FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2068304030> ?p ?o ?g. }

• W2068304030 endingPage "23183" @default.
• W2068304030 startingPage "23171" @default.
• W2068304030 abstract "Because HER-2 has been demonstrated in the nuclei of cancer cells, we hypothesized that it might interact with transcription factors that activate ERBB2 transcription. Macrohistone 2A1 (H2AFY; mH2A1) was found to interact with HER-2 in cancer cells that overexpress HER-2. Of the two human mH2A1 isoforms, mH2A1.2, but not mH2A1.1, interacted with HER-2 in human cancer cell lines. Overexpression of mH2A1.2, but not mH2A1.1, in cancer cells significantly increased HER-2 expression and tumorigenicity. Inhibition of HER-2 kinase activity diminished mH2A1 expression and mH2A1.2-induced ERBB2 transcription in cancer cells. Chromatin immunoprecipitation of mH2A1.2 in cancer cells stably transfected with mH2A1.2 showed enrichment of mH2A1.2 at the HER-2 promoter, suggesting a role for mH2A1.2 in driving HER-2 overexpression. The evolutionarily conserved macro domain of mH2A1.2 was sufficient for the interaction between HER-2 and mH2A1.2 and for mH2A1.2-induced ERBB2 transcription. Within the macro domain of mH2A1.2, a trinucleotide insertion (-EIS-) sequence not found in mH2A1.1 was essential for the interaction between HER-2 and mH2A1.2 as well as mH2A1.2-induced HER-2 expression and cell proliferation.Background: HER-2/c-erbB-2 is commonly overexpressed in cancers, but how its overexpression is achieved is not well understood.Results: HER-2 was found to interact with the atypical histone macroH2A1.2.Conclusion: HER-2 cooperates with macroH2A1.2 to drive HER-2 overexpression in cancer cells.Significance: The discovery of a novel interaction between mH2A1.2 and HER-2 reveals a unique mechanism by which oncogenes can broadly deregulate gene transcription in cancer cells. Because HER-2 has been demonstrated in the nuclei of cancer cells, we hypothesized that it might interact with transcription factors that activate ERBB2 transcription. Macrohistone 2A1 (H2AFY; mH2A1) was found to interact with HER-2 in cancer cells that overexpress HER-2. Of the two human mH2A1 isoforms, mH2A1.2, but not mH2A1.1, interacted with HER-2 in human cancer cell lines. Overexpression of mH2A1.2, but not mH2A1.1, in cancer cells significantly increased HER-2 expression and tumorigenicity. Inhibition of HER-2 kinase activity diminished mH2A1 expression and mH2A1.2-induced ERBB2 transcription in cancer cells. Chromatin immunoprecipitation of mH2A1.2 in cancer cells stably transfected with mH2A1.2 showed enrichment of mH2A1.2 at the HER-2 promoter, suggesting a role for mH2A1.2 in driving HER-2 overexpression. The evolutionarily conserved macro domain of mH2A1.2 was sufficient for the interaction between HER-2 and mH2A1.2 and for mH2A1.2-induced ERBB2 transcription. Within the macro domain of mH2A1.2, a trinucleotide insertion (-EIS-) sequence not found in mH2A1.1 was essential for the interaction between HER-2 and mH2A1.2 as well as mH2A1.2-induced HER-2 expression and cell proliferation. Background: HER-2/c-erbB-2 is commonly overexpressed in cancers, but how its overexpression is achieved is not well understood. Results: HER-2 was found to interact with the atypical histone macroH2A1.2. Conclusion: HER-2 cooperates with macroH2A1.2 to drive HER-2 overexpression in cancer cells. Significance: The discovery of a novel interaction between mH2A1.2 and HER-2 reveals a unique mechanism by which oncogenes can broadly deregulate gene transcription in cancer cells." @default.
• W2068304030 created "2016-06-24" @default.
• W2068304030 creator A5002936169 @default.
• W2068304030 creator A5006285042 @default.
• W2068304030 creator A5012555125 @default.
• W2068304030 creator A5013968780 @default.
• W2068304030 creator A5023325269 @default.
• W2068304030 creator A5049127223 @default.
• W2068304030 creator A5055463381 @default.
• W2068304030 creator A5076488105 @default.
• W2068304030 date "2012-06-01" @default.
• W2068304030 modified "2023-10-03" @default.
• W2068304030 title "The Atypical Histone MacroH2A1.2 Interacts with HER-2 Protein in Cancer Cells" @default.
• W2068304030 cites W1522147759 @default.
• W2068304030 cites W1541544453 @default.
• W2068304030 cites W1963879139 @default.
• W2068304030 cites W1964010757 @default.
• W2068304030 cites W1971589767 @default.
• W2068304030 cites W1973460244 @default.
• W2068304030 cites W1975658757 @default.
• W2068304030 cites W1979488703 @default.
• W2068304030 cites W1980877995 @default.
• W2068304030 cites W1993113643 @default.
• W2068304030 cites W1994824957 @default.
• W2068304030 cites W1994861590 @default.
• W2068304030 cites W1996275566 @default.
• W2068304030 cites W2018863876 @default.
• W2068304030 cites W2019267973 @default.
• W2068304030 cites W2023648132 @default.
• W2068304030 cites W2025525406 @default.
• W2068304030 cites W2034808255 @default.
• W2068304030 cites W2040142253 @default.
• W2068304030 cites W2074228092 @default.
• W2068304030 cites W2074465378 @default.
• W2068304030 cites W2076788485 @default.
• W2068304030 cites W2078611937 @default.
• W2068304030 cites W2089973951 @default.
• W2068304030 cites W2097091656 @default.
• W2068304030 cites W2105288740 @default.
• W2068304030 cites W2111693820 @default.
• W2068304030 cites W2112238332 @default.
• W2068304030 cites W2112807374 @default.
• W2068304030 cites W2121300496 @default.
• W2068304030 cites W2123648331 @default.
• W2068304030 cites W2132244795 @default.
• W2068304030 cites W2153309788 @default.
• W2068304030 cites W2157840751 @default.
• W2068304030 cites W2167398987 @default.
• W2068304030 cites W2169567788 @default.
• W2068304030 cites W45711525 @default.
• W2068304030 doi "https://doi.org/10.1074/jbc.m112.379412" @default.
• W2068304030 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3391143" @default.
• W2068304030 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22589551" @default.
• W2068304030 hasPublicationYear "2012" @default.
• W2068304030 type Work @default.
• W2068304030 sameAs 2068304030 @default.
• W2068304030 citedByCount "35" @default.
• W2068304030 countsByYear W20683040302012 @default.
• W2068304030 countsByYear W20683040302013 @default.
• W2068304030 countsByYear W20683040302014 @default.
• W2068304030 countsByYear W20683040302015 @default.
• W2068304030 countsByYear W20683040302016 @default.
• W2068304030 countsByYear W20683040302017 @default.
• W2068304030 countsByYear W20683040302018 @default.
• W2068304030 countsByYear W20683040302019 @default.
• W2068304030 countsByYear W20683040302020 @default.
• W2068304030 countsByYear W20683040302021 @default.
• W2068304030 countsByYear W20683040302022 @default.
• W2068304030 crossrefType "journal-article" @default.
• W2068304030 hasAuthorship W2068304030A5002936169 @default.
• W2068304030 hasAuthorship W2068304030A5006285042 @default.
• W2068304030 hasAuthorship W2068304030A5012555125 @default.
• W2068304030 hasAuthorship W2068304030A5013968780 @default.
• W2068304030 hasAuthorship W2068304030A5023325269 @default.
• W2068304030 hasAuthorship W2068304030A5049127223 @default.
• W2068304030 hasAuthorship W2068304030A5055463381 @default.
• W2068304030 hasAuthorship W2068304030A5076488105 @default.
• W2068304030 hasBestOaLocation W20683040301 @default.
• W2068304030 hasConcept C101762097 @default.
• W2068304030 hasConcept C104317684 @default.
• W2068304030 hasConcept C121608353 @default.
• W2068304030 hasConcept C134320426 @default.
• W2068304030 hasConcept C138885662 @default.
• W2068304030 hasConcept C150194340 @default.
• W2068304030 hasConcept C153911025 @default.
• W2068304030 hasConcept C179926584 @default.
• W2068304030 hasConcept C41895202 @default.
• W2068304030 hasConcept C502942594 @default.
• W2068304030 hasConcept C53345823 @default.
• W2068304030 hasConcept C54009773 @default.
• W2068304030 hasConcept C54355233 @default.
• W2068304030 hasConcept C64927066 @default.
• W2068304030 hasConcept C81885089 @default.
• W2068304030 hasConcept C83640560 @default.
• W2068304030 hasConcept C86339819 @default.
• W2068304030 hasConcept C86803240 @default.
• W2068304030 hasConcept C95444343 @default.
• W2068304030 hasConcept C96232424 @default.

• next