Mouse Hspb7 Knockout Project (CRISPR/Cas9)
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Cvhsp (HSPB7) Mouse Monoclonal Antibody [Clone ID: OTI1D11] Product Data
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for TA501310 cvHSP (HSPB7) Mouse Monoclonal Antibody [Clone ID: OTI1D11] Product data: Product Type: Primary Antibodies Clone Name: OTI1D11 Applications: FC, IF, WB Recommended Dilution: WB 1:2000, IF 1:100, FLOW 1:100 Reactivity: Human, Mouse, Rat Host: Mouse Isotype: IgG1 Clonality: Monoclonal Immunogen: Full length human recombinant protein of human HSPB7(NP_055239) produced in HEK293T cell. Formulation: PBS (PH 7.3) containing 1% BSA, 50% glycerol and 0.02% sodium azide. Concentration: 0.63 mg/ml Purification: Purified from mouse ascites fluids or tissue culture supernatant by affinity chromatography (protein A/G) Conjugation: Unconjugated Storage: Store at -20°C as received. Stability: Stable for 12 months from date of receipt. Predicted Protein Size: 18.4 kDa Gene Name: heat shock protein family B (small) member 7 Database Link: NP_055239 Entrez Gene 29818 MouseEntrez Gene 50565 RatEntrez Gene 27129 Human Q9UBY9 Synonyms: cvHSP This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 2 cvHSP (HSPB7) Mouse Monoclonal Antibody [Clone ID: OTI1D11] – TA501310 Product images: HEK293T cells were transfected with the pCMV6- ENTRY control (Cat# [PS100001], Left lane) or pCMV6-ENTRY HSPB7 (Cat# [RC202861], Right lane) cDNA for 48 hrs and lysed. Equivalent amounts of cell lysates (5 ug per lane) were separated by SDS-PAGE and immunoblotted with anti-HSPB7(Cat# TA501310). -
CSE642 Final Version
Eindhoven University of Technology MASTER Dimensionality reduction of gene expression data Arts, S. Award date: 2018 Link to publication Disclaimer This document contains a student thesis (bachelor's or master's), as authored by a student at Eindhoven University of Technology. Student theses are made available in the TU/e repository upon obtaining the required degree. The grade received is not published on the document as presented in the repository. The required complexity or quality of research of student theses may vary by program, and the required minimum study period may vary in duration. General rights Copyright and moral rights for the publications made accessible in the public portal are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. • Users may download and print one copy of any publication from the public portal for the purpose of private study or research. • You may not further distribute the material or use it for any profit-making activity or commercial gain Eindhoven University of Technology MASTER THESIS Dimensionality Reduction of Gene Expression Data Author: S. (Sako) Arts Daily Supervisor: dr. V. (Vlado) Menkovski Graduation Committee: dr. V. (Vlado) Menkovski dr. D.C. (Decebal) Mocanu dr. N. (Nikolay) Yakovets May 16, 2018 v1.0 Abstract The focus of this thesis is dimensionality reduction of gene expression data. I propose and test a framework that deploys linear prediction algorithms resulting in a reduced set of selected genes relevant to a specified case. Abstract In cancer research there is a large need to automate parts of the process of diagnosis, this is mainly to reduce cost, make it faster and more accurate. -
Pentosan Polysulfate Binds to STRO
Wu et al. Stem Cell Research & Therapy (2017) 8:278 DOI 10.1186/s13287-017-0723-y RESEARCH Open Access Pentosan polysulfate binds to STRO-1+ mesenchymal progenitor cells, is internalized, and modifies gene expression: a novel approach of pre-programing stem cells for therapeutic application requiring their chondrogenesis Jiehua Wu1,7, Susan Shimmon1,8, Sharon Paton2, Christopher Daly3,4,5, Tony Goldschlager3,4,5, Stan Gronthos6, Andrew C. W. Zannettino2 and Peter Ghosh1,5* Abstract Background: The pharmaceutical agent pentosan polysulfate (PPS) is known to induce proliferation and chondrogenesis of mesenchymal progenitor cells (MPCs) in vitro and in vivo. However, the mechanism(s) of action of PPS in mediating these effects remains unresolved. In the present report we address this issue by investigating the binding and uptake of PPS by MPCs and monitoring gene expression and proteoglycan biosynthesis before and after the cells had been exposed to limited concentrations of PPS and then re-established in culture in the absence of the drug (MPC priming). Methods: Immuno-selected STRO-1+ mesenchymal progenitor stem cells (MPCs) were prepared from human bone marrow aspirates and established in culture. The kinetics of uptake, shedding, and internalization of PPS by MPCs was determined by monitoring the concentration-dependent loss of PPS media concentrations using an enzyme-linked immunosorbent assay (ELISA) and the uptake of fluorescein isothiocyanate (FITC)-labelled PPS by MPCs. The proliferation of MPCs, following pre-incubation and removal of PPS (priming), was assessed using the Wst-8 assay 35 method, and proteoglycan synthesis was determined by the incorporation of SO4 into their sulphated glycosaminoglycans. -
Cardiac Signaling Genes Exhibit Unexpected Sequence Diversity in Sporadic Cardiomyopathy, Revealing HSPB7 Polymorphisms Associated with Disease Scot J
Research article Cardiac signaling genes exhibit unexpected sequence diversity in sporadic cardiomyopathy, revealing HSPB7 polymorphisms associated with disease Scot J. Matkovich,1 Derek J. Van Booven,1 Anna Hindes,1 Min Young Kang,1 Todd E. Druley,2,3 Francesco L.M. Vallania,3 Robi D. Mitra,3 Muredach P. Reilly,4 Thomas P. Cappola,4 and Gerald W. Dorn II1 1Center for Pharmacogenomics, Department of Medicine, 2Division of Pediatric Hematology and Oncology, Department of Pediatrics, and 3Center for Genome Sciences, Department of Genetics, Washington University School of Medicine, St. Louis, Missouri, USA. 4Penn Cardiovascular Institute, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA. Sporadic heart failure is thought to have a genetic component, but the contributing genetic events are poorly defined. Here, we used ultra-high-throughput resequencing of pooled DNAs to identify SNPs in 4 biologically relevant cardiac signaling genes, and then examined the association between allelic variants and incidence of sporadic heart failure in 2 large Caucasian populations. Resequencing of DNA pools, each containing DNA from approximately 100 individuals, was rapid, accurate, and highly sensitive for identifying common and rare SNPs; it also had striking advantages in time and cost efficiencies over individual resequencing using conventional Sanger methods. In 2,606 individuals examined, we identified a total of 129 separate SNPs in the 4 cardiac signaling genes, including 23 nonsynonymous SNPs that we believe to be novel. Comparison of allele frequencies between 625 Caucasian nonaffected controls and 1,117 Caucasian individuals with systolic heart failure revealed 12 SNPs in the cardiovascular heat shock protein gene HSPB7 with greater proportional representation in the systolic heart failure group; all 12 SNPs were confirmed in an independent replication study. -
Downregulation of the Tumor Suppressor HSPB7, Involved in the P53 Pathway, in Renal Cell Carcinoma by Hypermethylation
1490 INTERNATIONAL JOURNAL OF ONCOLOGY 44: 1490-1498, 2014 Downregulation of the tumor suppressor HSPB7, involved in the p53 pathway, in renal cell carcinoma by hypermethylation JIAYING LIN1,2, ZHENZHONG DENG1, CHIZU TANIKAWA1, TARO SHUIN3, TSUNEHARU MIKI4, KOICHI MATSUDA1 and YUSUKE NAKAMURA1,2 1Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, University of Tokyo, Tokyo 108-8639, Japan; 2Section of Hematology/Oncology, Department of Medicine, University of Chicago, Chicago, IL 60637, USA; 3Department of Urology, School of Medicine, Kochi University, Kochi 783-8505; 4Department of Urology, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan Received December 10, 2013; Accepted January 27, 2014 DOI: 10.3892/ijo.2014.2314 Abstract. In order to identify genes involved in renal carci- obesity, acquired cystic kidney disease and inherited suscepti- nogenesis, we analyzed the expression profile of renal cell bility (von Hippel-Lindau disease) (3,7,8) have been indicated, carcinomas (RCCs) using microarrays consisting of 27,648 but the etiological and pathological mechanisms of this disease cDNA or ESTs, and found a small heat shock protein, HSPB7, are still far from fully understood. to be significantly and commonly downregulated in RCC. Although local renal tumors can be surgically removed Subsequent quantitative PCR (qPCR) and immunohistochem- (9-11), distant metastasis is often observed even if the primary ical (IHC) analyses confirmed the downregulation of HSPB7 tumor is relatively small (12,13). Patients with metastatic in RCC tissues and cancer cell lines in both transcriptional RCC generally result in extremely poor outcomes with and protein levels. Bisulfite sequencing of a genomic region of overall median survival of around 13 months and the 5 year HSPB7 detected DNA hypermethylation of some segments of survival rate of <10% (13). -
Breast Cancer Type Classification Using Machine Learning
Journal of Personalized Medicine Article Breast Cancer Type Classification Using Machine Learning Jiande Wu and Chindo Hicks * Department of Genetics, School of Medicine, Louisiana State University Health Sciences Center, 533 Bolivar, New Orleans, LA 70112, USA; [email protected] * Correspondence: [email protected]; Tel.: +1-504-568-2657 Abstract: Background: Breast cancer is a heterogeneous disease defined by molecular types and subtypes. Advances in genomic research have enabled use of precision medicine in clinical man- agement of breast cancer. A critical unmet medical need is distinguishing triple negative breast cancer, the most aggressive and lethal form of breast cancer, from non-triple negative breast cancer. Here we propose use of a machine learning (ML) approach for classification of triple negative breast cancer and non-triple negative breast cancer patients using gene expression data. Methods: We performed analysis of RNA-Sequence data from 110 triple negative and 992 non-triple negative breast cancer tumor samples from The Cancer Genome Atlas to select the features (genes) used in the development and validation of the classification models. We evaluated four different classification models including Support Vector Machines, K-nearest neighbor, Naïve Bayes and Decision tree using features selected at different threshold levels to train the models for classifying the two types of breast cancer. For performance evaluation and validation, the proposed methods were applied to independent gene expression datasets. Results: Among the four ML algorithms evaluated, the Support Vector Machine algorithm was able to classify breast cancer more accurately into triple negative and non-triple negative breast cancer and had less misclassification errors than the other three algorithms evaluated. -
A Screen to Uncover Mediators of Resistance to Liver X Receptor Agonistic Cancer Therapy
Aus der Medizinische Klinik mit Schwerpunkt Hämatologie, Onkologie und Tumorimmunologie der Medizinischen Fakultät Charité – Universitätsmedizin Berlin DISSERTATION A screen to uncover mediators of resistance to liver X receptor agonistic cancer therapy - Ermittlung potenzieller Vermittler von Resistenz gegen die Liver-X Rezeptor agonistische Krebstherapie zur Erlangung des akademischen Grades Doctor medicinae (Dr. med.) vorgelegt der Medizinischen Fakultät Charité – Universitätsmedizin Berlin von Kimia Nathalie Tafreshian aus Stuttgart, Deutschland Datum der Promotion: 05.03.2021 I Table of contents TABLE OF FIGURES ....................................................................................................................... IV LIST OF TABLES ............................................................................................................................... V LIST OF ABBREVIATIONS ............................................................................................................ VI ABSTRACT ..................................................................................................................................... VIII 1. INTRODUCTION ........................................................................................................................ 1 Colorectal carcinoma ........................................................................................................................ 1 Drug resistance in cancer ................................................................................................................. -
A Genome-Wide Association Study of Idiopathic Dilated Cardiomyopathy in African Americans
Journal of Personalized Medicine Article A Genome-Wide Association Study of Idiopathic Dilated Cardiomyopathy in African Americans Huichun Xu 1,* ID , Gerald W. Dorn II 2, Amol Shetty 3, Ankita Parihar 1, Tushar Dave 1, Shawn W. Robinson 4, Stephen S. Gottlieb 4 ID , Mark P. Donahue 5, Gordon F. Tomaselli 6, William E. Kraus 5,7 ID , Braxton D. Mitchell 1,8 and Stephen B. Liggett 9,* 1 Division of Endocrinology, Diabetes and Nutrition, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA; [email protected] (A.P.); [email protected] (T.D.); [email protected] (B.D.M.) 2 Center for Pharmacogenomics, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA; [email protected] 3 Institute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA; [email protected] 4 Division of Cardiovascular Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA; [email protected] (S.W.R.); [email protected] (S.S.G.) 5 Division of Cardiology, Department of Medicine, Duke University Medical Center, Durham, NC 27708, USA; [email protected] (M.P.D.); [email protected] (W.E.K.) 6 Department of Medicine, Division of Cardiology, Johns Hopkins University, Baltimore, MD 21218, USA; [email protected] 7 Duke Molecular Physiology Institute, Duke University Medical Center, Durham, NC 27701, USA 8 Geriatrics Research and Education Clinical Center, Baltimore Veterans Administration -
Prognostic and Functional Significant of Heat Shock Proteins (Hsps)
biology Article Prognostic and Functional Significant of Heat Shock Proteins (HSPs) in Breast Cancer Unveiled by Multi-Omics Approaches Miriam Buttacavoli 1,†, Gianluca Di Cara 1,†, Cesare D’Amico 1, Fabiana Geraci 1 , Ida Pucci-Minafra 2, Salvatore Feo 1 and Patrizia Cancemi 1,2,* 1 Department of Biological Chemical and Pharmaceutical Sciences and Technologies (STEBICEF), University of Palermo, 90128 Palermo, Italy; [email protected] (M.B.); [email protected] (G.D.C.); [email protected] (C.D.); [email protected] (F.G.); [email protected] (S.F.) 2 Experimental Center of Onco Biology (COBS), 90145 Palermo, Italy; [email protected] * Correspondence: [email protected]; Tel.: +39-091-2389-7330 † These authors contributed equally to this work. Simple Summary: In this study, we investigated the expression pattern and prognostic significance of the heat shock proteins (HSPs) family members in breast cancer (BC) by using several bioinfor- matics tools and proteomics investigations. Our results demonstrated that, collectively, HSPs were deregulated in BC, acting as both oncogene and onco-suppressor genes. In particular, two different HSP-clusters were significantly associated with a poor or good prognosis. Interestingly, the HSPs deregulation impacted gene expression and miRNAs regulation that, in turn, affected important bio- logical pathways involved in cell cycle, DNA replication, and receptors-mediated signaling. Finally, the proteomic identification of several HSPs members and isoforms revealed much more complexity Citation: Buttacavoli, M.; Di Cara, of HSPs roles in BC and showed that their expression is quite variable among patients. In conclusion, G.; D’Amico, C.; Geraci, F.; we elaborated two panels of HSPs that could be further explored as potential biomarkers for BC Pucci-Minafra, I.; Feo, S.; Cancemi, P. -
Proteomic Analysis of Blood Exosomes from Healthy Females And
biomolecules Article Proteomic Analysis of Blood Exosomes from Healthy Females and Breast Cancer Patients Reveals an Association between Different Exosomal Bioactivity on Non-tumorigenic Epithelial Cell and Breast Cancer Cell Migration in Vitro Oleg Tutanov 1, Evgeniya Orlova 2, Ksenia Proskura 1,3, Alina Grigor’eva 1, Natalia Yunusova 4,5, Yuri Tsentalovich 6 , Antonina Alexandrova 2 and Svetlana Tamkovich 1,7,* 1 Laboratory of Molecular Medicine, Institute of Chemical Biology and Fundamental Medicine, Siberian Branch of Russian Academy of Sciences, 630090 Novosibirsk, Russia; [email protected] (O.T.); [email protected] (K.P.); [email protected] (A.G.) 2 Laboratory of Carcinogenesis Mechanisms, “N.N. Blokhin Cancer Research Center” of the Ministry of Health of the Russian Federation, 115478 Moscow, Russia; [email protected] (E.O.); [email protected] (A.A.) 3 Department of Mammology, Novosibirsk Regional Clinical Oncological Dispensary, 630108 Novosibirsk, Russia 4 Laboratory of Tumor Biochemistry, Cancer Research Institute, Тomsk National Research Medical Center, Russian Academy of Science, 634028 Tomsk, Russia; [email protected] 5 Department of Biochemistry and Molecular Biology, Siberian State Medical University, 634050 Tomsk, Russia 6 Laboratory of Proteomics and Metabolomics, International Tomography Center SB RAS, 630090 Novosibirsk, Russia; [email protected] 7 Department of Molecular Biology and Biotechnology, Novosibirsk State University, 630090 Novosibirsk, Russia * Correspondence: [email protected] Received: 26 February 2020; Accepted: 24 March 2020; Published: 25 March 2020 Abstract: Exosomes are important intercellular communication vehicles, secreted into body fluids by multiple cell types, including tumor cells. They contribute to the metastatic progression of tumor cells through paracrine signalling. -
Tubular P53 Regulates Multiple Genes to Mediate AKI
BASIC RESEARCH www.jasn.org Tubular p53 Regulates Multiple Genes to Mediate AKI † † † † † Dongshan Zhang,* Yu Liu,* Qingqing Wei, Yuqing Huo, Kebin Liu, Fuyou Liu,* and † Zheng Dong* *Departments of Emergency Medicine and Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China; and †Department of Cellular Biology and Anatomy, Vascular Biology Center and Department of Biochemistry and Molecular Biology, Georgia Regents University and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia ABSTRACT A pathogenic role of p53 in AKI was suggested a decade ago but remains controversial. Indeed, recent work indicates that inhibition of p53 protects against ischemic AKI in rats but exacerbates AKI in mice. One intriguing possibility is that p53 has cell type-specific roles in AKI. To determine the role of tubular p53, we generated two conditional gene knockout mouse models, in which p53 is specifically ablated from proximal tubules or other tubular segments, including distal tubules, loops of Henle, and medullary collecting ducts. Proximal tubule p53 knockout (PT-p53-KO) mice were resistant to ischemic and cisplatin nephrotoxic AKI, which was indicated by the analysis of renal function, histology, apoptosis, and inflammation. However, other tubular p53 knockout (OT-p53-KO) mice were sensitive to AKI. Mechanis- tically, AKI associated with the upregulation of several known p53 target genes, including Bax, p53- upregulated modulator of apoptosis-a, p21, and Siva, and this association was attenuated in PT-p53-KO mice. In global expression analysis, ischemic AKI induced 371 genes in wild-type kidney cortical tissues, but the induction of 31 of these genes was abrogated in PT-p53-KO tissues. -
Implications for Hspb7 in Muscle Atrophy Stephanie Wales Tobin1,2,3, Dabo Yang4, John Girgis4, Ali Farahzad1,2,3, Alexandre Blais4 and John C
© 2016. Published by The Company of Biologists Ltd | Journal of Cell Science (2016) 129, 4076-4090 doi:10.1242/jcs.190009 RESEARCH ARTICLE Regulation of Hspb7 by MEF2 and AP-1: implications for Hspb7 in muscle atrophy Stephanie Wales Tobin1,2,3, Dabo Yang4, John Girgis4, Ali Farahzad1,2,3, Alexandre Blais4 and John C. McDermott1,2,3,5,* ABSTRACT 2000; Prado et al., 2009). In the ubiquitin proteasome pathway, the Mycocyte enhancer factor 2 (MEF2) and activator protein 1 (AP-1) forkhead box protein (FoxO) family of transcription factors transcription complexes have been individually implicated in activates muscle atrophy through induction of two E3 ubiquitin myogenesis, but their genetic interaction has not previously been ligases, MAFbx/atrogin-1 and MuRF1 (also known as TRIM63) addressed. Using MEF2A, c-Jun and Fra-1 chromatin (Sandri et al., 2004). Current treatment programs for muscle immunoprecipitation sequencing (ChIP-seq) data and predicted AP- atrophy include activating the serine/threonine protein kinase (Akt) 1 consensus motifs, we identified putative common MEF2 and AP-1 pathway, which induces muscle hypertrophy by inactivating FoxO target genes, several of which are implicated in regulating the actin proteins (Stitt et al., 2004). However, Akt can be inhibited by β β cytoskeleton. Because muscle atrophy results in remodelling or myostatin, a member of the transforming growth factor (TGF- ) degradation of the actin cytoskeleton, we characterized the superfamily (Trendelenburg et al., 2009), superseding Akt expression of putative MEF2 and AP-1 target genes (Dstn, Flnc, activation as a treatment option. A new antibody recently Hspb7, Lmod3 and Plekhh2) under atrophic conditions using characterized to bind to both members (A and B) of the dexamethasone (Dex) treatment in skeletal myoblasts.