CCL2 has recently been shown to mediate iNKT cell migration into human neuroblastoma [28].
TNF is one of the few factors associated with PM that has been shown to mediate pathology.
N-terminal MEF2 and RUNX2 binding domains of HDAC4 have been shown to mediate these effects in vitro.
Hypoxia-induced factor 1 alpha (HIF-1a) has been shown to mediate the hypoxia-induced chondrogenic differentiation [50], [51].
Other efferents of the SN include GABAergic nigro-collicular pathways which have been shown to mediate fear/defense reactions [85].
Bim has been shown to mediate apoptosis during the negative selection of DP thymocytes [12], [31], [32].
It has been shown to mediate cell adhesion through homophilic interaction and some data suggest association with the cytoskeleton [73].
IRAK-M has previously been shown to mediate tolerance induced by several PAMPs, including LPS and peptidoglycan [14], [16].
In a therapeutic context, Akt has been shown to mediate striking neurotrophic and anti-apoptotic effects in vivo [21].
FIT proteins have been shown to mediate the partitioning of cellular triglyceride into lipid droplets, but not triglyceride biosynthesis.
In contrast, Fz receptors in vertebrates have so far been shown to mediate chemoattraction in response to Wnt [5], [6].
