Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.6.1.1 (adenylate cyclase)
 19,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fluorescein-labeled cholera toxin binds detectably to 40-60% of rat mesenteric lymph node cells and induces a temperature-dependent redistribution (patch and cap formation) of cell surface toxin receptors. The redistribution is inhibited by several "metabolic," "microtubule," and "microfilament" inhibitors, by concanavalin A, and by anticholera toxin IgG. Various studies indicate that cholera toxin is at least bivalent, and that this property may be related to both the induction of receptor redistribution and to the activation of adenylate cyclase. Membrane components which are probably identical to the sialo-glycolipid, GM1 ganglioside, appear to be mobile in the plane of the membrane. The possible role of toxin multivalency and receptor mobility in the mechanism of toxin action is considered.
 ...
PMID:Mobility of cholera toxin receptors on rat lymphocyte membranes. 106 63

The natural course of psoriasis is often modulated during pregnancy, indicating the regulatory effect of estrogen or progesterone on psoriasis. Interferon-induced protein of 10 kDa chemoattracts T helper 1 cells, and interferon-induced protein of 10 kDa production by keratinocytes is enhanced in psoriatic skin lesions. We examined in vitro effects of sex hormones on the interferon-induced protein of 10 kDa production by human keratinocytes. 17beta-estradiol inhibited interferon-gamma-induced interferon-induced protein of 10 kDa secretion, mRNA expression, and promoter activity. Interferon-stimulated response element on the promoter was responsible for the inhibition by 17beta-estradiol. Interferon-gamma-induced protein of 10 kDa production was also inhibited by anti-estrogens, ICI 182 780 and tamoxifen, and membrane-impermeable bovine serum albumin-conjugated 17beta-estradiol, suggesting the effects via membrane estrogen receptor, whereas 17alpha-estradiol, progesterone, and dihydrotestosterone had no effects. 17beta-estradiol and bovine serum albumin-conjugated 17beta-estradiol suppressed interferon-gamma-induced transcription through the interferon-stimulated response element and signal transducer and activator of transcription 1alpha binding to interferon-stimulated response element. 17beta-estradiol and bovine serum albumin-conjugated 17beta-estradiol suppressed interferon-gamma-induced tyrosine phosphorylation of signal transducer and activator of transcription 1alpha, and Janus tyrosine kinase 1 and 2. 17beta-estradiol-mediated suppression on the interferon-gamma-induced signal transducer and activator of transcription 1alpha activation and interferon-induced protein of 10 kDa synthesis was counteracted by adenylate cyclase inhibitor SQ22536. 17beta-estradiol, bovine serum albumin-conjugated 17beta-estradiol, ICI 182 780, and tamoxifen increased intracellular 3',5'-adenosine cyclic monophosphate level by activating adenylate cyclase in keratinocytes. Fluorescein isothiocyanate-labeled bovine serum albumin-conjugated 17beta-estradiol bound to the surface of keratinocytes, and mRNA for estrogen receptor beta but not for estrogen receptor alpha was detected in keratinocytes. These results suggest that 17beta-estradiol may interact with the membrane receptor on keratinocytes and generate 3',5'-adenosine cyclic monophosphate by activating adenylate cyclase, which may lead to the inhibition of interferon-gamma-induced signal transducer and activator of transcription 1alpha activation and interferon-induced protein of 10 kDa synthesis.
 ...
PMID:17beta-estradiol inhibits the production of interferon-induced protein of 10 kDa by human keratinocytes. 1260 54