Warning: Undefined variable $zfal in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Deprecated: str_replace(): Passing null to parameter #3 ($subject) of type array|string is deprecated in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 525
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 530
Warning: Undefined variable $sterm in C:\Inetpub\vhosts\kidney.de\httpdocs\mlpefetch.php on line 531
English Wikipedia
Nephropedia Template TP (
Twit Text
DeepDyve Pubget Overpricing |
lüll ATM: a mediator of multiple responses to genotoxic stress Rotman G; Shiloh YOncogene 1999[Nov]; 18 (45): 6135-44The ATM protein kinase is the product of the gene responsible for the pleiotropic recessive disorder ataxia-telangiectasia. ATM-deficient cells show enhanced sensitivity and greatly reduced responses to genotoxic agents that generate DNA double strand breaks (DSBs), such as ionizing radiation and radiomimetic chemicals, but exhibit normal responses to DNA adducts and base modifications induced by other agents. Therefore, DSBs are most likely the predominant signal for the activation of ATM-mediated pathways. Identification of the ATM gene triggered extensive research aimed at elucidating the numerous functions of its large multifaceted protein product. While ATM has both nuclear and cytoplasmic functions, this review will focus on its roles in the nucleus where it plays a central role in the very early stages of damage detection and serves as a master controller of cellular responses to DSBs. By activating key regulators of multiple signal transduction pathways, ATM mediates the efficient induction of a signaling network responsible for repair of the damage, and for cellular recovery and survival.|*Signal Transduction[MESH]|Animals[MESH]|Ataxia Telangiectasia Mutated Proteins[MESH]|Cell Cycle Proteins[MESH]|Cell Cycle/physiology/radiation effects[MESH]|Cell Survival[MESH]|Chromatin/genetics/metabolism[MESH]|DNA Damage/*genetics/*physiology/radiation effects[MESH]|DNA Repair/genetics/physiology[MESH]|DNA-Binding Proteins[MESH]|Humans[MESH]|Protein Serine-Threonine Kinases/*metabolism[MESH]|Tumor Suppressor Proteins[MESH] |