KU70 _ XRCC6
- Known as:
- KU70 _ XRCC6
- Catalog number:
- Y213694
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- KU70 _ XRCC6
Ask about this productRelated genes to: KU70 _ XRCC6
- Gene:
- ATP23 NIH gene
- Name:
- ATP23 metallopeptidase and ATP synthase assembly factor homolog
- Previous symbol:
- XRCC6BP1
- Synonyms:
- KUB3
- Chromosome:
- 12q14.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-01-09
- Date modifiied:
- 2016-11-09
- Gene:
- XRCC6 NIH gene
- Name:
- X-ray repair cross complementing 6
- Previous symbol:
- G22P1
- Synonyms:
- D22S731, D22S671, KU70, ML8
- Chromosome:
- 22q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1988-05-11
- Date modifiied:
- 2016-06-02
Related products to: KU70 _ XRCC6
5'-deoxyribose-5-phosphate lyase Ku70,5'-dRP lyase Ku70,70 kDa subunit of Ku antigen,ATP-dependent DNA helicase 2 subunit 1,ATP-dependent DNA helicase II 70 kDa subunit,CTC box-binding factor 75 kDa s5'-deoxyribose-5-phosphate lyase Ku70,5'-dRP_AP lyase Ku70,ATP-dependent DNA helicase 2 subunit 1,ATP-dependent DNA helicase II 70 kDa subunit,Chicken,DNA repair protein XRCC6,G22P1,Gallus gallus,Ku a5'-deoxyribose-5-phosphate lyase Ku70,5'-dRP_AP lyase Ku70,ATP-dependent DNA helicase 2 subunit 1,ATP-dependent DNA helicase II 70 kDa subunit,CTC box-binding factor 75 kDa subunit,CTC75,CTCBF,DNA repanti-Ku70anti-Ku70anti-Ku70anti-Ku70 (3D12)Anti-Ku70 produced in rabbit Antibodyanti-Ku70 (3D12)anti-Ku70 (3D12) type: Primary antibodies host: Mouseanti-Ku70 (4C2-1A6)anti-Ku70 (4C2-1A6), Mouse monoclonal to Ku70, Isotype IgG1, Host MouseAnti-Ku70 AntibodyAnti-Ku70 AntibodyAnti-Ku70 Antibody Related articles to: KU70 _ XRCC6
- Human glioblastomas are characterized by frequent DNA amplifications most often at chromosome regions 7p11.2 and 12q13-15. Although amplification is a well-known hallmark of glioblastoma genetics the function of most amplified genes in glioblastoma biology is not understood. Previously, we cloned Ku70-binding protein 3 (KUB3) from the amplified domain at 12q13-15. Here, we report that glioblastoma cell cultures with endogenous KUB3 gene amplification and with elevated KUB3 protein expression show an efficient double-strand break (DSB) repair after being irradiated with 1 Gy. A significantly less efficient DSB repair was found in glioma cell cultures without KUB3 amplification and expression. Furthermore, we found that a siRNA-mediated reduction of the endogenous KUB3 expression in glioblastoma cells resulted in a reduction of the repair efficiency. HeLa cells transfected with KUB3 showed an increased DSB repair in comparison to untreated HeLa cells. In addition, KUB3 seems to influence DSB efficiency via the DNA-PK-dependent repair pathway as shown by simultaneous inhibition of KUB3 and DNA-PK. The data provide the first evidence for a link between the level of KUB3 amplification and expression in glioma and DSB repair efficiency. - Source: PubMed
Publication date: 2013/05/13
Fischer UlrikeRheinheimer StefanieKrempler AndreaLöbrich MarkusMeese Eckart - DNA-dependent protein kinase (DNA-PK) plays a critical role in resealing DNA double-stand breaks by non-homologous end joining. Aside from DNA-PK, XRCC4 and DNA ligase IV, other proteins which play a role(s) in this repair pathway remain unknown; DNA-PK contains a catalytic subunit (DNA-PKcs) and a DNA binding subunit (Ku70 and Ku80). We isolated Ku70-binding proteins (KUB1-KUB4) using yeast two-hybrid analyses. Sequence analyses revealed KUB1 to be apolipoprotein J (apoJ), also known as X-ray-inducible transcript 8 (XIP8), testosterone-repressed prostate message-2 (TRPM-2) and clusterin. KUB2 is Ku80. KUB3 and KUB4 are unknown, >10 kb trans-cripts. Interactions of apoJ/XIP8 or KUB3 with Ku70 were confirmed by co-immunoprecipitation analyses in MCF-7:WS8 breast cancer or IMR-90 normal lung fibroblast cells, respectively. The interaction of apoJ/XIP8 with Ku70 was confirmed by far-western analyses. Stable over-expression of full-length apoJ/XIP8 in MCF-7:WS8 caused decreased Ku70/Ku80 DNA end binding that was restored by apoJ/XIP8 monoclonal antibodies. The role of apoJ/XIP8 in ionizing radiation resistance/sensitivity is under investigation. - Source: PubMed
Yang C RYeh SLeskov KOdegaard EHsu H LChang CKinsella T JChen D JBoothman D A