Cell transformation by c-fos requires an extended period of expression and is independent of the cell cycle.
about
Dominant negative c-jun inhibits activation of the cyclin D1 and cyclin E kinase complexesIsolation of an allele of reeler by insertional mutagenesisIdentification of a c-fos-induced gene that is related to the platelet-derived growth factor/vascular endothelial growth factor familyInduction of cyclin D1 by simian virus 40 small tumor antigenA transcriptome map of cellular transformation by the fos oncogeneDual mechanisms for lysophosphatidic acid stimulation of human ovarian carcinoma cellsThe Mos/MAP kinase pathway stabilizes c-Fos by phosphorylation and augments its transforming activity in NIH 3T3 cellsCrk and CrkL are required for cell transformation by v-fos and v-ras.AP-1 differentially expressed proteins Krp1 and fibronectin cooperatively enhance Rho-ROCK-independent mesenchymal invasion by altering the function, localization, and activity of nondifferentially expressed proteins.Inhibition of platelet-derived growth factor- and epidermal growth factor-mediated mitogenesis and signaling in 3T3 cells expressing delta Raf-1:ER, an estradiol-regulated form of Raf-1.The G10BP-1 gene encoding a GC box binding protein, is a target of Myc and Jun/Fos.Regulation of a multigenic invasion programme by the transcription factor, AP-1: re-expression of a down-regulated gene, TSC-36, inhibits invasion.Down-regulation of particulate protein kinase Cepsilon and up-regulation of nuclear activator protein-1 DNA binding in liver following in vivo exposure of B6C3F1 male mice to heptachlor epoxide.Alternative splicing of c-fos pre-mRNA: contribution of the rates of synthesis and degradation to the copy number of each transcript isoform and detection of a truncated c-Fos immunoreactive species.c-Fos accelerates hepatocyte conversion to a fibroblastoid phenotype through ERK-mediated upregulation of paxillin-Serine178 phosphorylation.c-Fos overexpression increases the proliferation of human hepatocytes by stabilizing nuclear Cyclin D1Functional analysis of newly discovered growth control genes: experimental approaches.Fos family members induce cell cycle entry by activating cyclin D1.An extracellular signal-regulated kinase 1- and 2-dependent program of chromatin trafficking of c-Fos and Fra-1 is required for cyclin D1 expression during cell cycle reentry.Multiple degradation pathways for Fos family proteins.SRF-dependent gene expression is required for PI3-kinase-regulated cell proliferation.JunB contributes to Id2 repression and the epithelial-mesenchymal transition in response to transforming growth factor-β.Invasion of normal human fibroblasts induced by v-Fos is independent of proliferation, immortalization, and the tumor suppressors p16INK4a and p53.The transcription factor AP-1 is required for EGF-induced activation of rho-like GTPases, cytoskeletal rearrangements, motility, and in vitro invasion of A431 cells.Raf-induced proliferation or cell cycle arrest is determined by the level of Raf activity with arrest mediated by p21Cip1.Identification of cJun-responsive genes in Rat-1a cells using multiple techniques: increased expression of stathmin is necessary for cJun-mediated anchorage-independent growth.Exposure of nerve growth factor-treated PC12 rat pheochromocytoma cells to a modulated radiofrequency field at 836.55 MHz: effects on c-jun and c-fos expression.Activated MEK stimulates expression of AP-1 components independently of phosphatidylinositol 3-kinase (PI3-kinase) but requires a PI3-kinase signal To stimulate DNA synthesis.The repertoire of fos and jun proteins expressed during the G1 phase of the cell cycle is determined by the duration of mitogen-activated protein kinase activation.Transcriptional activation of the fra-1 gene by AP-1 is mediated by regulatory sequences in the first intron.AP-1-mediated invasion requires increased expression of the hyaluronan receptor CD44.Separation of v-Src-induced mitogenesis and morphological transformation by inhibition of AP-1Mitochondrial membrane potential regulation is independent of c-fos expression.Neuregulin 1-Beta cytoprotective role in AML 12 mouse hepatocytes exposed to pentachlorophenolGrowth inhibition by the muscarinic M(3) acetylcholine receptor: evidence for p21(Cip1/Waf1) involvement in G(1) arrest.Attenuated expression of the serum responsive T1 gene in ras transformed fibroblasts due to the inhibition of c-fos gene activity.Cellular and viral Fos proteins are degraded by different proteolytic systems.Control of cell cycle gene expression in bone development and during c-Fos-induced osteosarcoma formation.Genomic instability-based transgenic models of prostate cancer.
P2860
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P2860
Cell transformation by c-fos requires an extended period of expression and is independent of the cell cycle.
description
1994 nî lūn-bûn
@nan
1994年の論文
@ja
1994年論文
@yue
1994年論文
@zh-hant
1994年論文
@zh-hk
1994年論文
@zh-mo
1994年論文
@zh-tw
1994年论文
@wuu
1994年论文
@zh
1994年论文
@zh-cn
name
Cell transformation by c-fos r ...... independent of the cell cycle.
@en
Cell transformation by c-fos r ...... independent of the cell cycle.
@nl
type
label
Cell transformation by c-fos r ...... independent of the cell cycle.
@en
Cell transformation by c-fos r ...... independent of the cell cycle.
@nl
prefLabel
Cell transformation by c-fos r ...... independent of the cell cycle.
@en
Cell transformation by c-fos r ...... independent of the cell cycle.
@nl
P2860
P356
P1476
Cell transformation by c-fos r ...... independent of the cell cycle.
@en
P2093
P2860
P304
P356
10.1128/MCB.14.6.4295
P407
P577
1994-06-01T00:00:00Z