Program in Molecular Medicine; UMass Metabolic Network; Davis Lab
Biochemistry, Biophysics, and Structural Biology | Cell and Developmental Biology | Cellular and Molecular Physiology | Enzymes and Coenzymes | Genetic Phenomena
Involution returns the lactating mammary gland to a quiescent state after weaning. The mechanism of involution involves collapse of the mammary epithelial cell compartment. To test whether the cJUN NH2-terminal kinase (JNK) signal transduction pathway contributes to involution, we established mice with JNK deficiency in the mammary epithelium. We found that JNK is required for efficient involution. JNK deficiency did not alter the STAT3/5 or SMAD2/3 signaling pathways that have been previously implicated in this process. Nevertheless, JNK promotes the expression of genes that drive involution, including matrix metalloproteases, cathepsins, and BH3-only proteins. These data demonstrate that JNK has a key role in mammary gland involution post lactation.
Gene expression, Kinases
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DOI of Published Version
Cell Death Differ. 2018 Mar 6. doi: 10.1038/s41418-018-0081-z. [Epub ahead of print] Link to article on publisher's site
Cell death and differentiation
Girnius NA, Edwards YJ, Davis RJ. (2018). The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution. University of Massachusetts Medical School Faculty Publications. https://doi.org/10.1038/s41418-018-0081-z. Retrieved from https://escholarship.umassmed.edu/faculty_pubs/1493
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.