File:Recombinational repair of DNA double-strand damage.jpg
Size of this preview: 562 × 600 pixels. Other resolutions: 225 × 240 pixels | 450 × 480 pixels | 1,016 × 1,084 pixels.
Original file (1,016 × 1,084 pixels, file size: 159 KB, MIME type: image/jpeg)
 | This is a file from the Wikimedia Commons. Information from its description page there is shown below. Commons is a freely licensed media file repository. You can help. |
Summary
| Description |
English: Recombinational repair of DNA double-strand damage - some key steps. ATM (ATM) is a protein kinase that is recruited and activated by DNA double-strand breaks. DNA double-strand damages also activate the Fanconi anemia core complex (FANCA/B/C/E/F/G/L/M).[1] The FA core complex monoubiquitinates the downstream targets FANCD2 and FANCI.[2] ATM activates (phosphorylates) CHEK2 and FANCD2[3] CHEK2 phosphorylates BRCA1.[4] Ubiquinated FANCD2 complexes with BRCA1 and RAD51.[5] The PALB2 protein acts as a hub,[6] bringing together BRCA1, BRCA2 and RAD51 at the site of a DNA double-strand break, and also binds to RAD51C, a member of the RAD51 paralog complex RAD51B-RAD51C-RAD51D-XRCC2 (BCDX2). The BCDX2 complex is responsible for RAD51 recruitment or stabilization at damage sites.[7] RAD51 plays a major role in homologous recombinational repair of DNA during double strand break repair. In this process, an ATP dependent DNA strand exchange takes place in which a template strand invades base-paired strands of homologous DNA molecules. RAD51 is involved in the search for homology and strand pairing stages of the process. |
| Date | |
| Source | Own work |
| Author | Chaya5260 |
Licensing
I, the copyright holder of this work, hereby publish it under the following license:
This file is licensed under the Creative Commons Attribution-Share Alike 4.0 International license.
- You are free:
- to share – to copy, distribute and transmit the work
- to remix – to adapt the work
- Under the following conditions:
- attribution – You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use.
- share alike – If you remix, transform, or build upon the material, you must distribute your contributions under the same or compatible license as the original.
- ↑ (2010). "Susceptibility pathways in Fanconi's anemia and breast cancer". N. Engl. J. Med. 362 (20): 1909–19. DOI:10.1056/NEJMra0809889. PMID 20484397. PMC: 3069698.
- ↑ (2009). "The Fanconi anemia protein FANCM is controlled by FANCD2 and the ATR/ATM pathways". J. Biol. Chem. 284 (38): 25560–8. DOI:10.1074/jbc.M109.007690. PMID 19633289. PMC: 2757957.
- ↑ (2011). "Coordinated action of the Fanconi anemia and ataxia telangiectasia pathways in response to oxidative damage". DNA Repair (Amst.) 10 (5): 518–25. DOI:10.1016/j.dnarep.2011.02.007. PMID 21466974.
- ↑ (2011). "Tumor suppressor CHK2: regulator of DNA damage response and mediator of chromosomal stability". Clin. Cancer Res. 17 (3): 401–5. DOI:10.1158/1078-0432.CCR-10-1215. PMID 21088254.
- ↑ (2002). "S-phase-specific interaction of the Fanconi anemia protein, FANCD2, with BRCA1 and RAD51". Blood 100 (7): 2414–20. DOI:10.1182/blood-2002-01-0278. PMID 12239151.
- ↑ (2014). "PALB2: the hub of a network of tumor suppressors involved in DNA damage responses". Biochim. Biophys. Acta 1846 (1): 263–75. DOI:10.1016/j.bbcan.2014.06.003. PMID 24998779. PMC: 4183126.
- ↑ (2013). "Rad51 paralog complexes BCDX2 and CX3 act at different stages in the BRCA1-BRCA2-dependent homologous recombination pathway". Mol. Cell. Biol. 33 (2): 387–95. DOI:10.1128/MCB.00465-12. PMID 23149936. PMC: 3554112.
File history
Click on a date/time to view the file as it appeared at that time.
| Date/Time | Thumbnail | Dimensions | User | Comment | |
|---|---|---|---|---|---|
| current | 23:54, 9 June 2016 | | 1,016 × 1,084 (159 KB) | Chaya5260 | User created page with UploadWizard |
File usage
The following 3 pages use this file:
