| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :1.2080739 |
| Here we demonstrate that c Abl interacts constitutively with Rad 51 . 1.2080739^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.56578379 |
| Interaction between c Abl and the Rad 51 protein has also provided support for involvement of c Abl in recombinational repair of DNA strand breaks . 0.56578379^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :1.2038741 |
| In assays using purified components , phosphorylation of Rad 51 by c Abl enhances complex formation between Rad 51 and Rad 52 , which cooperates with Rad 51 in recombination and repair . 1.2038741^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.61741252 |
| Complex regulation of HRR by cell cycle checkpoint and surveillance functions is suggested not only by direct interactions between human Rad 51 and p 53 , c Abl , and BRCA 2 , but also by very high recombination rates in p 53 deficient cells . . 0.61741252^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| Gleevec is a relatively specific inhibitor of c Abl , a tyrosine kinase that can play a role in the regulation Rad 51 . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| Abl tyrosine kinase is not essential for ataxia telangiectasia mutated functions in chromosomal maintenance . c Abl is activated by DNA damage in an ataxia telangiectasia mutated ( ATM ) dependent manner and plays important roles in growth arrest and apoptosis induced by DNA damage . c Abl also interacts physically and functionally with Rad 51 , a key molecule in homologous recombinational ( HR ) DNA repair . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| Here we demonstrate that RAD 51 is important for resistance to cisplatin and mitomycin C in cells expressing the BCR / ABL oncogenic tyrosine kinase . ^^^ BCR / ABL significantly enhances the expression of RAD 51 and several RAD 51 Paralogs . ^^^ Phosphorylation of the RAD 51 Tyr 315 residue by BCR / ABL appears essential for enhanced DSB repair and drug resistance . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| Two contrasting situations are discussed : one with up regulation ( expression of the oncogene BCR / ABL ) and one with a down regulation ( expression of the oncogene BCL 2 ) of RAD 51 , associated with apoptosis inhibition and tumour predisposition . . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| Ionizing radiation induced Rad 51 nuclear focus formation is cell cycle regulated and defective in both ATM ( / ) and c Abl ( / ) cells . ^^^ Furthermore , IR induced Rad 51 focus formation was defective in AT and c Abl ( / ) cells , but not wild type or NBS cells . ^^^ A decreased and delayed formation of Rad 51 foci containing nuclei was observed in AT cells upon IR , whereas in c Abl ( / ) cells a decreased but not delayed formation of Rad 51 foci containing nuclei was observed . ^^^ In conclusion , effective and prompt IR induced Rad 51 focus formation is cell cycle regulated and requires both ATM and c Abl . . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| PAT Plat was found to result in an extra number of slowly repairable DNA double strand breaks , inhibition of DNA protein kinase activity , dramatic nuclear relocalization of RAD 51 , hyperphosphorylation of the BRCA 1 protein , and activation of proto oncogenic c Abl tyrosine kinase . . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| Location of tyrosine 315 , a target for phosphorylation by cAbl tyrosine kinase , at the edge of the subunit subunit interface of the human Rad 51 filament . ^^^ Rad 51 is a key element of recombinational DNA repair and its activity is regulated by phosphorylation of the tyrosine residue at position 315 by cAbl kinase . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| BCR / ABL promotes interactions of BLM with RAD 51 , while simultaneous overexpression of BLM and RAD 51 in normal cells increases drug resistance . ^^^ These data suggest that BLM collaborates with RAD 51 to facilitate HRR and promotes the resistance of BCR / ABL positive leukemia cells to DNA damaging agents . . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| The mechanism of action appears to involve imatinib inhibition of c abl kinase activity with an associated decrease in CLB induced Rad 51 phosphorylation and CLB induced Rad 51 nuclear foci , suggesting that imatinib decreases Rad 51 related DNA repair of CLB induced DNA lesions . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| The ability of hypoxia to down regulate Rad 51 and other HR associated genes under hypoxia was not correlated to c Abl or c Myc gene expression , p 53 genotype or function , propensity for hypoxia mediated apoptosis , or specific changes in cell cycle distribution . ^^^ |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| NA |
|
| Interacting proteins: Q06609 and P00519 |
Pubmed |
SVM Score :0.0 |
| NA |
|