Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.13 (protein kinase C)
 49,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Steroid hormones modulate a variety of physiological functions in the hypothalamus. We attempted to identify steroid-regulated genes in the rat preoptic area-anterior hypothalamus by comparing differentially expressed mRNAs. Adult female rats were ovariectomized and, 1 week later, a silastic capsule containing 17beta-oestradiol (180 microg/ml) was subcutaneously implanted. After 2 days, a single injection of progesterone (1 mg) was administered at 10.00 h and rats were killed at 17.00 h on the same day. Differential-display polymerase chain reaction followed by Northern blot analysis showed that 10 clones were differentially regulated. Using homology search in Genbank, three genes were identified as sodium, potassium-ATPase beta1, protein kinase C-binding Nell-homologue protein and evectin-1. Further characterization of 10 clones showed that the expression patterns were tissue-specific and differentially regulated during puberty. Among these, mRNAs for protein kinase C-binding Nell-homologue protein, evectin-1 and human CGI-118 protein-like gene were induced after vagina opening, and differentially expressed during the oestrous cycle. Taken together, several steroid-regulated genes identified in the present study may play an important role in regulating hypothalamic functions, including puberty and the oestrous cycle.
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PMID:Analysis of steroid-induced genes in the rat preoptic area-anterior hypothalamus using a differential-display reverse transcriptase-polymerase chain reaction. 1141 40

The molecular mechanisms underlying entry of group B Streptococci (GBS) into human endothelial cells are not yet fully understood. This study is centered on the triggering of signaling cascade in human umbilical vein endothelial cells (HUVEC) during their interaction with different GBS serotypes/strains (type III: 80340-vagina and 90356-CSF and type V: 88641-vagina and 90186-blood). We have shown that the analyzed microorganisms adhere to HUVEC, but only those of the strains 90356-CSF, 88641-vagina and 90186-blood presented intracellular viability. Activation of PKC directly increased F-actin content and organization into stress fibers, and increased intracellular viability of GBS-III microorganisms. PKA inhibitor seems to promote surveillance of GBS type V microorganisms within HUVEC. These studies indicate that different molecules present at the cell surface of the GBS might induce different responses to HUVEC, interfering with the recruitment of cortical actin filaments.
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PMID:Signal transduction in human endothelial cells induced by their interaction with group B Streptococci. 1580 10

Nitric oxide (NO)-releasing microparticles were developed as a potential treatment option against various blood flow irregulations including sexual dysfunction, atherosclerosis and metal stent-induced restenosis. Polymeric microparticles containing diethylenetriamine diazeniumdiolate (DETA NONOate), a NO donor, were prepared using modified double-emulsion solvent evaporation method to maximize the loading efficacy and stability of DETA NONOate. The pharmacological effects of the NO-releasing microparticles were evaluated by examining the changes in the vaginal blood flow in rats. The effects of NO on the phosphorylation of protein kinase C (PKC) and mitogen activated protein (MAP) kinases in excised vaginal mucosa, such as extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK) and p38, were examined using immunoblotting technique to determine whether NO activates PKC, which subsequently plays an integral role in the formation of PKC-MAP kinase modules. The viability of vagina cells (VK2E6E7) upon exposure to NO-releasing microparticles was examined for cytotoxicity assessment. In contrast to rapid and short-term effects of non-formulated DETA NONOate, microparticles containing DETA NONOate exerted beneficial effects on the blood flow (148+/-13%) for an extended period of time, inducing a significant change at 5 min after its application and the maximum blood flow of 172+/-23% at 120 min. The enhanced vaginal blood flow was maintained for up to 210 min and gradually returned to the baseline afterward. The results of Western immunoblotting study displayed differential expression of MAP kinases (ERK1/2 and JNK) upon NO treatment, clearly demonstrating that PKC is involved in the blood flow regulation process. There were no significant changes in cell viability in vaginal cells upon exposure to NO-releasing microparticles as compared with the control. The results of this work supported that NO-releasing microparticles could improve the vaginal blood flow without causing cytotoxic effects and PKC-MAP kinase modules are involved in the NO-induced blood flow regulation process.
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PMID:Pharmacological activity and protein phosphorylation caused by nitric oxide-releasing microparticles. 1985 95

p50 is a member of the NF-kappaB family known to be involved in endometriosis. To gain insight into the roles of p50 in the development of endometriosis, we cross-transplanted endometrial fragments from p50 knockout mice to wild-type mice and vice versa, and also autotransplanted the fragments within the knockout and wild-type mice, inducing endometriosis. We then evaluated the size of the endometrial implants, and immunoreactivity to phosphorylated p65 (p-p65), PKCepsilon and TRPV1 in ectopic and eutopic endometrium as well as in vagina. We found that p50 deletion significantly reduces the size of endometrial implants. The immunoreactivity to p-p65 and PKCepsilon, but not TRPV1, was reduced in endometrial implants in p50 knockout mice. Deletion of p50 significantly reduced p-p65 and PKCepsilon, but not TRPV1, expression in eutopic endometrium and vagina. It also disrupts NF-kappaB activation and PKCepsilon expression in eutopic and vagina, suggesting the role of NF-kappaB in regulating PKCepsilon, which plays an important role in nociception. These data show that p50 is involved in the development of endometriosis and may be a promising therapeutic target.
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PMID:The role of nuclear factor-kappa-B p50 subunit in the development of endometriosis. 2119 37