Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.1 (protein kinase)
 81,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to investigate p38-mitogene-activated protein kinase (p38-MAPK), nuclear factor-kappa B (p65-NF-kB) and inducible nitric oxide synthase (iNOS) expression in an experimental model of varicocele in the rat testis. Male Wistar albino rats (n = 18) were divided into three equal groups: control group, sham operated group and left varicocele-induced group. Malondialdehyde (MDA), nitric oxide (NO) and reduced glutathione (GSH) levels were biochemically assessed, and the p38-MAPK and NF-kB activity, and iNOS expression were immunohistochemically studied in the right and left testicles of rats from each group. The GSH levels were significantly decreased, whereas the level of MDA and NO was significantly increased in the testicular tissues of rats in varicocele group compared with those of the control and sham groups. There was a marked staining for iNOS, p38-MAPK and p65-NF-kB expression in rats of varicocele group compared with the sham group. There was no positive staining in rats of control group. There were significant differences in biochemical, histological and immunohistochemical studies, but no significant differences were noted between other groups. p38-MAPK and p65-NF-kB activation, and iNOS expression have a significant role in varicocele-induced testicular dysfunction.
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PMID:Potential role of p38-mitogene-activated protein kinase and nuclear factor-kappa B expression in testicular dysfunction associated with varicocele: an experimental study. 2167 77

Diabetes is increasingly becoming a major cause of large-scale morbidity and mortality. Diabetes-induced oxidative stress alters numerous intracellular signaling pathways. Although testicular dysfunction is a major concern in diabetic men, the mechanistic alterations in the testes that lead to hypogonadism are not yet clear. Oxidative mitochondrial DNA damage, as indicated by 7,8-dihydro-8-oxo-2'-deoxyguanosine, and phosphorylation of p53 at ser315 residue (p-p53ser315) increased in a stage- and cell-specific manner in the testes of rats that were diabetic for 1 month (DM1). Prolongation of diabetes for 3 months (DM3) led to an increase in nuclear oxidative DNA damage in conjunction with a decrease in the expression of p-p53ser315. The nuclei of pachytene and preleptotene spermatocytes, steps 1, 11, and 12 spermatids, secondary spermatocytes and the Sertoli cells, and the meiotic figures showed an increase in the expression of p-p53ser315. An increase in the expression of a downstream target of p53 and protein 21(cyclin-dependent kinase interacting protein 1/wild-type p53-activated factor 1) (p21(CIP1/Waf1)) in both diabetic groups did not show any time-dependent effects but occurred concurrent with an upregulation of p-p53ser315 in DM1 and a downregulation of the protein in DM3. In diabetic groups, the expression of p21(CIP1/Waf1) was mainly cytoplasmic but also perinuclear in pachytene spermatocytes and round spermatids. The cytoplasmic localization of p21(CIP1/Waf1) may be suggestive of an antiapoptotic role for the protein. The perinuclear localization is probably related to the cell cycle arrest meant for DNA damage repair. Diabetes upregulates p21(CIP1/Waf1) signaling in testicular germ cells in association with alteration in p-p53ser315 expression, probably to counteract DNA damage-induced cell death.
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PMID:Diabetes-induced oxidative DNA damage alters p53-p21CIP1/Waf1 signaling in the rat testis. 2482 39