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10.4161/cc.27945 http://scihub22266oqcxt.onion/10.4161/cc.27945 C4013160!4013160!24553124     free     free     free       Cell+Cycle 2014 ; 13 (7): 1091-100 Nephropedia Template TP {{tp|p=24553124|t=2014. ATM controls proper mitotic spindle structure |pdf=|usr=}}{{24553124}} gab.com Text ATM controls proper mitotic spindle structure JO: Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=24553124 #FOAvip The recessive ataxia-telangiectasia (A-T) syndrome is characterized by cerebellar degeneration, immunodeficiency, cancer susceptibility, premature aging, and insulin-resistant diabetes and is caused by loss of function of the ATM kinase, a member of the phosphoinositide 3-kinase?like protein kinases (PIKKs) family. ATM plays a crucial role in the DNA damage response (DDR); however, the complexity of A-T features suggests that ATM may regulate other cellular functions. Here we show that ATM affects proper bipolar mitotic spindle structure independently of DNA damage. In addition, we find that in mitosis ATM forms a complex with the poly(ADP)ribose (PAR) polymerase Tankyrase (TNKS) 1, the spindle pole protein NuMA1, and breast cancer susceptibility protein BRCA1, another crucial DDR player. Our evidence indicates that the complex is required for efficient poly(ADP)ribosylation of NuMA1. We find further that a mutant NuMA1 version, non-phosphorylatable at potential ATM-dependent phosphorylation sites, is poorly PARylated and induces loss of spindle bipolarity. Our findings may help to explain crucial A-T features and provide further mechanistic rationale for TNKS inhibition in cancer therapy. Twit Text FOAVip ATM controls proper mitotic spindle structure ????Cell Cycle http://www.kidney.de/pget.php?&tw=1&pmid=24553124 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24553124 #FOAvip English Wikipedia <ref>{{Cite pmid|24553124}}</ref> ATM controls proper mitotic spindle structure #MMPMID24553124 Palazzo L; Della Monica R; Visconti R; Costanzo V; Grieco D Cell Cycle 2014[Apr]; 13 (7): 1091-100 PMID24553124show ga The recessive ataxia-telangiectasia (A-T) syndrome is characterized by cerebellar degeneration, immunodeficiency, cancer susceptibility, premature aging, and insulin-resistant diabetes and is caused by loss of function of the ATM kinase, a member of the phosphoinositide 3-kinase?like protein kinases (PIKKs) family. ATM plays a crucial role in the DNA damage response (DDR); however, the complexity of A-T features suggests that ATM may regulate other cellular functions. Here we show that ATM affects proper bipolar mitotic spindle structure independently of DNA damage. In addition, we find that in mitosis ATM forms a complex with the poly(ADP)ribose (PAR) polymerase Tankyrase (TNKS) 1, the spindle pole protein NuMA1, and breast cancer susceptibility protein BRCA1, another crucial DDR player. Our evidence indicates that the complex is required for efficient poly(ADP)ribosylation of NuMA1. We find further that a mutant NuMA1 version, non-phosphorylatable at potential ATM-dependent phosphorylation sites, is poorly PARylated and induces loss of spindle bipolarity. Our findings may help to explain crucial A-T features and provide further mechanistic rationale for TNKS inhibition in cancer therapy. äATM controls proper mitotic spindle structure (epmc).pdf DeepDyve Pubget Overpricing