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The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution
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 NH 2 -terminal kinase (JNK) signal transduction pathway contributes to involution, we established mice...
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Published in: | Cell death and differentiation 2018-09, Vol.25 (9), p.1702-1715 |
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creator | Girnius, Nomeda Edwards, Yvonne J. K. Davis, Roger J. |
description | 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 NH
2
-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. |
doi_str_mv | 10.1038/s41418-018-0081-z |
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subjects | 13/1 13/2 13/51 14/34 14/63 38/90 38/91 631/208/199 631/45/275 64/60 82/29 96/95 Apoptosis Biochemistry Biomedical and Life Sciences Cathepsins Cattle Cell Biology Cell Cycle Analysis Epithelial cells Epithelium Lactation Life Sciences Mammary gland Signal transduction Smad2 protein Stat3 protein Stem Cells Weaning |
title | The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution |
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