| Literature DB >> 25339611 |
Scott T Baker1, Shane M Turgeon2, Erik D Tulgren3, Jeanne Wigant3, Omeed Rahimi3, Karla J Opperman2, Brock Grill4.
Abstract
We show that loss-of-function mutations in kinases of the MLK-1 pathway (mlk-1, mek-1, and kgb-1/jnk) function cell-autonomously in neurons to suppress defects in synapse formation and axon termination caused by rpm-1 loss of function. Our genetic analysis also suggests that the phosphatase PPM-1, like RPM-1, is a potential inhibitor of kinases in the MLK-1 pathway.Entities:
Keywords: JNK; MAP kinase; RPM-1; axon; synapse
Mesh:
Substances:
Year: 2014 PMID: 25339611 PMCID: PMC4286679 DOI: 10.1534/genetics.114.170589
Source DB: PubMed Journal: Genetics ISSN: 0016-6731 Impact factor: 4.562