Mar 30, 2025 · MAP3K11 (Mitogen-Activated Protein Kinase Kinase Kinase 11) is a Protein Coding gene. Diseases associated with MAP3K11 include Dementia and Gastric Cancer. Among its related pathways are Signaling downstream of RAS mutants and G-protein signaling RAC1 in cellular process.

Mitogen-activated protein kinase kinase kinase 11 is an enzyme that in humans is encoded by the MAP3K11 gene. [5][6] The protein encoded by this gene is called MLK3 and it is a member of the serine/threonine kinase family. This kinase contains a SH3 domain and a …

MAP3K11 facilitates autophagy activity and is correlated with malignancy of oral squamous cell carcinoma. The role of mixed lineage kinase 3 (MLK3) in cancers. MLK3 Regulates Inflammatory Response via Activation of AP-1 Pathway in HEK293 and RAW264.7 Cells.

Activates the JUN N-terminal pathway. Required for serum-stimulated cell proliferation and for mitogen and cytokine activation of MAPK14 (p38), MAPK3 (ERK) and MAPK8 (JNK1) through …

Gene target information for MAP3K11 - mitogen-activated protein kinase kinase kinase 11 (human). Find diseases associated with this biological target and compounds tested against it in bioassay experiments.

Apr 7, 2020 · Mixed lineage kinase 3 (MLK3), also known as MAP3K11, was initially identified in a megakaryocytic cell line and is an emerging therapeutic target in cancer, yet its role in immune cells is not known. Here, we report that loss or pharmacological inhibition of MLK3 promotes activation and cytotoxicit …

Activates the JUN N-terminal pathway. Required for serum-stimulated cell proliferation and for mitogen and cytokine acti vation of MAPK14 (p38), MAPK3 (ERK) and MAPK8 (JNK1) through …

In this review, we outline the specific regulatory mechanisms of MAP3Ks in antiviral immunity and discuss the feasibility of targeting MAP3Ks for the treatment of virus-induced diseases. Keywords: Antiviral immunity, Antiviral therapy, IFN-I, MAP3Ks, NF-κB.

Together, our findings identify MAP3K11 as a critical target underlying miR-125b-driven transformation of pre-B cells and provide a rational to explore the consequences of enforced MAP3K11 activity in other types of blood cancers that associate with miR-125b overexpression.

Utilizing engineered tumour models we identified MAP3K11/GDF15 pathway activation as a potent inducer of cancer cachexia. Increased expression and high circulating levels of GDF15 acted as a key mediator of this process. In animal models, tumour‐produced GDF15 was sufficient to trigger the cachexia phenotype.