to act directly on stem cells to promote their proliferation and also in progeny precursors to determine absorptive versus secretory terminal differentiation pathways, although Notch signaling may actually enhance cell differentiation with other signaling pathways such as the Wnt-beta-catenin pathway promoting cell proliferation."
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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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"This may partially explain how the palmar skin achieves its increased thickness, as this result aligns with the literature, which shows that Notch signaling induces differentiation of the epidermis.In accordance with recent publications in murine skin, we find a surprising amount of co-expression of basal and differentiated markers within basal and suprabasal clusters (Figure S4)."
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For example, although previous reports illustrated that Notch signaling in mouse Sertoli cells promotes the differentiation of quiescent proSPG,
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scRNA‐seq revealed that receptors of Notch signaling, such as Notch2 and Notch3, are expressed in nearly all testicular somatic cell types, including Sertoli, Leydig, PTMs, and endothelial cells."
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"To test whether the DN thymocyte fraction exhibited any abnormality of Akt activity or FoxO phosphorylation in a setting more closely modeled on the Notch driven differentiation system, CD4 - CD8 - cells were cultured on OP9-DL1 stromal cells for 2 d. Although cell numbers were limiting even with Notch ligand, purified DN thymocytes cultured on Notch ligand bearing stromal cells exhibited substantially reduced phosphorylation of the Akt HM and of FoxO1/3a in Rictor deficient samples (XREF_FIG)."
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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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"(I) Overexpression of Active Notch (NACT) with the HLT driver induces non autonomous differentiation of crystal cells (ProPO, Red, not green), and inhibits expansion of HLT (Green) traced cells.Scale bar 10 mm.www.tandfonline.comFly209 organ is absent of cells actively expressing the activated Notch construct, suggesting that early Notch activation in blood progenitors affects their proliferation, quiescence, and survival."
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"Our FCM data revealed that Notch enhanced the proliferation of MSCs by decreasing the percentage of cells in the G0/G1 phase, and increasing the percentage of cells in the S phase In conclusion, we demonstrated that Notch signaling can potentiate the BMP9 induced osteogenic differentiation of MSCs."
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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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"Following the activation of Notch2 receptors, the Notch intracellular domain (NICD) of Notch receptor will translocate to the nucleus, associate with the DNA-binding protein RBPJκ, and mediate changes in gene transcription, such as Homolog of Hairy/Enhancer-of-Split (HES1) and Hairy/enhancer-of-split related with YRPW motif 1 (HEY1), to promote biliary differentiation (Fig. 5A)."
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"We directed via modulators of Wnt and Notch signaling differentiation of precursor mouse intestinal crypts into specialized organoids each containing ISC, enterocyte, goblet, or Paneth cells at relative proportions much higher than in situ as determined by mRNA expression and immunocytochemistry of cell type biomarkers."
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"To test whether cell intrinsic Notch signaling in thymic progenitors induces ILC2 differentiation, we ectopically expressed the intracellular domain of NOTCH1 (NICD1) in thymic CD34 + CD1a - progenitors, thereby inducing constitutive activation of NOTCH1 in these cells, and subjected these to co-culture on control OP9 cells."
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"Mitogen-activated protein kinase (MAPK) signaling, specifically involving extracellular signal-regulated kinases (ERK), jun N-terminal kinases (JNK), and p38MAPK, significantly contributes to AD-MSC osteogenesis [90], while Notch signaling interacts with BMP and Wnt pathways to inhibit chondrocyte differentiation in ECO and modulate the osteogenic differentiation process in IMO [83,91]."
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"In summary, we show that activation of Notch signaling in hPSC-derived neural crest is sufficient to direct the differentiation of brain mural cells, and establish an improved in vitro model that should facilitate improved understanding of brain mural cell development and function."
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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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"Against this background, it is imperative that a better understanding of the pathological process of OV be reached to facilitate the discovery of novel biomarkers for the successful prevention, diagnosis, and treatment of OV.There is mounting evidence that Notch can enhance the proliferation and differentiation of ovary stem/progenitor cells [3–6]."
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"In coculture systems, Delta like or Jagged Notch ligands within APCs were reported to promote skewing of T cell differentiation toward the T helper type 1 (Th1) or Th2 lineage, respectively, although dichotomous inductive effects of Delta like and Jagged Notch ligands were not detected in subsequent studies."
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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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"In addition, combined inhibition of Wnt, Notch, and epidermal growth factor receptor (EGFR) pathways, as well as combined inhibition of Wnt, Notch, and mitogen-associated protein kinase (MAPK), increase differentiation of Lgr5 + stem cells towards EECs and abolished differentiation of goblet cells and Paneth cells in intestinal Organoids [199] (Fig. 1)."
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"Therefore, we hypothesize that genetically modified iPSCs with Ag specific TCRs and survival related genes, followed by differentiation driven by Notch signaling, will enable the iPSCs to pass hematopoietic and T-lineage differentiation checkpoints, resulting in the development of highly reactive Ag specific CD8 + T cells."
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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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"Biological responses to HDAC inhibition were mediated, in part, by upregulating the noncanonical Notch ligand Delta and Notch like epidermal growth factor (EGF)-related receptor (DNER), which was found to inhibit GBM derived neurosphere formation, induce neurosphere cell differentiation, and inhibit the growth of neurosphere derived tumor xenografts."
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"In this study, we investigated cell autonomous roles of Notch signaling in osteoclast differentiation and function by altering Notch signaling during osteoclast differentiation using stimulation with immobilized ligands Jagged1 or Delta-like1 or by suppression with gamma-secretase inhibitor DAPT or transcriptional inhibitor SAHM1."
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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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"Notably, inhibition of Notch signaling is known to reduce the Lgr5-Hi cell population and the expression of stemness-associated genes such as Lgr5 and Olfm4.62 63 Ectopic expression of Notch in the Ngn3+ enteroendocrine progenitor cells, on the other hand, has been shown to drive differentiation toward enterocyte and goblet cell lineages.64 Thus, it is possible that iDKO Lgr5-Lo cells experience greater-than-usual Notch signals propelling their expansion and further differentiation along enterocyte and goblet cell lineages."
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"Analysis of Notch-differentiated lineages in vertebrate cerebellum have shown that Notch mediates cerebellar progenitor differentiation into excitatory and inhibitory cerebellar cell types (Zhang et al., 2021), but it is not yet known whether the resulting neurons integrate into shared or distinct circuits."
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"On the one hand, aberrantly low levels of Notch signaling in ISCs inhibit their proper differentiation into EBs; on the other hand, the higher Notch levels in EBs promote their excessive differentiation into enterocytes (ECs), leading to marked increases in abnormal ECs and decreased proliferation."
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"Furthermore, the Notch pathway is vital to induce the progenitor cell differentiation into secretory lineage cells, in which Hes1 and Atoh1 are the main transcription targets, and the fate of ISC was determined by up-regulating the expression of Hes1 and inhibiting atonal bHLH transcription factor 1 (Atoh1) (Zhou et al., 2021)."
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"Notch signaling is known to induce further differentiation of BCs from PCs at 17hpf prior to ingression of PMCs into the blastocoel (Materna and Davidson, 2012; Ohguro et al., 2011; Range et al., 2008; Sweet et al., 2002), so we reasoned that if Notch signaling was going to activate cell proliferation in BCs and PCs, this may occur at around 17hpf."
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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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"The NRG1 and Notch pathways are known to suppress the generation of fibroblast‐like cells and contribute to SC differentiation (reviewed in Jessen & 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)."
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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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"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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"Notch signaling is frequently reactivated together with other developmental and morphogenic signaling pathways upon organ injury to orchestrate the interplay, differentiation, and proliferation of distinct cell types and adult progenitors for tissue repair, deregulation of which may ultimately result in carcinogenesis."
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"Furthermore, proliferation of the skin, characterized by keratinocyte differentiation from basal to cornified keratinocytes followed by migration to the outer layer of skin, requires input from mitochondria via downstream transcriptional factors including C/EBP, Notch, and beta-catenin which together increase the differentiation of murine embryonic stem cells and induced pluripotent stem cells, as well as tissue-specific multipotent epithelial stem cells [13]."
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"We demonstrated that genetically modified iPSCs with Ag specific 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."
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"Such dysregulations switch the expression of cardiomyocytes into progenitor-like state in cardiac myxoma development by dysregulating Isl1, Baf60 complex, Wnt, FGF, Notch, Mef2c and others.The Nkx2-5 and MSX2 contribute predominantly to both proliferation and differentiation of Cardiac Progenitor Cells (CPCs), may possibly serve roles based on the microenvironment and the direction of cell circuitry in cardiac tumorigenesis."
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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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"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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"While it is well known that the Notch signaling is an evolutionarily conserved system that regulates proliferation and differentiation of BMSCs [XREF_BIBR, XREF_BIBR], the regulatory role of Notch signaling in the differentiation of BMSCs into GABAergic neuron like cells has not been examined."
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"Therefore, we conclude that LIN-12 and Notch signal instructs both vulval organogenesis and synaptic development of the egg laying circuit by regulating at least three sequential but independent developmental processes : the AC/VU decision, in which LIN-12 and Notch signaling promotes the differentiation of AC and VU cells; VPC specification, in which it determines the vulval precursor cell fates; and vm2 postsynaptic specification, in which it specifies the postsynaptic target cell and further regulates the muscle arm development."
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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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"This mechanism allows for the integration of nutritional signals through the IIS and TOR pathways with Notch mediated differentiation signals : High expression of TSC2 in ISCs prevents differentiation and is thus critical for stem cell maintenance, while reducing TSC activity in EBs is required and sufficient to promote differentiation into ECs."
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"A role for the primary cilium in NOTCH signaling was first identified in 2011 when the knockdown of IFT proteins in both cultured keratinocytes and embryonic epidermis cells led to significant NOTCH defects, while differentiation defects were cell-autonomous and rescued by activated NOTCH [75]."
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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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"However, a relevant study identified DEGs between high- and low-infiltrating M1 macrophages as predictors of HCC prognosis The activation of Notch signaling in HCC can mediate the differentiation of macrophages into M1 macrophages, thereby promoting inflammation and anti-tumor activity."
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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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"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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"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 initial studies in vitro and in injury models showed that Notch activated genes of the HRT (hairy related transcription factors) family could repress myocardin induced contractile protein expression, there were also several studies, showing that Notch activity promoted VSMC differentiation and contractile marker expression."
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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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"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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"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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"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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"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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"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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"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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"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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"Furthermore, since we found that activation of canonical Notch signaling did not induce osteogenic differentiation of MSCs in this study, it will be important to further identify the interactions between canonical Notch signaling and other signal-transduction pathways that result in enhanced osteogenesis and bone formation."
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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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"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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"We carried out a combination of transcriptomic analysis for TME subtypes estimation on TCGA‐STAD cohort and revealed a functional TME regulator HEYL which correlated with stromal component accumulation and activation of cancer‐related signatures in gastric cancer.HEYL was identified as a basic helix‐loop‐helix transcription factor and a direct target of Notch signaling that promotes neuronal differentiation in neural stem cells and specifically correlates with EMT in heart tissue."
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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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"Thus, given the crucial functions of Notch signaling in osteoblast maturation and differentiation, our finding that the Notch signaling pathway was altered in human bone with aging and specifically, that levels of both HES1 and HEY1 were significantly up-regulated in bone of old relative to young subjects, indicate that increased Notch signaling may contribute to impaired bone formation with aging."
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"Notch signaling is active in steady state airways and increased during repair Notch is required for differentiation, but not self-renewal, of airway basal cells Notch promotes luminal differentiation of mouse basal stem cells Our data suggest this mechanism is conserved in human basal cells Introduction."
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"These data also raise the possibility that Notch signaling directly regulates differentiation potential of a QSC rather than direct regulation of the quiescent state.scRNA-seq on cells from regenerating muscle suggests that Dll1 is expressed in a subset of differentiating, Myogenin cells and is important for self-renewal (Yartseva et al., 2020)."
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"Intriguingly, knocking down COUP-TFII in endothelial cells resulted in the increased expression of not only genes involved in Notch signaling but also smooth muscle lineage markers, 22 which correlated with the published results that Notch signaling promotes smooth muscle differentiation of epicardial cells."
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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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"In consideration of the same negative role of Notch signaling in osteoblast differentiation [XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR] as mTORC1 signaling and the positive correlation between Notch and mTORC1 [XREF_BIBR, XREF_BIBR, XREF_BIBR], we next investigated the potential role of the Notch pathway in the mechanism underlying the impaired differentiation potential of mTORC1 activated cells."
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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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"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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"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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"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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"Moreover, asymmetric cell division was shown to promote Notch signaling that further stimulated suprabasal terminal differentiation [XREF_BIBR] and importantly, loss of Notch in the skin disrupts the epidermal barrier and leads to increased proliferation and spontaneous tumor development [XREF_BIBR, XREF_BIBR]."
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"Airway BCs are not positively regulated by Notch during patterning, but sustained Notch inhibition prevents differentiation of MCCs and secretory cells in human ALI cultures, and leads to the thinning of the epithelium(Gomi et al., 2015; Rock et al., 2011), strongly suggesting a positive role for Notch in mammalian BCs maintenance as well."
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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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"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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"These results indicate that the phenotype of TAMs depends on the tumor, and their activation is highly dependent on the microenvironment, in which the Notch signal transduction pathway participates in TAM activation and promotes their differentiation into a pro-inflammatory phenotype."
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"For example, the GPI-anchored protein RECK regulates motor neuron differentiation in mammals by inhibiting Notch signaling; only when RECK is cleaved and released from the membrane can the ADAM10 metalloprotease access and cleave the Notch ligand thereby promoting differentiation (Corda et al., 2014)."
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"Next, we checked the ratios of glial-related cells between the two samples, we found that the ratios of radial glia and astrocyte decreased, but the ratios of intermediate progenitor and oligodendrocyte increased in pCAG-Cre; Rbpj dataset (Fig. 1K), consistent with our previous results that disrupted Notch signaling in RG cells accelerates the differentiation of stem cells and promotes the generation of oligodendrocyte at the expense of astrocyte (Fig. 1, A to D)."
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"Given the critical role of NOTCH signaling in esophageal squamous epithelial differentiation and homeostasis [27], it would be warranted to explore the role of NOTCH signaling in esophageal 3D organoids treated with both low- and high-LET radiation.Of particular interest was the increased stress phospho-protein expression for several phospho-proteins (pATF2, HSP27, MEK1, Msk1, and c-Jun) at the lower 0.1 Gy dose as compared to the higher 1 Gy dose for both Cs and Fe ion exposure (Figure 3)."
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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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"For example, repressing microglia activity at an early stage of the disease can result in inefficient myelin clearance, which impedes re-myelination [34], whereas inactivation of Notch signaling in OL lineage cells enhances their differentiation but compromises their proliferation."
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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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"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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"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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"These data confirm an early role of canonical Notch signaling in directing the expression of alternative differentiation programs starting from proliferative precursors in the VNO.Ectopic activation of Notch signaling has been previously shown to be able to alter cell fate (Jadhav et al., 2006)."
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"In short, in our study, the inhibition of Notch signaling by DAPT suppressed Th2 differentiation through down-regulating GATA3 and IL-4 (Figure 9) and promoted Th1 differentiation through up-regulating T-bet and IFN-γ in AkTM-sensitized mice.Increasing evidence suggests that the dysbiosis of gut microbiota is related to the development of food allergy [38,39,40]."
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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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"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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"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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"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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"Notch signaling can promote the differentiation of intestinal stem cells into absorptive progenitors (precursors of enterocytes) instead of secretory progenitors (precursors of goblet and Paneth cells); therefore, interruption of Notch signals could contribute to the higher percentage of enterocytes and lower percentages of goblet and Paneth cells in Fzd7 KO intestines."
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"Although this may be partially attributable to the strong tendency of these cells to remain within the basal layer, we also frequently did not detect K10 expression in dnMAMLexpressing cells positioned within the second and third suprabasal layers, suggesting that Notch promotes cell differentiation during wound healing."
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"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."