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Satellite cells and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Neil R.W. Martin, Adam P. Sharples
The Notch signalling pathway also plays a role in determining cell fate. Activation of the Notch pathway promotes myoblast proliferation and overexpression of the transmembrane receptor Notch-1 results in higher levels of Pax 7 in myoblasts and enhances satellite cell self-renewal (31, 32). By contrast, the Notch signalling inhibitor, Numb, promotes Myf-5 expression, myoblast differentiation and myotube formation (31). Numb is inherited asymmetrically when myoblast divide (31), potentially directing one daughter cell towards differentiation and another towards self-renewal. Numb localisation is also under the control of the Par complex (27), demonstrating how integrated cellular signalling can control satellite cell proliferation, differentiation and the return to quiescence.
Breast Cancer Stem Cells and Their Niche: Lethal Seeds in Lethal Soil
Published in Brian Leyland-Jones, Pharmacogenetics of Breast Cancer, 2020
Danuta Balicki, Brian Leyland-Jones, Max S. Wicha
The Notch signaling pathway plays an important role in regulating proliferation, survival, and differentiation of many cell types, including the regulation of self-renewal of adult stem cells and differentiation of progenitor cells along a particular lineage. These outcomes include increased survival or death, proliferation or growth arrest, and commitment to or blockage of differentiation. There are four mammalian Notch homologues, Notch 1 to 4, which interact with the DSL ligands: Delta, Delta-like, Jagged1, and Jagged2 in vertebrates (71).
Targeting Notch Pathways
Published in Gertjan J. L. Kaspers, Bertrand Coiffier, Michael C. Heinrich, Elihu Estey, Innovative Leukemia and Lymphoma Therapy, 2019
Jennifer O’Neil, A. Thomas Look
The discovery that activating mutations occur in over 50% of T-ALL patients has demonstrated the importance of this signaling pathway in the molecular pathogenesis of T-ALL. Inhibition of the Notch signaling pathway has opened up a new area for therapeutic intervention. γ-Secretase inhibitors hold promise as therapeutics for T-ALL and other malignances. These compounds will likely be most beneficial in combination with other drugs, either those currently used to treat T-ALL patients or other specific inhibitors of pathways downstream of Notch described in this chapter. Specific inhibitors of the Notch signaling pathway, such as antibodies or small molecules that specifically block Notchl signaling but not signaling by Notch 2–4, may be more effective and produce fewer side effects. The complexity of the Notch signaling pathway provides several additional points at which the pathway could be targeted including ligand binding, dimerization, proteolysis, and transcriptional activity.
Regulation of Notch Signaling Pathway to Innate Lymphoid Cells in Patients with Acute Myocardial Infarction
Published in Immunological Investigations, 2023
Haiwen Yu, Yongjie Wei, Yanyan Dong, Penglei Chen
The Notch signaling pathway is a cell signaling system that is conserved in a variety of eukaryotes (Castro et al. 2021) and controls a wide spectrum of developmental processes (Radtke et al. 2010; Yuan et al. 2010). Four Notch receptors (Notch1 ~ 4) and their ligands (such as Jagged1, Jagged2, and delta-like ligand 4) in mammals mediate cell-to-cell communication and proteolytic processing to promote signaling (Castro et al. 2021). Delta-like ligand negatively regulates angiogenic sprouting (Lobov et al. 2007). Whereas Jagged appears to have an opposing function by competing with delta-like ligand and participating in the recruitment of pericytes and sprouting (Qiu et al. 2016). Hairy and enhancer of split homolog 1 (Hes1) is one of the most important downstream target genes of Notch signaling and is widely expressed in human tissues, which are involved in immunoregulation both physiologically and pathologically, such as in cancers and inflammation (Rani et al. 2016; Wang et al. 2020). Notch signaling pathway plays important roles in various cellular mechanisms, such as cell fate determination, hematopoiesis, organ self-renewal, proliferation, and apoptosis (Castro et al. 2021). Notch signaling regulates atherosclerosis by controlling macrophage polarization and T-cell differentiation and activity (Vieceli Dalla Sega et al. 2019). However, the modulatory role of Notch signaling pathway in ACS is still not fully understood.
Decreasing lncRNA PVT1 causes Treg/Th17 imbalance via NOTCH signaling in immune thrombocytopenia
Published in Hematology, 2021
Ling Yu, Liqin Zhang, Zhiyong Jiang, Beiwei Yu
The Notch signaling pathway can regulate the fate of T lymphocytes and participate in T cell differentiation [27, 28]. In addition, the Notch signaling pathway also inhibits Treg cell differentiation and regulates Treg/Th17 balance [29, 30]. Furthermore, the NOTCH pathway is involved in ITP, and inhibition of Notch signaling activation can reverse the imbalance of Treg/Th17 cells in ITP, suggesting that blocking the NOTCH1 pathway may be an effective target for the treatment of ITP [31, 32]. Here, we found that NOTCH1 was decreased after overexpression of PVT1. Apart from that, overexpressing PVT1 induced the degradation of NOTCH1 and increased its ubiquitination. We also found that PVT1 could bind to NOTCH1. Collectively, increasing PVT1 expression might alleviate ITP by inhibiting the Notch1 pathway as well as the differentiation of Th7 cells.
The role of microRNA in cisplatin resistance or sensitivity
Published in Expert Opinion on Therapeutic Targets, 2020
Shanshan Wang, Ming-Yue Li, Yi Liu, Alexander C Vlantis, Jason YK Chan, Lingbin Xue, Bao-Guang Hu, Shucai Yang, Mo-Xian Chen, Shaoming Zhou, Wei Guo, Xianhai Zeng, Shuqi Qiu, C Andrew van Hasselt, Michael CF Tong, George G Chen
The Notch signaling pathway has been reported to play an essential role in cell proliferation, apoptosis, and progression of malignancies, but its functional role depending on specific cancer types or histologies. Several studies have suggested that Notch receptors can regulate the cell invasion and migration as well as EMT [25]. For example, the overexpression of Notch1 enhanced cell migration and invasion, leading to EMT in prostate cancer cells [26]. MiR-148a, an inhibitor of Notch1, suppressed tumor growth and malignancy in hepatocellular carcinoma [27]. Notch3 reported to be a candidate oncogene overexpressed in serous ovarian cancer, and was found to be significantly related to cancer metastasis and chemoresistance. Xu et al. demonstrated that one of the Notch3 regulate genes, SUSD2, promoted cancer metastasis and conferred cisplatin resistance in high-grade ovarian cancer by regulating the expression of EpCAM [28]. MiR-129-5p can inhibit NSCLC stemness and chemoresistance by directly targeting DLK1 that is one of the Notch signaling receptors. Ma et al. suggest that miR-129-5p and DLK1 can play a positive role in an effective treatment strategy for NSCLC [29].