Browse our anti-MAP3K3 (MAP3K3) Antibodies

Human Mitogen-Activated Protein Kinase Kinase Kinase 3 (MAP3K3) interaction partners

1. MEKK3 overexpression prevented the inhibitory effects of miR9 on the viability, migration and invasion of PC cells.

2. the data revealed the novel role and target of miR505 in NSCLC cells, which may provide novel insights regarding its role in the carcinogenesis of NSCLC and its potential values for clinical applications.

3. Its downstream target MAP3K3 could be a potential therapeutic target for NSCLC.

4. Expression of MEKK2 and MEKK3 inhibits medulloblastoma cell proliferation.

5. MEKK3 KO reduced both EMT and cell migration, the size of 3D colonies and the percentage of CD44(+)/CD24(+)/EpCAM(+) CSC, promoter recruitment of YAP/TAZ and the expression of their target genes.

6. All these suggest that the MAP3K M1P site is a potential interacting partner of MAP3K SH3 domain, which may mediate the intermolecular recognition between hPTTG1 and MAP3K.

7. Polymorphisms in MAP3K3, MMP24 and IGF1R are associated with greater height and act additively on height in children of an admixed population.

8. MAP3K3 overexpression is an independent poor prognostic indicator in ovarian carcinoma.

9. MAP3K3 may potentially not only serve as diagnostic/prognostic markers for patients with lung cancer but also provide an indicator for future investigations into immunomodulatory therapies for lung cancer.

10. studies identify gain of MEKK3 signalling and KLF2/4 function as causal mechanisms for cerebral cavernous malformations pathogenesis that may be targeted to develop new CCM therapeutics

11. High MEKK3 expression is associated with renal clear cell carcinoma.

12. MEKK3 expression was significantly higher in patients with renal clear cell carcinoma than in controls.

13. This study identified an NBR1-MEKK3 complex as a key regulator of JNK signaling and adipose tissue inflammation in obesity.

14. Our finding that Verrucous venous malformation contains a MAP3K3 mutation supports our impression that this lesion is a venous anomaly.

15. MEKK3 expression was positively correlated with survivin.

16. Inhibitors of apoptosis proteins regulate myogenic differentiation by directly suppressing MEKK2/3-MEK5-ERK5 signaling.

17. Alterations in MEKK3 expression occur in early stages of development of esophageal squamous cell carcinoma and are sustained during disease progression.

18. We provide evidence for an intimate mutual control of the IKK complex by mitogen-activated protein kinase kinase kinase 3 (MEKK3) and transforming growth factor beta activated kinase 1 (TAK1).

19. Proliferation of human IVD cells is regulated by exogenous and autocrine growth factors mainly via the MEK/ERK and PI-3K/Akt pathways.

20. The regulation of NHEJ by EGFR was only blocked when ERK was affected by siRNA but not when AKT was knocked down. These data indicate that EGFR modulates DSB repair by regulating NHEJ via MAPK signalling.

Mouse (Murine) Mitogen-Activated Protein Kinase Kinase Kinase 3 (MAP3K3) interaction partners

1. results suggest that MEKK3 plays important roles in platelet MAPK activation

2. The expression of MEKK3 in the midbrain is regulated by microRNA-124 in an experimental model of Parkinson's disease.

3. MiR-188 regulated MAP3K3 expression in bone marrow cells.MAP3K3 is involved in miR-188-induced promotion of bone marrow cells senescence.

4. this study shows that TAK1 negatively regulates lipopolysaccharide-induced cytokine secretion in myeloid cells by inhibiting MEKK3 activities

5. endothelial-specific loss of Mekk3, Klf2 or Klf4 markedly prevents cerebral cavernous malformation lesion formation, reverses the increase in Rho activity, and rescues lethality

6. CCM2:MEKK3-mediated regulation of Rho-ROCK signalling is required for maintenance of neurovascular integrity, a mechanism by which CCM2 loss leads to disease.

7. NBR1 is increased in adipose tissue macrophages in obese mice. The NBR1-MEKK3 complex is important in JNK activation in macrophages.

8. reveal a molecular mechanism by which CCM signaling controls endothelial gene expression during cardiovascular development

9. 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

10. 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.

11. 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.

12. 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.

13. 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.

14. 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.

15. mekk3 regulates interleukin-1 and toll-like receptor 4 signaling.

16. Selective activation of Map3k3 is essential for cyclic AMP-dependent UCP1 expression in adipocytes.

17. TLR8-mediated MEKK3-dependent IKKgamma phosphorylation might play an important role in the activation of IKK complex, leading to IkappaBalpha phosphorylation

18. 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

19. 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.

20. Data provide insights into the homeostatic interactions that maintain basal NF-kappaB levels by holding the enzymes MEKK3 and TAK1 in their inactive state.