p21ras-induced responsiveness of phosphatidylinositol turnover to bradykinin is a receptor number effect.
about
An interaction between p21ras and heat shock protein hsp60, a chaperonincAMP antagonizes p21ras-directed activation of extracellular signal-regulated kinase 2 and phosphorylation of mSos nucleotide exchange factorPlatelet-derived growth factor stimulates formation of active p21ras.GTP complex in Swiss mouse 3T3 cells.Identification of a protein associated with p21ras by chemical crosslinking.Cyclic AMP selectively enhances bradykinin receptor synthesis and expression in cultured arterial smooth muscle. Inhibition of angiotensin II and vasopressin response.Alterations of G-protein coupling function in phosphoinositide signaling pathways of cells transformed by ras and other membrane-associated and cytoplasmic oncogenes.The biochemistry of ras p21.The role of G proteins in transmembrane signalling.Possible involvement of normal p21 H-ras in the insulin/insulinlike growth factor 1 signal transduction pathway.Insulin stimulation of gene expression mediated by p21ras activation.Ras activation by insulin and epidermal growth factor through enhanced exchange of guanine nucleotides on p21ras.Differential pathways (phospholipase C and phospholipase D) of bradykinin-induced biphasic 1,2-diacylglycerol formation in non-transformed and K-ras-transformed NIH-3T3 fibroblasts. Involvement of intracellular Ca2+ oscillations in phosphatidylcholiEnhancement of kallikrein production and kinin sensitivity in T84 cells by growth in the nude mouse.Loss of bradykinin receptors and TPA-stimulated Na+ influx in SV40-transformed WI-38 cells.Transformation-specific decrease of phosphorylation of 80K protein, a substrate of protein kinase C, in NIH3T3 cells.Activation of inositol phospholipid breakdown by prostaglandin F2 alpha without any stimulation of proliferation in quiescent NIH-3T3 fibroblasts.Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts.Signal transduction in EJ-H-ras-transformed cells: de novo synthesis of diacylglycerol and subversion of agonist-stimulated inositol lipid metabolism.Regulation of Na+-H+ exchange in normal NIH-3T3 cells and in NIH-3T3 cells expressing the ras oncogene.The CDC42-specific inhibitor derived from ACK-1 blocks v-Ha-Ras-induced transformation.Effects of bradykinin on cell volume and intracellular pH in NIH 3T3 fibroblasts expressing the ras oncogene.
P2860
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P2860
p21ras-induced responsiveness of phosphatidylinositol turnover to bradykinin is a receptor number effect.
description
1988 nî lūn-bûn
@nan
1988 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
1988 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
1988年の論文
@ja
1988年論文
@yue
1988年論文
@zh-hant
1988年論文
@zh-hk
1988年論文
@zh-mo
1988年論文
@zh-tw
1988年论文
@wuu
name
p21ras-induced responsiveness ...... n is a receptor number effect.
@ast
p21ras-induced responsiveness ...... n is a receptor number effect.
@en
type
label
p21ras-induced responsiveness ...... n is a receptor number effect.
@ast
p21ras-induced responsiveness ...... n is a receptor number effect.
@en
prefLabel
p21ras-induced responsiveness ...... n is a receptor number effect.
@ast
p21ras-induced responsiveness ...... n is a receptor number effect.
@en
P2093
P2860
P356
P1476
p21ras-induced responsiveness ...... n is a receptor number effect.
@en
P2093
J de Gunzburg
R A Weinberg
P2860
P304
P356
10.1073/PNAS.85.16.5774
P407
P577
1988-08-01T00:00:00Z