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Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis.

Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Research Abstract Details 

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  • Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Abstract Text:

    tsung-cheng changTsung-Cheng Chang,erik a wentzelErik A Wentzel,oliver a kentOliver A Kent,kalyani ramachandranKalyani Ramachandran,michael mullendoreMichael Mullendore,kwang hyuck leeKwang Hyuck Lee,georg feldmannGeorg Feldmann,munekazu yamakuchiMunekazu Yamakuchi,marcella ferlitoMarcella Ferlito,charles j lowensteinCharles J Lowenstein,dan e arkingDan E Arking,michael a beerMichael A Beer,anirban maitraAnirban Maitra,joshua t mendellJoshua T Mendell,

    The p53 tumor suppressor protein is a critical regulator of the cellular response to cancer-initiating insults such as genotoxic stress. In this report, we demonstrate that microRNAs (miRNAs) are important components of the p53 transcriptional network. Global miRNA expression analyses identified a cohort of miRNAs that exhibit p53-dependent upregulation following DNA damage. One such miRNA, miR-34a, is commonly deleted in human cancers and, as shown here, frequently absent in pancreatic cancer cells. Characterization of the miR-34a primary transcript and promoter demonstrates that this miRNA is directly transactivated by p53. Expression of miR-34a causes dramatic reprogramming of gene expression and promotes apoptosis. Much like the known set of p53-regulated genes, miR-34a-responsive genes are highly enriched for those that regulate cell-cycle progression, apoptosis, DNA repair, and angiogenesis. Therefore, it is likely that an important function of miR-34a is the modulation and fine-tuning of the gene expression program initiated by p53.

    Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Publishing Authors By Initials

    tc changTC Chang,ea wentzelEA Wentzel,oa kentOA Kent,k ramachandranK Ramachandran,m mullendoreM Mullendore,kh leeKH Lee,g feldmannG Feldmann,m yamakuchiM Yamakuchi,m ferlitoM Ferlito,cj lowensteinCJ Lowenstein,de arkingDE Arking,ma beerMA Beer,a maitraA Maitra,jt mendellJT Mendell,

    For similar proteins: dna-binding proteins: tumor suppressor protein p53 research abstracts see: proteins: dna-binding proteins: tumor suppressor protein p53 research

    PUBMED ID PMID:

    MEDLINE DATE:

    Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Journal Published:

    PUBLICATION TYPE: Research Support, Non-U.S. Gov

    Journal: Molecular cell

    VOLUME: 26

    Page Numbers: 745-52

    Journal Abbreviation: Mol. Cell

    ISSN: 1097-2765

    DAY: 31

    MONTH: 05

    YEAR: 2007

    Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 9802571

    Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Keywords Mesh Terms:

    KEYWORDS: Tumor Suppressor Protein p53

    MESH TERMS: metabolism

    Chemical & Substance for Abstract: Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis. Information

    Substance Name: Tumor Suppressor Protein p53

    Registry Number: 0

    Grant and Affiliation Information for Transactivation of miR-34a by p53 broadly influences gene expression and promotes apoptosis.

    AFFILIATION: The McKusick-Nathans Institute of Genetic Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NCI

    GRANT: R01CA120185

    ACRONYM: CA

    MEDLINETA: Mol Cell

    REFSOURCE:

    DATABASENAME:

    ACCESSION NUMBER:

    Number Hits: 0

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