{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Shi Y"],"funding":["NIGMS NIH HHS"],"pagination":["5898-903"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC395895"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["101(16)"],"pubmed_abstract":["Ataxia-telangiectasia (A-T) is a syndrome of cancer susceptibility, immune dysfunction, and neurodegeneration that is caused by mutations in the A-T-mutated (ATM) gene. ATM has been implicated as a critical regulator of cellular responses to DNA damage, including the activation of cell cycle checkpoints and induction of apoptosis. Although defective cell cycle-checkpoint regulation and associated genomic instability presumably contribute to cancer susceptibility in A-T, the mechanism of neurodegeneration in A-T is not well understood. In addition, although ATM is required for the induction of the p53 transcriptional program in response to DNA damage, the identities of the relevant transcription factors that mediate ATM-dependent changes in gene expression remain largely undetermined. In th"],"journal":["Proceedings of the National Academy of Sciences of the United States of America"],"pubmed_title":["Direct regulation of CREB transcriptional activity by ATM in response to genotoxic stress."],"pmcid":["PMC395895"],"funding_grant_id":["GM67868-01","R01 GM067868"],"pubmed_authors":["Tibbetts RS","Venkataraman SL","Dodson GE","LeBlanc S","Shi Y","Mabb AM"],"additional_accession":[]},"is_claimable":false,"name":"Direct regulation of CREB transcriptional activity by ATM in response to genotoxic stress.","description":"Ataxia-telangiectasia (A-T) is a syndrome of cancer susceptibility, immune dysfunction, and neurodegeneration that is caused by mutations in the A-T-mutated (ATM) gene. ATM has been implicated as a critical regulator of cellular responses to DNA damage, including the activation of cell cycle checkpoints and induction of apoptosis. Although defective cell cycle-checkpoint regulation and associated genomic instability presumably contribute to cancer susceptibility in A-T, the mechanism of neurodegeneration in A-T is not well understood. In addition, although ATM is required for the induction of the p53 transcriptional program in response to DNA damage, the identities of the relevant transcription factors that mediate ATM-dependent changes in gene expression remain largely undetermined. In th","dates":{"release":"2004-01-01T00:00:00Z","publication":"2004 Apr","modification":"2025-04-04T11:00:12.994Z","creation":"2019-03-27T00:50:23Z"},"accession":"S-EPMC395895","cross_references":{"pubmed":["15073328"],"doi":["10.1073/pnas.0307718101"]}}