Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.1.1.3 (HSD)
 3,464 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

17 beta-Hydroxysteroid dehydrogenase (17 beta-HSD) IV is coded by 2.9 kb mRNA translated to an 80 kDa protein which is N-terminally cleaved to a 32 kDa enzyme. The 17 beta-HSD IV is dedicated to steroid inactivation and reveals only 25% amino acid similarity with 17 beta-HSD I-III enzymes. Despite five Asn-Xaa-Ser/Thr (Xaa = unspecified amino acid) sites in the 80 kDa protein the enzyme is not glycosylated. The porcine 32 kDa 17 beta-HSD IV forms dimers of 75 kDa. The highest 17 beta-HSD IV mRNA expression and specific activities are found in liver and kidney followed by ovary and testes. In porcine gonads the immunofluorescence assigned the 17 beta-HSD IV to granulosa cells and to Leydig and Sertoli cells. As shown by the treatment with phorbol-myristate-acetate in vitamin D-differentiated monocytic leukemia THP1 cells, steroid synthesis and inactivation are regulated differentially by the protein kinase C pathway: an increase in aromatase is accompanied by a decrease in 17 beta-HSD IV mRNA levels.
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PMID:Characterization of 17 beta-hydroxysteroid dehydrogenase IV. 894 81

Alpha-protein kinase 1, also known as alpha-kinase 1 (ALPK1), is associated with chronic kidney disease (CKD), myocardial infarction, gout and type 2 diabetes mellitus (DM). In addition to having an inductive effect on the proinflammatory cytokines in monocytic THP1 cells, ALPK1 is expressed abundantly in the mouse testes. Low testosterone levels are commonly associated with arthritis, CKD, type 2 DM, cardiovascular disease and inflammation. The testosterone's anti-inflammatory effect has been demonstrated to reduce proinflammatory cytokines and adhesion molecules. In this study, we found that ALPK1 transgenic mice showed lower levels of testosterone in both the testes and the serum. Decreasing endogenous ALPK1 enhanced testosterone levels and transcripts of testosterone-regulated genes (P450scc, 3beta-HSD, P450C17, 17beta-HSD, StAR, and INSL3) in TM3 Leydig cells. In contrast, increasing testosterone decreased ALPK1 in both TM3 and monocytic THP1 cells. This decrease was accompanied by a reduction of the proinflammatory cytokines. Increased ALPK1 levels attenuated the testosterone effects in THP1 cells. Finally, we also found that ALPK1 increased the release of TNF-alpha and TGF-beta1 in the human embryonic kidney 293 cells, while testosterone inhibited ALPK1 in the primary kidney cells. Taken together, this data suggests that the balance between ALPK1 and testosterone plays a critical role in the testosterone-mediated inhibition of proinflammatory cytokines.
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PMID:ALPK1 affects testosterone mediated regulation of proinflammatory cytokines production. 2627 47