Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.11.13 (
protein kinase C
)
49,245
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Basal level of asparagine synthetase mRNA in BALB3T3 cells was elevated when the cells were shifted from medium containing a high concentration (3.3 mM) of asparagine to one lacking asparagine. We then studied whether the expression of asparagine synthetase mRNA is also mediated through other asparagine-independent signaling pathways. BALB3T3 cells grown to near confluence were quiesced by serum-starvation, and various agents were then added to the culture to examine the enzyme activity and mRNA level of
asparagine synthetase
. 12-O-tetradecanoylphorbol-13-acetate (TPA), a direct activator of
protein kinase C
(
PKC
), elevated dose and time dependently the level of asparagine synthetase mRNA even in Eagle's minimum essential medium with alpha modification (MEM alpha) that contains protein-constituting 20 amino acids and is supplemented with 3.3 mM asparagine. Staurosporine and H-7,
PKC
inhibitors, strongly blocked the fetal bovine serum-dependent accumulation of asparagine synthetase mRNA. TPA could also enhance the activity of
asparagine synthetase
within 24 h at concentrations of more than 10 nM. These results suggest that expression of
asparagine synthetase
gene can be induced both through a pathway that involves
PKC
and through a pathway the origin of which is a reduced concentration of asparagine in BALB3T3 cells.
...
PMID:Expression of asparagine synthetase mRNA through asparagine independent signal transduction pathway that might involve protein kinase C in BALB3T3 cells. 857 80
During 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced differentiation of human promyelocytic leukemia HL-60 cells toward maturing monocytes/macrophages,
asparagine synthetase
(
ASNS
) mRNA expression declined time and dose-dependently. The effect of TPA was inhibited by inhibitors for
PKC
and MEK 1/2, but not by those for JNK and p38 MAPK. Combination treatment with TPA and asparaginase synergistically enhanced the growth retardation accompanied by apoptotic cell death characterized by internucleosomal DNA fragmentation. These data suggest the possible involvement of MEK1/2 MAPK in the inhibitory effect of TPA on
ASNS
mRNA expression and that the induction of the down-regulation of
ASNS
(via MEK1/2 activation) may be a new strategy for the treatment of leukemia blast cells.
...
PMID:Declined asparagine synthetase mRNA expression and enhanced sensitivity to asparaginase in HL-60 cells committed to monocytic differentiation. 1941 79
