Autocrine mechanism for v-sis transformation requires cell surface localization of internally activated growth factor receptors.
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Suramin rapidly alters cellular tyrosine phosphorylation in prostate cancer cell lines.Cloning, expression, characterization, and role in autocrine cell growth of cell surface retention sequence binding protein-1.17-beta estradiol elicits an autocrine leiomyoma cell proliferation: evidence for a stimulation of protein kinase-dependent pathway.Angiotensin II induces delayed mitogenesis and cellular proliferation in rat aortic smooth muscle cells. Correlation with the expression of specific endogenous growth factors and reversal by suramin.Clinical potential of novel therapeutic targets in breast cancer: CDK4/6, Src, JAK/STAT, PARP, HDAC, and PI3K/AKT/mTOR pathways.Expression of ras oncogenes in cultured human cells alters the transcriptional and posttranscriptional regulation of cytokine genes.Suramin, an experimental chemotherapeutic drug, activates the receptor for epidermal growth factor and promotes growth of certain malignant cells.The N-terminal propiece of interleukin 1 alpha is a transforming nuclear oncoproteinThe v-sis oncoprotein loses transforming activity when targeted to the early Golgi complexModulation of keratinocyte growth factor and its receptor in reepithelializing human skin.Disruption of transforming growth factor beta signaling by a novel ligand-dependent mechanismThe v-sis protein retains biological activity as a type II membrane protein when anchored by various signal-anchor domains, including the hydrophobic domain of the bovine papilloma virus E5 oncoprotein.Stromal platelet-derived growth factor receptor α (PDGFRα) provides a therapeutic target independent of tumor cell PDGFRα expression in lung cancer xenografts.Intracellular retention of membrane-anchored v-sis protein abrogates autocrine signal transductionA glutamine residue in the membrane-associating domain of the bovine papillomavirus type 1 E5 oncoprotein mediates its binding to a transmembrane component of the vacuolar H(+)-ATPase.The K-fgf/hst oncogene induces transformation through an autocrine mechanism that requires extracellular stimulation of the mitogenic pathwayPlatelet-derived growth factor receptor can mediate tumorigenic transformation by the bovine papillomavirus E5 protein.Dominant-negative mutants of platelet-derived growth factor revert the transformed phenotype of human astrocytoma cellsStable association between the bovine papillomavirus E5 transforming protein and activated platelet-derived growth factor receptor in transformed mouse cells.Imatinib as effective therapy for dermatofibrosarcoma protuberans: proof of concept of the autocrine hypothesis for cancer.Platelet-derived growth factor: mechanism of action and possible in vivo function.E5 oncoprotein retained in the endoplasmic reticulum/cis Golgi still induces PDGF receptor autophosphorylation but does not transform cellsG protein-coupled receptor signalling in the cardiac nuclear membrane: evidence and possible roles in physiological and pathophysiological function.Human neuroblastoma cells express alpha and beta platelet-derived growth factor receptors coupling with neurotrophic and chemotactic signaling.Identification of a cell retention signal in the B-chain of platelet-derived growth factor and in the long splice version of the A-chain.Transforming growth factor-beta 1 mutations in Camurati-Engelmann disease lead to increased signaling by altering either activation or secretion of the mutant protein.Structural and functional analysis of a chimeric protein COL1A1-PDGFB generated by the translocation t(17;22)(q22;q13.1) in Dermatofibrosarcoma protuberans (DP).Platelet-derived growth factor. Structure, function and implications in normal and malignant cell growth.Suramin enters and accumulates in low pH intracellular compartments of v-sis-transformed NIH 3T3 cells.Activation of the platelet-derived growth factor receptor by the bovine papillomavirus E5 transforming protein.Differences in binding to the solid substratum and extracellular matrix may explain isoform-specific paracrine effects of platelet-derived growth factor.Reversion of autocrine transformation by a dominant negative platelet-derived growth factor mutant.Tumorigenic conversion of human mesothelial cells as a consequence of platelet-derived growth factor-A chain overexpression.Cell transformation by kFGF requires secretion but not glycosylation.Cell surface retention sequence binding protein-1 interacts with the v-sis gene product and platelet-derived growth factor beta-type receptor in simian sarcoma virus-transformed cells.Compartmentalization of autocrine signal transduction pathways in Sis-transformed NIH 3T3 cells.
P2860
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P2860
Autocrine mechanism for v-sis transformation requires cell surface localization of internally activated growth factor receptors.
description
1989 nî lūn-bûn
@nan
1989 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1989 թվականի հոտեմբերին 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
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@ast
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@en
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@nl
type
label
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@ast
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@en
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@nl
prefLabel
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@ast
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@en
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@nl
P2093
P2860
P356
P1476
Autocrine mechanism for v-sis ...... vated growth factor receptors.
@en
P2093
P2860
P304
P356
10.1073/PNAS.86.20.8063
P407
P577
1989-10-01T00:00:00Z