Immortalization by c-myc, H-ras, and Ela oncogenes induces differential cellular gene expression and growth factor responses
about
Hepatitis C virus core protein cooperates with ras and transforms primary rat embryo fibroblasts to tumorigenic phenotypeIdentification of a region of simian virus 40 large T antigen required for cell transformationRescue of cells from ras oncogene-induced growth arrest by a second, complementing, oncogene.Ras-mediated cell cycle arrest is altered by nuclear oncogenes to induce Schwann cell transformation.Possible role of arginase-1 in concomitant tumor immunityAn essential domain of the c-myc protein interacts with a nuclear factor that is also required for E1A-mediated transformationThe c-myc-regulated gene mrl encodes plasminogen activator inhibitor 1Posttranscriptional regulation of cellular gene expression by the c-myc oncogene.Induction of sensitivity to the cytotoxic action of tumor necrosis factor alpha by adenovirus E1A is independent of transformation and transcriptional activationDifferential induction of cytolytic susceptibility by E1A, myc, and ras oncogenes in immortalized cells.The amino-terminal region of the adenovirus serotype 5 E1a protein performs two separate functions when expressed in primary baby rat kidney cells.Reviewing once more the c-myc and Ras collaboration: converging at the cyclin D1-CDK4 complex and challenging basic concepts of cancer biology.The N-terminal region of the adenovirus type 5 E1A proteins can repress expression of cellular genes via two distinct but overlapping domains.Overexpression of an activated rasG gene during growth blocks the initiation of Dictyostelium development.Cyclin D2 and Ha-Ras transformed rat embryo fibroblasts exhibit a novel deregulation of cell size control and early S phase arrest in low serum.Negative autoregulation of c-myc transcription.Common target for 12-O-tetradecanoylphorbol-13-acetate and ras in the transcriptional enhancer of the growth factor-inducible JE gene.Establishment and characterization of two immortalized cell lines of the osteoblastic lineage.Stromal influences on transformation of human mammary epithelial cells overexpressing c-myc and SV40T.Mechanism of endogenous myc gene down-regulation in E mu-N-myc tumors.Adenovirus 5 E1A is responsible for increased expression of insulin receptor substrate 4 in established adenovirus 5-transformed cell lines and interacts with IRS components activating the PI3 kinase/Akt signalling pathway.
P2860
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P2860
Immortalization by c-myc, H-ras, and Ela oncogenes induces differential cellular gene expression and growth factor responses
description
1987 nî lūn-bûn
@nan
1987年の論文
@ja
1987年論文
@yue
1987年論文
@zh-hant
1987年論文
@zh-hk
1987年論文
@zh-mo
1987年論文
@zh-tw
1987年论文
@wuu
1987年论文
@zh
1987年论文
@zh-cn
name
Immortalization by c-myc, H-ra ...... on and growth factor responses
@en
type
label
Immortalization by c-myc, H-ra ...... on and growth factor responses
@en
prefLabel
Immortalization by c-myc, H-ra ...... on and growth factor responses
@en
P2860
P356
P1476
Immortalization by c-myc, H-ra ...... on and growth factor responses
@en
P2093
P2860
P304
P356
10.1128/MCB.7.11.3899
P407
P577
1987-11-01T00:00:00Z