MAP2K4: A Protein Regulator of Cell Signaling (G6416)

Target Name: MAP2K4

NCBI ID: G6416

MAP2K4

MAP2K4: A Protein Regulator of Cell Signaling

MAP2K4 (MAP2K4_HUMAN) is a protein that is expressed in various tissues of the human body. It is a key regulator of cell signaling pathways, particularly in the context of the MAPK/ERK signaling pathway. This pathway is involved in many cellular processes, including cell growth, differentiation, and response to stimuli.MAP2K4 plays a crucial role in the regulation of this pathway, as it is a key component of the MAPK/ERK signaling complex.

MAP2K4 is a 21-kDa protein that is expressed in a variety of tissues, including muscle, heart, brain, and pancreas. It is primarily localized to the cytoplasm of cells and is also found in the cell nucleus.MAP2K4 is a GTPase-activating protein (GAP), which means that it can activate the protein GTPase-activating protein (GAP) in response to GTP binding.GAP is a protein that plays a critical role in the regulation of cellular signaling pathways. It is a scaffold that can interact with various signaling proteins, including MAP2K4.

MAP2K4 is involved in many cellular processes that are critical for the survival and proper function of the cell. For example, it is involved in the regulation of cell growth, which is critical for the development and maintenance of tissues and organs.MAP2K4 also plays a role in the regulation of cell differentiation, which is the process by which cells become specialized cells with unique functions.

MAP2K4 is also involved in the regulation of cellular responses to stimuli, including the regulation of pain perception. When a cell is exposed to mechanical or thermal stimulation, MAP2K4 is activated and involved in cell signal transduction pathways, involved in the generation and production of pain perception. conduction.

MAP2K4 is a potential drug target and may be a biomarker for a variety of diseases. For example, altered levels of MAP2K4 have been observed in a variety of diseases, including cancer, neurodegenerative diseases, and cardiovascular disease. Additionally, altered levels of MAP2K4 have been associated with certain medications, including some anti-cancer drugs.

In conclusion, MAP2K4 is a protein that plays a crucial role in the regulation of cell signaling pathways, including the MAPK/ERK signaling pathway. It is a potential drug target and may be a biomarker for a variety of diseases. Further research is needed to fully understand the role of MAP2K4 in cellular signaling and its potential as a therapeutic target.

Protein Name: Mitogen-activated Protein Kinase Kinase 4

Functions: Dual specificity protein kinase which acts as an essential component of the MAP kinase signal transduction pathway. Essential component of the stress-activated protein kinase/c-Jun N-terminal kinase (SAP/JNK) signaling pathway. With MAP2K7/MKK7, is the one of the only known kinase to directly activate the stress-activated protein kinase/c-Jun N-terminal kinases MAPK8/JNK1, MAPK9/JNK2 and MAPK10/JNK3. MAP2K4/MKK4 and MAP2K7/MKK7 both activate the JNKs by phosphorylation, but they differ in their preference for the phosphorylation site in the Thr-Pro-Tyr motif. MAP2K4 shows preference for phosphorylation of the Tyr residue and MAP2K7/MKK7 for the Thr residue. The phosphorylation of the Thr residue by MAP2K7/MKK7 seems to be the prerequisite for JNK activation at least in response to pro-inflammatory cytokines, while other stimuli activate both MAP2K4/MKK4 and MAP2K7/MKK7 which synergistically phosphorylate JNKs. MAP2K4 is required for maintaining peripheral lymphoid homeostasis. The MKK/JNK signaling pathway is also involved in mitochondrial death signaling pathway, including the release cytochrome c, leading to apoptosis. Whereas MAP2K7/MKK7 exclusively activates JNKs, MAP2K4/MKK4 additionally activates the p38 MAPKs MAPK11, MAPK12, MAPK13 and MAPK14

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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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