Ε Phosphorylation of a Common Site in CD3 Domain Binding Via
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UNDERSTANDING THE GENETICS UNDERLYING MASTITIS USING A MULTI-PRONGED APPROACH A Dissertation Presented to the Faculty of the Graduate School of Cornell University In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy by Asha Marie Miles December 2019 © 2019 Asha Marie Miles UNDERSTANDING THE GENETICS UNDERLYING MASTITIS USING A MULTI-PRONGED APPROACH Asha Marie Miles, Ph. D. Cornell University 2019 This dissertation addresses deficiencies in the existing genetic characterization of mastitis due to granddaughter study designs and selection strategies based primarily on lactation average somatic cell score (SCS). Composite milk samples were collected across 6 sampling periods representing key lactation stages: 0-1 day in milk (DIM), 3- 5 DIM, 10-14 DIM, 50-60 DIM, 90-110 DIM, and 210-230 DIM. Cows were scored for front and rear teat length, width, end shape, and placement, fore udder attachment, udder cleft, udder depth, rear udder height, and rear udder width. Independent multivariable logistic regression models were used to generate odds ratios for elevated SCC (≥ 200,000 cells/ml) and farm-diagnosed clinical mastitis. Within our study cohort, loose fore udder attachment, flat teat ends, low rear udder height, and wide rear teats were associated with increased odds of mastitis. Principal component analysis was performed on these traits to create a single new phenotype describing mastitis susceptibility based on these high-risk phenotypes. Cows (N = 471) were genotyped on the Illumina BovineHD 777K SNP chip and considering all 14 traits of interest, a total of 56 genome-wide associations (GWA) were performed and 28 significantly associated quantitative trait loci (QTL) were identified. -
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. -
Eps8l2 (F-8): Sc-514673
SAN TA C RUZ BI OTEC HNOL OG Y, INC . Eps8L2 (F-8): sc-514673 BACKGROUND APPLICATIONS Eps8L2 (epidermal growth factor receptor kinase substrate 8-like protein 2), Eps8L2 (F-8) is recommended for detection of Eps8L2 of human origin by also known as EPS8R2 or PP13181, is a 715 amino acid protein that localizes Western Blotting (starting dilution 1:100, dilution range 1:100-1:1000), to the cytoplasm and belongs to the Eps8 (epidermal growth factor receptor immunoprecipitation [1-2 µg per 100-500 µg of total protein (1 ml of cell pathway substrate 8) family. Expressed in placenta and fibroblasts, Eps8L2 lysate)], immunofluorescence (starting dilution 1:50, dilution range 1:50- functions to stimulate the guanine exchange activity of Sos 1 (son of seven - 1:500) and solid phase ELISA (starting dilution 1:30, dilution range 1:30- less homolog 1), a protein that promotes the exchange of Ras-bound GDP 1:3000). for GTP. Additionally, Eps8L2 is thought to associate with Actin and, via this Suitable for use as control antibody for Eps8L2 siRNA (h): sc-96954, Eps8L2 association, may play a role in membrane ruffling and remodeling of the shRNA Plasmid (h): sc-96954-SH and Eps8L2 shRNA (h) Lentiviral Particles: Actin cytoskeleton. Through its ability to regulate protein activation and cyto- sc-96954-V. skeleton dynamics, Eps8L2 may participate in cell growth and differentiation events within the cell. Eps8L2, a protein that is expressed as two isoforms Molecular Weight of Eps8L2: 81 kDa. due to alternative splicing, contains one PID (phosphotyrosine interaction) Positive Controls: A-431 whole cell lysate: sc-2201, HeLa whole cell lysate: domain and one SH3 domain. -
Human Induced Pluripotent Stem Cell–Derived Podocytes Mature Into Vascularized Glomeruli Upon Experimental Transplantation
BASIC RESEARCH www.jasn.org Human Induced Pluripotent Stem Cell–Derived Podocytes Mature into Vascularized Glomeruli upon Experimental Transplantation † Sazia Sharmin,* Atsuhiro Taguchi,* Yusuke Kaku,* Yasuhiro Yoshimura,* Tomoko Ohmori,* ‡ † ‡ Tetsushi Sakuma, Masashi Mukoyama, Takashi Yamamoto, Hidetake Kurihara,§ and | Ryuichi Nishinakamura* *Department of Kidney Development, Institute of Molecular Embryology and Genetics, and †Department of Nephrology, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan; ‡Department of Mathematical and Life Sciences, Graduate School of Science, Hiroshima University, Hiroshima, Japan; §Division of Anatomy, Juntendo University School of Medicine, Tokyo, Japan; and |Japan Science and Technology Agency, CREST, Kumamoto, Japan ABSTRACT Glomerular podocytes express proteins, such as nephrin, that constitute the slit diaphragm, thereby contributing to the filtration process in the kidney. Glomerular development has been analyzed mainly in mice, whereas analysis of human kidney development has been minimal because of limited access to embryonic kidneys. We previously reported the induction of three-dimensional primordial glomeruli from human induced pluripotent stem (iPS) cells. Here, using transcription activator–like effector nuclease-mediated homologous recombination, we generated human iPS cell lines that express green fluorescent protein (GFP) in the NPHS1 locus, which encodes nephrin, and we show that GFP expression facilitated accurate visualization of nephrin-positive podocyte formation in -
EPS8L1 293T Cell Transient Overexpression Lysate(Denatured)
Produktinformation Diagnostik & molekulare Diagnostik Laborgeräte & Service Zellkultur & Verbrauchsmaterial Forschungsprodukte & Biochemikalien Weitere Information auf den folgenden Seiten! See the following pages for more information! Lieferung & Zahlungsart Lieferung: frei Haus Bestellung auf Rechnung SZABO-SCANDIC Lieferung: € 10,- HandelsgmbH & Co KG Erstbestellung Vorauskassa Quellenstraße 110, A-1100 Wien T. +43(0)1 489 3961-0 Zuschläge F. +43(0)1 489 3961-7 [email protected] • Mindermengenzuschlag www.szabo-scandic.com • Trockeneiszuschlag • Gefahrgutzuschlag linkedin.com/company/szaboscandic • Expressversand facebook.com/szaboscandic EPS8L1 293T Cell Transient Overexpression Lysate(Denatured) Catalog # : H00054869-T01 規格 : [ 100 uL ] List All Specification Application Image Transfected 293T Western Blot Cell Line: Plasmid: pCMV-EPS8L1 full-length Host: Human Theoretical MW 60.72 (kDa): Quality Control Transient overexpression cell lysate was tested with Anti-EPS8L1 Testing: antibody (H00054869-B01) by Western Blots. SDS-PAGE Gel EPS8L1 transfected lysate. Western Blot Lane 1: EPS8L1 transfected lysate ( 60.72 KDa) Lane 2: Non-transfected lysate. Storage Buffer: 1X Sample Buffer (50 mM Tris-HCl, 2% SDS, 10% glycerol, 300 mM 2- mercaptoethanol, 0.01% Bromophenol blue) Storage Store at -80°C. Aliquot to avoid repeated freezing and thawing. Instruction: MSDS: Download Applications Page 1 of 2 2016/5/23 Western Blot Gene Information Entrez GeneID: 54869 GeneBank NM_139204.1 Accession#: Protein NP_631943.1 Accession#: Gene Name: EPS8L1 Gene Alias: DRC3,EPS8R1,FLJ20258,MGC23164,MGC4642,PP10566 Gene EPS8-like 1 Description: Gene Ontology: Hyperlink Gene Summary: This gene encodes a protein that is related to epidermal growth factor receptor pathway substrate 8 (EPS8), a substrate for the epidermal growth factor receptor. The function of this protein is unknown. -
The Human Gene Connectome As a Map of Short Cuts for Morbid Allele Discovery
The human gene connectome as a map of short cuts for morbid allele discovery Yuval Itana,1, Shen-Ying Zhanga,b, Guillaume Vogta,b, Avinash Abhyankara, Melina Hermana, Patrick Nitschkec, Dror Friedd, Lluis Quintana-Murcie, Laurent Abela,b, and Jean-Laurent Casanovaa,b,f aSt. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY 10065; bLaboratory of Human Genetics of Infectious Diseases, Necker Branch, Paris Descartes University, Institut National de la Santé et de la Recherche Médicale U980, Necker Medical School, 75015 Paris, France; cPlateforme Bioinformatique, Université Paris Descartes, 75116 Paris, France; dDepartment of Computer Science, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel; eUnit of Human Evolutionary Genetics, Centre National de la Recherche Scientifique, Unité de Recherche Associée 3012, Institut Pasteur, F-75015 Paris, France; and fPediatric Immunology-Hematology Unit, Necker Hospital for Sick Children, 75015 Paris, France Edited* by Bruce Beutler, University of Texas Southwestern Medical Center, Dallas, TX, and approved February 15, 2013 (received for review October 19, 2012) High-throughput genomic data reveal thousands of gene variants to detect a single mutated gene, with the other polymorphic genes per patient, and it is often difficult to determine which of these being of less interest. This goes some way to explaining why, variants underlies disease in a given individual. However, at the despite the abundance of NGS data, the discovery of disease- population level, there may be some degree of phenotypic homo- causing alleles from such data remains somewhat limited. geneity, with alterations of specific physiological pathways under- We developed the human gene connectome (HGC) to over- come this problem. -
Dissertation Thesis Phd Dysregulated Trophoblast-Specific Gene
Dysregulated trophoblast-specific gene expression mediated by retroviral regulatory sequences contributes to preeclampsia (PE) Dissertation zur Erlangung des akademischen Grades Doctor of Philosophy (PhD) im Fach Biologie eingereicht an der Lebenswissenschaftlichen Fakultät der Humboldt-Universität zu Berlin von Master of Science Rabia Anwar Präsident der Humboldt-Universität zu Berlin Prof. Dr.-Ing. Dr. Sabine Kunst Dekan der der Lebenswissenschaftlichen Fakultät Prof. Dr. Bernhard Grimm Gutachter: 1. Prof. Dr. Ana Pombo 2. Prof. Dr. Kai Schmidt-Ott 3. Dr. Zsuzsanna Izsvák Tag der mündlichen Prüfung: 30th September 2020 i Content Content Summary ................................................................................................................................... 1 Zusammenfassung .................................................................................................................... 3 1. Background and Introduction......................................................................................... 5 1.1. Preeclampsia (PE) ............................................................................................................. 5 1.2. Healthy pregnancy ............................................................................................................ 6 1.2.1. Placenta development in a healthy pregnancy ................................................................. 6 1.2.2. Placenta tissue composition ............................................................................................ -
Essential Role for Abi1 in Embryonic Survival and WAVE2 Complex Integrity
Essential role for Abi1 in embryonic survival and WAVE2 complex integrity Patrycja M. Dubieleckaa,1, Kathrin I. Ladweinb,1, Xiaoling Xionga, Isabelle Migeottec, Anna Chorzalskaa, Kathryn V. Andersonc, Janet A. Sawickid, Klemens Rottnerb,e, Theresia E. Stradalb,f, and Leszek Kotulaa,2 aLaboratory of Cell Signaling, New York Blood Center, New York, NY 10065; bHelmholtz Centre for Infection Research, D-38124 Braunschweig, Germany; cDevelopmental Biology Program, Sloan-Kettering Institute, New York, NY 10065; dLankenau Institute for Medical Research, Wynnewood, PA 19096; eInstitute of Genetics, University of Bonn, 53117 Bonn, Germany; and fInstitute for Molecular Cell Biology, University of Münster, D-48149 Münster, Germany Edited* by Hilary Koprowski, Thomas Jefferson University, Philadelphia, PA, and approved March 15, 2011 (received for review November 11, 2010) Abl interactor 1 (Abi1) plays a critical function in actin cytoskeleton activation to actin polymerization that drives lamellipodia pro- dynamics through participation in the WAVE2 complex. To gain trusion at the plasma membrane (13, 14). WAVE1 and WAVE3 a better understanding of the specific role of Abi1, we generated were proposed to have roles analogous to WAVE2 in the complex (8). Although the function of WAVE3 is less defined, the critical a conditional Abi1-KO mouse model and MEFs lacking Abi1 expres- fl sion. Abi1-KO cells displayed defective regulation of the actin cyto- role of the other two WAVEs in dorsal ruf e formation was demonstrated (15, 16). Mechanistically, it is proposed that native skeleton, and this dysregulation was ascribed to altered activity of WAVE2 complex is inactive (17–19) but is activated at the the WAVE2 complex. -
Characterization of in Vivo Resistance to Osimertinib and JNJ-61186372
Published OnlineFirst August 22, 2017; DOI: 10.1158/1535-7163.MCT-17-0413 Cancer Biology and Translational Studies Molecular Cancer Therapeutics Characterization of In Vivo Resistance to Osimertinib and JNJ-61186372, an EGFR/Met Bispecific Antibody, Reveals Unique and Consensus Mechanisms of Resistance Kristina B. Emdal1, Antje Dittmann1, Raven J. Reddy1, Rebecca S. Lescarbeau1, Sheri L. Moores2, Sylvie Laquerre2, and Forest M. White1 Abstract Approximately 10% of non–small cell lung cancer (NSCLC) targeting EGFR/Met antibody, JNJ-61186372. Tumor-specific patients in the United States and 40% of NSCLC patients in Asia increases in tyrosine-phosphorylated peptides from EGFR family have activating epidermal growth factor receptor (EGFR) muta- members, Shc1 and Gab1 or Src family kinase (SFK) substrates tions and are eligible to receive targeted anti-EGFR therapy. were observed, underscoring a differential ability of tumors to Despite an extension of life expectancy associated with this uniquely escape EGFR inhibition. Although most resistant tumors treatment, resistance to EGFR tyrosine kinase inhibitors and within each treatment group displayed a marked inhibition of anti-EGFR antibodies is almost inevitable. To identify additional EGFR as well as SFK signaling, the combination of EGFR inhibi- signaling routes that can be cotargeted to overcome resistance, we tion (osimertinib) and SFK inhibition (saracatinib or dasatinib) quantified tumor-specific molecular changes that govern resistant led to further decrease in cell growth in vitro. This result suggests cancer cell growth and survival. Mass spectrometry–based quan- that residual SFK signaling mediates therapeutic resistance and titative proteomics was used to profile in vivo signaling changes in that elimination of this signal through combination therapy may 41 therapy-resistant tumors from four xenograft NSCLC models. -
Divergent Dysregulation of Gene Expression in Murine Models Of
Kong et al. Molecular Autism 2014, 5:16 http://www.molecularautism.com/content/5/1/16 RESEARCH Open Access Divergent dysregulation of gene expression in murine models of fragile X syndrome and tuberous sclerosis Sek Won Kong1,5†, Mustafa Sahin2†, Christin D Collins3, Mary H Wertz2, Malcolm G Campbell5, Jarrett D Leech2, Dilja Krueger4, Mark F Bear4, Louis M Kunkel3 and Isaac S Kohane1,5* Abstract Background: Fragile X syndrome and tuberous sclerosis are genetic syndromes that both have a high rate of comorbidity with autism spectrum disorder (ASD). Several lines of evidence suggest that these two monogenic disorders may converge at a molecular level through the dysfunction of activity-dependent synaptic plasticity. Methods: To explore the characteristics of transcriptomic changes in these monogenic disorders, we profiled genome-wide gene expression levels in cerebellum and blood from murine models of fragile X syndrome and tuberous sclerosis. Results: Differentially expressed genes and enriched pathways were distinct for the two murine models examined, with the exception of immune response-related pathways. In the cerebellum of the Fmr1 knockout (Fmr1-KO) model, the neuroactive ligand receptor interaction pathway and gene sets associated with synaptic plasticity such as long-term potentiation, gap junction, and axon guidance were the most significantly perturbed pathways. The phosphatidylinositol signaling pathway was significantly dysregulated in both cerebellum and blood of Fmr1-KO mice. In Tsc2 heterozygous (+/−) mice, immune system-related pathways, genes encoding ribosomal proteins, and glycolipid metabolism pathways were significantly changed in both tissues. Conclusions: Our data suggest that distinct molecular pathways may be involved in ASD with known but different genetic causes and that blood gene expression profiles of Fmr1-KO and Tsc2+/− mice mirror some, but not all, of the perturbed molecular pathways in the brain. -
Understanding SOS (Son of Sevenless) Stéphane Pierre, Anne-Sophie Bats, Xavier Coumoul
Understanding SOS (Son of Sevenless) Stéphane Pierre, Anne-Sophie Bats, Xavier Coumoul To cite this version: Stéphane Pierre, Anne-Sophie Bats, Xavier Coumoul. Understanding SOS (Son of Sevenless). Bio- chemical Pharmacology, Elsevier, 2011, 82 (9), pp.1049-1056. 10.1016/j.bcp.2011.07.072. hal- 02190799 HAL Id: hal-02190799 https://hal.archives-ouvertes.fr/hal-02190799 Submitted on 22 Jul 2019 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. *Manuscript Click here to view linked References Understanding SOS (Son of Sevenless). 1 1,2,‡ 1,2,3,‡ 1,2, † 2 Stéphane PIERRE , Anne-Sophie BATS , Xavier COUMOUL 3 4 5 1 6 INSERM UMR-S 747, Toxicologie Pharmacologie et Signalisation Cellulaire, 45 rue des 7 Saints Pères, 75006 Paris France 8 9 10 2 Université Paris Descartes, Centre universitaire des Saints-Pères, 45 rue des Saints Pères, 11 12 75006 Paris France 13 14 3 15 AP-HP, Hôpital Européen Georges Pompidou, Service de Chirurgie Gynécologique 16 17 Cancérologique, 75015 Paris France 18 19 ‡ These authors contributed equally to this work. 20 21 † 22 Address correspondence to: Xavier Coumoul, INSERM UMR-S 747, 45 rue des Saints-Pères 23 24 75006 Paris France; Phone: +33 1 42 86 33 59; Fax: +33 1 42 86 38 68; E-mail: 25 26 [email protected] 27 28 29 30 31 Key words: Son of Sevenless. -
Identification of Core Genes Involved in the Progression of Cervical
International Journal of Molecular Sciences Article Identification of Core Genes Involved in the Progression of Cervical Cancer Using an Integrative mRNA Analysis Marina Dudea-Simon 1, Dan Mihu 1, Alexandru Irimie 2,3, Roxana Cojocneanu 4, Schuyler S. Korban 5, Radu Oprean 6, Cornelia Braicu 4,* and Ioana Berindan-Neagoe 4,7 1 2nd Obstetrics and Gynecology Department, “Iuliu Hatieganu” University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania; [email protected] (M.D.-S.); [email protected] (D.M.) 2 Department of Surgery, “Prof. Dr. Ion Chiricuta” Oncology Institute, 400015 Cluj-Napoca, Romania; [email protected] 3 Department of Surgical Oncology and Gynecological Oncology, Iuliu Hatieganu University of Medicine and Pharmacy, 400012 Cluj-Napoca, Romania 4 Research Center for Functional Genomics, Biomedicine and Translational Medicine, Iuliu Hatieganu University of Medicine and Pharmacy, 23 Marinescu Street, 400337 Cluj-Napoca, Romania; [email protected] (R.C.); [email protected] (I.B.-N.) 5 Department of Natural and Environmental Sciences, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA; [email protected] 6 Analytical Chemistry Department, Iuliu Hatieganu University of Medicine and Pharmacy, 4, Louis Pasteur Street, 400349 Cluj-Napoca, Romania; [email protected] 7 Department of Functional Genomics and Experimental Pathology, “Prof. Dr. Ion Chiricu¸tă” Oncology Institute, 34-36 Republicii Street, 400015 Cluj-Napoca, Romania * Correspondence: [email protected] Received: 5 September 2020; Accepted: 1 October 2020; Published: 3 October 2020 Abstract: In spite of being a preventable disease, cervical cancer (CC) remains at high incidence, and it has a significant mortality rate. Although hijacking of the host cellular pathway is fundamental for developing a better understanding of the human papillomavirus (HPV) pathogenesis, a major obstacle is identifying the central molecular targets involved in HPV-driven CC.