The Cdc42/Par6/aPKC polarity complex regulates apoptosis-induced compensatory proliferation in epithelia.

ABSTRACT:

Background

In response to stress- or tissue-damage-induced apoptosis, unaffected epithelial cells undergo compensatory proliferation to maintain the integrity of the epithelium. Proximal signals regulating this response are not fully understood, but c-Jun N-terminal kinase (JNK) activity appears to be critical for both apoptosis and compensatory proliferation. Disruption of epithelial cell apical-basal polarity occurs in early cancer development and is often correlated with increased proliferation by means not fully characterized. We considered whether disruption of the various polarity complexes could provide signals identifying damaged epithelial cells and thus lead to apoptosis-induced compensatory proliferation.

Results

We identify the Cdc42/Par6/atypical protein kinase

SUBMITTER: Warner SJ 

PROVIDER: S-EPMC2910247 | biostudies-literature | 2010 Apr

REPOSITORIES: biostudies-literature