Abstract:
:Gap junctions (GJs) traverse apposing membranes of neighboring cells to mediate intercellular communication by passive diffusion of signaling molecules. We have shown previously that cells endocytose GJs utilizing the clathrin machinery. Endocytosis generates cytoplasmic double-membrane vesicles termed annular gap junctions or connexosomes. However, the signaling pathways and protein modifications that trigger GJ endocytosis are largely unknown. Treating mouse embryonic stem cell colonies - endogenously expressing the GJ protein connexin43 (Cx43) - with epidermal growth factor (EGF) inhibited intercellular communication by 64% and activated both, MAPK and PKC signaling cascades to phosphorylate Cx43 on serines 262, 279/282, and 368. Upon EGF treatment Cx43 phosphorylation transiently increased up to 4-fold and induced efficient (66.4%) GJ endocytosis as evidenced by a 5.9-fold increase in Cx43/clathrin co-precipitation.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Fong JT,Nimlamool W,Falk MMdoi
10.1016/j.febslet.2014.01.048subject
Has Abstractpub_date
2014-03-03 00:00:00pages
836-44issue
5eissn
0014-5793issn
1873-3468pii
S0014-5793(14)00078-7journal_volume
588pub_type
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