 Connection
Mitchell Mcgill to Hepatocytes
This is a "connection" page, showing publications Mitchell Mcgill has written about Hepatocytes.
|
|
| |
Connection Strength |
|
 |
|
 |
| |
2.214 |
|
|
|
-
Jaeschke H, McGill MR. Cytochrome P450-derived versus mitochondrial oxidant stress in acetaminophen hepatotoxicity. Toxicol Lett. 2015 Jun 15; 235(3):216-7.
Score: 0.464
-
Smith AK, Ropella GEP, McGill MR, Krishnan P, Dutta L, Kennedy RC, Jaeschke H, Hunt CA. Contrasting model mechanisms of alanine aminotransferase (ALT) release from damaged and necrotic hepatocytes as an example of general biomarker mechanisms. PLoS Comput Biol. 2020 06; 16(6):e1007622.
Score: 0.166
-
Kennedy RC, Smith AK, Ropella GEP, McGill MR, Jaeschke H, Hunt CA. Propagation of Pericentral Necrosis During Acetaminophen-Induced Liver Injury: Evidence for Early Interhepatocyte Communication and Information Exchange. Toxicol Sci. 2019 05 01; 169(1):151-166.
Score: 0.154
-
Ewing LE, Skinner CM, Quick CM, Kennon-McGill S, McGill MR, Walker LA, ElSohly MA, Gurley BJ, Koturbash I. Hepatotoxicity of a Cannabidiol-Rich Cannabis Extract in the Mouse Model. Molecules. 2019 Apr 30; 24(9).
Score: 0.154
-
Bhushan B, Chavan H, Borude P, Xie Y, Du K, McGill MR, Lebofsky M, Jaeschke H, Krishnamurthy P, Apte U. Dual Role of Epidermal Growth Factor Receptor in Liver Injury and Regeneration after Acetaminophen Overdose in Mice. Toxicol Sci. 2017 02; 155(2):363-378.
Score: 0.129
-
Du K, McGill MR, Xie Y, Jaeschke H. Benzyl alcohol protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes but causes mitochondrial dysfunction and cell death at higher doses. Food Chem Toxicol. 2015 Dec; 86:253-61.
Score: 0.121
-
Xie Y, McGill MR, Du K, Dorko K, Kumer SC, Schmitt TM, Ding WX, Jaeschke H. Mitochondrial protein adducts formation and mitochondrial dysfunction during N-acetyl-m-aminophenol (AMAP)-induced hepatotoxicity in primary human hepatocytes. Toxicol Appl Pharmacol. 2015 Dec 01; 289(2):213-22.
Score: 0.120
-
Woolbright BL, McGill MR, Yan H, Jaeschke H. Bile Acid-Induced Toxicity in HepaRG Cells Recapitulates the Response in Primary Human Hepatocytes. Basic Clin Pharmacol Toxicol. 2016 Feb; 118(2):160-7.
Score: 0.119
-
Miyakawa K, Joshi N, Sullivan BP, Albee R, Brandenberger C, Jaeschke H, McGill MR, Scott MA, Ganey PE, Luyendyk JP, Roth RA. Platelets and protease-activated receptor-4 contribute to acetaminophen-induced liver injury in mice. Blood. 2015 Oct 08; 126(15):1835-43.
Score: 0.118
-
Xie Y, McGill MR, Dorko K, Kumer SC, Schmitt TM, Forster J, Jaeschke H. Mechanisms of acetaminophen-induced cell death in primary human hepatocytes. Toxicol Appl Pharmacol. 2014 Sep 15; 279(3):266-274.
Score: 0.110
-
Ramachandran A, McGill MR, Xie Y, Ni HM, Ding WX, Jaeschke H. Receptor interacting protein kinase 3 is a critical early mediator of acetaminophen-induced hepatocyte necrosis in mice. Hepatology. 2013 Dec; 58(6):2099-108.
Score: 0.105
-
McGill MR, Lebofsky M, Norris HR, Slawson MH, Bajt ML, Xie Y, Williams CD, Wilkins DG, Rollins DE, Jaeschke H. Plasma and liver acetaminophen-protein adduct levels in mice after acetaminophen treatment: dose-response, mechanisms, and clinical implications. Toxicol Appl Pharmacol. 2013 Jun 15; 269(3):240-9.
Score: 0.101
-
Woolbright BL, Ramachandran A, McGill MR, Yan HM, Bajt ML, Sharpe MR, Lemasters JJ, Jaeschke H. Lysosomal instability and cathepsin B release during acetaminophen hepatotoxicity. Basic Clin Pharmacol Toxicol. 2012 Dec; 111(6):417-25.
Score: 0.097
-
Ni HM, McGill MR, Chao X, Woolbright BL, Jaeschke H, Ding WX. Caspase Inhibition Prevents Tumor Necrosis Factor-a-Induced Apoptosis and Promotes Necrotic Cell Death in Mouse Hepatocytes in?Vivo and in?Vitro. Am J Pathol. 2016 10; 186(10):2623-36.
Score: 0.032
-
Ni HM, McGill MR, Chao X, Du K, Williams JA, Xie Y, Jaeschke H, Ding WX. Removal of acetaminophen protein adducts by autophagy protects against acetaminophen-induced liver injury in mice. J Hepatol. 2016 08; 65(2):354-62.
Score: 0.031
-
Maes M, McGill MR, da Silva TC, Abels C, Lebofsky M, Maria Monteiro de Ara?jo C, Tiburcio T, Veloso Alves Pereira I, Willebrords J, Crespo Yanguas S, Farhood A, Beschin A, Van Ginderachter JA, Zaidan Dagli ML, Jaeschke H, Cogliati B, Vinken M. Involvement of connexin43 in acetaminophen-induced liver injury. Biochim Biophys Acta. 2016 06; 1862(6):1111-21.
Score: 0.031
-
Michaut A, Le Guillou D, Moreau C, Bucher S, McGill MR, Martinais S, Gicquel T, Morel I, Robin MA, Jaeschke H, Fromenty B. A cellular model to study drug-induced liver injury in nonalcoholic fatty liver disease: Application to acetaminophen. Toxicol Appl Pharmacol. 2016 Feb 01; 292:40-55.
Score: 0.031
-
Du K, Xie Y, McGill MR, Jaeschke H. Pathophysiological significance of c-jun N-terminal kinase in acetaminophen hepatotoxicity. Expert Opin Drug Metab Toxicol. 2015; 11(11):1769-79.
Score: 0.030
-
Du K, McGill MR, Xie Y, Bajt ML, Jaeschke H. Resveratrol prevents protein nitration and release of endonucleases from mitochondria during acetaminophen hepatotoxicity. Food Chem Toxicol. 2015 Jul; 81:62-70.
Score: 0.029
-
Du K, Williams CD, McGill MR, Xie Y, Farhood A, Vinken M, Jaeschke H. The gap junction inhibitor 2-aminoethoxy-diphenyl-borate protects against acetaminophen hepatotoxicity by inhibiting cytochrome P450 enzymes and c-jun N-terminal kinase activation. Toxicol Appl Pharmacol. 2013 Dec 15; 273(3):484-91.
Score: 0.026
-
Xie Y, Williams CD, McGill MR, Lebofsky M, Ramachandran A, Jaeschke H. Purinergic receptor antagonist A438079 protects against acetaminophen-induced liver injury by inhibiting p450 isoenzymes, not by inflammasome activation. Toxicol Sci. 2013 Jan; 131(1):325-35.
Score: 0.024
-
Jaeschke H, McGill MR, Ramachandran A. Pathophysiological relevance of proteomics investigations of drug-induced hepatotoxicity in HepG2 cells. Toxicol Sci. 2011 Jun; 121(2):428-30; author reply 431-3.
Score: 0.022
|
Connection Strength
The connection strength for concepts is the sum of the scores for each matching publication.
Publication scores are based on many factors, including how long ago they were written and whether the person is a first or senior author.
|