Abstract:
:Gap junctions are present in both vertebrates and invertebrates from nematodes to mammals. Although the importance of gap junctions has been documented in many biological processes, the molecular mechanisms underlying gap junction dynamics remain unclear. Here, using the C. elegans PLM neurons as a model, we show that UNC-44/ankyrin acts upstream of UNC-33/CRMP in regulation of a potential kinesin VAB-8 to control gap junction dynamics, and loss-of-function in the UNC-44/UNC-33/VAB-8 pathway suppresses the turnover of gap junction channels. Therefore, we first show a signal pathway including ankyrin, CRMP, and kinesin in regulating gap junctions.
journal_name
PLoS Genetjournal_title
PLoS geneticsauthors
Meng L,Chen CH,Yan Ddoi
10.1371/journal.pgen.1005948subject
Has Abstractpub_date
2016-03-25 00:00:00pages
e1005948issue
3eissn
1553-7390issn
1553-7404pii
PGENETICS-D-15-02350journal_volume
12pub_type
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