GJB4: A Potential Drug Target for NASH and Other Form of Liver Disease

Target Name: GJB4

NCBI ID: G127534

GJB4: A Potential Drug Target for NASH and Other Form of Liver Disease

GJB4 (Glycophorin A, also known as CX30.3) is a protein that is expressed in the liver and other organs. It is a member of the Glycophorin A family, which is known for their role in intracellular signaling and modulation of cellular processes. GJB4 has been shown to play a role in the regulation of inflammation, fibrosis, and autophagy, and is therefore considered a potential drug target (or biomarker).

GJB4 was first identified in the late 1990s as a liver protein that was expressed in high levels in individuals with nonalcoholic steatohepatitis (NASH), a type of liver disease that is characterized by the buildup of fat in the liver. Studies have since shown that individuals with NASH are more likely to have increased levels of GJB4 in their liver, and that inhibiting GJB4 has the potential to be a therapeutic approach for treating NASH.

In addition to its role in NASH, GJB4 has also been shown to be involved in a variety of other cellular processes. For example, GJB4 has been shown to play a role in the regulation of cell adhesion, by which cells stick together and form tissues . It has also been shown to be involved in the regulation of cellular signaling pathways, including the TGF-β pathway, which is involved in cell growth, differentiation, and fibrosis.

GJB4 has also been shown to be involved in the regulation of inflammation and immune cell function. Studies have shown that GJB4 is expressed in immune cells, including T cells and macrophages, and that it plays a role in the regulation of their activity. For example , GJB4 has been shown to inhibit the activity of T cells, which are a key part of the immune system and play a role in the regulation of inflammation.

In addition to its role in immune cells, GJB4 has also been shown to be involved in the regulation of fibrosis, which is the thickening of connective tissue that occurs in response to injury or inflammation. Studies have shown that GJB4 is involved in the regulation of fibrosis, by which it promotes the growth and thickening of connective tissue.

GJB4 has also been shown to be involved in the regulation of autophagy, which is the process by which cells break down and recycle their own damaged or unnecessary parts. Studies have shown that GJB4 is involved in the regulation of autophagy, by which it promotes the formation of autophagosomes, which are the structures that break down and recycle damaged or unnecessary parts.

GJB4 has been shown to have a variety of potential therapeutic applications, including the treatment of NASH and other forms of liver disease. For example, studies have shown that inhibiting GJB4 can protect against the development of NASH in animal models, and that this may be achieved by inhibiting the activity of GJB4 in immune cells. In addition, GJB4 has been shown to be involved in the regulation of fibrosis and autophagy, and targeting these processes may be a promising approach for the treatment of fibrosed tissues and other forms of organ damage.

In conclusion, GJB4 is a protein that is expressed in the liver and other organs, and has been shown to play a role in a variety of cellular processes. Its potential as a drug target or biomarker makes it an attractive target for the development of new treatments for NASH and other forms of liver disease. Further research is needed to fully understand the role of GJB4 in cellular processes and its potential as a therapeutic approach.

Protein Name: Gap Junction Protein Beta 4

Functions: Structural component of gap junctions (By similarity). Gap junctions are dodecameric channels that connect the cytoplasm of adjoining cells. They are formed by the docking of two hexameric hemichannels, one from each cell membrane (By similarity). Small molecules and ions diffuse from one cell to a neighboring cell via the central pore (By similarity)

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