Autoregulation of fos: the dyad symmetry element as the major target of repression.
about
Expression cloning of a novel zinc finger protein that binds to the c-fos serum response elementSynergism in ternary complex formation between the dimeric glycoprotein p67SRF, polypeptide p62TCF and the c-fos serum response elementMutual transrepression of Fos and the glucocorticoid receptor: involvement of a functional domain in Fos which is absent in FosBPhosphorylation of the c-Fos transrepression domain by mitogen-activated protein kinase and 90-kDa ribosomal S6 kinasec-fos transcriptional activation and repression correlate temporally with the phosphorylation status of TCFComparative analysis of the ternary complex factors Elk-1, SAP-1a and SAP-2 (ERP/NET)Human DNA polymerase alpha gene: sequences controlling expression in cycling and serum-stimulated cellsPromoter function and structure of the growth factor-inducible immediate early gene cyr61Loss of cellular adhesion to matrix induces p53-independent expression of PTEN tumor suppressorIdentification of multiple SRF N-terminal phosphorylation sites affecting DNA binding propertiesLFB1/HNF1 acts as a repressor of its own transcriptionc-FOS suppresses ovarian cancer progression by changing adhesionNegative and positive regulation by transcription factor cAMP response element-binding protein is modulated by phosphorylation.AP-1 factors play an important role in transformation induced by the v-rel oncogene.Postinduction repression of the beta-interferon gene is mediated through two positive regulatory domains.Structure and mapping of the fosB gene. FosB downregulates the activity of the fosB promoterGene regulation and genetic susceptibility to neoplastic transformation: AP-1 and p80 expression in JB6 cellsERK-associated changes of AP-1 proteins during fear extinction.Transcription factor binding and spacing constraints in the human beta-actin proximal promoter.Dual Specificity Phosphatase 5, a Specific Negative Regulator of ERK Signaling, Is Induced by Serum Response Factor and Elk-1 Transcription FactorCRISP-3, a protein with homology to plant defense proteins, is expressed in mouse B cells under the control of Oct2Net-b, a Ras-insensitive factor that forms ternary complexes with serum response factor on the serum response element of the fos promoterLoss of serum response element-binding activity and hyperphosphorylation of serum response factor during cellular aging.Negative regulation of the BZLF1 promoter of Epstein-Barr virus.Adenovirus E4orf4 protein reduces phosphorylation of c-Fos and E1A proteins while simultaneously reducing the level of AP-1Transcriptional activation and repression by Fos are independent functions: the C terminus represses immediate-early gene expression via CArG elements.The serum response factor is extensively modified by phosphorylation following its synthesis in serum-stimulated fibroblasts.Altered transcriptional activity of c-fos promoter plasmids in v-raf-transformed NIH 3T3 cells.Natural and synthetic DNA elements with the CArG motif differ in expression and protein-binding properties.p67SRF is a constitutive nuclear protein implicated in the modulation of genes required throughout the G1 period.Oncogene N-ras mediates selective inhibition of c-fos induction by nerve growth factor and basic fibroblast growth factor in a PC12 cell lineFunctional analysis of an isolated fos promoter element with AP-1 site homology reveals cell type-specific transcriptional properties.Epstein-Barr virus BZLF1 trans activator induces the promoter of a cellular cognate gene, c-fos.Inhibitory effect of myristylation on transrepression by FBR (Gag-Fos) proteinNegative autoregulation of the neu gene is mediated by a novel enhancer.Ternary complex formation over the c-fos serum response element: p62TCF exhibits dual component specificity with contacts to DNA and an extended structure in the DNA-binding domain of p67SRF.Interference between pathway-specific transcription factors: glucocorticoids antagonize phorbol ester-induced AP-1 activity without altering AP-1 site occupation in vivo.Both products of the fosB gene, FosB and its short form, FosB/SF, are transcriptional activators in fibroblasts.The SIF binding element confers sis/PDGF inducibility onto the c-fos promoter.The collagenase gene promoter contains a TPA and oncogene-responsive unit encompassing the PEA3 and AP-1 binding sites.
P2860
Q24294405-1B211F86-7CF1-4432-97F4-7B19AF85AE7EQ24307673-F3C248D9-9D98-4570-95DD-A14440D90461Q24556543-E5105C3E-5134-4229-BEEB-1119A1DEEE66Q24564046-22BF61EF-0181-4E89-8159-AA6D6B714EE5Q24564617-04908A72-958D-4645-8C18-E120925B1E0FQ24568248-729CB1F9-386D-4936-BFFA-94E16B78E864Q24603946-A70BC1FE-764F-4C42-9A2D-1DE4A1B3127DQ24631079-33AAE758-19BC-4569-9591-77390E74CC6EQ24797910-CCBC1D64-96E7-4249-A051-3600BF21E566Q28319216-15C04428-1315-44DF-9483-C24799674D26Q28567475-57572D3C-FEB0-4C81-A7AD-A5AF426773E4Q30570979-E8871CEC-8856-41B3-94C8-389B9BCFCFD4Q33617959-C9147C79-79D6-4702-828A-142BD4725D97Q33786606-206215B3-ACB6-4C39-BED5-74E537D59910Q33832054-4EF79281-406E-45B7-84D6-8B24AA9AE122Q35012543-3232552F-5539-485C-86D2-71B9B4829F16Q35034208-39EC94D1-96FA-413D-9663-14132FA2D6D3Q35062606-C2C15BB0-7A8A-47BE-AAD2-224CF2A2AA72Q35801189-F3F7B18E-E77E-4DEB-B129-A6697C5001ACQ35874878-38998A41-DFA2-491E-8198-DA315AFD8A6EQ36563487-117C6BCE-1F77-4233-BFB4-1A20FC64CB18Q36572771-106A64BD-34DC-4C56-904F-CAC762339D16Q36658009-ADFB457B-FE0C-4A9C-AF73-1F01505B3F7DQ36701157-6569EF31-5F33-4898-AEAC-155ACCE34F71Q36702140-0F9693CF-9A7E-4036-A5FD-A7136716E39EQ36720751-D4492E80-E78A-4B66-8F57-28120921A116Q36731769-8FA0FB2F-93A2-4324-B6CC-93C54417BC8EQ36733951-6B896AE5-5AB2-4DEE-BD17-ADAB4E73DDF9Q36744632-C6A4BF40-AA20-4659-AD02-ACAE5D11A3A8Q36745246-1AF1098D-4512-4602-8138-B4716B588889Q36755516-00C3B653-AC8C-4692-9979-47B2FF5D9ADBQ36774210-33603FF6-99AF-4ACC-A13B-A2D6D0F3F274Q36783282-EBC1D333-5342-4F0A-B636-13EBA3D2AED3Q36813511-193EE717-F03D-4B95-919E-51D096DA1CA7Q36817452-68AD8F16-BE9A-4B65-B998-4ABE7F1A9824Q38326992-ED613775-CA3E-4AD7-8119-B208D43E0B86Q38328562-A7939EE0-36E6-49F9-B89F-D917B846BF55Q38332525-DFEE8F49-83C7-4B53-8945-AFC880A2ADB6Q38338025-330DDD11-7F8E-4451-801F-1BA74BB7F983Q38340236-A3FB3A3C-7E35-4EDD-B372-68E7FFFC53B0
P2860
Autoregulation of fos: the dyad symmetry element as the major target of repression.
description
1989 nî lūn-bûn
@nan
1989 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած
@hyw
1989 թվականի սեպտեմբերին հրատարակված գիտական հոդված
@hy
1989年の論文
@ja
1989年論文
@yue
1989年論文
@zh-hant
1989年論文
@zh-hk
1989年論文
@zh-mo
1989年論文
@zh-tw
1989年论文
@wuu
name
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@ast
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@en
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@nl
type
label
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@ast
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@en
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@nl
prefLabel
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@ast
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@en
Autoregulation of fos: the dyad symmetry element as the major target of repression.
@nl
P2093
P2860
P1433
P1476
Autoregulation of fos: the dyad symmetry element as the major target of repression
@en
P2093
Herrlich P
Rahmsdorf HJ
Rahmsdorf U
Schönthal A
P2860
P304
P356
10.1002/J.1460-2075.1989.TB08394.X
P407
P577
1989-09-01T00:00:00Z