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)
Growth of human mammary tumor cells ZR-75-1 is stimulated by estradiol (E2), epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I). In these cells ribosomal protein S6 kinase is activated by EGF, IGF-I, insulin and phorbol 12-myristate 13-acetate (TPA) but not by E2. The human mammary tumor cell line MDA-MB 231, which is E2-receptor negative, has receptors for EGF, IGF-I and insulin but is unresponsive to these factors in terms of growth and S6 kinase activation. The role of
protein kinase C
(
PKC
) in the activation of S6 kinase by growth factors and TPA was investigated in ZR-75-1 cells. Down regulation of
PKC
activity by treatment with TPA for 48-h blocks the stimulation of S6 kinase by TPA but leaves the activation by EGF, IGF-I and insulin unaffected. In intact ZR-75-1 cells staurosporine blocks activation of S6 kinase by EGF and TPA, however with different IC50. The results show that S6 kinase is not activated by estradiol, that its activation by EGF,
IGE
-I and insulin does not depend on the presence of
PKC
activity and that its activation by TPA is mediated by a different (
PKC
-dependent) pathway.
...
PMID:Regulation of ribosomal protein S6 kinase in human mammary tumor cells: effect of estrogen, growth factors and phorbol ester. 327 21
Primary generalized epilepsy
may be the result of maldevelopment of central nervous system and each seizure may be the consequence of a neuronal maladaptation to an unknown stimulus using the paleospinothalamical tract due to an overexpression of brain-derived neurotrophic factor and neurotrophin-3. The subsequent protein kinase C epsilon (PKC-epsilon) activation and intracellular Ca(2+) release causes a nociceptive hypersensitization and an increased cortical hyperexcitability because of increased frequency of synchronous Ca(2+) oscillations, cortical maldevelopment at the level of synapses and an attenuation of GABA(A) receptor mediated responses in reticular thalamic nucleus. Valproate may exert its antiepileptic effect as a
PKC
-epsilon inhibitor, and using with a
PKC
-epsilon activator that cannot pass blood brain barrier, its side effects may become avoidable.
...
PMID:The epsilon theory: a novel synthesis of the underlying molecular and electrophysiological mechanisms of primary generalized epilepsy and the possible mechanism of action of valproate. 1560 53
