WASF2 Antibody Cat

Total Page:16

File Type:pdf, Size:1020Kb

WASF2 Antibody Cat WASF2 Antibody Cat. No.: 57-800 WASF2 Antibody Specifications HOST SPECIES: Rabbit SPECIES REACTIVITY: Human HOMOLOGY: Predicted species reactivity based on immunogen sequence: Bovine, Mouse This WASF2 antibody is generated from rabbits immunized with a KLH conjugated IMMUNOGEN: synthetic peptide between 162-190 amino acids from the Central region of human WASF2. TESTED APPLICATIONS: WB APPLICATIONS: For WB starting dilution is: 1:1000 PREDICTED MOLECULAR 54 kDa WEIGHT: Properties This antibody is purified through a protein A column, followed by peptide affinity PURIFICATION: purification. CLONALITY: Polyclonal ISOTYPE: Rabbit Ig CONJUGATE: Unconjugated October 2, 2021 1 https://www.prosci-inc.com/wasf2-antibody-57-800.html PHYSICAL STATE: Liquid BUFFER: Supplied in PBS with 0.09% (W/V) sodium azide. CONCENTRATION: batch dependent Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies STORAGE CONDITIONS: care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures. Additional Info OFFICIAL SYMBOL: WASF2 Wiskott-Aldrich syndrome protein family member 2, WASP family protein member 2, ALTERNATE NAMES: Protein WAVE-2, Verprolin homology domain-containing protein 2, WASF2, WAVE2 ACCESSION NO.: Q9Y6W5 PROTEIN GI NO.: 59800456 GENE ID: 10163 USER NOTE: Optimal dilutions for each application to be determined by the researcher. Background and References This gene encodes a member of the Wiskott-Aldrich syndrome protein family. The gene product is a protein that forms a multiprotein complex that links receptor kinases and actin. Binding to actin occurs through a C-terminal verprolin homology domain in all family members. The multiprotein complex serves to tranduce signals that involve BACKGROUND: changes in cell shape, motility or function. The published map location (PMID:10381382) has been changed based on recent genomic sequence comparisons, which indicate that the expressed gene is located on chromosome 1, and a pseudogene may be located on chromosome X. REFERENCES: 1) Takahashi, K., et al. Cell. Signal. 22(3):510-518(2010) 2) Lebensohn, A.M., et al. Mol. Cell 36(3):512-524(2009) 3) Cai, X., et al. Lung Cancer 65(3):299-305(2009) 4) Morimura, S., et al. Biochem. Biophys. Res. Commun. 382(3):614-619(2009) ANTIBODIES FOR RESEARCH USE ONLY. For additional information, visit ProSci's Terms & Conditions Page. October 2, 2021 2 https://www.prosci-inc.com/wasf2-antibody-57-800.html.
Recommended publications
  • Genome-Wide Analysis of Host-Chromosome Binding Sites For
    Lu et al. Virology Journal 2010, 7:262 http://www.virologyj.com/content/7/1/262 RESEARCH Open Access Genome-wide analysis of host-chromosome binding sites for Epstein-Barr Virus Nuclear Antigen 1 (EBNA1) Fang Lu1, Priyankara Wikramasinghe1, Julie Norseen1,2, Kevin Tsai1, Pu Wang1, Louise Showe1, Ramana V Davuluri1, Paul M Lieberman1* Abstract The Epstein-Barr Virus (EBV) Nuclear Antigen 1 (EBNA1) protein is required for the establishment of EBV latent infection in proliferating B-lymphocytes. EBNA1 is a multifunctional DNA-binding protein that stimulates DNA replication at the viral origin of plasmid replication (OriP), regulates transcription of viral and cellular genes, and tethers the viral episome to the cellular chromosome. EBNA1 also provides a survival function to B-lymphocytes, potentially through its ability to alter cellular gene expression. To better understand these various functions of EBNA1, we performed a genome-wide analysis of the viral and cellular DNA sites associated with EBNA1 protein in a latently infected Burkitt lymphoma B-cell line. Chromatin-immunoprecipitation (ChIP) combined with massively parallel deep-sequencing (ChIP-Seq) was used to identify cellular sites bound by EBNA1. Sites identified by ChIP- Seq were validated by conventional real-time PCR, and ChIP-Seq provided quantitative, high-resolution detection of the known EBNA1 binding sites on the EBV genome at OriP and Qp. We identified at least one cluster of unusually high-affinity EBNA1 binding sites on chromosome 11, between the divergent FAM55 D and FAM55B genes. A con- sensus for all cellular EBNA1 binding sites is distinct from those derived from the known viral binding sites, sug- gesting that some of these sites are indirectly bound by EBNA1.
    [Show full text]
  • UCSD MOLECULE PAGES Doi:10.6072/H0.MP.A002549.01 Volume 1, Issue 2, 2012 Copyright UC Press, All Rights Reserved
    UCSD MOLECULE PAGES doi:10.6072/H0.MP.A002549.01 Volume 1, Issue 2, 2012 Copyright UC Press, All rights reserved. Review Article Open Access WAVE2 Tadaomi Takenawa1, Shiro Suetsugu2, Daisuke Yamazaki3, Shusaku Kurisu1 WASP family verprolin-homologous protein 2 (WAVE2, also called WASF2) was originally identified by its sequence similarity at the carboxy-terminal VCA (verprolin, cofilin/central, acidic) domain with Wiskott-Aldrich syndrome protein (WASP) and N-WASP (neural WASP). In mammals, WAVE2 is ubiquitously expressed, and its two paralogs, WAVE1 (also called suppressor of cAMP receptor 1, SCAR1) and WAVE3, are predominantly expressed in the brain. The VCA domain of WASP and WAVE family proteins can activate the actin-related protein 2/3 (Arp2/3) complex, a major actin nucleator in cells. Proteins that can activate the Arp2/3 complex are now collectively known as nucleation-promoting factors (NPFs), and the WASP and WAVE families are a founding class of NPFs. The WAVE family has an amino-terminal WAVE homology domain (WHD domain, also called the SCAR homology domain, SHD) followed by the proline-rich region that interacts with various Src-homology 3 (SH3) domain proteins. The VCA domain located at the C-terminus. WAVE2, like WAVE1 and WAVE3, constitutively forms a huge heteropentameric protein complex (the WANP complex), binding through its WHD domain with Abi-1 (or its paralogs, Abi-2 and Abi-3), HSPC300 (also called Brick1), Nap1 (also called Hem-2 and NCKAP1), Sra1 (also called p140Sra1 and CYFIP1; its paralog is PIR121 or CYFIP2). The WANP complex is recruited to the plasma membrane by cooperative action of activated Rac GTPases and acidic phosphoinositides.
    [Show full text]
  • Systems Analysis Implicates WAVE2&Nbsp
    JACC: BASIC TO TRANSLATIONAL SCIENCE VOL.5,NO.4,2020 ª 2020 THE AUTHORS. PUBLISHED BY ELSEVIER ON BEHALF OF THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION. THIS IS AN OPEN ACCESS ARTICLE UNDER THE CC BY-NC-ND LICENSE (http://creativecommons.org/licenses/by-nc-nd/4.0/). PRECLINICAL RESEARCH Systems Analysis Implicates WAVE2 Complex in the Pathogenesis of Developmental Left-Sided Obstructive Heart Defects a b b b Jonathan J. Edwards, MD, Andrew D. Rouillard, PHD, Nicolas F. Fernandez, PHD, Zichen Wang, PHD, b c d d Alexander Lachmann, PHD, Sunita S. Shankaran, PHD, Brent W. Bisgrove, PHD, Bradley Demarest, MS, e f g h Nahid Turan, PHD, Deepak Srivastava, MD, Daniel Bernstein, MD, John Deanfield, MD, h i j k Alessandro Giardini, MD, PHD, George Porter, MD, PHD, Richard Kim, MD, Amy E. Roberts, MD, k l m m,n Jane W. Newburger, MD, MPH, Elizabeth Goldmuntz, MD, Martina Brueckner, MD, Richard P. Lifton, MD, PHD, o,p,q r,s t d Christine E. Seidman, MD, Wendy K. Chung, MD, PHD, Martin Tristani-Firouzi, MD, H. Joseph Yost, PHD, b u,v Avi Ma’ayan, PHD, Bruce D. Gelb, MD VISUAL ABSTRACT Edwards, J.J. et al. J Am Coll Cardiol Basic Trans Science. 2020;5(4):376–86. ISSN 2452-302X https://doi.org/10.1016/j.jacbts.2020.01.012 JACC: BASIC TO TRANSLATIONALSCIENCEVOL.5,NO.4,2020 Edwards et al. 377 APRIL 2020:376– 86 WAVE2 Complex in LVOTO HIGHLIGHTS ABBREVIATIONS AND ACRONYMS Combining CHD phenotype–driven gene set enrichment and CRISPR knockdown screening in zebrafish is an effective approach to identifying novel CHD genes.
    [Show full text]
  • Supporting Information
    Supporting Information Edgar et al. 10.1073/pnas.1601895113 SI Methods (Actimetrics), and recordings were analyzed using LumiCycle Mice. Sample size was determined using the resource equation: Data Analysis software (Actimetrics). E (degrees of freedom in ANOVA) = (total number of exper- – Cell Cycle Analysis of Confluent Cell Monolayers. NIH 3T3, primary imental animals) (number of experimental groups), with −/− sample size adhering to the condition 10 < E < 20. For com- WT, and Bmal1 fibroblasts were sequentially transduced − − parison of MuHV-4 and HSV-1 infection in WT vs. Bmal1 / with lentiviral fluorescent ubiquitin-based cell cycle indicators mice at ZT7 (Fig. 2), the investigator did not know the genotype (FUCCI) mCherry::Cdt1 and amCyan::Geminin reporters (32). of the animals when conducting infections, bioluminescence Dual reporter-positive cells were selected by FACS (Influx Cell imaging, and quantification. For bioluminescence imaging, Sorter; BD Biosciences) and seeded onto 35-mm dishes for mice were injected intraperitoneally with endotoxin-free lucif- subsequent analysis. To confirm that expression of mCherry:: Cdt1 and amCyan::Geminin correspond to G1 (2n DNA con- erin (Promega E6552) using 2 mg total per mouse. Following < ≤ anesthesia with isofluorane, they were scanned with an IVIS tent) and S/G2 (2 n 4 DNA content) cell cycle phases, Lumina (Caliper Life Sciences), 15 min after luciferin admin- respectively, cells were stained with DNA dye DRAQ5 (abcam) and analyzed by flow cytometry (LSR-Fortessa; BD Biosci- istration. Signal intensity was quantified using Living Image ences). To examine dynamics of replicative activity under ex- software (Caliper Life Sciences), obtaining maximum radiance perimental confluent conditions, synchronized FUCCI reporter for designated regions of interest (photons per second per − − − monolayers were observed by time-lapse live cell imaging over square centimeter per Steradian: photons·s 1·cm 2·sr 1), relative 3 d (Nikon Eclipse Ti-E inverted epifluorescent microscope).
    [Show full text]
  • Analysis of the Complex Interaction of Cdr1as‑Mirna‑Protein and Detection of Its Novel Role in Melanoma
    ONCOLOGY LETTERS 16: 1219-1225, 2018 Analysis of the complex interaction of CDR1as‑miRNA‑protein and detection of its novel role in melanoma LIHUAN ZHANG*, YUAN LI*, WENYAN LIU, HUIFENG LI and ZHIWEI ZHU College of Life Sciences, Shanxi Agricultural University, Taigu, Shanxi 030801, P.R. China Received May 15, 2017; Accepted April 9, 2018 DOI: 10.3892/ol.2018.8700 Abstract. Despite improvements in the prevention, diagnosis has been detected in several species, including viruses (2), and treatment of melanoma having developed rapidly, the role plants (4), archaea (5)[Salzman, 2013 #198; Memczak, 2013 of circular RNA CDR1 antisense RNA (CDR1as) in melanoma #291] and animals (6). In eukaryotic cells, circRNA has remains to be elucidated. The aim of the present study was to attracted attention due to its unique characteristics, including predict the novel roles of CDR1as in melanoma through novel high stability, specificity and evolutionary conservation (7). bioinformatics analysis. In the present study, the circ2Traits The majority of circRNAs are derived from exons of coding database was used to supply information on CDR1as in cancer. regions, 3'UTRs, 5'UTRs, introns, intergenetic regions and CircNet, circBase and circInteractome databases were used to antisense RNAs (8). CircRNAs, which have attracted attention detect the co-expression of CDR1as, microRNAs and proteins. in recent years, can be produced by canonical and nonca- Furthermore, the functions and pathways of the associated nonical splicing as distinguished from the linear RNAs (9). proteins were predicted using the Database for Annotation, Through high-throughput sequencing, three types of circRNAs Visualization and Integrated Discovery. Gene Ontology have been identified: Exonic circRNAs (7), circular intronic enrichment analysis suggested that the proteins associated RNAs (ciRNAs) (9), and retained-intron circular RNAs or with CDR1as were mainly regulated in the cytoplasm as exon-intron circRNAs (elciRNAs) (10).
    [Show full text]
  • Noncoding Rnas As Novel Pancreatic Cancer Targets
    NONCODING RNAS AS NOVEL PANCREATIC CANCER TARGETS by Amy Makler A Thesis Submitted to the Faculty of The Charles E. Schmidt College of Science In Partial Fulfillment of the Requirements for the Degree of Master of Science Florida Atlantic University Boca Raton, FL August 2018 Copyright 2018 by Amy Makler ii ACKNOWLEDGEMENTS I would first like to thank Dr. Narayanan for his continuous support, constant encouragement, and his gentle, but sometimes critical, guidance throughout the past two years of my master’s education. His faith in my abilities and his belief in my future success ensured I continue down this path of research. Working in Dr. Narayanan’s lab has truly been an unforgettable experience as well as a critical step in my future endeavors. I would also like to extend my gratitude to my committee members, Dr. Binninger and Dr. Jia, for their support and suggestions regarding my thesis. Their recommendations added a fresh perspective that enriched our initial hypothesis. They have been indispensable as members of my committee, and I thank them for their contributions. My parents have been integral to my successes in life and their support throughout my education has been crucial. They taught me to push through difficulties and encouraged me to pursue my interests. Thank you, mom and dad! I would like to thank my boyfriend, Joshua Disatham, for his assistance in ensuring my writing maintained a logical progression and flow as well as his unwavering support. He was my rock when the stress grew unbearable and his encouraging words kept me pushing along.
    [Show full text]
  • Wasf2: a Novel Target of Intermittent Parathyroid Hormone Administration
    INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE 31: 1243-1247, 2013 Wasf2: A novel target of intermittent parathyroid hormone administration MAKI UYAMA1,2, MASAMITSU KAWANAMI2 and MASATO TAMURA1 Departments of 1Biochemistry and Molecular Biology, 2Periodontology and Endodontology, Graduate School of Dental Medicine, Hokkaido University, Sapporo 060-8586, Japan Received December 20, 2012; Accepted February 21, 2013 DOI: 10.3892/ijmm.2013.1315 Abstract. Systemic intermittent administration of parathyroid continuously secrete an excess of hormone. Such continuous hormone (PTH) stimulates bone formation in animals and secretion of PTH induces bone resorption by stimulation of humans, and recombinant human PTH1-34 (teriparatide) receptor activator of nuclear factor (NF)-κB ligand (RANKL) is used clinically for the treatment of osteoporosis. In this and inhibition of osteoprotegerin (OPG) in osteoblasts (2). study, we investigated the regulation of gene expression by The effects of PTH on osteoblasts are known to be mediated intermittent PTH administration in MC3T3-E1 osteoblastic via binding of PTH to the seven membrane-spanning G cells. We found that intermittent PTH1-34 administration protein-coupled receptor, PTH receptor 1 (PTHR1), and downregulated Wiskott-Aldrich syndrome protein family activation of both the cyclic AMP (cAMP)-dependent protein member (Wasf) 2 mRNA expression. Wnt inhibitor, IWP-2, kinase A (PKA) pathway and the phosphoinositide-dependent and protein kinase C inhibitor, Go6976, inhibited this down- protein kinase C (PKC) pathway (3). Intermittent PTH regulation. However, continuous PTH did not affect Wasf2 administration in mice has been shown to increase osteoblast expression. Transfection of Wasf2 siRNA reduced bone numbers by stimulating survival signaling, preventing their sialoprotein (BSP) mRNA expression in a similar manner apoptosis, and thus increasing bone formation (4).
    [Show full text]
  • 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.
    [Show full text]
  • Microrna-1253 Regulation of WASF2 (WAVE2) and Its Relevance to Racial Health Disparities
    G C A T T A C G G C A T genes Article MicroRNA-1253 Regulation of WASF2 (WAVE2) and Its Relevance to Racial Health Disparities Mercy A. Arkorful 1, Nicole Noren Hooten 2 , Yongqing Zhang 3, Amirah N. Hewitt 2, Lori Barrientos Sanchez 2, Michele K. Evans 2 and Douglas F. Dluzen 1,* 1 Department of Biology, Morgan State University, Baltimore, MD 21251, USA; [email protected] 2 Laboratory of Epidemiology and Population Science, National Institute on Aging, Baltimore, MD 21224, USA; [email protected] (N.N.H.); [email protected] (A.N.H.); [email protected] (L.B.S.); [email protected] (M.K.E.) 3 Laboratory of Genetics and Genomics, National Institute on Aging, Baltimore, MD 21224, USA; [email protected] * Correspondence: [email protected]; Tel.: +443-885-4462 Received: 16 April 2020; Accepted: 18 May 2020; Published: 20 May 2020 Abstract: The prevalence of hypertension among African Americans (AAs) in the US is among the highest of any demographic and affects over two-thirds of AA women. Previous data from our laboratory suggest substantial differential gene expression (DGE) of mRNAs and microRNAs (miRNAs) exists within peripheral blood mononuclear cells (PBMCs) isolated from AA and white women with or without hypertension. We hypothesized that DGE by race may contribute to racial differences in hypertension. In a reanalysis of our previous dataset, we found that the Wiskott–Aldrich syndrome protein Verprolin-homologous protein 2 (WASF2 (also known as WAVE2)) is differentially expressed in AA women with hypertension, along with several other members of the actin cytoskeleton signaling pathway that plays a role in cell shape and branching of actin filaments.
    [Show full text]
  • Noise Genetics: Inferring Protein Function by Correlating Phenotype with Protein Levels and Localization in Individual Human Cells
    Noise Genetics: Inferring Protein Function by Correlating Phenotype with Protein Levels and Localization in Individual Human Cells Shlomit Farkash-Amar1, Anat Zimmer1, Eran Eden1, Ariel Cohen1, Naama Geva-Zatorsky1, Lydia Cohen1, Ron Milo2, Alex Sigal1, Tamar Danon1, Uri Alon1* 1 Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel, 2 Department of Plant Sciences, Weizmann Institute of Science, Rehovot, Israel Abstract To understand gene function, genetic analysis uses large perturbations such as gene deletion, knockdown or over- expression. Large perturbations have drawbacks: they move the cell far from its normal working point, and can thus be masked by off-target effects or compensation by other genes. Here, we offer a complementary approach, called noise genetics. We use natural cell-cell variations in protein level and localization, and correlate them to the natural variations of the phenotype of the same cells. Observing these variations is made possible by recent advances in dynamic proteomics that allow measuring proteins over time in individual living cells. Using motility of human cancer cells as a model system, and time-lapse microscopy on 566 fluorescently tagged proteins, we found 74 candidate motility genes whose level or localization strongly correlate with motility in individual cells. We recovered 30 known motility genes, and validated several novel ones by mild knockdown experiments. Noise genetics can complement standard genetics for a variety of phenotypes. Citation: Farkash-Amar S, Zimmer A, Eden E, Cohen A, Geva-Zatorsky N, et al. (2014) Noise Genetics: Inferring Protein Function by Correlating Phenotype with Protein Levels and Localization in Individual Human Cells. PLoS Genet 10(3): e1004176.
    [Show full text]
  • 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.
    [Show full text]
  • Heat-Shock Factor 2 Is a Suppressor of Prostate Cancer Invasion
    Oncogene (2016) 35, 1770–1784 OPEN © 2016 Macmillan Publishers Limited All rights reserved 0950-9232/16 www.nature.com/onc ORIGINAL ARTICLE Heat-shock factor 2 is a suppressor of prostate cancer invasion JK Björk1,2,4, M Åkerfelt1,2,4, J Joutsen1,3, MC Puustinen1,3, F Cheng1,3, L Sistonen1,3,4 and M Nees1,4 Heat-shock factors (HSFs) are key transcriptional regulators in cell survival. Although HSF1 has been identified as a driver of carcinogenesis, HSF2 has not been explored in malignancies. Here, we report that HSF2 suppresses tumor invasion of prostate cancer (PrCa). In three-dimensional organotypic cultures and the in vivo xenograft chorioallantoic membrane model HSF2 knockdown perturbs organoid differentiation and promotes invasiveness. Gene expression profiling together with functional studies demonstrated that the molecular mechanism underlying the effect on tumor progression originates from HSF2 steering the switch between acinar morphogenesis and invasion. This is achieved by the regulation of genes connected to, for example, GTPase activity, cell adhesion, extracellular matrix and actin cytoskeleton dynamics. Importantly, low HSF2 expression correlates with high Gleason score, metastasis and poor survival of PrCa patients, highlighting the clinical relevance of our findings. Finally, the study was expanded beyond PrCa, revealing that the expression of HSF2 is decreased in a wide range of cancer types. This study provides the first evidence for HSF2 acting as a suppressor of invasion in human malignancies. Oncogene (2016) 35, 1770–1784; doi:10.1038/onc.2015.241; published online 29 June 2015 INTRODUCTION HSF1 was highlighted in a cohort of breast cancer patients, Prostate cancer (PrCa) is the most commonly diagnosed male showing correlation between high HSF1 expression and 15 cancer in Western countries.1 Gleason grading, which is based on decreased survival.
    [Show full text]