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Effects and Mechanisms of Eps8 on the Biological Behaviour of Malignant Tumours (Review)
824 ONCOLOGY REPORTS 45: 824-834, 2021 Effects and mechanisms of Eps8 on the biological behaviour of malignant tumours (Review) KAILI LUO1, LEI ZHANG2, YUAN LIAO1, HONGYU ZHOU1, HONGYING YANG2, MIN LUO1 and CHEN QING1 1School of Pharmaceutical Sciences and Yunnan Key Laboratory of Pharmacology for Natural Products, Kunming Medical University, Kunming, Yunnan 650500; 2Department of Gynecology, Yunnan Tumor Hospital and The Third Affiliated Hospital of Kunming Medical University; Kunming, Yunnan 650118, P.R. China Received August 29, 2020; Accepted December 9, 2020 DOI: 10.3892/or.2021.7927 Abstract. Epidermal growth factor receptor pathway substrate 8 1. Introduction (Eps8) was initially identified as the substrate for the kinase activity of EGFR, improving the responsiveness of EGF, which Malignant tumours are uncontrolled cell proliferation diseases is involved in cell mitosis, differentiation and other physiological caused by oncogenes and ultimately lead to organ and body functions. Numerous studies over the last decade have demon- dysfunction (1). In recent decades, great progress has been strated that Eps8 is overexpressed in most ubiquitous malignant made in the study of genes and signalling pathways in tumours and subsequently binds with its receptor to activate tumorigenesis. Eps8 was identified by Fazioli et al in NIH-3T3 multiple signalling pathways. Eps8 not only participates in the murine fibroblasts via an approach that allows direct cloning regulation of malignant phenotypes, such as tumour proliferation, of intracellular substrates for receptor tyrosine kinases (RTKs) invasion, metastasis and drug resistance, but is also related to that was designed to study the EGFR signalling pathway. Eps8 the clinicopathological characteristics and prognosis of patients. -
Insights Into Functional Connectivity in Mammalian Signal Transduction Pathways by Pairwise
bioRxiv preprint doi: https://doi.org/10.1101/2019.12.30.891200; this version posted December 30, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Insights into Functional Connectivity in Mammalian Signal Transduction Pathways by Pairwise Comparison of Protein Interaction Partners of Critical Signaling Hubs Chilakamarti V. Ramana * Department of Medicine, Dartmouth-Hitchcock Medical Center, Lebanon, NH 03766, USA *Correspondence should be addressed: Chilakamarti V .Ramana, Telephone. (603)-738-2507, E-mail: [email protected] ORCID ID: /0000-0002-5153-8252 1 bioRxiv preprint doi: https://doi.org/10.1101/2019.12.30.891200; this version posted December 30, 2019. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. Abstract Growth factors and cytokines activate signal transduction pathways and regulate gene expression in eukaryotes. Intracellular domains of activated receptors recruit several protein kinases as well as transcription factors that serve as platforms or hubs for the assembly of multi-protein complexes. The signaling hubs involved in a related biologic function often share common interaction proteins and target genes. This functional connectivity suggests that a pairwise comparison of protein interaction partners of signaling hubs and network analysis of common partners and their expression analysis might lead to the identification of critical nodes in cellular signaling. -
The Role of the Src Homology-2 Domain Containing Protein B (SHB) in B Cells
M WELSH and others Role of SHB in b cells 56:1 R21–R31 Review The role of the Src Homology-2 domain containing protein B (SHB) in b cells Correspondence † Michael Welsh, Maria Jamalpour, Guangxiang Zang and Bjo¨rn Åkerblom should be addressed to M Welsh Department of Medical Cell Biology, Uppsala University, PO Box 571, Husargatan 3, SE-75123 Uppsala, Sweden Email †G Zang is now at Department of Medical Biosciences, Umea˚ University, Umea˚ , Sweden [email protected] Abstract This review will describe the SH2-domain signaling protein Src Homology-2 domain Key Words containing protein B (SHB) and its role in various physiological processes relating in " signal transduction particular to glucose homeostasis and b cell function. SHB operates downstream of several " insulin secretion tyrosine kinase receptors and assembles signaling complexes in response to receptor " vascular activation by interacting with other signaling proteins via its other domains (proline-rich, " islet cells phosphotyrosine-binding and tyrosine-phosphorylation sites). The subsequent responses " immune system are context-dependent. Absence of Shb in mice has been found to exert effects on hematopoiesis, angiogenesis and glucose metabolism. Specifically, first-phase insulin secretion in response to glucose was impaired and this effect was related to altered characteristics of focal adhesion kinase activation modulating signaling through Akt, ERK, b catenin and cAMP. It is believed that SHB plays a role in integrating adaptive responses to various stimuli by simultaneously modulating cellular responses in different cell-types, thus Journal of Molecular Journal of Molecular Endocrinology playing a role in maintaining physiological homeostasis. Endocrinology (2016) 56, R21–R31 Introduction The limited replicative capacity of human pancreatic (bTC1 cells) after serum-stimulation, the Src Homology-2 b cells contributes significantly to the development of domain containing adapter protein B (SHB) was identified diabetes mellitus and thus comprises a major hurdle for (Welsh et al. -
EPS8, an Adaptor Protein Acts As an Oncoprotein in Human Cancer
Chapter 5 EPS8, an Adaptor Protein Acts as an Oncoprotein in Human Cancer Ming-Chei Maa and Tzeng-Horng Leu Additional information is available at the end of the chapter http://dx.doi.org/10.5772/54906 1. Introduction A spectrum of cellular activities including proliferation, differentiation and metabolism are controlled by growth factors and hormones. The effects of many growth factors are mediated and achieved via transmembrane receptor tyrosine kinases [1,2]. Following ligand binding, the intrinsic catalytic activity of the growth factor receptor tyrosine kinases (RTKs) is augmented. The autophosphorylated RTKs then transmit signals through their ability to recruit and/or phosphorylate intracellular substrates. Thus, identification and characterization of proteins that associate with and/or become tyrosyl phosphorylated by RTKs become critical to delineate RTKs-mediated signaling pathways. A variety of methodologies have been developed and applied to search for substrates of tyrosine kinases including RTKs [3-8]. Here, we focus on EGFR pathway substrate no. 8 (Eps8), a putative target of epidermal growth factor (EGF) receptor (EGFR), and discuss its biological function as well as its implication in human cancers. Given Eps8-elicited effects contribute to neoplasm, its potential as a therapeutic target for cancer treatment is anticipated. 1.1. The identification of Eps8 To dissect EGFR-mediated signaling, Di Fiore’s laboratory took advantage of immuno- affinity purification of an entire set of proteins phosphorylated in EGF-treated EGFR- overexpressing cells, followed by generation of antisera against the purified protein pool. With these antisera, bacterial expression libraries were immunologically screened. Several murine cDNAs (eps clones) representing genes encoding substrates for EGFR were obtained [7,8]. -
The Clinical Aspect of Adaptor Molecules in T Cell Signaling: Lessons Learnt from Inborn Errors of Immunity
MINI REVIEW published: 12 August 2021 doi: 10.3389/fimmu.2021.701704 The Clinical Aspect of Adaptor Molecules in T Cell Signaling: Lessons Learnt From Inborn Errors of Immunity Yael Dinur-Schejter 1,2,3*, Irina Zaidman 1,2, Hagar Mor-Shaked 1,4 and Polina Stepensky 1,2 1 Faculty of Medicine, Hebrew University of Jerusalem, Jerusalem, Israel, 2 The Bone Marrow Transplantation and Cancer Immunotherapy Department, Hadassah Ein Kerem Medical Center, Jerusalem, Israel, 3 Allergy and Clinical Immunology Unit, Hadassah Ein-Kerem Medical Center, Jerusalem, Israel, 4 Monique and Jacques Roboh Department of Genetic Research, Hadassah Ein Kerem Medical Center, Jerusalem, Israel Adaptor molecules lack enzymatic and transcriptional activities. Instead, they exert their function by linking multiple proteins into intricate complexes, allowing for transmitting and fine-tuning of signals. Many adaptor molecules play a crucial role in T-cell signaling, following engagement of the T-cell receptor (TCR). In this review, we focus on Linker of Edited by: Activation of T cells (LAT) and SH2 domain-containing leukocyte protein of 76 KDa (SLP- Anne Spurkland, 76). Monogenic defects in these adaptor proteins, with known roles in T-cell signaling, University of Oslo, Norway have been described as the cause of human inborn errors of immunity (IEI). We describe Reviewed by: Martha Jordan, the current knowledge based on defects in cell lines, murine models and human patients. University of Pennsylvania, Germline mutations in Adhesion and degranulation adaptor protein (ADAP), have not United States resulted in a T-cell defect. Stephen Charles Bunnell, Tufts University School of Medicine, Keywords: adaptor molecules, ADAP, LAT, SLP-76, T-cell signaling, primary immune deficiency United States *Correspondence: Yael Dinur-Schejter [email protected] INTRODUCTION Specialty section: Engagement of the T cell receptor (TCR) triggers a signaling cascade responsible for T-cell This article was submitted to activation, maturation and differentiation. -
Phenotype Informatics
Freie Universit¨atBerlin Department of Mathematics and Computer Science Phenotype informatics: Network approaches towards understanding the diseasome Sebastian Kohler¨ Submitted on: 12th September 2012 Dissertation zur Erlangung des Grades eines Doktors der Naturwissenschaften (Dr. rer. nat.) am Fachbereich Mathematik und Informatik der Freien Universitat¨ Berlin ii 1. Gutachter Prof. Dr. Martin Vingron 2. Gutachter: Prof. Dr. Peter N. Robinson 3. Gutachter: Christopher J. Mungall, Ph.D. Tag der Disputation: 16.05.2013 Preface This thesis presents research work on novel computational approaches to investigate and characterise the association between genes and pheno- typic abnormalities. It demonstrates methods for organisation, integra- tion, and mining of phenotype data in the field of genetics, with special application to human genetics. Here I will describe the parts of this the- sis that have been published in peer-reviewed journals. Often in modern science different people from different institutions contribute to research projects. The same is true for this thesis, and thus I will itemise who was responsible for specific sub-projects. In chapter 2, a new method for associating genes to phenotypes by means of protein-protein-interaction networks is described. I present a strategy to organise disease data and show how this can be used to link diseases to the corresponding genes. I show that global network distance measure in interaction networks of proteins is well suited for investigat- ing genotype-phenotype associations. This work has been published in 2008 in the American Journal of Human Genetics. My contribution here was to plan the project, implement the software, and finally test and evaluate the method on human genetics data; the implementation part was done in close collaboration with Sebastian Bauer. -
Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared Amongst Δγ T, Innate Lymphoid, and Th Cells
Downloaded from http://www.jimmunol.org/ by guest on September 26, 2021 δγ is online at: average * The Journal of Immunology , 10 of which you can access for free at: 2016; 197:1460-1470; Prepublished online 6 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600643 http://www.jimmunol.org/content/197/4/1460 Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared amongst T, Innate Lymphoid, and Th Cells You Jeong Lee, Gabriel J. Starrett, Seungeun Thera Lee, Rendong Yang, Christine M. Henzler, Stephen C. Jameson and Kristin A. Hogquist J Immunol cites 41 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2016/07/06/jimmunol.160064 3.DCSupplemental This article http://www.jimmunol.org/content/197/4/1460.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2016 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 26, 2021. The Journal of Immunology Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared amongst gd T, Innate Lymphoid, and Th Cells You Jeong Lee,* Gabriel J. -
Genome-Wide Association Analysis of the Genetic Basis for Sheath Blight Resistance in Rice
Zhang et al. Rice (2019) 12:93 https://doi.org/10.1186/s12284-019-0351-5 ORIGINAL ARTICLE Open Access Genome-Wide Association Analysis of the Genetic Basis for Sheath Blight Resistance in Rice Fan Zhang, Dan Zeng, Cong-Shun Zhang, Jia-Ling Lu, Teng-Jun Chen, Jun-Ping Xie and Yong-Li Zhou* Abstract Background: Sheath blight (ShB), caused by Rhizoctonia solani Kühn, is one of the most destructive rice diseases. Developing ShB-resistant rice cultivars represents the most economical and environmentally sound strategy for managing ShB. Results: To characterize the genetic basis for ShB resistance in rice, we conducted association studies for traits related to ShB resistance, namely culm length (CL), lesion height (LH), and relative lesion height (RLH). Combined a single locus genome-wide scan and a multi-locus method using 2,977,750 single-nucleotide polymorphisms to analyse 563 rice accessions, we detected 134, 562, and 75 suggestive associations with CL, LH, and RLH, respectively. The adjacent signals associated with RLH were merged into 27 suggestively associated loci (SALs) based on the estimated linkage disequilibrium blocks. More than 44% of detected RLH-SALs harboured multiple QTLs/genes associated with ShB resistance, while the other RLH-SALs were putative novel ShB resistance loci. A total of 261 ShB resistance putative functional genes were screened from 23 RLH-SALs according to bioinformatics and haplotype analyses. Some of the annotated genes were previously reported to encode defence-related and pathogenesis-related proteins, suggesting that quantitative resistance to ShB in rice is mediated by SA- and JA- dependent signalling pathways. -
The Role of the Src Homology-2 Domain Containing Protein B (SHB) in B Cells
M WELSH and others Role of SHB in b cells 56:1 R21–R31 Review The role of the Src Homology-2 domain containing protein B (SHB) in b cells Correspondence † Michael Welsh, Maria Jamalpour, Guangxiang Zang and Bjo¨rn Åkerblom should be addressed to M Welsh Department of Medical Cell Biology, Uppsala University, PO Box 571, Husargatan 3, SE-75123 Uppsala, Sweden Email †G Zang is now at Department of Medical Biosciences, Umea˚ University, Umea˚ , Sweden [email protected] Abstract This review will describe the SH2-domain signaling protein Src Homology-2 domain Key Words containing protein B (SHB) and its role in various physiological processes relating in " signal transduction particular to glucose homeostasis and b cell function. SHB operates downstream of several " insulin secretion tyrosine kinase receptors and assembles signaling complexes in response to receptor " vascular activation by interacting with other signaling proteins via its other domains (proline-rich, " islet cells phosphotyrosine-binding and tyrosine-phosphorylation sites). The subsequent responses " immune system are context-dependent. Absence of Shb in mice has been found to exert effects on hematopoiesis, angiogenesis and glucose metabolism. Specifically, first-phase insulin secretion in response to glucose was impaired and this effect was related to altered characteristics of focal adhesion kinase activation modulating signaling through Akt, ERK, b catenin and cAMP. It is believed that SHB plays a role in integrating adaptive responses to various stimuli by simultaneously modulating cellular responses in different cell-types, thus Journal of Molecular Journal of Molecular Endocrinology playing a role in maintaining physiological homeostasis. Endocrinology (2016) 56, R21–R31 Introduction The limited replicative capacity of human pancreatic (bTC1 cells) after serum-stimulation, the Src Homology-2 b cells contributes significantly to the development of domain containing adapter protein B (SHB) was identified diabetes mellitus and thus comprises a major hurdle for (Welsh et al. -
Gene Expression Profiling in Fibromyalgia Indicates An
Journal of Clinical Medicine Article Gene Expression Profiling in Fibromyalgia Indicates an Autoimmune Origin of the Disease and Opens New Avenues for Targeted Therapy 1 1 2, 1, , Marzia Dolcino , Elisa Tinazzi , Antonio Puccetti y and Claudio Lunardi * y 1 Department of Medicine, University of Verona, Piazzale L.A. Scuro 10, 37134 Verona, Italy; [email protected] (M.D.); [email protected] (E.T.) 2 Department of Experimental Medicine, Section of Histology, University of Genova, Via G.B. Marsano 10, 16132 Genova, Italy; [email protected] * Correspondence: [email protected] These authors contributed equally to this work. y Received: 29 April 2020; Accepted: 7 June 2020; Published: 10 June 2020 Abstract: Fibromyalgia is a chronic disorder characterized by widespread pain and by several non-pain symptoms. Autoimmunity, small fiber neuropathy and neuroinflammation have been suggested to be involved in the pathogenesis of the disease. We have investigated the gene expression profile in peripheral blood mononuclear cells obtained from ten patients and ten healthy subjects. Of the 545,500 transcripts analyzed, 1673 resulted modulated in fibromyalgic patients. The majority of these genes are involved in biological processes and pathways linked to the clinical manifestations of the disease. Moreover, genes involved in immunological pathways connected to interleukin-17 and to Type I interferon signatures were also modulated, suggesting that autoimmunity plays a role in the disease. We then aimed at identifying differentially expressed Long non-coding RNAs (LncRNAs) functionally connected to modulated genes both directly and via microRNA targeting. Only two LncRNAs of the 298 found modulated in patients, were able to target the most highly connected genes in the fibromyalgia interactome, suggesting their involvement in crucial gene regulation. -
Haplotyping Small Hive Beetle (Aethina Tumida) Reveals NA1 and NA2 Distribution in Rhode Island Apis Mellifera Hives Katelyn St
Rhode Island College Digital Commons @ RIC Honors Projects Overview Honors Projects 2017 Haplotyping Small Hive Beetle (Aethina Tumida) Reveals NA1 and NA2 Distribution in Rhode Island Apis Mellifera Hives Katelyn St. George [email protected] Follow this and additional works at: https://digitalcommons.ric.edu/honors_projects Part of the Biology Commons Recommended Citation St. George, Katelyn, "Haplotyping Small Hive Beetle (Aethina Tumida) Reveals NA1 and NA2 Distribution in Rhode Island Apis Mellifera Hives" (2017). Honors Projects Overview. 135. https://digitalcommons.ric.edu/honors_projects/135 This Honors is brought to you for free and open access by the Honors Projects at Digital Commons @ RIC. It has been accepted for inclusion in Honors Projects Overview by an authorized administrator of Digital Commons @ RIC. For more information, please contact [email protected]. Haplotyping small hive beetle 3 HAPLOTYPING SMALL HIVE BEETLE (AETHINA TUMIDA) REVEALS NA1 AND NA2 DISTRIBUTION IN RHODE ISLAND APIS MELLIFERA HIVES By Katelyn St. George An Undergraduate Thesis Submitted in Partial Fulfillment of the Requirements for the Awarding of Departmental Honors in the Department of Biology The Faculty of Arts and Sciences Rhode Island College 2017 Haplotyping small hive beetle 4 ABSTRACT The small hive beetle (Aethina tumida) is a parasite of honeybee hives (Apis mellifera) and native to South Africa. Invasive in North America since 1996, the species has spread to hives throughout the continent, including many in Rhode Island and nearby states. To better understand migration patterns for this invasive species, we haplotyped small hive beetles (SHB) based on mitochondrial Cytochrome Oxidase Part 1 (COI) gene sequences. -
BMC Immunology
BMC Immunology This Provisional PDF corresponds to the article as it appeared upon acceptance. Fully formatted PDF and full text (HTML) versions will be made available soon. Shb deficient mice display an augmented TH2 response in peripheral CD4+ T cells BMC Immunology 2011, 12:3 doi:10.1186/1471-2172-12-3 Karin Gustafsson ([email protected]) Gabriela Calounova ([email protected]) Fredrik Hjelm ([email protected]) Vitezslav Kriz ([email protected]) Birgitta Heyman ([email protected]) Kjell-Olov Gronvik ([email protected]) Gustavo Mostoslavsky ([email protected]) Michael Welsh ([email protected]) ISSN 1471-2172 Article type Research article Submission date 10 December 2010 Acceptance date 11 January 2011 Publication date 11 January 2011 Article URL http://www.biomedcentral.com/1471-2172/12/3 Like all articles in BMC journals, this peer-reviewed article was published immediately upon acceptance. It can be downloaded, printed and distributed freely for any purposes (see copyright notice below). Articles in BMC journals are listed in PubMed and archived at PubMed Central. For information about publishing your research in BMC journals or any BioMed Central journal, go to http://www.biomedcentral.com/info/authors/ © 2011 Gustafsson et al. ; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided