Anti-MTA2 Monoclonal Antibody, Clone FQS9648(3) (DCABH-5548) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use

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Anti-MTA2 monoclonal antibody, clone FQS9648(3) (DCABH-5548) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Rabbit monoclonal to MTA2 Antigen Description The p53 tumor suppressor gene integrates numerous signals that control cell life and death. There are several proteins that are involved in the p53 pathway, including Chk2, p53R2, p53AIP1, Noxa, PIDD, and MTA2. The transcriptional activity of p53 is modulated by protein stability and acetylation. MTA2, also termed MTA1L1, was found to be a subunit of nucleosome remodeling and deacetylating (NuRD) complex. MTA2 modulates the enzymatic activity of the histone deacetylase complex and its expression reduces the levels of acetylated p53. Deacetylation of p53 by MTA2 represses p53 dependent transcriptional activation and modulates p53 mediated cell growth arrest and apoptosis. MTA2 is ubiquitously expressed in human tissues. Isotype IgG Source/Host Rabbit Species Reactivity Human Clone FQS9648(3) Purity Tissue culture supernatant Conjugate Unconjugated Applications ICC/IF, Flow Cyt, IHC-P, WB Positive Control MCF7, HeLa and SW480 cell lysates. Paraffin-embedded Human kidney and Human colonic carcinoma tissue. HeLa cells. Format Liquid Size 100 μl Buffer Preservative: 0.01% Sodium azide; Constituents: 50% Glycerol, 0.05% BSA Preservative 0.01% Sodium Azide Storage Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term. Avoid freeze / thaw cycle. 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved Ship Shipped at 4°C. GENE INFORMATION Gene Name MTA2 metastasis associated 1 family, member 2 [ Homo sapiens ] Official Symbol MTA2 Synonyms MTA2; metastasis associated 1 family, member 2; metastasis associated gene family, member 2 , MTA1L1; metastasis-associated protein MTA2; MTA1 L1; MTA1-L1 protein; metastasis- associated 1-like 1; metastasis-associated protein 2; metastasis -associated gen Entrez Gene ID 9219 Protein Refseq NP_004730 UniProt ID A0A024R534 Chromosome Location 11q12-q13.1 Pathway EGFR1 Signaling Pathway, organism-specific biosystem; Signaling events mediated by HDAC Class I, organism-specific biosystem; Function RNA polymerase II transcription factor binding; histone deacetylase activity; metal ion binding; protein binding; sequence-specific DNA binding; sequence-specific DNA binding transcription factor activity; transcription factor binding transcription factor 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 2 © Creative Diagnostics All Rights Reserved.

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Anti-MTA2 Monoclonal Antibody, Clone NUB3-387 (DCABH-8980) This Product Is for Research Use Only and Is Not Intended for Diagnostic Use
Anti-MTA2 monoclonal antibody, clone NUB3-387 (DCABH-8980) This product is for research use only and is not intended for diagnostic use. PRODUCT INFORMATION Product Overview Mouse monoclonal to MTA2 Antigen Description The p53 tumor suppressor gene integrates numerous signals that control cell life and death. There are several proteins that are involved in the p53 pathway, including Chk2, p53R2, p53AIP1, Noxa, PIDD, and MTA2. The transcriptional activity of p53 is modulated by protein stability and acetylation. MTA2, also termed MTA1L1, was found to be a subunit of nucleosome remodeling and deacetylating (NuRD) complex. MTA2 modulates the enzymatic activity of the histone deacetylase complex and its expression reduces the levels of acetylated p53. Deacetylation of p53 by MTA2 represses p53 dependent transcriptional activation and modulates p53 mediated cell growth arrest and apoptosis. MTA2 is ubiquitously expressed in human tissues. Immunogen Synthetic peptide: RRAARRPNLPLKVKPT conjugated to KLH, corresponding to amino acids 626-641 of Human MTA2 Isotype IgG1 Source/Host Mouse Species Reactivity Mouse, Rat, Hamster, Cow, Dog, Human, Monkey Clone NUB3-387 Purification This antibody is a purified IgG. Conjugate Unconjugated Applications ELISA, WB, IP, ICC/IF Positive Control ICC/IF: HEK-293T cells transfected with MTA2 expression vector WB: 293T total cell extract. Format Liquid Size 100 μl Buffer Preservative: 15mM Sodium Azide; Constituents: 10mM PBS, pH 7.4 Preservative 15mM Sodium Azide Storage Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C or -80°C. Avoid repeated freeze 45-1 Ramsey Road, Shirley, NY 11967, USA Email: [email protected] Tel: 1-631-624-4882 Fax: 1-631-938-8221 1 © Creative Diagnostics All Rights Reserved / thaw cycles.
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Regulation of Apoptosis by P53-Inducible Transmembrane Protein Containing Sushi Domain
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Role and Regulation of the P53-Homolog P73 in the Transformation of Normal Human Fibroblasts
Role and regulation of the p53-homolog p73 in the transformation of normal human fibroblasts Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Bayerischen Julius-Maximilians-Universität Würzburg vorgelegt von Lars Hofmann aus Aschaffenburg Würzburg 2007 Eingereicht am Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Dr. Martin J. Müller Gutachter: Prof. Dr. Michael P. Schön Gutachter : Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am Erklärung Hiermit erkläre ich, dass ich die vorliegende Arbeit selbständig angefertigt und keine anderen als die angegebenen Hilfsmittel und Quellen verwendet habe. Diese Arbeit wurde weder in gleicher noch in ähnlicher Form in einem anderen Prüfungsverfahren vorgelegt. Ich habe früher, außer den mit dem Zulassungsgesuch urkundlichen Graden, keine weiteren akademischen Grade erworben und zu erwerben gesucht. Würzburg, Lars Hofmann Content SUMMARY ................................................................................................................ IV ZUSAMMENFASSUNG ............................................................................................. V 1. INTRODUCTION ................................................................................................. 1 1.1. Molecular basics of cancer .......................................................................................... 1 1.2. Early research on tumorigenesis ................................................................................. 3 1.3. Developing
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Mutational Profile and Prognostic Significance of TP53 in Diffuse Large
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P53aip1 Regulates the Mitochondrial Apoptotic Pathway1
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Addressing the Issue of Missing Heritability: the Importance of Apoptosis in Hereditary Breast and Ovarian Cancer and Functional Assessment of Tp53i3-S252*
Wayne State University Wayne State University Dissertations January 2020 Addressing The Issue Of Missing Heritability: The Importance Of Apoptosis In Hereditary Breast And Ovarian Cancer And Functional Assessment Of Tp53i3-S252* Sophia Chaudhry Wayne State University Follow this and additional works at: https://digitalcommons.wayne.edu/oa_dissertations Part of the Genetics Commons Recommended Citation Chaudhry, Sophia, "Addressing The Issue Of Missing Heritability: The Importance Of Apoptosis In Hereditary Breast And Ovarian Cancer And Functional Assessment Of Tp53i3-S252*" (2020). Wayne State University Dissertations. 2382. https://digitalcommons.wayne.edu/oa_dissertations/2382 This Open Access Dissertation is brought to you for free and open access by DigitalCommons@WayneState. It has been accepted for inclusion in Wayne State University Dissertations by an authorized administrator of DigitalCommons@WayneState. ADDRESSING THE ISSUE OF MISSING HERITABILITY: THE IMPORTANCE OF APOPTOSIS IN HEREDITARY BREAST AND OVARIAN CANCER AND FUNCTIONAL ASSESSMENT OF TP53I3-S252* by SOPHIA RASUL CHAUDHRY DISSERTATION Submitted to the Graduate School of Wayne State University, Detroit, Michigan in partial fulfillment of the requirements for the degree of DOCTOR OF PHILOSOPHY 2020 MAJOR: MOLECULAR GENETICS AND GENOMICS Approved By: ____________________________________ Advisor Date ____________________________________ ____________________________________ ____________________________________ DEDICATION I dedicate this work to my parents, my siblings and my nieces and nephew. All have been a positive force and motivation in becoming the scientist I am today. ii ACKNOWLEDGMENTS There are many people who deserve recognition for helping me complete my doctoral work. One of the most challenging parts of my time as a graduate student finding the right lab. I was very lucky to be accepted into the lab headed by Dr.
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Etude De 2 Gènes Cibles De La Protéine P53 : Siah (Seven in Absentia Human Homologue) Et Tsap6 (Tumor Suppressor Activated Pathway 6) Séverine Beaucourt
Etude de 2 gènes cibles de la protéine P53 : siah (seven in absentia human homologue) et tsap6 (tumor suppressor activated pathway 6) Séverine Beaucourt To cite this version: Séverine Beaucourt. Etude de 2 gènes cibles de la protéine P53 : siah (seven in absentia human homologue) et tsap6 (tumor suppressor activated pathway 6). Biologie cellulaire. Université Paris Sud - Paris XI, 2005. Français. tel-00157749 HAL Id: tel-00157749 https://tel.archives-ouvertes.fr/tel-00157749 Submitted on 27 Jun 2007 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. "I am satisfied with the mystery of life's eternity and with the awareness of--and glimpse into--the marvelous construction of the existing world together with the steadfast determination to comprehend a portion, be it ever so tiny, of the reason that manifests itself in nature. This is the basis of cosmic religiosity, and it appears to me that the most important function of art and science is to awaken this feeling among the receptive and keep it alive." Albert Einstein Avant-propos Je souhaiterais avant toute chose remercier Adam Telerman et Robert Amson pour m'avoir fait confiance tout au long de ces années, et surtout à mon arrivée au laboratoire lorsque je cherchais un stage qui devait marquer la "fin de mes études".
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P53aip1 Regulates the Mitochondrial Apoptotic Pathway1
[CANCER RESEARCH 62, 2883–2889, May 15, 2002] p53AIP1 Regulates the Mitochondrial Apoptotic Pathway1 Koichi Matsuda, Koji Yoshida, Yoichi Taya, Kozo Nakamura, Yusuke Nakamura,2 and Hirofumi Arakawa Human Genome Center, Institute of Medical Science, University of Tokyo, Minato-ku, Tokyo 108-8639 [K. M., K. Y., Y. N., H. A.], and Department of Orthopedic Surgery, Faculty of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033 [K. M., K. N.], and National Cancer Center Research Institute, Chuo-ku, Tokyo 104-0045 [Y.T.], Japan ABSTRACT family have been reported as anti- or proapoptotic players; all of them possess at least one of the four domains. We identified recently the p53AIP1 gene, a novel p53 target that Although p53-dependent apoptosis is thought to be the most im- mediates p53-dependent apoptosis. In the experiments reported here, portant feature of tumor suppression by p53, a large part of that ectopic expression of p53AIP1 induced down-regulation of mitochondrial ⌬⌿m and release of cytochrome c from mitochondria in human cells. mechanism remains to be explained. Several target genes have been Immunoprecipitation and immunostaining experiments indicated interac- isolated as attractive candidates for p53-dependent apoptosis, includ- tion between p53AIP1 and bcl-2 proteins at mitochondria. Overexpression ing bax (23), PIG3 (24, 25), Killer/DR5 (26), Fas (27, 28), Noxa (29), of bcl-2 blocked the down-regulation of mitochondrial ⌬⌿m and the PERP (30), and PUMA (31, 32). Bax, Noxa, and PUMA are mito- proapoptotic activity of p53AIP1. Our results implicate p53AIP1 as a chondrial proteins and members of the bcl-2 family, because they pivotal mediator of the p53-dependent mitochondrial apoptotic pathway.
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Stress Via P53 Pathway Causes Apoptosis by Mitochondrial Noxa
Oncogene (2008) 27, 741–754 & 2008 Nature Publishing Group All rights reserved 0950-9232/08 $30.00 www.nature.com/onc ORIGINAL ARTICLE Stress via p53 pathway causes apoptosis by mitochondrialNoxa upregulation in doxorubicin-treated neuroblastoma cells K Kurata1, R Yanagisawa1, M Ohira2, M Kitagawa3, A Nakagawara2 and T Kamijo1,2 1Department of Pediatrics, Shinshu University School of Medicine, Matsumoto, Nagano, Japan; 2Division of Biochemistry, Chiba Cancer Center Research Institute, Chuoh-ku, Chiba, Japan and 3Department of Biochemistry, Hamamatsu University School of Medicine, Hamamatsu, Shizuoka, Japan In this study, we employed a panel of cell lines to determine which survival has been improved by recent therapies, whether p53-dependent cell death in neuroblastoma (NB) high-risk NB is still one of the most difﬁcult tumors to cells is caused by apoptotic cellular function, and we cure, with only 30% long-term survival despite intensive further studied the molecular mechanism of apoptosis multimodal therapy. New treatments and a better induced via the p53-dependent pathway. We obtained understanding of drug resistance mechanisms are evidence that a type of p53-dependent stress, doxorubicin required for the improvement of the survival rate. A (Doxo) administration, causes accumulation of p53 in the noteworthy ﬁnding of NB research is that mutations of nucleus of NB cells and phosphorylation of several serine p53 tumor suppressor have been reported in less than residues in both Doxo-sensitive and -resistant cell lines. 2% of NBs out of 340 tested (Tweddle et al., 2001). Upregulation of p53-downstream molecules in cells and Instead of mutation, cytoplasmic sequestration of p53 upregulation of Noxa in the mitochondrial fraction were has been proposed as an alternative mechanism of observed only in Doxo-sensitive NB cells.
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Allelic Imbalance at Chromosome 11 in Head and Neck Squamous Cell Carcinoma in an Indian Patient Population
512 ORIGINAL ARTICLE J Clin Pathol: first published as 10.1136/jcp.56.7.512 on 1 July 2003. Downloaded from Allelic imbalance at chromosome 11 in head and neck squamous cell carcinoma in an Indian patient population G Mondal, A Tripathi, N Bhattacharya, N Sikdar, A Roy, A Sengupta, B Roy, C K Panda, S Roychoudhury ............................................................................................................................. J Clin Pathol 2003;56:512–518 Background: Genetic instability of chromosome 11 is a frequent event in many solid tumours, includ- See end of article for ing head and neck squamous cell carcinoma (HNSCC). authors’ affiliations Aims: To perform allelic imbalance analysis of cytogenetically mapped altered regions of human chro- ....................... mosome 11 in patients with HNSCC from eastern India. Methods: Correspondence to: Genomic alterations were investigated using highly polymorphic microsatellite markers in Dr S Roychoudhury, both HNSCC and leukoplakia tissues. Human Genetics and Results: Microsatellite markers D11S1758 from 11p13–15 and D11S925 from 11q23.3–24 had the Genomics Division, Indian highest frequency (38% and 32%, respectively) of loss of heterozygosity among all the markers ana- Institute of Chemical lysed. Allelic loss at the marker D11S925 was seen in both leukoplakia and in all stages of HNSCC Biology, 4, Raja S. C. Mullick Road, Kolkata 700 tumour tissues suggesting that it is an early event in HNSCC tumorigenesis. Microsatellite size altera- 032, India; tion was also found to be high (> 20%) in several markers. In leukoplakia samples microsatellite insta- [email protected] bility was seen at a higher frequency than loss of the allele, indicating such alterations might initiate the Accepted for publication process of tumorigenesis in HNSCC.
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