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elegans p38 MAPK pathway, consisting of DLK-1 (a DLK-type MAPKKK), MKK-4 (a MLK4-type MAPKK) and PMK-3 (a p38-type MAPK), regulates presynaptic development.
Several studies have demonstrated that the homologues of DLK-1 are required for axon regeneration in both Drosophila melanogaster and mice.
An RNAi screen for regulators of axon regeneration identified the MAPKKK DLK-1. (43) It was later demonstrated that activation of the p38 MAPK pathway consisting of DLK-1, MKK-4 and PMK-3 is required for axon regeneration of motor and mechanosensory neurons (Fig.
For example, DLK-1 and MLK-1 are both targeted for ubiquitin-mediated degradation by the E3 ubiquitin ligase RPM-1.
First, RPM-1 was found to interact genetically and biochemically with Rab activator GLO-4 and kinase DLK-1, both of which are necessary for the axon overextension phenotype .
The hiw synaptic overgrowth and axon guidance phenotypes both depend on the action of the Drosophila homolog of DLK-1, Wallenda, as its mutation suppresses the hiw phenotype [53, 55].
Grill et al., "Regulation of a DLK-1 and p38 MAP kinase pathway by the ubiquitin ligase RPM-1 is required for presynaptic development," Cell, vol.
Jin, "The DLK-1 kinase promotes mRNA stability and local translation in C.
While initially all these cells were termed unrestricted somatic stem cells, further research revealed significant differences between the cell lines, such as the competence for adipogenic differentiation and expression of the preadipocyte marker delta like 1 homologue (DLK-1)  and expression of the homeobox (HOX) genes .
The discrimination of USSC from CB MSC by the expression of DLK-1 and the inverse correlation with the adipogenic differentiation capacity was the first evidence for two distinct stromal cell populations in cord blood .
The aim of this study was to further assess the function of DLK-1 and its soluble form, known as fetal antigen 1(FA1) , in regard to a potential biological diversity between USSC and CB MSC which might have impact on future clinical use.
When the researchers 'overexpressed' the dlk-1 gene in worms - making it more active than normal - broken nerves in the worms regenerated much more quickly than expected.
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