Mispairing C57BL/6 Substrains of Genetically Engineered Mice and Wild-Type Controls Can Lead to Confounding Results as It Did in Studies of JNK2 in Acetaminophen and Concanavalin A Liver Injury-Reference-Cited by-同舟云学术

Mispairing C57BL/6 Substrains of Genetically Engineered Mice and Wild-Type Controls Can Lead to Confounding Results as It Did in Studies of JNK2 in Acetaminophen and Concanavalin A Liver Injury

Published:2011-06-20 Issue:6 Volume:24 Page:794-796
ISSN:0893-228X
Container-title:Chemical Research in Toxicology
language:en
Short-container-title:Chem. Res. Toxicol.

Author:

Bourdi Mohammed,Davies John S.,Pohl Lance R.

Publisher

American Chemical Society (ACS)

Subject

Toxicology,General Medicine

Link

https://pubs.acs.org/doi/pdf/10.1021/tx200143x

Reference22 articles.

1. Deletion of Apoptosis Signal-Regulating Kinase 1 Attenuates Acetaminophen-Induced Liver Injury by Inhibiting c-Jun N-Terminal Kinase Activation

2. c-Jun N-Terminal Kinase Plays a Major Role in Murine Acetaminophen Hepatotoxicity

3. Critical role of c-jun (NH2) terminal kinase in paracetamol- induced acute liver failure

4. Alcohol trait and transcriptional genomic analysis of C57BL/6 substrains

5. Genetic Differences among C57BL/6 Substrains

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