Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.3390/ijms16011008 http://scihub22266oqcxt.onion/10.3390/ijms16011008 25569083!4307287!25569083     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25569083&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Int+J+Mol+Sci 2015 ; 16 (1): 1008-29 Nephropedia Template TP {{tp|p=25569083|t=2015. Elucidating mechanisms of toxicity using phenotypic data from primary human cell systems--a chemical biology approach for thrombosis-related side effects |pdf=|usr=}}{{25569083}} gab.com Text Elucidating mechanisms of toxicity using phenotypic data from primary human cell systems--a chemical biology approach for thrombosis-related side effects JO: Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25569083 #FOAvip Here we describe a chemical biology approach for elucidating potential toxicity mechanisms for thrombosis-related side effects. This work takes advantage of a large chemical biology data set comprising the effects of known, well-characterized reference agents on the cell surface levels of tissue factor (TF) in a primary human endothelial cell-based model of vascular inflammation, the BioMAP(R) 3C system. In previous work with the Environmental Protection Agency (EPA) for the ToxCast program, aryl hydrocarbon receptor (AhR) agonists and estrogen receptor (ER) antagonists were found to share an usual activity, that of increasing TF levels in this system. Since human exposure to compounds in both chemical classes is associated with increased incidence of thrombosis-related side effects, we expanded this analysis with a large number of well-characterized reference compounds in order to better understand the underlying mechanisms. As a result, mechanisms for increasing (AhR, histamine H1 receptor, histone deacetylase or HDAC, hsp90, nuclear factor kappa B or NFkappaB, MEK, oncostatin M receptor, Jak kinase, and p38 MAPK) and decreasing (vacuolar ATPase or V-ATPase) and mTOR) TF expression levels were uncovered. These data identify the nutrient, lipid, bacterial, and hypoxia sensing functions of autophagy as potential key regulatory points controlling cell surface TF levels in endothelial cells and support the mechanistic hypothesis that these functions are associated with thrombosis-related side effects in vivo. Twit Text FOAVip Elucidating mechanisms of toxicity using phenotypic data from primary human cell systems--a chemical biology approach for thrombosis-related side effects ????Int J Mol Sci http://www.kidney.de/pget.php?&tw=1&pmid=25569083 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25569083 #FOAvip English Wikipedia <ref>{{Cite pmid|25569083}}</ref> Elucidating mechanisms of toxicity using phenotypic data from primary human cell systems--a chemical biology approach for thrombosis-related side effects #MMPMID25569083 Berg EL; Polokoff MA; O'Mahony A; Nguyen D; Li X Int J Mol Sci 2015[Jan]; 16 (1): 1008-29 PMID25569083show ga Here we describe a chemical biology approach for elucidating potential toxicity mechanisms for thrombosis-related side effects. This work takes advantage of a large chemical biology data set comprising the effects of known, well-characterized reference agents on the cell surface levels of tissue factor (TF) in a primary human endothelial cell-based model of vascular inflammation, the BioMAP(R) 3C system. In previous work with the Environmental Protection Agency (EPA) for the ToxCast program, aryl hydrocarbon receptor (AhR) agonists and estrogen receptor (ER) antagonists were found to share an usual activity, that of increasing TF levels in this system. Since human exposure to compounds in both chemical classes is associated with increased incidence of thrombosis-related side effects, we expanded this analysis with a large number of well-characterized reference compounds in order to better understand the underlying mechanisms. As a result, mechanisms for increasing (AhR, histamine H1 receptor, histone deacetylase or HDAC, hsp90, nuclear factor kappa B or NFkappaB, MEK, oncostatin M receptor, Jak kinase, and p38 MAPK) and decreasing (vacuolar ATPase or V-ATPase) and mTOR) TF expression levels were uncovered. These data identify the nutrient, lipid, bacterial, and hypoxia sensing functions of autophagy as potential key regulatory points controlling cell surface TF levels in endothelial cells and support the mechanistic hypothesis that these functions are associated with thrombosis-related side effects in vivo. |*Models, Biological[MESH] |Autophagy[MESH] |Biomarkers/metabolism[MESH] |Cells, Cultured[MESH] |Endothelial Cells/cytology/*drug effects/metabolism[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism[MESH] |Organic Chemicals/*toxicity[MESH] |Receptors, Aryl Hydrocarbon/agonists/metabolism[MESH] |Receptors, Estrogen/antagonists & inhibitors/metabolism[MESH] |TOR Serine-Threonine Kinases/metabolism[MESH] |Thromboplastin/metabolism[MESH]Elucidating mechanisms of toxicity using phenotypic data from primary (epmc).pdf DeepDyve Pubget Overpricing