Ataxia-Telangiectasia Mutated Kinase: Role in Myocardial Remodeling.
| Title: | Ataxia-Telangiectasia Mutated Kinase: Role in Myocardial Remodeling. |
|---|---|
| Authors: | Thrasher P; Department of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.; Singh M; Department of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.; Singh K; Department of Biomedical Sciences, James H Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.; James H Quillen Veterans Affairs Medical Center, Mountain Home, TN, USA. |
| Source: | Journal of rare diseases research & treatment [J Rare Dis Res Treat] 2017; Vol. 2 (1), pp. 32-37. Date of Electronic Publication: 2016 Dec 16. |
| Publication Type: | Journal Article |
| Language: | English |
| Journal Info: | Publisher: Sciaccess, Inc Country of Publication: United States NLM ID: 101692909 Publication Model: Print-Electronic Cited Medium: Print NLM ISO Abbreviation: J Rare Dis Res Treat Subsets: PubMed not MEDLINE |
| Imprint Name(s): | Original Publication: Grand Rapids, MI : Sciaccess, Inc. |
| Abstract: | Ataxia-telangiectasia mutated kinase (ATM) is a serine/threonine kinase. Mutations in the ATM gene cause a rare autosomal multisystemic disease known as Ataxia-telangiectasia (AT). Individuals with mutations in both copies of the ATM gene suffer from increased susceptibility to ionizing radiation, predisposition to cancer, insulin resistance, immune deficiency, and premature aging. Patients with one mutated allele make-up ~1.4 to 2% of the general population. These individuals are spared from most of the symptoms of the disease. However, they are predisposed to developing cancer or ischemic heart disease, and die 7-8 years earlier than the non-carriers. DNA double-strand breaks activate ATM, and active ATM is known to phosphorylate an extensive array of proteins involved in cell cycle arrest, DNA repair, and apoptosis. The importance of ATM in the regulation of DNA damage response signaling is fairly well-established. This review summarizes the role of ATM in the heart, specifically in cardiac remodeling following β-adrenergic receptor stimulation and myocardial infarction. |
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| Grant Information: | I01 BX000640 United States BX BLRD VA; I01 BX002332 United States BX BLRD VA; R15 HL129140 United States HL NHLBI NIH HHS |
| Contributed Indexing: | Keywords: Apoptosis; Ataxia-telangiectasia mutated kinase; Fibrosis; Hypertrophy; Myocardial infarction; Myocardial remodeling; β-adrenergic receptor |
| Entry Date(s): | Date Created: 20171121 Latest Revision: 20231112 |
| Update Code: | 20260130 |
| PubMed Central ID: | PMC5690556 |
| PMID: | 29152614 |
| Database: | MEDLINE |
Journal Article