Matches in SemOpenAlex for { <https://semopenalex.org/work/W2065342358> ?p ?o ?g. }
Showing items 1 to 100 of
100
with 100 items per page.
- W2065342358 endingPage "11203" @default.
- W2065342358 startingPage "11197" @default.
- W2065342358 abstract "The gene encoding UDP-GlcNAc:dolichol phosphate N-acetylglucosamine-1-phosphate transferase (GPT), the enzyme that initiates the pathway for the biosynthesis of asparagine-linked glycoproteins, is ubiquitously expressed in eukaryotic cells. However, its expression in the mammary gland is developmentally and hormonally regulated; transcription of the mouse mammary GPT gene is stimulated by the lactogenic hormones, insulin, glucocorticoid, and prolactin. The involvement of cis-acting elements in regulating the expression of the mouse GPT (mGPT) gene was investigated by transient transfections of various GPT promoter/luciferase (Luc) constructs into primary mouse mammary epithelial cells. A series of 5′-deletions of the GPT promoter identified a distal negative regulatory region (base pairs −1057 to −968) and deletion of this region results in enhanced hormonal induction (~7-fold) with no effect on basal promoter activity. Electrophoretic mobility shift assays (EMSA) performed with nuclear extracts from different developmental stages of mouse mammary gland demonstrated that the binding activity of the nuclear proteins to the distal negative regulatory region was predominant in virgin stage as compared with pregnant and lactating stages. EMSA performed with nuclear extracts from virgin explants showed that the binding activity was markedly decreased after cultivation with the combination of the three lactogenic hormones. DNase I footprinting analysis identified two pentamer direct repeat motifs, AGGAA and GAAAC, within the negative regulatory region. EMSA competition experiments showed that mutations within the direct repeats failed to compete for binding of the nuclear proteins to labeled wild type oligonucleotide. Transcription from the promoter containing the mutated direct repeats was increased greatly, consistent with the conclusion that these motifs functions in vivo to repress GPT gene expression. These data suggest the importance of the negative regulatory region in hormonal control of mGPT gene expression in mammary gland. The gene encoding UDP-GlcNAc:dolichol phosphate N-acetylglucosamine-1-phosphate transferase (GPT), the enzyme that initiates the pathway for the biosynthesis of asparagine-linked glycoproteins, is ubiquitously expressed in eukaryotic cells. However, its expression in the mammary gland is developmentally and hormonally regulated; transcription of the mouse mammary GPT gene is stimulated by the lactogenic hormones, insulin, glucocorticoid, and prolactin. The involvement of cis-acting elements in regulating the expression of the mouse GPT (mGPT) gene was investigated by transient transfections of various GPT promoter/luciferase (Luc) constructs into primary mouse mammary epithelial cells. A series of 5′-deletions of the GPT promoter identified a distal negative regulatory region (base pairs −1057 to −968) and deletion of this region results in enhanced hormonal induction (~7-fold) with no effect on basal promoter activity. Electrophoretic mobility shift assays (EMSA) performed with nuclear extracts from different developmental stages of mouse mammary gland demonstrated that the binding activity of the nuclear proteins to the distal negative regulatory region was predominant in virgin stage as compared with pregnant and lactating stages. EMSA performed with nuclear extracts from virgin explants showed that the binding activity was markedly decreased after cultivation with the combination of the three lactogenic hormones. DNase I footprinting analysis identified two pentamer direct repeat motifs, AGGAA and GAAAC, within the negative regulatory region. EMSA competition experiments showed that mutations within the direct repeats failed to compete for binding of the nuclear proteins to labeled wild type oligonucleotide. Transcription from the promoter containing the mutated direct repeats was increased greatly, consistent with the conclusion that these motifs functions in vivo to repress GPT gene expression. These data suggest the importance of the negative regulatory region in hormonal control of mGPT gene expression in mammary gland." @default.
- W2065342358 created "2016-06-24" @default.
- W2065342358 creator A5003943272 @default.
- W2065342358 creator A5018970596 @default.
- W2065342358 creator A5069076350 @default.
- W2065342358 creator A5075033726 @default.
- W2065342358 date "1996-05-01" @default.
- W2065342358 modified "2023-10-16" @default.
- W2065342358 title "Negative Regulatory Element Involved in the Hormonal Regulation of GlcNAc-1-P Transferase Gene in Mouse Mammary Gland" @default.
- W2065342358 cites W1486018587 @default.
- W2065342358 cites W1488947327 @default.
- W2065342358 cites W1495825919 @default.
- W2065342358 cites W1518755252 @default.
- W2065342358 cites W1529450128 @default.
- W2065342358 cites W1547218808 @default.
- W2065342358 cites W1550544725 @default.
- W2065342358 cites W1558516755 @default.
- W2065342358 cites W1575935170 @default.
- W2065342358 cites W1589386825 @default.
- W2065342358 cites W1596938063 @default.
- W2065342358 cites W1599042760 @default.
- W2065342358 cites W1614268180 @default.
- W2065342358 cites W1764572032 @default.
- W2065342358 cites W1837711156 @default.
- W2065342358 cites W1960160624 @default.
- W2065342358 cites W1981765089 @default.
- W2065342358 cites W1993243592 @default.
- W2065342358 cites W2011467252 @default.
- W2065342358 cites W2013980278 @default.
- W2065342358 cites W2015502095 @default.
- W2065342358 cites W2019328934 @default.
- W2065342358 cites W2027216583 @default.
- W2065342358 cites W2039057191 @default.
- W2065342358 cites W2041639550 @default.
- W2065342358 cites W2043287133 @default.
- W2065342358 cites W2048422948 @default.
- W2065342358 cites W2075232957 @default.
- W2065342358 cites W2081530554 @default.
- W2065342358 cites W2112823160 @default.
- W2065342358 cites W2117126022 @default.
- W2065342358 cites W2118673410 @default.
- W2065342358 cites W2151443440 @default.
- W2065342358 cites W2152708819 @default.
- W2065342358 cites W4553897 @default.
- W2065342358 doi "https://doi.org/10.1074/jbc.271.19.11197" @default.
- W2065342358 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8626667" @default.
- W2065342358 hasPublicationYear "1996" @default.
- W2065342358 type Work @default.
- W2065342358 sameAs 2065342358 @default.
- W2065342358 citedByCount "16" @default.
- W2065342358 countsByYear W20653423582014 @default.
- W2065342358 countsByYear W20653423582022 @default.
- W2065342358 crossrefType "journal-article" @default.
- W2065342358 hasAuthorship W2065342358A5003943272 @default.
- W2065342358 hasAuthorship W2065342358A5018970596 @default.
- W2065342358 hasAuthorship W2065342358A5069076350 @default.
- W2065342358 hasAuthorship W2065342358A5075033726 @default.
- W2065342358 hasConcept C101762097 @default.
- W2065342358 hasConcept C104317684 @default.
- W2065342358 hasConcept C150194340 @default.
- W2065342358 hasConcept C153911025 @default.
- W2065342358 hasConcept C165864922 @default.
- W2065342358 hasConcept C183978625 @default.
- W2065342358 hasConcept C27153228 @default.
- W2065342358 hasConcept C2778061764 @default.
- W2065342358 hasConcept C55493867 @default.
- W2065342358 hasConcept C86339819 @default.
- W2065342358 hasConcept C86803240 @default.
- W2065342358 hasConceptScore W2065342358C101762097 @default.
- W2065342358 hasConceptScore W2065342358C104317684 @default.
- W2065342358 hasConceptScore W2065342358C150194340 @default.
- W2065342358 hasConceptScore W2065342358C153911025 @default.
- W2065342358 hasConceptScore W2065342358C165864922 @default.
- W2065342358 hasConceptScore W2065342358C183978625 @default.
- W2065342358 hasConceptScore W2065342358C27153228 @default.
- W2065342358 hasConceptScore W2065342358C2778061764 @default.
- W2065342358 hasConceptScore W2065342358C55493867 @default.
- W2065342358 hasConceptScore W2065342358C86339819 @default.
- W2065342358 hasConceptScore W2065342358C86803240 @default.
- W2065342358 hasIssue "19" @default.
- W2065342358 hasLocation W20653423581 @default.
- W2065342358 hasOpenAccess W2065342358 @default.
- W2065342358 hasPrimaryLocation W20653423581 @default.
- W2065342358 hasRelatedWork W1652539077 @default.
- W2065342358 hasRelatedWork W1930517486 @default.
- W2065342358 hasRelatedWork W1975471112 @default.
- W2065342358 hasRelatedWork W2064205709 @default.
- W2065342358 hasRelatedWork W2100604934 @default.
- W2065342358 hasRelatedWork W2103327128 @default.
- W2065342358 hasRelatedWork W2111182449 @default.
- W2065342358 hasRelatedWork W2167465117 @default.
- W2065342358 hasRelatedWork W2172226517 @default.
- W2065342358 hasRelatedWork W2193318419 @default.
- W2065342358 hasVolume "271" @default.
- W2065342358 isParatext "false" @default.
- W2065342358 isRetracted "false" @default.
- W2065342358 magId "2065342358" @default.
- W2065342358 workType "article" @default.