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The cJUN NH2-terminal kinase (JNK) pathway contributes to mouse mammary gland remodeling during involution.

Cell death and differentiation | 2018

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.

Pubmed ID: 29511338 RIS Download

Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK107220
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK112698
  • Agency: Howard Hughes Medical Institute, United States

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