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MiR-188 regulated MAP3K3 expression in bone marrow cells.MAP3K3 is involved in miR-188-induced promotion of bone marrow cells senescence.
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this study shows that TAK1 negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 activities
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endothelial-specific loss of Mekk3, Klf2 or Klf4 markedly prevents cerebral cavernous malformation lesion formation, reverses the increase in Rho activity, and rescues lethality
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CCM2:MEKK3-mediated regulation of Rho-ROCK signalling is required for maintenance of neurovascular integrity, a mechanism by which CCM2 loss leads to disease.
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NBR1 is increased in adipose tissue macrophages in obese mice. The NBR1-MEKK3 complex is important in JNK activation in macrophages.
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reveal a molecular mechanism by which CCM signaling controls endothelial gene expression during cardiovascular development
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MEKK2 alone can suppress T-cell TGF-beta responses. MEKK2 or MEKK3 can cause ERK1/2 to phosphorylate SMAD2/3 and suppress R-SMAD-dependent transcription. MEKK2 and MEKK3 play overlapping roles in regulating Th-cell differentiation via TGF-beta
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Using Mekk3-deficient murine T cells, the authors concluded MEKK3 expression is required for mounting optimal T cell responses in vivo and is involved in mediating the TCR-dependent Rac1/2 signals for IFN-gamma production through the MAPK pathways.
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The signaling defect of elevated interleukin (IL)-12 overproducing cells in nonobese diabetic mice could be attributed to, at least partially, the overexpression of a single MAP3K, namely MEKK3.
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Strikingly, chimeric mice transplanted with Mekk3(Deltaflox/-) BM exhibited a reduction in tumor growth and vessel density compared with mice transplanted with Mekk3(Deltaflox/+) BM cells.
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PB1 domain mediates the association of MEKK2 and MEKK3 with MEK5 and that the respective PB1 domains of these kinases are critical for regulation of the ERK5 pathway.
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Results show that MEKK3 is essential in the rapid activation of NF-kappaB, whereas MEKK2 is important in controlling the delayed activation of NF-kappaB in response to stimulation with the cytokines TNF-alpha and IL-1alpha.
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mekk3 regulates interleukin-1 and toll-like receptor 4 signaling.
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Selective activation of Map3k3 is essential for cyclic AMP-dependent UCP1 expression in adipocytes.
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TLR8-mediated MEKK3-dependent IKKgamma phosphorylation might play an important role in the activation of IKK complex, leading to IkappaBalpha phosphorylation
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The TAK1-independent MEKK3-dependent pathway involves IKKgamma phosphorylation and IKKalpha activation, resulting in NFkappaB activation through IkappaBalpha phosphorylation and subsequent dissociation from NFkappaB but without IkappaBalpha degradation
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Results suggest that MEKK3 is critical for Ang1/Tie2 signaling to control endothelial cell(EC) proliferation, and is required for EC to interact with myocardium during embryogenesis. However, MEKK3 is not essential for tumor growth and angiogenesis.
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Data provide insights into the homeostatic interactions that maintain basal NF-kappaB levels by holding the enzymes MEKK3 and TAK1 in their inactive state.
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identifies a potentially important regulatory step in MEKK3 signaling via dephosphorylation of Thr(294), which reduces 14-3-3 binding correlating with MEKK3 pathway activation
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MEKK3 activity is sufficient for epithelial to mesenchymal transition during endocardial cushion morphogenesis.
