by forming a complex with MEKK4 in skeletal muscle fibers Gadd45a increases MEKK4 protein kinase activity which is both sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a-mediated skeletal muscle fiber atrophy.
Results define MEKK4 as a signaling hub for FGF4 activation of JNK that is required for maintenance of trophoblast stem cells in an undifferentiated state.
GSK3beta binding to MEKK4 blocks MEKK4 dimerization that is required for MEKK4 activation effectively inhibiting MEKK4 stimulation of the JNK and p38 MAPK pathways
MEKK4 transcripts was reported in early myocardium endocardium and in cardiac cushion cells that have executed epithelial to mesenchymal transformation (EMT) suggesting that MEKK4 may function during production of the cushion mesenchyme; MEKK4 regulates epithelial-to-mesenchymal transition in the endocardial cushions of the developing heart.
During Th1 differentiation the GADD45beta/GADD45gamma/MEKK4 pathway integrates upstream signals transduced by both T cell receptor and IL12/STAT4 leading to augmented interferon-gamma production in a process independent of STAT4.
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