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Accession Number ADA570974
Title Characterization of RACK7 as a Novel Factor Involved in BRCA1 Mutation Mediated Breast Cancer.
Publication Date Oct 2012
Media Count 72p
Personal Author A. Rommel I. M. Verma M. Preyer Q. Zhu
Abstract Though BRCA1 has been shown to play a role in DNA end resection, likely critical in the cell s decision to undergo homologous recombination or non-homologous end joining repair pathways, much of BRCA1 function remains unknown. To identify genes that cooperate with BRCA1 in DNA damage response and tumor suppression, we performed a lentiviral vector based cDNA library screen. ZMYND8 (zinc finger Mynd-type containing 8), previously Rack7 (receptor for activated C kinase) or Prkcbp1 (protein kinase C binding protein 1), was identified in our screen as a candidate gene that could modulate the DNA damage hypersensitivity in cells lacking BRCA1. Biochemical data indicates that ZMYND8 might be involved in chromatin reorganization surrounding a stalled fork, which may be vital in preventing collapse and granting genomic stability. Overexpression of ZMYND8 in breast, ovarian, and several other malignancies, could be a novel mechanism to overcome replica-tion stress resulting from BRCA1 dysfunction. This suggests that ZMYND8 and BRCA1 could function epistatically, a phenomenon we continue to investigate using our lab-generated mouse models. In conclusion, our novel findings demonstrate that ZMYND8 is required to prevent the reversal of stalled replication forks, and thereby contributes to the preservation genomic stability under replication stress.
Keywords Atm
Brca1 tumor suppresors
Breast cancer
Deoxyribonucleic acids
Dna damage response
Dna double strand break
Dna(Deoxyribonucleic acids)
Gene expression
Genomic stability
In vivo analysis
Phosphorus transferases
Prkcbp1(Protein kinase c binding protein 1)
Rack7 peptides
Receptor sites(Physiology)
Replication forks
Replication stresses
Transgenic mouse models
Zmynd8 peptides

Source Agency Non Paid ADAS
NTIS Subject Category 57F - Cytology, Genetics, & Molecular Biology
57E - Clinical Medicine
Corporate Author Salk Inst. for Biological Studies, La Jolla, CA.
Document Type Technical report
Title Note Final rept. 15 Sep 2010-14 Sep 2012.
NTIS Issue Number 1315
Contract Number W81XWH-10-1-0963

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