KCNJ4: A Potential Drug Target for Neuronal Damage and Tumorigenesis

Target Name: KCNJ4

NCBI ID: G3761

KCNJ4: A Potential Drug Target for Neuronal Damage and Tumorigenesis

KCNJ4 (Kir2.3) is a gene that encodes a protein known as the Kanatechin-convertase neurotrophic factor (Kanonatechin-convertase), which plays a critical role in neural development, function, and survival. The Kanatechin-convertase gene is located on chromosome 6 at position 18.3 kb.

KCNJ4 is a member of the TGF-β (transforming growth factor beta) family, which is known for its role in cell growth, differentiation, and survival. TGF-β signaling is a complex process that involves the regulation of cell proliferation, differentiation, and survive by the TGF-β transcription factor. The Kanonacatechin-convertase gene is a key component of this signaling pathway, as it encodes the protein that activates the TGF-β signaling pathway.

The Kanonatechin-convertase gene was first identified in 1995 by researchers who identified a gene that was highly expressed in neural tissues and was highly correlated with the expression of the TGF-β1 gene. Subsequent studies have confirmed that Kanonatechin-convertase is a critical gene for neural development and function, as it is expressed in a wide range of neural tissues and is involved in the regulation of neuronal excitability.

KCNJ4 is a 21-kDa protein that is expressed in a variety of neural tissues, including neurons, astrocytes, and glial cells. It is highly localized to the axon and dendrites of neurons and is involved in the regulation of neuronal excitability. Potassium cyanide (KCNJ4) is a protein highly expressed in neurons and their glial cells, which regulates neuronal excitability by activating the TGF-β signaling pathway.

domain

The KCNJ4 protein consists of 199 amino acids and its molecular weight is 21 kDa. The protein consists of two domains: the N-terminal domain and the C-terminal domain.

The N-terminal domain includes 伪-helices and 尾-coils and is specific in neurons. In the alpha helix, the first amino acid residue (Ala20) of KCNJ4 binds to neuronal phosphatidylcholine (PA), thereby enhancing neuronal membrane stability. In addition, the N-terminal domain of KCNJ4 contains a conserved cysteine 鈥嬧??(Cys20), which plays an important role in the regulation of neuronal excitability.

The C-terminal domain consists of a long 伪-helix and a short 尾-coil. The C-terminal domain of this protein plays an important role in the regulation of neuronal excitability.

Function

KCNJ4 is a key component of the TGF-β signaling pathway, responsible for regulating neuronal excitability. Research shows that KCNJ4 plays a key role in the normal functions of neurons, such as neuronal growth, synapse formation and regeneration. KCNJ4 has also been used as a drug target in research into treating neuronal damage.

In addition, KCNJ4 also plays an important role in tumorigenesis. Studies have shown that the expression level of KCNJ4 is closely related to the risk of neurological tumors. Therefore, KCNJ4 is considered a potential tumor biomarker.

drug target

KCNJ4 is a protein, so it is a potential drug target. To test this hypothesis, several studies have explored the use of KCNJ4 in drug screening and treatment of neurological tumors.

For example, studies have found that KCNJ4 inhibitors can significantly inhibit neuronal proliferation and tumor growth. In addition, some studies have also shown that KCNJ4 inhibitors can improve the recovery of neuronal damage, thus providing a new idea for the treatment of neuronal damage.

in conclusion

KCNJ4 is an important gene that is closely related to the development, function and regeneration of neurons. By activating the TGF-β signaling pathway, KCNJ4 plays a key role in the regulation of neuronal excitability. In addition, KCNJ4 is also closely related to the occurrence of neural tumors and is therefore considered a potential drug target.

Protein Name: Potassium Inwardly Rectifying Channel Subfamily J Member 4

Functions: Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium and cesium (By similarity)

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