Effects of dexamethasone, heat shock, and serum responses on the inhibition of hsc70 synthesis by antisense RNA in NIH 3T3 cells

1995 ◽  
Vol 164 (2) ◽  
pp. 344-355 ◽  
Author(s):  
Ting Li ◽  
Lawrence E. Hightower
Keyword(s):  
Heat Shock ◽  
Antisense Rna ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

scholarly journals Alpha B-crystallin expression in mouse NIH 3T3 fibroblasts: glucocorticoid responsiveness and involvement in thermal protection.

1993 ◽  
Vol 13 (3) ◽  
pp. 1824-1835 ◽  
Author(s):  
A Aoyama ◽  
E Fröhli ◽  
R Schäfer ◽  
R Klemenz
Keyword(s):  
Heat Shock ◽  
Thermal Protection ◽  
Cell Clone ◽  
Ectopic Expression ◽  
Small Heat Shock Protein ◽  
Ras Oncogene ◽  
3T3 Cells ◽  
3T3 Fibroblasts ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

alpha B-crystallin, a major soluble protein of vertebrate eye lenses, is a small heat shock protein which transiently accumulates in response to heat shock and other kinds of stress in mouse NIH 3T3 fibroblasts. Ectopic expression of an alpha B-crystallin cDNA clone renders NIH 3T3 cells thermoresistant. alpha B-crystallin accumulates in response to the synthetic glucocorticoid hormone dexamethasone. Dexamethasone-treated NIH 3T3 cells become thermoresistant to the same extent as they accumulate alpha B-crystallin. A cell clone in which alpha B-crystallin is superinduced upon heat shock acquires augmented thermotolerance. Expression of the ras oncogene causes a rapid but transient accumulation of alpha B-crystallin within 1 day. Later, sustained ras oncogene expression suppresses the dexamethasone-mediated alpha B-crystallin accumulation. Thus, oncogenic transformation triggered by the ras oncogene interferes with hormone-mediated accumulation of alpha B-crystallin and concomitant acquisition of thermoresistance. Other known heat shock proteins do not accumulate in response to ectopic alpha B-crystallin expression or to dexamethasone treatment. These results indicate that alpha B-crystallin can protect NIH 3T3 fibroblasts from thermal shock.

Altered heat-shock response in mouse NIH 3T3 cells expressing either v-FOS or Ha-RAS 1 oncogen

1992 ◽  
Vol 76 (2) ◽  
pp. 228-228
Author(s):  
N. Fabre ◽  
C. Diaz ◽  
P. Mehlen ◽  
J.P. Magaud ◽  
A.P. Arrigo
Keyword(s):  
Heat Shock ◽  
Heat Shock Response ◽  
3T3 Cells ◽  
Shock Response ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

scholarly journals Redox Factor-1 (Ref-1) Mediates the Activation of AP-1 in HeLa and NIH 3T3 Cells in Response to Heat Shock

1999 ◽  
Vol 274 (24) ◽  
pp. 16959-16964 ◽  
Author(s):  
David A. Diamond ◽  
Azemat Parsian ◽  
Clayton R. Hunt ◽  
Sam Lofgren ◽  
Douglas R. Spitz ◽  
...  
Keyword(s):  
Heat Shock ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

scholarly journals Heat Shock Protein Hsp72 Is a Negative Regulator of Apoptosis Signal-Regulating Kinase 1

2002 ◽  
Vol 22 (22) ◽  
pp. 7721-7730 ◽  
Author(s):  
Hee-Sae Park ◽  
Ssang-Goo Cho ◽  
Chang Kyun Kim ◽  
Hyun Sub Hwang ◽  
Kyung Tae Noh ◽  
...  
Keyword(s):  
Heat Shock ◽  
Protein Kinase ◽  
Heat Shock Protein ◽  
Mapk Signaling ◽  
Negative Regulator ◽  
Physical Interaction ◽  
3T3 Cells ◽  
Mild Heat ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

ABSTRACT Heat shock protein 72 (Hsp72) is thought to protect cells against cellular stress. The protective role of Hsp72 was investigated by determining the effect of this protein on the stress-activated protein kinase signaling pathways. Prior exposure of NIH 3T3 cells to mild heat shock (43°C for 20 min) resulted in inhibition of H2O2-induced activation of apoptosis signal-regulating kinase 1 (ASK1). Overexpression of Hsp72 also inhibited H2O2-induced activation of ASK1 as well as that of downstream kinases in the p38 mitogen-activated protein kinase (MAPK) signaling cascade. Recombinant Hsp72 bound directly to ASK1 and inhibited ASK1 activity in vitro. Furthermore, coimmunoprecipitation analysis revealed a physical interaction between endogenous Hsp72 and ASK1 in NIH 3T3 cells exposed to mild heat shock. Hsp72 blocked both the homo-oligomerization of ASK1 and ASK1-dependent apoptosis. Hsp72 antisense oligonucleotides prevented the inhibitory effects of mild heat shock on H2O2-induced ASK1 activation and apoptosis. These observations suggest that Hsp72 functions as an endogenous inhibitor of ASK1.

scholarly journals Expression of chimeric tRNA-driven antisense transcripts renders NIH 3T3 cells highly resistant to Moloney murine leukemia virus replication.

1990 ◽  
Vol 10 (12) ◽  
pp. 6512-6523 ◽  
Author(s):  
B A Sullenger ◽  
T C Lee ◽  
C A Smith ◽  
G E Ungers ◽  
E Gilboa
Keyword(s):  
Murine Leukemia Virus ◽  
Antisense Rna ◽  
Leukemia Virus ◽  
Retroviral Vector ◽  
Moloney Murine Leukemia Virus ◽  
3T3 Cells ◽  
Antisense Transcripts ◽  
Nih 3T3 ◽  
Murine Leukemia ◽  
Nih 3T3 Cells

NIH 3T3 cells infected with Moloney murine leukemia virus (MoMLV) express high levels of virus-specific RNA. To inhibit replication of the virus, we stably introduced chimeric tRNA genes encoding antisense templates into NIH 3T3 cells via a retroviral vector. Efficient expression of hybrid tRNA-MoMLV antisense transcripts and inhibition of MoMLV replication were dependent on the use of a particular type of retroviral vector, the double-copy vector, in which the chimeric tRNA gene was inserted in the 3' long terminal repeat. MoMLV replication was inhibited up to 97% in cells expressing antisense RNA corresponding to the gag gene and less than twofold in cells expressing antisense RNA corresponding to the pol gene. RNA and protein analyses suggest that inhibition was exerted at the level of translation. These results suggest that RNA polymerase III-based antisense inhibition systems can be used to inhibit highly expressed viral genes and render cells resistant to viral replication via intracellular immunization strategies.

Expression of chimeric tRNA-driven antisense transcripts renders NIH 3T3 cells highly resistant to Moloney murine leukemia virus replication

1990 ◽  
Vol 10 (12) ◽  
pp. 6512-6523
Author(s):  
B A Sullenger ◽  
T C Lee ◽  
C A Smith ◽  
G E Ungers ◽  
E Gilboa
Keyword(s):  
Murine Leukemia Virus ◽  
Antisense Rna ◽  
Leukemia Virus ◽  
Retroviral Vector ◽  
Moloney Murine Leukemia Virus ◽  
3T3 Cells ◽  
Antisense Transcripts ◽  
Nih 3T3 ◽  
Murine Leukemia ◽  
Nih 3T3 Cells

NIH 3T3 cells infected with Moloney murine leukemia virus (MoMLV) express high levels of virus-specific RNA. To inhibit replication of the virus, we stably introduced chimeric tRNA genes encoding antisense templates into NIH 3T3 cells via a retroviral vector. Efficient expression of hybrid tRNA-MoMLV antisense transcripts and inhibition of MoMLV replication were dependent on the use of a particular type of retroviral vector, the double-copy vector, in which the chimeric tRNA gene was inserted in the 3' long terminal repeat. MoMLV replication was inhibited up to 97% in cells expressing antisense RNA corresponding to the gag gene and less than twofold in cells expressing antisense RNA corresponding to the pol gene. RNA and protein analyses suggest that inhibition was exerted at the level of translation. These results suggest that RNA polymerase III-based antisense inhibition systems can be used to inhibit highly expressed viral genes and render cells resistant to viral replication via intracellular immunization strategies.

Alpha B-crystallin expression in mouse NIH 3T3 fibroblasts: glucocorticoid responsiveness and involvement in thermal protection

1993 ◽  
Vol 13 (3) ◽  
pp. 1824-1835
Author(s):  
A Aoyama ◽  
E Fröhli ◽  
R Schäfer ◽  
R Klemenz
Keyword(s):  
Heat Shock ◽  
Thermal Protection ◽  
Cell Clone ◽  
Ectopic Expression ◽  
Small Heat Shock Protein ◽  
Ras Oncogene ◽  
3T3 Cells ◽  
3T3 Fibroblasts ◽  
Nih 3T3 ◽  
Nih 3T3 Cells

alpha B-crystallin, a major soluble protein of vertebrate eye lenses, is a small heat shock protein which transiently accumulates in response to heat shock and other kinds of stress in mouse NIH 3T3 fibroblasts. Ectopic expression of an alpha B-crystallin cDNA clone renders NIH 3T3 cells thermoresistant. alpha B-crystallin accumulates in response to the synthetic glucocorticoid hormone dexamethasone. Dexamethasone-treated NIH 3T3 cells become thermoresistant to the same extent as they accumulate alpha B-crystallin. A cell clone in which alpha B-crystallin is superinduced upon heat shock acquires augmented thermotolerance. Expression of the ras oncogene causes a rapid but transient accumulation of alpha B-crystallin within 1 day. Later, sustained ras oncogene expression suppresses the dexamethasone-mediated alpha B-crystallin accumulation. Thus, oncogenic transformation triggered by the ras oncogene interferes with hormone-mediated accumulation of alpha B-crystallin and concomitant acquisition of thermoresistance. Other known heat shock proteins do not accumulate in response to ectopic alpha B-crystallin expression or to dexamethasone treatment. These results indicate that alpha B-crystallin can protect NIH 3T3 fibroblasts from thermal shock.

scholarly journals Heat shock induces the release of fibroblast growth factor 1 from NIH 3T3 cells.

1992 ◽  
Vol 89 (22) ◽  
pp. 10691-10695 ◽  
Author(s):  
A. Jackson ◽  
S. Friedman ◽  
X. Zhan ◽  
K. A. Engleka ◽  
R. Forough ◽  
...  
Keyword(s):  
Growth Factor ◽  
Heat Shock ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth ◽  
3T3 Cells ◽  
Nih 3T3 ◽  
Nih 3T3 Cells
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