Paxillin is the target of c-Jun N-terminal kinase in Schwann cells and regulates migration

An alternatively spliced zebrafishjnk1atranscript has an essential and non-redundant role in development of the first heart field derived proximal ventricular chamber

“…Importantly, we have shown that the migratory pattern of cardiomyocytes is disturbed in the absence of Jnk1a. A role for Jnk1 in cell movement is widely recognised in the metastatic spread of cancer [34] and is required in Schwann cell migration [35], dependent on paxillin at focal adhesions [36]. It is possible to imagine that some cells may become lost during migration, and in isolation undergo cell death or differentiate into other tissues.…”

Neural-specific deletion of the focal adhesion adaptor protein paxillin slows migration speed and delays cortical layer formation

“…Interestingly, one of the downstream factors of the Rac1 pathway is Jun N-terminal kinase (JNK), which is also required for neuronal migration and leading process formation (Kawauchi et al, 2003). JNK phosphorylates microtubules associated with the protein DCX (Gdalyahu et al, 2004) and MAP1B (Kawauchi et al, 2005), as well as paxillin at S178 (Miyamoto et al, 2012). Thus, a model emerges in which paxillin and FAK could function to regulate small GTPase activity, leading to JNK activation and the phosphorylation and modification of microtubule stabilizing proteins.…”

Transglutaminase-2 in cell adhesion

“…6,12,41 Various studies have shown that pJNK can be a kinase for Ser 178 of paxillin. 7,42 Our in-vitro kinase screening assay (data unpublished) with a panel of 229 kinases shows that JNK is a relatively powerful kinase for recombinant human paxillin substrate.…”