4bxo

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m (Protected "4bxo" [edit=sysop:move=sysop])
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'''Unreleased structure'''
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{{STRUCTURE_4bxo| PDB=4bxo | SCENE= }}
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===Architecture and DNA recognition elements of the Fanconi anemia FANCM- FAAP24 complex===
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{{ABSTRACT_PUBMED_23932590}}
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The entry 4bxo is ON HOLD until Paper Publication
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==Disease==
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[[http://www.uniprot.org/uniprot/FANCM_HUMAN FANCM_HUMAN]] Fanconi anemia. The disease is caused by mutations affecting the gene represented in this entry.
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Authors: Coulthard, R., Deans, A., Swuec, P., Bowles, M., Purkiss, A., Costa, A., West, S., McDonald, N.
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==Function==
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[[http://www.uniprot.org/uniprot/FANCM_HUMAN FANCM_HUMAN]] ATPase required for FANCD2 ubiquitination, a key reaction in DNA repair. Binds to ssDNA but not to dsDNA. Recruited to forks stalled by DNA interstrand cross-links, and required for cellular resistance to such lesions.<ref>PMID:16116422</ref> <ref>PMID:16116434</ref> [REFERENCE:7][REFERENCE:8] [[http://www.uniprot.org/uniprot/FAP24_HUMAN FAP24_HUMAN]] Plays a role in DNA repair through recruitment of the FA core complex to damaged DNA. Regulates FANCD2 monoubiquitination upon DNA damage. Induces chromosomal instability as well as hypersensitivity to DNA cross-linking agents, when repressed. Targets FANCM/FAAP24 complex to the DNA, preferentially to single strand DNA.
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Description: Architecture and DNA recognition elements of the Fanconi anemia FANCM-FAAP24 complex
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==About this Structure==
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[[4bxo]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4BXO OCA].
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==Reference==
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<ref group="xtra">PMID:023932590</ref><references group="xtra"/><references/>
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[[Category: Homo sapiens]]
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[[Category: RNA helicase]]
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[[Category: Bowles, M.]]
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[[Category: Costa, A.]]
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[[Category: Coulthard, R.]]
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[[Category: Deans, A.]]
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[[Category: McDonald, N.]]
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[[Category: Purkiss, A.]]
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[[Category: Swuec, P.]]
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[[Category: West, S.]]
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[[Category: Dna binding]]
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[[Category: Hydrolase-dna complex]]
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[[Category: Pseudo-nuclease]]

Revision as of 07:29, 28 August 2013

Template:STRUCTURE 4bxo

Contents

Architecture and DNA recognition elements of the Fanconi anemia FANCM- FAAP24 complex

Template:ABSTRACT PUBMED 23932590

Disease

[FANCM_HUMAN] Fanconi anemia. The disease is caused by mutations affecting the gene represented in this entry.

Function

[FANCM_HUMAN] ATPase required for FANCD2 ubiquitination, a key reaction in DNA repair. Binds to ssDNA but not to dsDNA. Recruited to forks stalled by DNA interstrand cross-links, and required for cellular resistance to such lesions.[1] [2] [REFERENCE:7][REFERENCE:8] [FAP24_HUMAN] Plays a role in DNA repair through recruitment of the FA core complex to damaged DNA. Regulates FANCD2 monoubiquitination upon DNA damage. Induces chromosomal instability as well as hypersensitivity to DNA cross-linking agents, when repressed. Targets FANCM/FAAP24 complex to the DNA, preferentially to single strand DNA.

About this Structure

4bxo is a 4 chain structure with sequence from Homo sapiens. Full crystallographic information is available from OCA.

Reference

  • Coulthard R, Deans AJ, Swuec P, Bowles M, Costa A, West SC, McDonald NQ. Architecture and DNA Recognition Elements of the Fanconi Anemia FANCM-FAAP24 Complex. Structure. 2013 Aug 6. pii: S0969-2126(13)00255-4. doi:, 10.1016/j.str.2013.07.006. PMID:23932590 doi:10.1016/j.str.2013.07.006
  1. ↑ Meetei AR, Medhurst AL, Ling C, Xue Y, Singh TR, Bier P, Steltenpool J, Stone S, Dokal I, Mathew CG, Hoatlin M, Joenje H, de Winter JP, Wang W. A human ortholog of archaeal DNA repair protein Hef is defective in Fanconi anemia complementation group M. Nat Genet. 2005 Sep;37(9):958-63. Epub 2005 Aug 21. PMID:16116422 doi:ng1626
  2. ↑ Mosedale G, Niedzwiedz W, Alpi A, Perrina F, Pereira-Leal JB, Johnson M, Langevin F, Pace P, Patel KJ. The vertebrate Hef ortholog is a component of the Fanconi anemia tumor-suppressor pathway. Nat Struct Mol Biol. 2005 Sep;12(9):763-71. Epub 2005 Aug 21. PMID:16116434 doi:10.1038/nsmb981

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