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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2007.1
- 수록면
- 116 - 124 (9page)
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Purpose: Mutations in the ATM (ataxia-telangiectasia mutated) gene, which encodes a 370 kd protein with a kinase catalytic domain, predisposes people to cancers, and these mutations are also linked to ataxia-telangiectasia (A-T). The histone acetylaion/deacetylation- dependent chromatin remodeling can activate the ATM kinase-mediated DNA damage signal pathway (in an accompanying work, Lee, 2007). This has led us to study whether this modification can impinge on the ATM-mediated DNA damage response via transcriptional modulation in order to understand the function of ATM in the regulation of gene transcription.
Materials and Methods: To identify the genes whose expression is regulated by ATM in response to histone deaceylase (HDAC) inhibition, we performed an analysis of oligonucleotide microarrays with using the appropriate cell lines, isogenic A-T (ATM) and control (ATM+) cells, following treatment with a HDAC inhibitor TSA.
Results: Treatment with TSA reprograms the differential gene expression profile in response to HDAC inhibition in ATM cells and ATM+ cells. We analyzed the genes that are regulated by TSA in the ATM-dependent manner, and we classified these genes into different functional categories, including those involved in cell cycle/DNA replication, DNA repair, apoptosis, growth/differentiation, cell- cell adhesion, signal transduction, metabolism and transcription.
Conclusion: We found that while some genes are regulated by TSA without regard to ATM, the patterns of gene regulation are differentially regulated in an ATM-dependent manner. Taken together, these finding indicate that ATM can regulate the transcription of genes that play critical roles in the molecular response to DNA damage, and this response is modulated through an altered HDAC inhibition-mediated gene expression. (Cancer Res Treat. 2007;39:116-124)
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참고문헌 (25)
참고문헌 신청
Ayesh S / 2002 / Possible physiological role of H19 RNA 35 : 63 ~ 74
Bakkenist CJ / 2003 / DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation 421 : 499 ~ 506
Bruno T / 2006 / Che-1 phosphorylation by ATM/ATR and Chk2-kinases activates p53 transcription and the G2/M checkpoint 10 : 473 ~ 486
Chen CS / 2007 / Histone deacetylase inhibitors sensitize prostate cancer cells to agent that produce DNA double-strand breaks by targeting Ku70 acetylation 67 : 5318 ~ 5327
Cheng L / 1999 / Expression in normal human tissues of five nucleotide excision repair genes measured simultaneously by multiplex reverse transcriptase-polymerase chain reac
Bakkenist CJ / 2003 / DNA damage activates ATM through intermolecular autophosphorylation and dimer dissociation 421 : 499 ~ 506
Bruno T / 2006 / Che-1 phosphorylation by ATM/ATR and Chk2-kinases activates p53 transcription and the G2/M checkpoint 10 : 473 ~ 486
Chen CS / 2007 / Histone deacetylase inhibitors sensitize prostate cancer cells to agent that produce DNA double-strand breaks by targeting Ku70 acetylation 67 : 5318 ~ 5327
Cheng L / 1999 / Expression in normal human tissues of five nucleotide excision repair genes measured simultaneously by multiplex reverse transcriptase-polymerase chain reac
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New Approaches to Functional Process Discovery in HPV 16-Associated Cervical Cancer Cells by Gene Ontology
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