FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2345949512> ?p ?o ?g. }

• W2345949512 endingPage "4992" @default.
• W2345949512 startingPage "4985" @default.
• W2345949512 abstract "Research Article15 December 1993free access Repression of adenovirus E1A enhancer activity by a novel zinc finger-containing DNA-binding protein related to the GLI-Kruppel protein. C. Fognani C. Fognani Department of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author G. Della Valle G. Della Valle Department of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author L.E. Babiss L.E. Babiss Department of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author C. Fognani C. Fognani Department of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author G. Della Valle G. Della Valle Department of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author L.E. Babiss L.E. Babiss Department of Molecular Cell Biology, Rockefeller University, New York, NY 10021. Search for more papers by this author Author Information C. Fognani1, G. Della Valle1 and L.E. Babiss1 1Department of Molecular Cell Biology, Rockefeller University, New York, NY 10021. The EMBO Journal (1993)12:4985-4992https://doi.org/10.1002/j.1460-2075.1993.tb06192.x PDFDownload PDF of article text and main figures. ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinked InMendeleyWechatReddit Figures & Info We have previously shown that expression of the E1A oncogene is negatively regulated in rodent fibroblast cells by a nuclear factor (phi AP3) that binds to the E1A promoter region just upstream of the canonical enhancer element. To understand how phi AP3 can regulate E1A gene transcription by inactivation of the enhancer function, we have used an oligonucleotide probe containing a binding site for this protein to clone the mouse phi AP3 gene. DNA sequence analysis of the 2.3 kb cDNA revealed the presence of six well-conserved zinc finger DNA-binding motifs, which were highly related to those found in the GLI-Kruppel family of human zinc finger proteins. Analysis of the tissue distribution of the phi AP3 mRNA suggested that its expression was ubiquitous but at variable levels, most likely as a result of post-transcriptional regulation of mRNA stability. The phi AP3 factor is a nuclear phosphoprotein; the extent of its phosphorylation is regulated during the cell cycle. Preferential binding of the hyperphosphorylated form of this protein to DNA was observed. Co-expression of the phi AP3 cDNA and a luciferase reporter gene under the control of the E1A promoter/enhancer in several human cell lines resulted in repression of E1A enhancer activity. In contrast, when the phi AP3 binding site upstream of the enhancer was mutated, no inhibition of enhancer function was observed. Based on these observations we conclude that we have cloned the cellular phi AP3 gene, and that the DNA-binding activity of this protein is regulated during the cell cycle. Previous ArticleNext Article Volume 12Issue 131 December 1993In this issue RelatedDetailsLoading ..." @default.
• W2345949512 created "2016-06-24" @default.
• W2345949512 creator A5005828835 @default.
• W2345949512 creator A5080365505 @default.
• W2345949512 creator A5082465845 @default.
• W2345949512 date "1993-12-01" @default.
• W2345949512 modified "2023-10-18" @default.
• W2345949512 title "Repression of adenovirus E1A enhancer activity by a novel zinc finger-containing DNA-binding protein related to the GLI-Kruppel protein." @default.
• W2345949512 cites W123775848 @default.
• W2345949512 cites W1485934418 @default.
• W2345949512 cites W1579796122 @default.
• W2345949512 cites W1775647714 @default.
• W2345949512 cites W1812146242 @default.
• W2345949512 cites W1912385731 @default.
• W2345949512 cites W1924824038 @default.
• W2345949512 cites W1925053557 @default.
• W2345949512 cites W1965372133 @default.
• W2345949512 cites W1966156883 @default.
• W2345949512 cites W1972042181 @default.
• W2345949512 cites W1980807416 @default.
• W2345949512 cites W1987703174 @default.
• W2345949512 cites W1993243592 @default.
• W2345949512 cites W1997403350 @default.
• W2345949512 cites W2007281794 @default.
• W2345949512 cites W2017244785 @default.
• W2345949512 cites W2020611359 @default.
• W2345949512 cites W2026548183 @default.
• W2345949512 cites W2031013042 @default.
• W2345949512 cites W2033371710 @default.
• W2345949512 cites W2068446924 @default.
• W2345949512 cites W2071781833 @default.
• W2345949512 cites W2072276788 @default.
• W2345949512 cites W2076222750 @default.
• W2345949512 cites W2079327210 @default.
• W2345949512 cites W2089723533 @default.
• W2345949512 cites W2092216600 @default.
• W2345949512 cites W2094154951 @default.
• W2345949512 cites W2095138452 @default.
• W2345949512 cites W2121542842 @default.
• W2345949512 cites W2134812217 @default.
• W2345949512 cites W2149031125 @default.
• W2345949512 cites W2339231403 @default.
• W2345949512 cites W2403980878 @default.
• W2345949512 cites W311062589 @default.
• W2345949512 doi "https://doi.org/10.1002/j.1460-2075.1993.tb06192.x" @default.
• W2345949512 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/413759" @default.
• W2345949512 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8262041" @default.
• W2345949512 hasPublicationYear "1993" @default.
• W2345949512 type Work @default.
• W2345949512 sameAs 2345949512 @default.
• W2345949512 citedByCount "23" @default.
• W2345949512 crossrefType "journal-article" @default.
• W2345949512 hasAuthorship W2345949512A5005828835 @default.
• W2345949512 hasAuthorship W2345949512A5080365505 @default.
• W2345949512 hasAuthorship W2345949512A5082465845 @default.
• W2345949512 hasBestOaLocation W23459495121 @default.
• W2345949512 hasConcept C104317684 @default.
• W2345949512 hasConcept C111936080 @default.
• W2345949512 hasConcept C153911025 @default.
• W2345949512 hasConcept C24284526 @default.
• W2345949512 hasConcept C54355233 @default.
• W2345949512 hasConcept C86339819 @default.
• W2345949512 hasConcept C86803240 @default.
• W2345949512 hasConceptScore W2345949512C104317684 @default.
• W2345949512 hasConceptScore W2345949512C111936080 @default.
• W2345949512 hasConceptScore W2345949512C153911025 @default.
• W2345949512 hasConceptScore W2345949512C24284526 @default.
• W2345949512 hasConceptScore W2345949512C54355233 @default.
• W2345949512 hasConceptScore W2345949512C86339819 @default.
• W2345949512 hasConceptScore W2345949512C86803240 @default.
• W2345949512 hasIssue "13" @default.
• W2345949512 hasLocation W23459495121 @default.
• W2345949512 hasLocation W23459495122 @default.
• W2345949512 hasLocation W23459495123 @default.
• W2345949512 hasOpenAccess W2345949512 @default.
• W2345949512 hasPrimaryLocation W23459495121 @default.
• W2345949512 hasRelatedWork W2030987915 @default.
• W2345949512 hasRelatedWork W2031686190 @default.
• W2345949512 hasRelatedWork W2041177404 @default.
• W2345949512 hasRelatedWork W2109930126 @default.
• W2345949512 hasRelatedWork W2141204992 @default.
• W2345949512 hasRelatedWork W2239249333 @default.
• W2345949512 hasRelatedWork W2325880119 @default.
• W2345949512 hasRelatedWork W2735826995 @default.
• W2345949512 hasRelatedWork W2900649558 @default.
• W2345949512 hasRelatedWork W4243361172 @default.
• W2345949512 hasVolume "12" @default.
• W2345949512 isParatext "false" @default.
• W2345949512 isRetracted "false" @default.
• W2345949512 magId "2345949512" @default.
• W2345949512 workType "article" @default.