1d4u: Difference between revisions
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{{STRUCTURE_1d4u| PDB=1d4u | SCENE= }} | {{STRUCTURE_1d4u| PDB=1d4u | SCENE= }} | ||
===INTERACTIONS OF HUMAN NUCLEOTIDE EXCISION REPAIR PROTEIN XPA WITH RPA70 AND DNA: CHEMICAL SHIFT MAPPING AND 15N NMR RELAXATION STUDIES=== | |||
{{ABSTRACT_PUBMED_10563794}} | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/XPA_HUMAN XPA_HUMAN]] Defects in XPA are a cause of xeroderma pigmentosum complementation group A (XP-A) [MIM:[http://omim.org/entry/278700 278700]]; also known as xeroderma pigmentosum type 1 (XP1). XP-A is a rare human autosomal recessive disease characterized by solar sensitivity, high predisposition for developing cancers on areas exposed to sunlight and, in some cases, neurological abnormalities. Group A patients show the most severe skin symptoms and progressive neurological disorders.<ref>PMID:1339397</ref><ref>PMID:1372103</ref><ref>PMID:9671271</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/XPA_HUMAN XPA_HUMAN]] Involved in DNA excision repair. Initiates repair by binding to damaged sites with various affinities, depending on the photoproduct and the transcriptional state of the region. Required for UV-induced CHEK1 phosphorylation and the recruitment of CEP164 to cyclobutane pyrimidine dimmers (CPD), sites of DNA damage after UV irradiation.<ref>PMID:19197159</ref> | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:010563794</ref><references group="xtra"/> | <ref group="xtra">PMID:010563794</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Buchko, G W.]] | [[Category: Buchko, G W.]] | ||
Revision as of 07:45, 25 March 2013
INTERACTIONS OF HUMAN NUCLEOTIDE EXCISION REPAIR PROTEIN XPA WITH RPA70 AND DNA: CHEMICAL SHIFT MAPPING AND 15N NMR RELAXATION STUDIESINTERACTIONS OF HUMAN NUCLEOTIDE EXCISION REPAIR PROTEIN XPA WITH RPA70 AND DNA: CHEMICAL SHIFT MAPPING AND 15N NMR RELAXATION STUDIES
Template:ABSTRACT PUBMED 10563794
DiseaseDisease
[XPA_HUMAN] Defects in XPA are a cause of xeroderma pigmentosum complementation group A (XP-A) [MIM:278700]; also known as xeroderma pigmentosum type 1 (XP1). XP-A is a rare human autosomal recessive disease characterized by solar sensitivity, high predisposition for developing cancers on areas exposed to sunlight and, in some cases, neurological abnormalities. Group A patients show the most severe skin symptoms and progressive neurological disorders.[1][2][3]
FunctionFunction
[XPA_HUMAN] Involved in DNA excision repair. Initiates repair by binding to damaged sites with various affinities, depending on the photoproduct and the transcriptional state of the region. Required for UV-induced CHEK1 phosphorylation and the recruitment of CEP164 to cyclobutane pyrimidine dimmers (CPD), sites of DNA damage after UV irradiation.[4]
About this StructureAbout this Structure
1d4u is a 1 chain structure with sequence from Homo sapiens. Full experimental information is available from OCA.
ReferenceReference
- ↑ Buchko GW, Daughdrill GW, de Lorimier R, Rao B K, Isern NG, Lingbeck JM, Taylor JS, Wold MS, Gochin M, Spicer LD, Lowry DF, Kennedy MA. Interactions of human nucleotide excision repair protein XPA with DNA and RPA70 Delta C327: chemical shift mapping and 15N NMR relaxation studies. Biochemistry. 1999 Nov 16;38(46):15116-28. PMID:10563794
- ↑ Satokata I, Tanaka K, Okada Y. Molecular basis of group A xeroderma pigmentosum: a missense mutation and two deletions located in a zinc finger consensus sequence of the XPAC gene. Hum Genet. 1992 Mar;88(6):603-7. PMID:1339397
- ↑ Satokata I, Tanaka K, Yuba S, Okada Y. Identification of splicing mutations of the last nucleotides of exons, a nonsense mutation, and a missense mutation of the XPAC gene as causes of group A xeroderma pigmentosum. Mutat Res. 1992 Mar;273(2):203-12. PMID:1372103
- ↑ States JC, McDuffie ER, Myrand SP, McDowell M, Cleaver JE. Distribution of mutations in the human xeroderma pigmentosum group A gene and their relationships to the functional regions of the DNA damage recognition protein. Hum Mutat. 1998;12(2):103-13. PMID:9671271 doi:<103::AID-HUMU5>3.0.CO;2-6 10.1002/(SICI)1098-1004(1998)12:2<103::AID-HUMU5>3.0.CO;2-6
- ↑ Pan YR, Lee EY. UV-dependent interaction between Cep164 and XPA mediates localization of Cep164 at sites of DNA damage and UV sensitivity. Cell Cycle. 2009 Feb 15;8(4):655-64. Epub 2009 Feb 14. PMID:19197159