Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.14.99.3 (heme oxygenase)
 4,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activation of the heme oxygenase (HO) gene during development of mouse male germ cells was examined by nuclear run-off assay. Results showed that the HO gene was activated in male germ cells, especially in spermatogonia and that the mRNA was stored throughout meiosis. In contrast, Western blotting analysis revealed that HO was expressed during spermatogenesis to spermatocytes. As the mouse HO gene is known to have a 12-o-tetradecanoyl-phorbol 13-acetate(TPA)-responsive element (TRE) in its upstream region and is activated by TPA in mouse M1 cells, we also examined the activation of the nuclear proto-oncogenes fos and jun, which are activators of TRE. Both genes were found to be activated with expression of their protein products only in spermatogonia. Moreover activation of fos, jun and HO genes in spermatogonia was strongly inhibited by a c-kinase inhibitor. These results suggest that the HO gene is activated at the spermatogonia stage by a fos/jun heterodimer complex (AP1) through c-kinase activation.
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PMID:Transcriptional control of the heme oxygenase gene during mouse spermatogenesis. 822 5

It has been known for a long time that heme oxygenase (HO) is a key enzyme in heme catabolism, and it was found to act as an oxidative-stress protein to produce carbon monoxide, which has similar actions to those of nitrogen monoxide. We examined transcriptional control of the HO gene in mouse M1 (myeloleukemia) cells during treatment with lipopolysaccharide (LPS; an oxidative reagent). Since the promoter region of this gene in human cells contains a 12-O-tetradecanoyl- phorbol-13-acetate(TPA)-responsive element (TRE) and a nuclear-factor-kappa B-responsive element. HO mRNA expression might be regulated by an oxidative activation pathway. We investigated activation of the HO gene after treatment of M1 cells with LPS. Upon treatment with LPS, H2O2 was produced, the nuclear proto-oncogenes fos and jun were activated, then the HO gene was activated. The extent of transcriptional activation of the fos, jun and HO genes in M1 cells treated with LPS was strongly reduced by a scavenger of oxygen radicals (N-acetyl-L-cysteine), but a specific inhibitor of protein kinase C only reduced transcriptional activation by 10-20%. These results suggest that LPS may be an oxidative reagent. Some oxidative reagents (e.g., H2O2) are strong activators of NF-kappa B, and therefore we treated M1 cells with H2O2. Essentially the same extends of transcriptional activation of the fos, jun and HO genes were observed as those observed after LPS treatment. Super-shift assays with DNA that contained the TRE motif revealed that the Fos and Jun proteins from nuclei of M1 cells treated with LPS and H2O2 bound weakly to the TRE motif, and, in assays with DNA that contained the NF-kappa B motif, nuclear protein from M1 cells treated with H2O2 or LPS bound strongly to the NF-kappa B motif. These results strongly suggest that the HO gene in M1 cells is mainly activated by LPS through oxidative activation of NF-kappa B due to production of H2O2.
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PMID:Lipopolysaccharide activates transcription of the heme oxygenase gene in mouse M1 cells through oxidative activation of nuclear factor kappa B. 877 98