Protein kinase D2 potentiates MEK/ERK/RSK signaling, c-Fos accumulation and DNA synthesis induced by bombesin in Swiss 3T3 cells

2007 ◽  
Vol 211 (3) ◽  
pp. 781-790 ◽  
Author(s):  
James Sinnett-Smith ◽  
Elena Zhukova ◽  
Osvaldo Rey ◽  
Enrique Rozengurt
Keyword(s):  
Protein Kinase ◽  
Dna Synthesis ◽  
3T3 Cells ◽  
Swiss 3T3

scholarly journals Protein Kinase D Potentiates DNA Synthesis Induced by Gq-coupled Receptors by Increasing the Duration of ERK Signaling in Swiss 3T3 Cells

2004 ◽  
Vol 279 (16) ◽  
pp. 16883-16893 ◽  
Author(s):  
James Sinnett-Smith ◽  
Elena Zhukova ◽  
Nena Hsieh ◽  
Xiaohua Jiang ◽  
Enrique Rozengurt
Keyword(s):  
Protein Kinase ◽  
Dna Synthesis ◽  
Erk Signaling ◽  
Protein Kinase D ◽  
3T3 Cells ◽  
Swiss 3T3

S1691 Endogenous Protein Kinase D Contributes to Gq-Coupled Receptor Induction of DNA Synthesis in Swiss 3T3 Cells

2008 ◽  
Vol 134 (4) ◽  
pp. A-251
Author(s):  
James Sinnett-Smith ◽  
Rodrigo O. Jacamo ◽  
Robert K. Kui ◽  
Yunzu M. Wang ◽  
Enrique Rozengurt
Keyword(s):  
Protein Kinase ◽  
Dna Synthesis ◽  
Protein Kinase D ◽  
3T3 Cells ◽  
Endogenous Protein ◽  
Swiss 3T3

Microinjection of smg/rap1/Krev-1 p21 into Swiss 3T3 cells induces DNA synthesis and morphological changes

1992 ◽  
Vol 12 (8) ◽  
pp. 3407-3414
Author(s):  
Y Yoshida ◽  
M Kawata ◽  
Y Miura ◽  
T Musha ◽  
T Sasaki ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Laser Scanning ◽  
Morphological Changes ◽  
Stress Fibers ◽  
Confocal Laser ◽  
3T3 Cells ◽  
Membrane Ruffling ◽  
Ras P21 ◽  
Swiss 3T3 ◽  
Gamma S

Microinjection of either Ki-rasVal-12 p21 or the GDP-bound form of Ki-ras p21 plus smg GDP dissociation stimulator (GDS), a stimulatory GDP/GTP exchange protein for Ki-ras p21, smg/rap1/Krev-1 p21, and rho p21, into quiescent Swiss 3T3 cells induced DNA synthesis irrespective of the presence or absence of insulin. The guanosine 5'-(3-O-thio)triphosphate (GTP gamma S)-bound form of smg p21B or the GDP-bound form of smg p21B plus smg GDS also induced DNA synthesis but only in the presence of insulin. Either the GDP-bound form of Ki-ras p21 or the same form of smg p21B alone was inactive, but smg GDS alone was slightly active only in the presence of insulin. The morphology of the cells was analyzed by scanning electron, phase-contrast, and confocal laser scanning microscopies. Ki-rasVal-12 p21 induced membrane ruffling irrespective of the presence or absence of insulin. The GTP gamma S-bound form of smg p21B showed the same effect only in the presence of insulin. Either the GDP-bound form of Ki-ras p21, the same form of smg p21B, or smg GDS alone was inactive. Upon microinjection of Ki-rasVal-12 p21, stress fibers markedly decreased and the cells became round and piled up. In contrast, upon microinjection of the GTP gamma S-bound form of smg p21B, stress fibers did not markedly decrease and the cells neither became round nor piled up. These results indicate that both ras p21 and smg p21 are mitogenic in Swiss 3T3 cells but that their actions are slightly different.

scholarly journals Bombesin and platelet-derived growth factor stimulate formation of inositol phosphates and Ca2+ mobilization in Swiss 3T3 cells by different mechanisms

1989 ◽  
Vol 258 (1) ◽  
pp. 177-185 ◽  
Author(s):  
D M Blakeley ◽  
A N Corps ◽  
K D Brown
Keyword(s):  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Phorbol Esters ◽  
Inositol Phosphates ◽  
Platelet Derived Growth Factor ◽  
3T3 Cells ◽  
Kinase C ◽  
Swiss 3T3 ◽  
Stimulation Of

Highly purified platelet-derived growth factor (PDGF) or recombinant PDGF stimulate DNA synthesis in quiescent Swiss 3T3 cells. The dose-response curves for the natural and recombinant factors were similar, with half-maximal responses at 2-3 ng/ml and maximal responses at approx. 10 ng/ml. Over this dose range, both natural and recombinant PDGF stimulated a pronounced accumulation of [3H]inositol phosphates in cells labelled for 72 h with [3H]inositol. In addition, mitogenic concentrations of PDGF stimulated the release of 45Ca2+ from cells prelabelled with the radioisotope. However, in comparison with the response to the peptide mitogens bombesin and vasopressin, a pronounced lag was evident in both the generation of inositol phosphates and the stimulation of 45Ca2+ efflux in response to PDGF. Furthermore, although the bombesin-stimulated efflux of 45Ca2+ was independent of extracellular Ca2+, the PDGF-stimulated efflux was markedly inhibited by chelation of external Ca2+ by using EGTA. Neither the stimulation of formation of inositol phosphates nor the stimulation of 45Ca2+ efflux in response to PDGF were affected by tumour-promoting phorbol esters such as 12-O-tetradecanoylphorbol 13-acetate (TPA). In contrast, TPA inhibited phosphoinositide hydrolysis and 45Ca2+ efflux stimulated by either bombesin or vasopressin. Furthermore, whereas formation of inositol phosphates in response to both vasopressin and bombesin was increased in cells in which protein kinase C had been down-modulated by prolonged exposure to phorbol esters, the response to PDGF was decreased in these cells. These results suggest that, in Swiss 3T3 cells, PDGF receptors are coupled to phosphoinositidase activation by a mechanism that does not exhibit protein kinase C-mediated negative-feedback control and which appears to be fundamentally different from the coupling mechanism utilized by the receptors for bombesin and vasopressin.

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