FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2013036524> ?p ?o ?g. }

• W2013036524 endingPage "806" @default.
• W2013036524 startingPage "793" @default.
• W2013036524 abstract "Rad14p is a DNA damage recognition factor in nucleotide excision repair. Intriguingly, we show here that Rad14p associates with the promoter of a galactose-inducible GAL1 gene after transcriptional induction in the absence of DNA lesion. Such an association of Rad14p facilitates the recruitment of TBP, TFIIH, and RNA polymerase II to the GAL1 promoter. Furthermore, the association of RNA polymerase II with the GAL1 promoter is significantly decreased in the absence of Rad14p, when the coding sequence was deleted. These results support the role of Rad14p in transcriptional initiation. Consistently, the level of GAL1 mRNA is significantly decreased in the absence of Rad14p. Similar results are also obtained at other galactose-inducible GAL genes such as GAL7 and GAL10. Likewise, Rad14p promotes transcription of other non-GAL genes such as CUP1, CTT1, and STL1 after transcriptional induction. However, the effect of Rad14p on the steady-state levels of transcription of GAL genes or constitutively active genes such as ADH1, PGK1, PYK1, and RPS5 is not observed. Thus, Rad14p promotes initial transcription but does not appear to regulate the steady-state level. Collectively, our results unveil a new role of Rad14p in stimulating transcription in addition to its well-known function in nucleotide excision repair.Background: Although Rad14p has well known functions in NER, its role in transcription is not clearly known.Results: We demonstrate that Rad14p associates with active gene in absence of lesion and promotes transcription.Conclusion: Our results support a new role of Rad14p in transcriptional regulation in addition to its well known function in NER.Significance: This study implicates Rad14p as a new regulator of gene expression. Rad14p is a DNA damage recognition factor in nucleotide excision repair. Intriguingly, we show here that Rad14p associates with the promoter of a galactose-inducible GAL1 gene after transcriptional induction in the absence of DNA lesion. Such an association of Rad14p facilitates the recruitment of TBP, TFIIH, and RNA polymerase II to the GAL1 promoter. Furthermore, the association of RNA polymerase II with the GAL1 promoter is significantly decreased in the absence of Rad14p, when the coding sequence was deleted. These results support the role of Rad14p in transcriptional initiation. Consistently, the level of GAL1 mRNA is significantly decreased in the absence of Rad14p. Similar results are also obtained at other galactose-inducible GAL genes such as GAL7 and GAL10. Likewise, Rad14p promotes transcription of other non-GAL genes such as CUP1, CTT1, and STL1 after transcriptional induction. However, the effect of Rad14p on the steady-state levels of transcription of GAL genes or constitutively active genes such as ADH1, PGK1, PYK1, and RPS5 is not observed. Thus, Rad14p promotes initial transcription but does not appear to regulate the steady-state level. Collectively, our results unveil a new role of Rad14p in stimulating transcription in addition to its well-known function in nucleotide excision repair. Background: Although Rad14p has well known functions in NER, its role in transcription is not clearly known. Results: We demonstrate that Rad14p associates with active gene in absence of lesion and promotes transcription. Conclusion: Our results support a new role of Rad14p in transcriptional regulation in addition to its well known function in NER. Significance: This study implicates Rad14p as a new regulator of gene expression." @default.
• W2013036524 created "2016-06-24" @default.
• W2013036524 creator A5020924075 @default.
• W2013036524 creator A5080308532 @default.
• W2013036524 creator A5084946819 @default.
• W2013036524 date "2013-01-01" @default.
• W2013036524 modified "2023-09-29" @default.
• W2013036524 title "Functional Analysis of Rad14p, a DNA Damage Recognition Factor in Nucleotide Excision Repair, in Regulation of Transcription in Vivo" @default.
• W2013036524 cites W1526737460 @default.
• W2013036524 cites W1535395598 @default.
• W2013036524 cites W1537981848 @default.
• W2013036524 cites W1964783227 @default.
• W2013036524 cites W1964961771 @default.
• W2013036524 cites W1966072209 @default.
• W2013036524 cites W1967190671 @default.
• W2013036524 cites W1969175894 @default.
• W2013036524 cites W1971214797 @default.
• W2013036524 cites W1974697229 @default.
• W2013036524 cites W1983456026 @default.
• W2013036524 cites W1988733863 @default.
• W2013036524 cites W1992082799 @default.
• W2013036524 cites W1996899465 @default.
• W2013036524 cites W1997909925 @default.
• W2013036524 cites W2002721894 @default.
• W2013036524 cites W2007986017 @default.
• W2013036524 cites W2012350378 @default.
• W2013036524 cites W2013230822 @default.
• W2013036524 cites W2015063900 @default.
• W2013036524 cites W2017118719 @default.
• W2013036524 cites W2017519940 @default.
• W2013036524 cites W2021581979 @default.
• W2013036524 cites W2023348831 @default.
• W2013036524 cites W2024754737 @default.
• W2013036524 cites W2037104046 @default.
• W2013036524 cites W2039876512 @default.
• W2013036524 cites W2041514249 @default.
• W2013036524 cites W2044428414 @default.
• W2013036524 cites W2044513395 @default.
• W2013036524 cites W2060899717 @default.
• W2013036524 cites W2066040575 @default.
• W2013036524 cites W2071783675 @default.
• W2013036524 cites W2073806145 @default.
• W2013036524 cites W2073894791 @default.
• W2013036524 cites W2080554706 @default.
• W2013036524 cites W2084744430 @default.
• W2013036524 cites W2085301101 @default.
• W2013036524 cites W2087196090 @default.
• W2013036524 cites W2088703460 @default.
• W2013036524 cites W2093920124 @default.
• W2013036524 cites W2094973595 @default.
• W2013036524 cites W2097621806 @default.
• W2013036524 cites W2097692009 @default.
• W2013036524 cites W2101598171 @default.
• W2013036524 cites W2111347231 @default.
• W2013036524 cites W2112159784 @default.
• W2013036524 cites W2112652171 @default.
• W2013036524 cites W2116287534 @default.
• W2013036524 cites W2120408898 @default.
• W2013036524 cites W2124227044 @default.
• W2013036524 cites W2127024810 @default.
• W2013036524 cites W2128541424 @default.
• W2013036524 cites W2128935473 @default.
• W2013036524 cites W2131602976 @default.
• W2013036524 cites W2133832693 @default.
• W2013036524 cites W2134422799 @default.
• W2013036524 cites W2140447069 @default.
• W2013036524 cites W2145049521 @default.
• W2013036524 cites W2147185637 @default.
• W2013036524 cites W2148181192 @default.
• W2013036524 cites W2156354811 @default.
• W2013036524 cites W2158602038 @default.
• W2013036524 cites W2165125584 @default.
• W2013036524 cites W2166444458 @default.
• W2013036524 cites W2167389868 @default.
• W2013036524 cites W2169333620 @default.
• W2013036524 cites W2170519372 @default.
• W2013036524 cites W2184130964 @default.
• W2013036524 cites W4232123327 @default.
• W2013036524 cites W4360795053 @default.
• W2013036524 doi "https://doi.org/10.1074/jbc.m112.413716" @default.
• W2013036524 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3543029" @default.
• W2013036524 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23188830" @default.
• W2013036524 hasPublicationYear "2013" @default.
• W2013036524 type Work @default.
• W2013036524 sameAs 2013036524 @default.
• W2013036524 citedByCount "9" @default.
• W2013036524 countsByYear W20130365242014 @default.
• W2013036524 countsByYear W20130365242017 @default.
• W2013036524 countsByYear W20130365242019 @default.
• W2013036524 countsByYear W20130365242020 @default.
• W2013036524 countsByYear W20130365242022 @default.
• W2013036524 crossrefType "journal-article" @default.
• W2013036524 hasAuthorship W2013036524A5020924075 @default.
• W2013036524 hasAuthorship W2013036524A5080308532 @default.
• W2013036524 hasAuthorship W2013036524A5084946819 @default.
• W2013036524 hasBestOaLocation W20130365241 @default.
• W2013036524 hasConcept C101762097 @default.
• W2013036524 hasConcept C104317684 @default.

• next