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http://scihub22266oqcxt.onion/ 1000507!ä!1000507 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\1000507.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cancer+Res 1976 ; 36 (12): 4647-51 Nephropedia Template TP {{tp|p=1000507|t=1976. Effect of hepatocarcinogens on the binding of glucocorticoid-receptor complex in rat liver nuclei |pdf=|usr=}}{{1000507}} gab.com Text Effect of hepatocarcinogens on the binding of glucocorticoid-receptor complex in rat liver nuclei JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=1000507 #FOAvip The effects of a number of carcinogens and hepatotoxins on the binding kinetics of the interactions of glucocorticoidcytosol receptor complex with nuclear acceptor sites in rat liver were investigated. Both the apparent sites in rat liver were investigated. Both the apparent concentration of nuclear binding sites and the Kd were significantly diminished following treatment of rats with sublethal doses of the carcinogens aflatoxin B1, diethylnitrosamine, dimethylnitrosamine, thioacetamide, 3'-methyl-4-dimethylaminoazobenzene, 4-dimethylaminoazobenzene, and 3-methylcholanthrene. Treatment with actinomycin D resulted in a slight reduction in the apparent concentration of nuclear acceptor sites but had no effect on the nuclear binding Kd. The hepatotoxic but noncarcinogenic analgesic, acetaminophen, as well as the weakly toxic aflatoxin B1 cognate, aflatoxin B2, were without effect on the kinetics or binding capacity of glucocorticoid-nuclear acceptor site interaction. These experiments suggest that chemically induced alteration of functional glucocorticoid binding sites on chromatin may be involved in the biochemical effects produced in liver by carcinogens of several chemical types. This experimental model may provide a useful approach for further elucidation of early events in carcinogenesis. Twit Text FOAVip Effect of hepatocarcinogens on the binding of glucocorticoid-receptor complex in rat liver nuclei ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=1000507 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=1000507 #FOAvip English Wikipedia <ref>{{Cite pmid|1000507}}</ref> Effect of hepatocarcinogens on the binding of glucocorticoid-receptor complex in rat liver nuclei #MMPMID1000507 Kensler TW; Busby WF Jr; Davidson NE; Wogan GN Cancer Res 1976[Dec]; 36 (12): 4647-51 PMID1000507show ga The effects of a number of carcinogens and hepatotoxins on the binding kinetics of the interactions of glucocorticoidcytosol receptor complex with nuclear acceptor sites in rat liver were investigated. Both the apparent sites in rat liver were investigated. Both the apparent concentration of nuclear binding sites and the Kd were significantly diminished following treatment of rats with sublethal doses of the carcinogens aflatoxin B1, diethylnitrosamine, dimethylnitrosamine, thioacetamide, 3'-methyl-4-dimethylaminoazobenzene, 4-dimethylaminoazobenzene, and 3-methylcholanthrene. Treatment with actinomycin D resulted in a slight reduction in the apparent concentration of nuclear acceptor sites but had no effect on the nuclear binding Kd. The hepatotoxic but noncarcinogenic analgesic, acetaminophen, as well as the weakly toxic aflatoxin B1 cognate, aflatoxin B2, were without effect on the kinetics or binding capacity of glucocorticoid-nuclear acceptor site interaction. These experiments suggest that chemically induced alteration of functional glucocorticoid binding sites on chromatin may be involved in the biochemical effects produced in liver by carcinogens of several chemical types. This experimental model may provide a useful approach for further elucidation of early events in carcinogenesis. |*Receptors, Glucocorticoid/drug effects[MESH] |*Receptors, Steroid[MESH] |Alkylation[MESH] |Animals[MESH] |Binding Sites[MESH] |Carcinogens/metabolism/*pharmacology[MESH] |Cell Nucleus/metabolism[MESH] |Cytosol/metabolism[MESH] |DNA/metabolism[MESH] |Dactinomycin/pharmacology[MESH] |Dexamethasone/*metabolism[MESH] |Kinetics[MESH] |Liver/drug effects/*metabolism[MESH] |Male[MESH]Effect of hepatocarcinogens on the binding of glucocorticoid-receptor (epmc).pdf DeepDyve Pubget Overpricing