ERCC8 (gene): Difference between revisions

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{{Infobox_gene}}
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'''DNA excision repair protein ERCC-8''' is a [[protein]] that in humans is encoded by the ''ERCC8'' [[gene]].<ref name="pmid8596535">{{cite journal | vauthors = Itoh T, Shiomi T, Shiomi N, Harada Y, Wakasugi M, Matsunaga T, Nikaido O, Friedberg EC, Yamaizumi M | title = Rodent complementation group 8 (ERCC8) corresponds to Cockayne syndrome complementation group A | journal = Mutat Res | volume = 362 | issue = 2 | pages = 167–74 |date=April 1996 | pmid = 8596535 | pmc =  | doi =  10.1016/0921-8777(95)00046-1}}</ref><ref name="entrez">{{cite web | title = Entrez Gene: ERCC8 excision repair cross-complementing rodent repair deficiency, complementation group 8| url = https://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=1161| accessdate = }}</ref>
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This gene encodes a WD repeat protein, which interacts with the [[Cockayne syndrome type B]] (CSB) and [[p44 protein]]s, the latter being a subunit of the RNA polymerase II [[transcription factor II H]]. Mutations in this gene have been identified in patients with the hereditary disease [[Cockayne syndrome]] (CS). CS is an accelerated aging disorder characterized by [[photosensitivity]], impaired development and multi-system progressive degeneration. The CS cells are abnormally sensitive to ultraviolet radiation and are defective in the repair of transcriptionally active genes. Multiple alternatively [[Protein splicing|splice]]d transcript variants encoding different isoforms have been found for this gene.<ref name="entrez" />
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CS arises from [[germline]] [[mutation]]s in either of two [[gene]]s ''CSA(ERCC8)'' or ''CSB([[ERCC6]])''. ''CSA'' mutations generally give rise to a more moderate form of CS than ''CSB'' mutations.<ref name="pmid26616585">{{cite journal |vauthors=Iyama T, Wilson DM |title=Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome |journal=J. Mol. Biol. |volume=428 |issue=1 |pages=62–78 |year=2016 |pmid=26616585 |pmc=4738086 |doi=10.1016/j.jmb.2015.11.020 |url=}}</ref>  Mutations in the ''CSA'' gene account for about 20% of CS cases.<ref name="pmid24781187">{{cite journal |vauthors=Koch S, Garcia Gonzalez O, Assfalg R, Schelling A, Schäfer P, Scharffetter-Kochanek K, Iben S |title=Cockayne syndrome protein A is a transcription factor of RNA polymerase I and stimulates ribosomal biogenesis and growth |journal=Cell Cycle |volume=13 |issue=13 |pages=2029–37 |year=2014 |pmid=24781187 |pmc=4111694 |doi=10.4161/cc.29018 |url=}}</ref>
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==Function==


<!-- The GNF_Protein_box is automatically maintained by Protein Box Bot.  See Template:PBB_Controls to Stop updates. -->
CSA and CSB proteins are thought to function in [[transcription (biology)|transcription]] and [[DNA repair]], most notably in transcription-coupled nucleotide excision repair. CSA and CSB-deficient cells exhibit a lack of preferential repair of UV-induced [[pyrimidine dimer|cyclobutane pyrimidine dimers]] in actively transcribed genes, consistent with a failed transcription coupled nucleotide excision repair response.<ref name="pmid8290349">{{cite journal |vauthors=van Hoffen A, Natarajan AT, Mayne LV, van Zeeland AA, Mullenders LH, Venema J |title=Deficient repair of the transcribed strand of active genes in Cockayne's syndrome cells |journal=Nucleic Acids Res. |volume=21 |issue=25 |pages=5890–5 |year=1993 |pmid=8290349 |pmc=310470 |doi= 10.1093/nar/21.25.5890|url=}}</ref>  Within the cell, the CSA protein localizes to sites of [[DNA damage (naturally occurring)|DNA damage]], particularly [[Crosslinking of DNA|inter-strand cross-links]], double-strand breaks and some mono-adducts.<ref name="pmid26616585"/>
{{GNF_Protein_box
| image = 
| image_source = 
| PDB =
| Name = Excision repair cross-complementing rodent repair deficiency, complementation group 8
| HGNCid = 3439
  | Symbol = ERCC8
| AltSymbols =; CKN1; CSA
| OMIM = 609412
| ECnumber = 
| Homologene = 62
| MGIid = 1919241
| GeneAtlas_image1 = PBB_GE_ERCC8_205162_at_tn.png
| Function = {{GNF_GO|id=GO:0005515 |text = protein binding}}
| Component = {{GNF_GO|id=GO:0000109 |text = nucleotide-excision repair complex}} {{GNF_GO|id=GO:0005634 |text = nucleus}} {{GNF_GO|id=GO:0016363 |text = nuclear matrix}}
| Process = {{GNF_GO|id=GO:0006283 |text = transcription-coupled nucleotide-excision repair}} {{GNF_GO|id=GO:0006350 |text = transcription}} {{GNF_GO|id=GO:0006355 |text = regulation of transcription, DNA-dependent}} {{GNF_GO|id=GO:0007605 |text = sensory perception of sound}}
| Orthologs = {{GNF_Ortholog_box
    | Hs_EntrezGene = 1161
    | Hs_Ensembl = ENSG00000049167
    | Hs_RefseqProtein = NP_000073
    | Hs_RefseqmRNA = NM_000082
    | Hs_GenLoc_db =
    | Hs_GenLoc_chr = 5
    | Hs_GenLoc_start = 60205415
    | Hs_GenLoc_end = 60276648
    | Hs_Uniprot = Q13216
    | Mm_EntrezGene = 71991
    | Mm_Ensembl = ENSMUSG00000021694
    | Mm_RefseqmRNA = NM_028042
    | Mm_RefseqProtein = NP_082318
    | Mm_GenLoc_db = 
    | Mm_GenLoc_chr = 13
    | Mm_GenLoc_start = 109279483
    | Mm_GenLoc_end = 109316111
    | Mm_Uniprot = Q3TZV2
  }}
}}
'''Excision repair cross-complementing rodent repair deficiency, complementation group 8''', also known as '''ERCC8''', is a human [[gene]].<ref name="entrez">{{cite web | title = Entrez Gene: ERCC8 excision repair cross-complementing rodent repair deficiency, complementation group 8| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=1161| accessdate = }}</ref>


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==Interactions==
{{PBB_Summary
ERCC8 (gene) has been shown to [[Protein-protein interaction|interact]] with [[XAB2]].<ref name=pmid10944529>{{cite journal |vauthors=Nakatsu Y, Asahina H, Citterio E, Rademakers S, Vermeulen W, Kamiuchi S, Yeo JP, Khaw MC, Saijo M, Kodo N, Matsuda T, Hoeijmakers JH, Tanaka K |date=November 2000  |title=XAB2, a novel tetratricopeptide repeat protein involved in transcription-coupled DNA repair and transcription |journal=J. Biol. Chem. |volume=275 |issue=45 |pages=34931–7 |publisher= |location = UNITED STATES| issn = 0021-9258| pmid = 10944529 |doi = 10.1074/jbc.M004936200 | bibcode = | oclc =| id = | url = | language = | format = | accessdate = | laysummary = | laysource = | laydate = | quote = }}</ref>
| section_title =  
| summary_text = This gene encodes a WD repeat protein, which interacts with Cockayne syndrome type B (CSB) protein and with p44 protein, a subunit of the RNA polymerase II transcription factor IIH. Mutations in this gene have been identified in patients with hereditary disease Cockayne syndrome (CS). The CS cells are abnormally sensitive to ultraviolet radiation and are defective in the repair of transcriptionally active genes. Multiple alternatively spliced transcript variants encoding different isoforms have been found for this gene.<ref name="entrez">{{cite web | title = Entrez Gene: ERCC8 excision repair cross-complementing rodent repair deficiency, complementation group 8| url = http://www.ncbi.nlm.nih.gov/sites/entrez?Db=gene&Cmd=ShowDetailView&TermToSearch=1161| accessdate = }}</ref>
}}


==References==
==References==
{{reflist|2}}
{{reflist}}
 
==Further reading==
==Further reading==
{{refbegin | 2}}
{{refbegin | 2}}
{{PBB_Further_reading  
{{PBB_Further_reading  
| citations =  
| citations =  
*{{cite journal  | author=van Gool AJ, van der Horst GT, Citterio E, Hoeijmakers JH |title=Cockayne syndrome: defective repair of transcription? |journal=EMBO J. |volume=16 |issue= 14 |pages= 4155-62 |year= 1997 |pmid= 9250659 |doi=  }}
*{{cite journal  | vauthors=van Gool AJ, van der Horst GT, Citterio E, Hoeijmakers JH |title=Cockayne syndrome: defective repair of transcription? |journal=EMBO J. |volume=16 |issue= 14 |pages= 4155–62 |year= 1997 |pmid= 9250659 |doi=10.1093/emboj/16.14.4155  | pmc=1170041 }}
*{{cite journal  | author=Henning KA, Li L, Iyer N, ''et al.'' |title=The Cockayne syndrome group A gene encodes a WD repeat protein that interacts with CSB protein and a subunit of RNA polymerase II TFIIH. |journal=Cell |volume=82 |issue= 4 |pages= 555-64 |year= 1995 |pmid= 7664335 |doi= }}
*{{cite journal  | vauthors=Henning KA, Li L, Iyer N |title=The Cockayne syndrome group A gene encodes a WD repeat protein that interacts with CSB protein and a subunit of RNA polymerase II TFIIH |journal=Cell |volume=82 |issue= 4 |pages= 555–64 |year= 1995 |pmid= 7664335 |doi=10.1016/0092-8674(95)90028-4  |displayauthors=etal  }}
*{{cite journal  | author=Itoh T, Shiomi T, Shiomi N, ''et al.'' |title=Rodent complementation group 8 (ERCC8) corresponds to Cockayne syndrome complementation group A. |journal=Mutat. Res. |volume=362 |issue= 2 |pages= 167-74 |year= 1996 |pmid= 8596535 |doi= }}
*{{cite journal  | vauthors=Bregman DB, Halaban R, van Gool AJ |title=UV-induced ubiquitination of RNA polymerase II: a novel modification deficient in Cockayne syndrome cells |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=93 |issue= 21 |pages= 11586–90 |year= 1996 |pmid= 8876179 |doi=10.1073/pnas.93.21.11586  | pmc=38101  |displayauthors=1 |bibcode=1996PNAS...9311586B }}
*{{cite journal  | author=Bregman DB, Halaban R, van Gool AJ, ''et al.'' |title=UV-induced ubiquitination of RNA polymerase II: a novel modification deficient in Cockayne syndrome cells. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=93 |issue= 21 |pages= 11586-90 |year= 1996 |pmid= 8876179 |doi=  }}
*{{cite journal  | vauthors=Selby CP, Sancar A |title=Human transcription-repair coupling factor CSB/ERCC6 is a DNA-stimulated ATPase but is not a helicase and does not disrupt the ternary transcription complex of stalled RNA polymerase II |journal=J. Biol. Chem. |volume=272 |issue= 3 |pages= 1885–90 |year= 1997 |pmid= 8999876 |doi=10.1074/jbc.272.3.1885 }}
*{{cite journal  | author=Selby CP, Sancar A |title=Human transcription-repair coupling factor CSB/ERCC6 is a DNA-stimulated ATPase but is not a helicase and does not disrupt the ternary transcription complex of stalled RNA polymerase II. |journal=J. Biol. Chem. |volume=272 |issue= 3 |pages= 1885-90 |year= 1997 |pmid= 8999876 |doi=  }}
*{{cite journal  | vauthors=Nakatsu Y, Asahina H, Citterio E |title=XAB2, a novel tetratricopeptide repeat protein involved in transcription-coupled DNA repair and transcription |journal=J. Biol. Chem. |volume=275 |issue= 45 |pages= 34931–7 |year= 2001 |pmid= 10944529 |doi= 10.1074/jbc.M004936200  |displayauthors=etal }}
*{{cite journal  | author=Nakatsu Y, Asahina H, Citterio E, ''et al.'' |title=XAB2, a novel tetratricopeptide repeat protein involved in transcription-coupled DNA repair and transcription. |journal=J. Biol. Chem. |volume=275 |issue= 45 |pages= 34931-7 |year= 2001 |pmid= 10944529 |doi= 10.1074/jbc.M004936200 }}
*{{cite journal  | vauthors=Kamiuchi S, Saijo M, Citterio E |title=Translocation of Cockayne syndrome group A protein to the nuclear matrix: possible relevance to transcription-coupled DNA repair |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 1 |pages= 201–6 |year= 2002 |pmid= 11782547 |doi= 10.1073/pnas.012473199  | pmc=117539 |displayauthors=1 |bibcode=2002PNAS...99..201K |url=https://repub.eur.nl/pub/3192/eur_hoeijmakers_9110.pdf }}
*{{cite journal  | author=Kamiuchi S, Saijo M, Citterio E, ''et al.'' |title=Translocation of Cockayne syndrome group A protein to the nuclear matrix: possible relevance to transcription-coupled DNA repair. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 1 |pages= 201-6 |year= 2002 |pmid= 11782547 |doi= 10.1073/pnas.012473199 }}
*{{cite journal  | vauthors=Strausberg RL, Feingold EA, Grouse LH |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899–903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899  | pmc=139241 |displayauthors=1 |bibcode=2002PNAS...9916899M }}
*{{cite journal  | author=Strausberg RL, Feingold EA, Grouse LH, ''et al.'' |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899-903 |year= 2003 |pmid= 12477932 |doi= 10.1073/pnas.242603899 }}
*{{cite journal  | vauthors=Groisman R, Polanowska J, Kuraoka I |title=The ubiquitin ligase activity in the DDB2 and CSA complexes is differentially regulated by the COP9 signalosome in response to DNA damage |journal=Cell |volume=113 |issue= 3 |pages= 357–67 |year= 2003 |pmid= 12732143 |doi=10.1016/S0092-8674(03)00316-7  |displayauthors=etal  }}
*{{cite journal  | author=Groisman R, Polanowska J, Kuraoka I, ''et al.'' |title=The ubiquitin ligase activity in the DDB2 and CSA complexes is differentially regulated by the COP9 signalosome in response to DNA damage. |journal=Cell |volume=113 |issue= 3 |pages= 357-67 |year= 2003 |pmid= 12732143 |doi= }}
*{{cite journal  | vauthors=Cao H, Williams C, Carter M, Hegele RA |title=CKN1 (MIM 216400): mutations in Cockayne syndrome type A and a new common polymorphism |journal=J. Hum. Genet. |volume=49 |issue= 1 |pages= 61–3 |year= 2004 |pmid= 14661080 |doi= 10.1007/s10038-003-0107-2 }}
*{{cite journal  | author=Cao H, Williams C, Carter M, Hegele RA |title=CKN1 (MIM 216400): mutations in Cockayne syndrome type A and a new common polymorphism. |journal=J. Hum. Genet. |volume=49 |issue= 1 |pages= 61-3 |year= 2004 |pmid= 14661080 |doi= 10.1007/s10038-003-0107-2 }}
*{{cite journal  | vauthors=Ota T, Suzuki Y, Nishikawa T |title=Complete sequencing and characterization of 21,243 full-length human cDNAs |journal=Nat. Genet. |volume=36 |issue= 1 |pages= 40–5 |year= 2004 |pmid= 14702039 |doi= 10.1038/ng1285  |displayauthors=etal  }}
*{{cite journal  | author=Ota T, Suzuki Y, Nishikawa T, ''et al.'' |title=Complete sequencing and characterization of 21,243 full-length human cDNAs. |journal=Nat. Genet. |volume=36 |issue= 1 |pages= 40-5 |year= 2004 |pmid= 14702039 |doi= 10.1038/ng1285 }}
*{{cite journal  | vauthors=Gerhard DS, Wagner L, Feingold EA |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC) |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121–7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504  | pmc=528928  |displayauthors=etal  }}
*{{cite journal  | author=Gerhard DS, Wagner L, Feingold EA, ''et al.'' |title=The status, quality, and expansion of the NIH full-length cDNA project: the Mammalian Gene Collection (MGC). |journal=Genome Res. |volume=14 |issue= 10B |pages= 2121-7 |year= 2004 |pmid= 15489334 |doi= 10.1101/gr.2596504 }}
*{{cite journal  | vauthors=Ridley AJ, Colley J, Wynford-Thomas D, Jones CJ |title=Characterisation of novel mutations in Cockayne syndrome type A and xeroderma pigmentosum group C subjects |journal=J. Hum. Genet. |volume=50 |issue= 3 |pages= 151–4 |year= 2005 |pmid= 15744458 |doi= 10.1007/s10038-004-0228-2 }}
*{{cite journal  | author=Ridley AJ, Colley J, Wynford-Thomas D, Jones CJ |title=Characterisation of novel mutations in Cockayne syndrome type A and xeroderma pigmentosum group C subjects. |journal=J. Hum. Genet. |volume=50 |issue= 3 |pages= 151-4 |year= 2005 |pmid= 15744458 |doi= 10.1007/s10038-004-0228-2 }}
*{{cite journal  | vauthors=Sarker AH, Tsutakawa SE, Kostek S |title=Recognition of RNA polymerase II and transcription bubbles by XPG, CSB, and TFIIH: insights for transcription-coupled repair and Cockayne Syndrome |journal=Mol. Cell |volume=20 |issue= 2 |pages= 187–98 |year= 2006 |pmid= 16246722 |doi= 10.1016/j.molcel.2005.09.022  |displayauthors=etal  }}
*{{cite journal  | author=Sarker AH, Tsutakawa SE, Kostek S, ''et al.'' |title=Recognition of RNA polymerase II and transcription bubbles by XPG, CSB, and TFIIH: insights for transcription-coupled repair and Cockayne Syndrome. |journal=Mol. Cell |volume=20 |issue= 2 |pages= 187-98 |year= 2006 |pmid= 16246722 |doi= 10.1016/j.molcel.2005.09.022 }}
*{{cite journal  | vauthors=Groisman R, Kuraoka I, Chevallier O |title=CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome |journal=Genes Dev. |volume=20 |issue= 11 |pages= 1429–34 |year= 2006 |pmid= 16751180 |doi= 10.1101/gad.378206  | pmc=1475755  |displayauthors=etal  }}
*{{cite journal  | author=Groisman R, Kuraoka I, Chevallier O, ''et al.'' |title=CSA-dependent degradation of CSB by the ubiquitin-proteasome pathway establishes a link between complementation factors of the Cockayne syndrome. |journal=Genes Dev. |volume=20 |issue= 11 |pages= 1429-34 |year= 2006 |pmid= 16751180 |doi= 10.1101/gad.378206 }}
*{{cite journal  | vauthors=Fousteri M, Vermeulen W, van Zeeland AA, Mullenders LH |title=Cockayne syndrome A and B proteins differentially regulate recruitment of chromatin remodeling and repair factors to stalled RNA polymerase II in vivo |journal=Mol. Cell |volume=23 |issue= 4 |pages= 471–82 |year= 2006 |pmid= 16916636 |doi= 10.1016/j.molcel.2006.06.029 }}
*{{cite journal  | author=Fousteri M, Vermeulen W, van Zeeland AA, Mullenders LH |title=Cockayne syndrome A and B proteins differentially regulate recruitment of chromatin remodeling and repair factors to stalled RNA polymerase II in vivo. |journal=Mol. Cell |volume=23 |issue= 4 |pages= 471-82 |year= 2006 |pmid= 16916636 |doi= 10.1016/j.molcel.2006.06.029 }}
*{{cite journal  | vauthors=Saijo M, Hirai T, Ogawa A |title=Functional TFIIH is required for UV-induced translocation of CSA to the nuclear matrix |journal=Mol. Cell. Biol. |volume=27 |issue= 7 |pages= 2538–47 |year= 2007 |pmid= 17242193 |doi= 10.1128/MCB.01288-06 | pmc=1899911  |displayauthors=etal  }}
*{{cite journal  | author=Saijo M, Hirai T, Ogawa A, ''et al.'' |title=Functional TFIIH is required for UV-induced translocation of CSA to the nuclear matrix. |journal=Mol. Cell. Biol. |volume=27 |issue= 7 |pages= 2538-47 |year= 2007 |pmid= 17242193 |doi= 10.1128/MCB.01288-06 }}
*{{cite journal  | vauthors=D'Errico M, Parlanti E, Teson M |title=The role of CSA in the response to oxidative DNA damage in human cells |journal=Oncogene |volume=26 |issue= 30 |pages= 4336–43 |year= 2007 |pmid= 17297471 |doi= 10.1038/sj.onc.1210232 |displayauthors=etal  }}
*{{cite journal | author=D'Errico M, Parlanti E, Teson M, ''et al.'' |title=The role of CSA in the response to oxidative DNA damage in human cells. |journal=Oncogene |volume=26 |issue= 30 |pages= 4336-43 |year= 2007 |pmid= 17297471 |doi= 10.1038/sj.onc.1210232 }}
}}
}}
{{refend}}
{{refend}}


{{protein-stub}}
==External links==
{{WikiDoc Sources}}
* [https://www.ncbi.nlm.nih.gov/books/NBK1342/  GeneReviews/NCBI/NIH/UW entry on Cockayne syndrome]
 
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{{DNA repair}}
 
 
{{gene-5-stub}}

Latest revision as of 15:24, 4 November 2018

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Identifiers
Aliases
External IDsGeneCards: [1]
Orthologs
SpeciesHumanMouse
Entrez

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Ensembl

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UniProt

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RefSeq (mRNA)

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RefSeq (protein)

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Location (UCSC)n/an/a
PubMed searchn/an/a
Wikidata
View/Edit Human

DNA excision repair protein ERCC-8 is a protein that in humans is encoded by the ERCC8 gene.[1][2]

This gene encodes a WD repeat protein, which interacts with the Cockayne syndrome type B (CSB) and p44 proteins, the latter being a subunit of the RNA polymerase II transcription factor II H. Mutations in this gene have been identified in patients with the hereditary disease Cockayne syndrome (CS). CS is an accelerated aging disorder characterized by photosensitivity, impaired development and multi-system progressive degeneration. The CS cells are abnormally sensitive to ultraviolet radiation and are defective in the repair of transcriptionally active genes. Multiple alternatively spliced transcript variants encoding different isoforms have been found for this gene.[2]

CS arises from germline mutations in either of two genes CSA(ERCC8) or CSB(ERCC6). CSA mutations generally give rise to a more moderate form of CS than CSB mutations.[3] Mutations in the CSA gene account for about 20% of CS cases.[4]

Function

CSA and CSB proteins are thought to function in transcription and DNA repair, most notably in transcription-coupled nucleotide excision repair. CSA and CSB-deficient cells exhibit a lack of preferential repair of UV-induced cyclobutane pyrimidine dimers in actively transcribed genes, consistent with a failed transcription coupled nucleotide excision repair response.[5] Within the cell, the CSA protein localizes to sites of DNA damage, particularly inter-strand cross-links, double-strand breaks and some mono-adducts.[3]

Interactions

ERCC8 (gene) has been shown to interact with XAB2.[6]

References

  1. ↑ Itoh T, Shiomi T, Shiomi N, Harada Y, Wakasugi M, Matsunaga T, Nikaido O, Friedberg EC, Yamaizumi M (April 1996). "Rodent complementation group 8 (ERCC8) corresponds to Cockayne syndrome complementation group A". Mutat Res. 362 (2): 167–74. doi:10.1016/0921-8777(95)00046-1. PMID 8596535.
  2. ↑ 2.0 2.1 "Entrez Gene: ERCC8 excision repair cross-complementing rodent repair deficiency, complementation group 8".
  3. ↑ 3.0 3.1 Iyama T, Wilson DM (2016). "Elements That Regulate the DNA Damage Response of Proteins Defective in Cockayne Syndrome". J. Mol. Biol. 428 (1): 62–78. doi:10.1016/j.jmb.2015.11.020. PMC 4738086. PMID 26616585.
  4. ↑ Koch S, Garcia Gonzalez O, Assfalg R, Schelling A, Schäfer P, Scharffetter-Kochanek K, Iben S (2014). "Cockayne syndrome protein A is a transcription factor of RNA polymerase I and stimulates ribosomal biogenesis and growth". Cell Cycle. 13 (13): 2029–37. doi:10.4161/cc.29018. PMC 4111694. PMID 24781187.
  5. ↑ van Hoffen A, Natarajan AT, Mayne LV, van Zeeland AA, Mullenders LH, Venema J (1993). "Deficient repair of the transcribed strand of active genes in Cockayne's syndrome cells". Nucleic Acids Res. 21 (25): 5890–5. doi:10.1093/nar/21.25.5890. PMC 310470. PMID 8290349.
  6. ↑ Nakatsu Y, Asahina H, Citterio E, Rademakers S, Vermeulen W, Kamiuchi S, Yeo JP, Khaw MC, Saijo M, Kodo N, Matsuda T, Hoeijmakers JH, Tanaka K (November 2000). "XAB2, a novel tetratricopeptide repeat protein involved in transcription-coupled DNA repair and transcription". J. Biol. Chem. UNITED STATES. 275 (45): 34931–7. doi:10.1074/jbc.M004936200. ISSN 0021-9258. PMID 10944529.

Further reading

External links



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