MAP3K8: A Protein At The Center of Immune, Cell Death and Disease

Target Name: MAP3K8

NCBI ID: G1326

MAP3K8

MAP3K8: A Protein At The Center of Immune, Cell Death and Disease

MAP3K8 (TPL2) is a protein that is expressed in various tissues throughout the body. It is a key regulator of the immune response and has been implicated in a number of diseases, including cancer.

One of the key functions of MAP3K8 is its role in the regulation of inflammation. It is part of the MAPK/ERK signaling pathway, which is a critical pathway that regulates cellular responses to stress and damage. When cells are exposed to stress or damage, the MAPK/ERK pathway is activated, leading to the production of signaling molecules that promote cell proliferation and survival.

MAP3K8 has also been shown to play a role in the regulation of cell death. It is a driver of the production of pro-apoptotic proteins, which are proteins that cause cells to die. This process is important for the regulation of cell growth and the removal of damaged or dysfunctional cells.

In addition to its role in inflammation and cell death, MAP3K8 has also been implicated in a number of other diseases. For example, it has been shown to be involved in the development of cancer, and to contribute to the development of neurodegenerative diseases.

Given its involvement in so many important cellular processes, MAP3K8 is an attractive target for drug development. Researchers are currently working to develop drugs that can inhibit the activity of MAP3K8 and prevent it from contributing to the development of disease. These drugs may be used to treat a wide range of conditions, including cancer, neurodegenerative diseases, and autoimmune disorders.

In conclusion, MAP3K8 is a protein that plays a critical role in the regulation of many important cellular processes. It is an attractive target for drug development due to its involvement in a wide range of diseases. Further research is needed to fully understand the role of MAP3K8 in cellular processes and to develop effective drugs that can inhibit its activity.

Protein Name: Mitogen-activated Protein Kinase Kinase Kinase 8

Functions: Required for lipopolysaccharide (LPS)-induced, TLR4-mediated activation of the MAPK/ERK pathway in macrophages, thus being critical for production of the pro-inflammatory cytokine TNF-alpha (TNF) during immune responses. Involved in the regulation of T-helper cell differentiation and IFNG expression in T-cells. Involved in mediating host resistance to bacterial infection through negative regulation of type I interferon (IFN) production. In vitro, activates MAPK/ERK pathway in response to IL1 in an IRAK1-independent manner, leading to up-regulation of IL8 and CCL4. Transduces CD40 and TNFRSF1A signals that activate ERK in B-cells and macrophages, and thus may play a role in the regulation of immunoglobulin production. May also play a role in the transduction of TNF signals that activate JNK and NF-kappa-B in some cell types. In adipocytes, activates MAPK/ERK pathway in an IKBKB-dependent manner in response to IL1B and TNF, but not insulin, leading to induction of lipolysis. Plays a role in the cell cycle. Isoform 1 shows some transforming activity, although it is much weaker than that of the activated oncogenic variant

The "MAP3K8 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about MAP3K8 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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