DF6720-MSMB Antibody

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Affinity Biosciences website:www.affbiotech.com order:[email protected] MSMB Antibody Cat.#: DF6720 Concn.: 1mg/ml Mol.Wt.: 13kDa Size: 50ul,100ul,200ul Source: Rabbit Clonality: Polyclonal Application: WB 1:500-1:2000, IHC 1:50-1:200, ELISA(peptide) 1:20000-1:40000 *The optimal dilutions should be determined by the end user. Reactivity: Human,Mouse Purification: The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific). Specificity: MSMB Antibody detects endogenous levels of total MSMB. Immunogen: A synthesized peptide derived from human MSMB, corresponding to a region within the internal amino acids. Uniprot: P08118 Description: The protein encoded by this gene is a member of the immunoglobulin binding factor family. It is synthesized by the epithelial cells of the prostate gland and secreted into the seminal plasma. This protein has inhibin-like activity. It may have a role as an autocrine paracrine factor in uterine, breast and other female reproductive tissues. The expression of the encoded protein is found to be decreased in prostate cancer. Two alternatively spliced transcript variants encoding different isoforms are described for this gene. The use of alternate polyadenylation sites has been found for this gene. Storage Condition and Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM Buffer: NaCl, 0.02% sodium azide and 50% glycerol.Store at -20 °C.Stable for 12 months from date of receipt. Western blot analysis of HepG2 cell lysates, using MSMB Antibody. The lane on the left was treated with the antigen- specific peptide. 1 / 2 Affinity Biosciences website:www.affbiotech.com order:[email protected] DF6720 at 1/100 staining Mouse liver tissue by IHC-P. The sample was formaldehyde fixed and a heat mediated antigen retrieval step in citrate buffer was performed. The sample was then blocked and incubated with the antibody for 1.5 hours at 22°C. An HRP conjugated goat anti-rabbit antibody was used as the secondary antibody. IMPORTANT: For western blot, incubate membrane with diluted primary Ab in 5% w/v milk , 1X TBS, 0.1% Tween®20 at 4°C with gentle shaking, overnight. For Research Use Only. Not for use in diagnostic and therapeutic procedures. Not for resale without express authorization. 2 / 2 Powered by TCPDF (www.tcpdf.org).

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Contribution of MSMB Promoter Region Gene Polymorphism to Early-Onset Prostate Cancer Risk in Mexican Males
www.oncotarget.com Oncotarget, 2019, Vol. 10, (No. 7), pp: 738-748 Research Paper Contribution of MSMB promoter region gene polymorphism to early-onset prostate cancer risk in Mexican males Silvia Juliana Trujillo-Cáceres1, Luisa Torres-Sánchez1, Ana I. Burguete-García2, Yaneth Citlalli Orbe Orihuela2, Ruth Argelia Vázquez-Salas3, Esmeralda Álvarez- Topete4 and Rocío Gómez4 1Centro de Investigación en Salud Poblacional, Instituto Nacional de Salud Pública (INSP), Cuernavaca, Morelos, Mexico 2Centro de Investigación en Enfermedades Infecciosas, INSP, Cuernavaca, Morelos, Mexico 3Conacyt-Centro de Investigación en Salud Poblacional, INSP, Cuernavaca, Morelos, Mexico 4Departamento de Toxicología, Cinvestav-IPN, Mexico City, Mexico Correspondence to: Luisa Torres-Sánchez, email: [email protected] Keywords: genetic polymorphisms; MSMB; prostate cancer; rs10993994; sexually transmitted diseases Received: July 13, 2018 Accepted: December 16, 2018 Published: January 22, 2019 Copyright: Trujillo-Cáceres et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. ABSTRACT Sexually transmitted infections and its contribution to prostate cancer (PC) development have been relevant in different populations. MSMB gene polymorphism (rs10993994) has exhibited an association both with PC as well as the susceptibility to sexually transmitted infections. Hitherto, these conditions have been not studied in Mexico yet, neither if sexually transmitted infections could modify the MSMB and PC association. Herein, socio-demographic features, sexually transmitted infections records, the reproductive backgrounds, and the genetic characterisation were analysed in 322 incident PC cases and 628 population healthy controls from Mexico City.
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Association of Imputed Prostate Cancer Transcriptome with Disease Risk Reveals Novel Mechanisms
Corrected: Author Correction ARTICLE https://doi.org/10.1038/s41467-019-10808-7 OPEN Association of imputed prostate cancer transcriptome with disease risk reveals novel mechanisms Nima C. Emami1,2, Linda Kachuri2, Travis J. Meyers2, Rajdeep Das3,4, Joshua D. Hoffman2, Thomas J. Hoffmann 2,5, Donglei Hu 5,6,7, Jun Shan8, Felix Y. Feng3,4,7, Elad Ziv5,6,7, Stephen K. Van Den Eeden 3,8 & John S. Witte1,2,3,5,7 1234567890():,; Here we train cis-regulatory models of prostate tissue gene expression and impute expression transcriptome-wide for 233,955 European ancestry men (14,616 prostate cancer (PrCa) cases, 219,339 controls) from two large cohorts. Among 12,014 genes evaluated in the UK Biobank, we identify 38 associated with PrCa, many replicating in the Kaiser Permanente RPGEH. We report the association of elevated TMPRSS2 expression with increased PrCa risk (independent of a previously-reported risk variant) and with increased tumoral expression of the TMPRSS2:ERG fusion-oncogene in The Cancer Genome Atlas, suggesting a novel germline-somatic interaction mechanism. Three novel genes, HOXA4, KLK1, and TIMM23, additionally replicate in the RPGEH cohort. Furthermore, 4 genes, MSMB, NCOA4, PCAT1, and PPP1R14A, are associated with PrCa in a trans-ethnic meta-analysis (N = 9117). Many genes exhibit evidence for allele-speciﬁc transcriptional activation by PrCa master-regulators (including androgen receptor) in Position Weight Matrix, Chip-Seq, and Hi-C experimental data, suggesting common regulatory mechanisms for the associated genes. 1 Program in Biological and Medical Informatics, University of California San Francisco, San Francisco, CA 94158, USA.
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Alterations in LMTK2, MSMB and HNF1B Gene Expression Are Associated with the Development of Prostate Cancer BMC Cancer 2010, 10:315
Harries et al. BMC Cancer 2010, 10:315 http://www.biomedcentral.com/1471-2407/10/315 RESEARCH ARTICLE Open Access AlterationsResearch article in LMTK2, MSMB and HNF1B gene expression are associated with the development of prostate cancer Lorna W Harries*1, John RB Perry2, Paul McCullagh3 and Malcolm Crundwell4 Abstract Background: Genome wide association studies (GWAS) have identified several genetic variants that are associated with prostate cancer. Most of these variants, like other GWAS association signals, are located in non-coding regions of potential candidate genes, and thus could act at the level of the mRNA transcript. Methods: We measured the expression and isoform usage of seven prostate cancer candidate genes in benign and malignant prostate by real-time PCR, and correlated these factors with cancer status and genotype at the GWAS risk variants. Results: We determined that levels of LMTK2 transcripts in prostate adenocarcinomas were only 32% of those in benign tissues (p = 3.2 × 10-7), and that an independent effect of genotype at variant rs6465657 on LMTK2 expression in benign (n = 39) and malignant tissues (n = 21) was also evident (P = 0.002). We also identified that whilst HNF1B(C) and MSMB2 comprised the predominant isoforms in benign tissues (90% and 98% of total HNF1B or MSMB expression), HNF1B(B) and MSMB1 were predominant in malignant tissue (95% and 96% of total HNF1B or MSMB expression; P = 1.7 × 10-7 and 4 × 10-4 respectively), indicating major shifts in isoform usage. Conclusions: Our results indicate that the amount or nature of mRNA transcripts expressed from the LMTK2, HNF1B and MSMB candidate genes is altered in prostate cancer, and provides further evidence for a role for these genes in this disorder.
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Inform Network Support Rare Chromosome Disorder Support Group The Stables, Station Road West, Oxted, Surrey RH8 9EE, United Kingdom Tel: +44(0)1883 723356 [email protected] I www.rarechromo.org Join Unique for family links, information and support. Unique is a charity without government funding, existing entirely on donations and grants. If you can, please make a donation via our website at http://www.rarechromo.org/donate Please help us to help you! 10q11.22q11.23 Facebook groups www.facebook.com/groups/chromosome10disorder/ www.facebook.com/groups/152331614838414/ Deletions and Unique mentions other organisations’ message boards and websites to help families looking for information. This does not imply that we endorse their content or have any responsibility for it. Microdeletions This information guide is not a substitute for personal medical advice. Families should consult a medically qualified clinician in all matters relating to genetic diagnosis, management and health. Information on genetic changes is a very fast-moving field and while the information in this guide is believed to be the best available at the time of publication, some facts may later change. Unique does its best to keep abreast of changing information and to review its published guides as needed. This booklet was compiled by Unique (AP) and reviewed by Dr Corrina Powell, Specialist Registrar in Clinical Genetics, and Rosa Spencer- Tansley, Trainee Genetic Counsellor, Leicester Royal Infirmary Clinical Genetics Department ,UK. Version 1 2019 (AP) Copyright © Unique 2020 Rare Chromosome Disorder Support Group Charity Number 1110661 Registered in England and Wales Company Number 5460413 rarechromo.org 20 Genetic information Genetic information genetic Detailed 10q11.22q11.23 microdeletions Chromosome Position Important Microdeletion A 10q11.2q11.23 microdeletion is a rare genetic condition caused by the loss of a 10 Mb genes examples small piece of genetic material from one of the body’s 46 chromosomes – chromosome 10.
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Mapping of Natural Signal Transduction Modulators on Drug Targets Relevant to Prostate Cancer Jayalakshmi T*1, P.B
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Comprehensive Resequence Analysis of a 97 Kb Region of Chromosome 10Q11.2 Containing the MSMB Gene Associated with Prostate Cancer
Hum Genet (2009) 126:743–750 DOI 10.1007/s00439-009-0723-9 ORIGINAL INVESTIGATION Comprehensive resequence analysis of a 97 kb region of chromosome 10q11.2 containing the MSMB gene associated with prostate cancer Meredith Yeager Æ Zuoming Deng Æ Joseph Boland Æ Casey Matthews Æ Jennifer Bacior Æ Victor Lonsberry Æ Amy Hutchinson Æ Laura A. Burdett Æ Liqun Qi Æ Kevin B. Jacobs Æ Jesus Gonzalez-Bosquet Æ Sonja I. Berndt Æ Richard B. Hayes Æ Robert N. Hoover Æ Gilles Thomas Æ David J. Hunter Æ Michael Dean Æ Stephen J. Chanock Received: 30 June 2009 / Accepted: 17 July 2009 / Published online: 31 July 2009 Ó The Author(s) 2009. This article is published with open access at Springerlink.com Abstract Genome-wide association studies of prostate technology to resequence a *97-kb region that includes the cancer have identified single nucleotide polymorphism area surrounding MSMB (chr10: 51,168,025–51,265,101) in (SNP) markers in a region of chromosome 10q11.2, har- 36 prostate cancer cases, 26 controls of European origin, boring the microseminoprotein-b (MSMB) gene. Both the and 8 unrelated CEPH individuals in order to identify gene product of MSMB, the prostate secretory protein 94 additional variants to investigate in functional studies. We (PSP94) and its binding protein (PSPBP), have been pre- identified 241 novel polymorphisms within this region, viously investigated as serum biomarkers for prostate including 142 in the 51-kb block of linkage disequilibrium cancer progression. Recent functional work has shown that (LD) that contains rs10993994 and the proximal promoter different alleles of the significantly associated SNP in the of MSMB.
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Mutation Analysis of the MSMB Gene in Familial Prostate Cancer
British Journal of Cancer (2010) 102, 414 – 418 & 2010 Cancer Research UK All rights reserved 0007 – 0920/10 $32.00 www.bjcancer.com Mutation analysis of the MSMB gene in familial prostate cancer ,1 1 1 2 1 3 2 Z Kote-Jarai* , D Leongamornlert , M Tymrakiewicz , H Field , M Guy , AA Al Olama , J Morrison , L O’Brien1, R Wilkinson1, A Hall1, E Sawyer1, K Muir4, F Hamdy5, J Donovan6, D Neal7,8, D Easton3 and R Eeles1,9 1 2 Translational Cancer Genetics Team, The Institute of Cancer Research, 15 Cotswold Road, Sutton, Surrey SM2 5NG, UK; Department of Oncology. 3 University of Cambridge, Strangeways Laboratory, Worts Causeway, Cambridge CB1 8RN, UK; CR-UK Genetic Epidemiology Unit, University of 4 Cambridge, Strangeways Laboratory, Worts Causeway, Cambridge CB1 8RN, UK; University of Nottingham Medical School, Queens Medical Centre, Nottingham NG7 2UH, UK; 5Nuffield Department of Surgery, University of Oxford, Oxford OX3 9DU, UK; 6Department of Social Medicine, University of Bristol, Canynge Hall, Whiteladies Road, Bristol, UK; 7Surgical Oncology (Uro-Oncology: S4), Departments of Oncology and Surgery, University of 8 Cambridge, Box 279, Addenbrooke’s Hospital, Hills Road, Cambridge CB2 2QQ, UK; Cancer Research UK Cambridge Research Institute & Li Ka 9 Shing Centre, Robinson Way, Cambridge CB2 0RE, UK; The Royal Marsden NHS Foundation Trust, Downs Road, Sutton, Surrey SM2 5PT, UK & Fulham Road, London SW3 6JJ, UK BACKGROUND: MSMB, a gene coding for b-microseminoprotein, has been identified as a candidate susceptibility gene for prostate cancer (PrCa) in two genome-wide association studies (GWAS). SNP rs10993994 is 2 bp upstream of the transcription initiation site of MSMB and was identified as an associated PrCa risk variant.
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