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dBrms1 Acts as a Positive Regulator of notch signaling in Drosophila Wing

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Journal of Genetics and Genomics 2014年第6期41卷 317-325页

作者： Qinghai Zhang Yan Zhang Longfei Wu Yongfei Yang Xue Li Lei Gao Xiaomeng Hou Yihui Wu Guoli Hou Zhouhua Li Xinhua Lin State Key Laboratory of Biomembrane and Membrane Biotechnology Institute of Zoology Chinese Academy of Sciences University of Chinese Academy of Sciences School of Life Sciences Capital Normal University Division of Developmental Biology Cincinnati Children’s Hospital Medical Center

The highly conserved notch signaling is precisely regulated at different steps in a series of developmental events. However, little is known about the regulation of notch receptor at transcriptional level. Here, we demonstrate that dBrmsl is involved in regulating notch signaling in Drosophila wing. We show that knockdown of dBrmsl by RNA interference （RNAi） in wing disc suppresses the expression of notch signaling target genes wingless （wg）, cut and Enhancer of split m8 [E（spl）m8]. Consistently, the levels of Wg and Cut are reduced in the dBrmsl mutant clones. Importantly, loss of dBrmsl leads to significant reduction of notch proteins. Furthermore, depletion of dBrmsl results in apparent downregulation of notch transcription in the wing disc. Moreover, we find that dBrmsl is functionally conserved with human Breast cancer metastasis suppressor 1 like （hBRMSIL） in the modulation of notch signaling. Taken together, our data provide important insights into the biological function of dBrmsl in regulating notch signaling.

关键词： notch signaling Drosophila Wing disc notch transcription dBrmsl

notch signaling in female cancers: a multifaceted node to overcome drug resistance

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Cancer Drug Resistance 2021年第4期4卷 805-836页

作者： Maria V.Giuli Angelica Mancusi Eugenia Giuliani Isabella Screpanti Saula Checquolo Laboratory of Molecular Pathology Department of Molecular MedicineSapienza UniversityRome 00161Italy Scientific Direction San Gallicano Dermatological Institute IRCCSRome 00144Italy Department of Medico-Surgical Sciences and Biotechnology Sapienza UniversityLatina 04100Italy Center for Life Nano Science@Sapienza Istituto Italiano di TecnologiaRome 00161Italy

Drug resistance is one of the main challenges in cancer therapy,including in the treatment of female-specific malignancies,which account for more than 60%of cancer cases among ***,elucidating the underlying molecular mechanisms is an urgent need in gynecological cancers to foster novel therapeutic ***,notch signaling,including either receptors or ligands,has emerged as a promising candidate given its multifaceted role in almost all of the hallmarks of *** the connection between notch pathway and drug resistance in the afore-mentioned tumor contexts,several studies focused on the notch-dependent regulation of the cancer stem cell(CSC)subpopulation or the induction of the epithelial-to-mesenchymal transition(EMT),both features implicated in either intrinsic or acquired ***,the present review provides an up-to-date overview of the published results on notch signaling and EMT-or CSC-driven drug ***,other drug resistance-related mechanisms are examined such as the involvement of the notch pathway in drug efflux and tumor ***,there is a long way to go before every facet will be fully understood;nevertheless,some small pieces are falling neatly into ***,the main aim of this review is to provide strong evidence in support of notch signaling inhibition as an effective strategy to evade or reverse resistance in female-specific cancers.

关键词： notch signaling drug resistance female-specific cancers cancer stem cells epithelial-to-mesenchymal transition drug efflux tumor microenvironment

Retinal regeneration requires dynamic notch signaling

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Neural Regeneration Research 2022年第6期17卷 1199-1209页

作者： Leah J.Campbell Jaclyn L.Levendusky Shannon A.Steines David R.Hyde Department of Biological Sciences Center for Zebrafish ResearchCenter for Stem Cells and Regenerative MedicineUniversity of Notre DameNotre DameINUSA

Retinal damage in the adult zebrafish induces Müller glia reprogramming to produce neuronal progenitor cells that proliferate and differentiate into retinal *** signaling,which is a fundamental mechanism known to drive cell-cell communication,is required to maintain Müller glia in a quiescent state in the undamaged retina,and repression of notch signaling is necessary for Müller glia to reenter the cell *** dynamic regulation of notch signaling following retinal damage also directs proliferation and neurogenesis of the Müller glia-derived progenitor cells in a robust regeneration *** contrast,mammalian Müller glia respond to retinal damage by entering a prolonged gliotic state that leads to additional neuronal death and permanent vision *** the dynamic regulation of notch signaling in the zebrafish retina may aid efforts to stimulate Müller glia reprogramming for regeneration of the diseased human *** findings identified DeltaB and notch3 as the ligand-receptor pair that serves as the principal regulators of zebrafish Müller glia *** addition,multi-omics datasets and functional studies indicate that additional notch receptors,ligands,and target genes regulate cell proliferation and neurogenesis during the regeneration time ***,our understanding of notch signaling during retinal regeneration is *** fully appreciate the complex regulation of notch signaling that is required for successful retinal regeneration,investigation of additional aspects of the pathway,such as post-translational modification of the receptors,ligand endocytosis,and interactions with other fundamental pathways is *** we review various modes of notch signaling regulation in the context of the vertebrate retina to put recent research in perspective and to identify open areas of inquiry.

关键词： differentiation gliosis Müller glia neuronal progenitor cell notch signaling proliferation quiescence retinal development retinal regeneration zebrafish

Role of notch signaling in regulating innate immunity and inflammation in health and disease

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Protein & Cell 2016年第3期7卷 159-174页

作者： Yingli Shang Sinead Smith Xiaoyu Hu School of Medicine and Institute for Immunology Tsinghua University Beijing 100084 China Department of Clinical Medicine Trinity College Dublin Dublin 2 Ireland

The notch signaling pathway is conserved from Drosophila to mammals and is critically involved in developmental processes. In the immune system, it has been established that notch signaling regulates multiple steps of T and B cell development in both central and peripheral lymphoid organs. Relative to the well documented role of notch signaling in lymphocyte development, less is known about its role in regulating myeloid lineage development and function, especially in the context of acute and chronic inflammation. In this review article, we will describe the evidence accumulated during the recent years to support a key regulatory role of the notch pathway in innate immune and inflammatory responses and discuss the potential implications of such regulation for pathogenesis and therapy of inflammatory disorders.

关键词： inflammation innate immunity macrophages notch signaling RBP-J

MicroRNA miR-252-5p regulates the notch signaling pathway by targeting Rab6 in Drosophila wing development

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Insect Science 2023年第5期30卷 1431-1444页

作者： Do-Hwan Lim Min-Seok Choi Ji Won Jeon Young Sik Lee School of Systems Biomedical Science Soongsil UniversitySeoulRepublic of Korea College of Life Sciences and Biotechnology Korea UniversitySeoulRepublic of Korea Institute of Animal Molecular Biotechnology Korea UniversitySeoulRepublic of Korea

The notch signaling pathway plays a central role in the development of various ***,dysregulation of microRNAs(miRNAs),which are crucial regulators of gene expression,can disrupt signaling pathways at all stages of *** notch signaling is involved in wing development in Drosophila,the mechanism underlying miRNA-based regulation of the notch signaling pathway is ***,we report that loss of Drosophila miR-252 increases the size of adult wings,whereas the overexpression of miR-252 in specific compartments of larval wing discs leads to patterning defects in the adult *** miR-252 overexpression-induced wing phenotypes were caused by aberrant notch signaling with intracellular accumulation of the full-length notch receptor during development,which could be due to defects in intracellular notch trafficking associated with its recycling to the plasma membrane and autophagy-mediated ***,we identified Rab6 as a direct target of miR-252-5p;Rab6 encodes a small Ras-like GTPase that regulates endosomal trafficking *** with this finding,RNAi-mediated downregulation of Rab6 led to similar defects in both wing patterning and notch ***,co-overexpression of Rab6 completely rescued the wing phenotype associated with miR-252 overexpression,further supporting that Rab6 is a biologically relevant target of miR-252-5p in the context of wing ***,our data indicate that the miR-252-5p-Rab6 regulatory axis is involved in Drosophila wing development by controlling the notch signaling pathway.

关键词： Drosophila miR-252-5p notch signaling Rab6 wing development

Dysregulation of notch signaling related genes in oral lichen planus

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Asian Pacific Journal of Tropical Biomedicine 2017年第7期7卷 666-669页

作者： Nunthawan Nowwarote Thanaphum Osathanon Mineralized Tissue Research Unit Faculty of Dentistry Chulalongkorn University Bangkok 10330 Thailand Department of Anatomy Faculty of Dentistry Chulalongkorn University Bangkok 10330 Thailand Craniofacial Genetics and Stem Cells Research Group Faculty of Dentistry Chulalongkorn University Bangkok 10330 Thailand

Objective: To investigate a dysregulation of notch signaling in oral lichen planus(OLP)using public available microarray ***: A m RNA expression profiling dataset from Gene Expression Omnibus was downloaded. Differential gene expression between OLP and normal oral epithelium was examined using Network Analyst. The dysregulated genes related to notch signaling were ***: Thirteen genes in notch signaling pathway were significantly differential expressed between OLP and normal epithelium. OLP samples significantly increased the m RNA levels of HEYL, APH1 B, CNTN1 and PSEN2. Whilst, ITCH, HES1, TLE2, DLK2,DTX2, notch3, JAG2, RFNG, and SPEN were downregulated in OLP ***: notch signaling was dysregulated and may participate in pathophysiologic process in OLP.

关键词： notch signaling Oral lichen planus Expression analysis Genes

notch signaling regulates expression of Mcl-1 andapoptosis in PPD-treated macrophages

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Cellular & Molecular Immunology 2013年第5期10卷 444-452页

作者： Tanapat P alaga Siriluk Ratanabunyong Thitiporn Pattarakankul Naunpun Sangphech Wipawee Wongchana Yukihiro Hadae Patipark Kueanjinda Department of Microbiology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand Interdisciplinary Program in Medical Microbiology Graduate School Chulalongkorn University Bangkok 10330 Thailand Graduate Program in Industrial Microbiology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand Graduate Program in Biotechnology Faculty of Science Chulalongkorn University Bangkok 10330 Thailand International Center for Biotechnology Osaka University Osaka 565-0871 Japan

Macrophages are cellular targets for infection by bacteria and viruses. The fate of infected macrophages plays a key role in determining the outcome of the host immune response. Apoptotic cell death of macrophages is considered to be a protective host defense that eliminates pathogens and infected cells. In this study, we investigated the involvement of notch signaling in regulating apoptosis in macrophages treated with tuberculin purified protein derivative （PPD）. Murine bone marrow-derived macrophages （BMMs） treated with PPD or infected with Mycobacterium bovis Bacillus Calmette-Guerin （BCG） induced upregulation of notch1. This upregulation correlated well with the upregulation of the anti-apoptotic gene mcl-1 both at the transcriptional and translational levels. Decreased levels of notch I and Mcl- 1 were observed in BMM treated with PPD when a gamma secretase inhibitor （GSI）, which inhibits the processing of notch receptors, was used. Moreover, silencing notch1 in the macrophage-like cell line RAW264.7 decreased Mcl-1 protein expression, suggesting that notch1 is critical for Mcl-1 expression in macrophages. A significant increase in apoptotic cells was observed upon treatment of BMM with PPD in the presence of GSI compared to the vehicle-control treated cells. Finally, analysis of the mcl-1 promoter in humans and mice revealed a conserved potential CSURBP-Jκ binding site. The association of notch I with the mcl-1 promoter was confirmed by chromatin immunoprecipitation. Taken together, these results indicate that notch I inhibits apoptosis of macrophages stimulated with PPD by directly controlling the mcl-1 promoter.

关键词： apoptosis BCG macrophage Mcl-1 notch signaling PPD

Bevacizumab modulates retinal pigment epithelial-tomesenchymal transition via regulating notch signaling

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International Journal of Ophthalmology(English edition) 2015年第2期8卷 245-249页

作者： Jing-Jing Zhang San-Jun Chu Xiao-Lei Sun Ting Zhang Wei-Yun Shi Qingdao University Medical College Shandong Provincial Key Laboratory of Ophthalmology Shandong Eye Institute Shandong Academy of Medical Sciences

AIM: To investigate the effect of bevacizumab treatment on notch signaling and the induction of epithelial-of-mesenchymal transition(EMT) in human retinal pigment epithelial cells(ARPE-19) in ***: In vitro cultivated ARPE-19 cells were treated with 0.25 mg/m L bevacizumab for 12, 24, and 48 *** morphology changes were observed under an inverted microscope. The expression of zonula occludens-1(ZO-1), vimentin and notch-1 intracellular domain(NICD) was examined by *** m RNA levels of ZO-1, α-SMA, notch-1, notch-2,notch-4, Dll4, Jagged-1, RBP-Jk and Hes-1 expression were evaluated with quantitative real-time polymerase chain reaction(q RT-PCR). The protein levels of α-SMA,NICD, Hes-1 and Dll-4 expression were examined with Western ***: Bevacizumab stimulation increased the expression of α-SMA and vimentin in ARPE-19 cells which changed into spindle-shaped fibroblast-like ***, the m RNA expression of Hes-1 increased and the protein expression of Hes-1 and NICD also increased, which notch signaling was activated. The m RNA expression of notch-1, Jagged-1 and RBP-Jk increased at 48 h, and while Dll4 m RNA and protein expression did not change after bevacizumab ***: Jagged-1/notch-1 signaling may play a critical role in bevacizumab-induced EMT in ARPE-19 cells, which provides a novel insight into the pathogenesis of intravitreal bevacizumab-associated complication.

关键词： bevacizumab notch signaling epithelial-tomesenchymal transition retinal pigment epithelial cells

The roles and activation of endocardial notch signaling in heart regeneration

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Cell Regeneration 2021年第1期10卷 27-34页

作者： Huicong Li Cheng Chang Xueyu Li Ruilin Zhang School of Life Sciences Fudan UniversityShanghaiChina School of Basic Medical Sciences Wuhan UniversityWuhanChina

As a highly conserved signaling pathway in metazoans,the notch pathway plays important roles in embryonic development and tissue ***,cardiac injury and regeneration have become an increasingly popular topic for biomedical research,and notch signaling has been shown to exert crucial functions during heart regeneration as *** this review,we briefly summarize the molecular functions of the endocardial notch pathway in several cardiac injury and stress *** there is an increase in appreciating the importance of endocardial notch signaling in heart regeneration,the mechanism of its activation is not fully *** review highlights recent findings on the activation of the endocardial notch pathway by hemodynamic blood flow change in larval zebrafish ventricle after partial ablation,a process involving primary cilia,mechanosensitive ion channel Trpv4 and mechanosensitive transcription factor Klf2.

关键词： Heart regeneration notch signaling Hemodynamic alteration klf2 Primary cilium Ion channel