- 细胞因子
- Dihydropyrimidinase and Proteins
- Regulatory proteins
- 授予称号
- Peptide Substrates
- Isoform Specific Antibodies
- Deacetylase & Demethylase Proteins
- Acetyl & Methyltransferase Proteins
- siRNA Controls
- Cell Stress and Chaperone Proteins
- 激酶
- 双加氧酶与蛋白质
- Transcription Proteins
- Carbohydrate Kinases
- 表观遗传酶抑制剂
- Growth Factors
- 脂类激酶
- Phospholipase C and Proteins
- Mutant Kinases
- Oligo Substrates
- Fluorescent and Color Proteins
Overview:
ATMisamasterregulatorfordsDNAbreakrepair,whichbelongstothephosphoinositide3-kinase(PI(3)K)superfamily.Unlikeotherlipidkinases,ATMphosphorylatesproteins.ATMispresentinundamagedcellsasaninactivedimer,whichisactivatedlikelyinresponsetochangesinchromatinstructure.ExposureofcellstoionizingrADIationtriggersATMkinaseactivity,leadingtocellcyclearrestintheG1,SorG2phase.SeveralsubstratesoftheATMkinaseparticipateintheseIR-inducedcell-cyclearrests.Theseincludep53,MDM2andCHK2intheG1checkpoint;NBS1,BRCA1,FancD2andSMC1inthetransientIR-inducedS-phasearrest;andBRCA1andhRAD17duringtheG2/Mcheckpoint.ATMismutatedinthehereditarydiseaseataxia-telangiectasia.
References:
1.BakkeNIST,C.J.,etal.:DNAdamageactivatesATMthroughintermolecularautophosphorylationanddimerdissociation.Nature.2003:421;499-506.2.KitagawaR,etal.:PhosphorylationofSMC1isacriticaldownstreameventintheATM-NBS1-BRCA1pathway.GenesDev.2004:18(12);1423-38.3.Falck,J.etal.:ConservedmodesofrecruitmentofATM,ATRandDNA-PKcstositesofDNAdamage.Nature.2005:434;605-611.
