The abnormal activation of Notch signaling is closely related to the development of acute leukemia (AL). The core elements of the Notch signaling system include Notch receptors, Notch ligands, CSL DNA-binding proteins, and effectors like target genes. Any factors, which affect ligands, receptors, signal transducers and effectors, can influence the signal transduction of Notch signaling greatly. Based on the role of Notch signaling in AL, several targeted drugs against Notch upstream signaling have been developed. However, due to the complexity and pleiotropic effects of Notch upstream signaling, these targeted drugs display strong side effects. Thus, Hes (Hairy Enhancer of Split) factors as a primary Notch effector, also play an important role in the pathogenesis of AL. This review summarizes recent progresses on Notch-Hes signaling in AL, hopping to provide references for further excavation of the Notch-Hes signaling, and lay foundations for developing the next generation of targeted drugs.
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http://dx.doi.org/10.7534/j.issn.1009-2137.2017.01.043 | DOI Listing |
Endocr Metab Immune Disord Drug Targets
January 2025
Amity Institute of Pharmacy, Amity University Haryana Chemistry Gurugram India.
Objectives: In the last two decades, scientists have gained a better understanding of several aspects of pituitary development. The signaling pathways that govern pituitary morphology and development have been identified, and the compensatory relationships among them are now known.
Aims: This paper aims to emphasize the wide variety of relationships between Pituitary Gland and Stem cells in hormone Production and disease prevention.
Medicine (Baltimore)
November 2024
Department of Orthopaedics, Beijing Ditan Hospital Affiliated to Capital Medical University, Chaoyang District, Beijing, China.
Acquired immunodeficiency syndrome is a systemic infectious disease caused by human immunodeficiency virus infection, which could attack the bones and heart. However, the relationship between Nuclear Complex Associated 3 Homolog (NOC3L) and DEAD box helicase 17 (DDX17) and acquired immunodeficiency complicated with viral myocarditis and osteoporosis is unclear. The acquired immune deficiency dataset GSE140713, GSE147162 and the osteoporosis dataset (GSE230665), and viral myocarditis dataset (GSE150392) configuration files were generated from gene expression omnibus.
View Article and Find Full Text PDFZhongguo Zhong Yao Za Zhi
December 2024
School of Traditional Chinese Medicine, Binzhou Medical College Yantai 264003, China Institute of Basic Medicine, Xiyuan Hospital, China Academy of Chinese Medical Sciences Beijing 100091, China.
This article explored the specific mechanism by which ginsenoside Rg_1 regulates cellular autophagy to attenuate hypoxia/reoxygenation(H/R) injury in HL-1 cardiomyocytes through the microRNA155(miR-155)/neurogenic gene Notch homologous protein 1(Notch1)/hairy and enhancer of split 1(Hes1) pathway. An HL-1 cell model with H/R injury was constructed, and ginsenoside Rg_1 and/or Notch1 inhibitor DAPT and miR-155 mimics were used to treat cells. Cell counting kit(CCK)-8 was used to detect the relative viability of HL-1 cells with H/R injury.
View Article and Find Full Text PDFPflugers Arch
January 2025
School of Physical Education and Sport of Ribeirão Preto, University of São Paulo (USP), Avenida Bandeirantes, 3900, Monte Alegre, Ribeirão Preto, São Paulo, 14040-907, Brazil.
The Notch signaling pathway is crucial for skeletal muscle development, regeneration, inflammation, and aging. This study investigated the association between interleukin-10 (IL-10) and the Notch pathway in C2C12 cells, as well as explored the effects of combined endurance and resistance exercise on the Notch and autophagy pathways in the skeletal muscle of senescence-accelerated mouse-resistant 1 Sedentary (SAMR1 CT), SAMR1 exercised (SAMR1 EX), senescence-accelerated prone mouse 8 Sedentary (SAMP8 CT), and SAMP8 exercised (SAMP8 EX). C2C12 myoblasts were transfected with siIL-10.
View Article and Find Full Text PDFInjured epithelial organs must rapidly replace damaged cells to restore barrier integrity and physiological function. In response, injury-born stem cell progeny differentiate faster compared to healthy-born counterparts, yet the mechanisms that pace differentia-tion are unclear. Using the adult Drosophila intestine, we find that injury speeds cell differentiation by altering the lateral inhibition circuit that transduces a fate-determin-ing Notch signal.
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