HCAR2 (Puma-g) as A Potential Drug Target and Biomarker for Cancer Treatment

Target Name: HCAR2

NCBI ID: G338442

HCAR2 (Puma-g) as A Potential Drug Target and Biomarker for Cancer Treatment

HCAR2 (Puma-g) is a protein that is expressed in human tissues and is known for its role in the development and progression of various diseases, including cancer. The protein is a potential drug target (or biomarker) and is currently being studied in various clinical trials to determine its effectiveness in treating cancer.

HCAR2 (Puma-g) is a transmembrane protein that is characterized by its ability to interact with various signaling molecules, including TGF-β1, NF-kappa-B, and PI3K. TGF-β1 is a well-known transcription factor that is involved in the regulation of cell growth, while NF-kappa-B and PI3K are involved in the regulation of inflammation and signaling, respectively.

Research has shown that HCAR2 (Puma-g) is involved in the regulation of cell proliferation, migration, and survival. Studies have also shown that HCAR2 (Puma-g) is overexpressed in various human diseases, including cancer, and that its levels are correlated with the severity of these diseases.

Due to its involvement in the regulation of cell growth and survival, HCAR2 (Puma-g) has been identified as a potential drug target (or biomarker) for the treatment of various diseases, including cancer. One of the main reasons for this is the fact that HCAR2 (Puma-g) is known to be involved in the regulation of cell signaling pathways, which are the key mechanisms that coordinate the functions of cells.

For example, studies have shown that HCAR2 (Puma-g) is involved in the regulation of TGF-β1 signaling, which is involved in the regulation of cell growth, cell division, and cell survival. Similarly, HCAR2 (Puma-g) is also involved in the regulation of NF-kappa-B and PI3K signaling pathways, which are involved in inflammation and signaling, respectively.

In addition to its involvement in cell signaling pathways, HCAR2 (Puma-g) is also known to play a role in the regulation of cell adhesion. Adhesion is the process by which cells stick together and form tissues, and it is a critical aspect of cell biology. Studies have shown that HCAR2 (Puma-g) is involved in the regulation of cell adhesion, and that its levels are involved in the development and maintenance of tight junctions, which are a type of cell adhesion structure.

Another study has shown that HCAR2 (Puma-g) is involved in the regulation of cell apoptosis, which is the process by which cells die when they have reached their maximum lifespan. Apoptosis is a natural and important aspect of cell biology, as it helps to remove damaged or dysfunctional cells from the body. Studies have shown that HCAR2 (Puma-g) is involved in the regulation of cell apoptosis, and that its levels are involved in the development and progression of various diseases, including cancer.

Due to its involvement in the regulation of cell signaling pathways, HCAR2 (Puma-g) has been identified as a potential drug target (or biomarker) for the treatment of various diseases, including cancer. One of the main advantages of targeting HCAR2 (Puma-g) is that it is involved in the regulation of multiple signaling pathways, which makes it a more versatile and effective drug target than some other targets. For example, HCAR2 (Puma-g) can be targeted with small molecules, antibodies, or other therapeutic agents that are designed to interact with its specific functions.

In addition to its potential as a drug target, HCAR2 (Puma-g) is also being studied as a biomarker for the diagnosis and prognosis of various diseases. Studies have shown that the levels of HCAR2 (Puma-g) are involved in the regulation of cell growth and survival, and that these levels can be used as

Protein Name: Hydroxycarboxylic Acid Receptor 2

Functions: Acts as a high affinity receptor for both nicotinic acid (also known as niacin) and (D)-beta-hydroxybutyrate and mediates increased adiponectin secretion and decreased lipolysis through G(i)-protein-mediated inhibition of adenylyl cyclase. This pharmacological effect requires nicotinic acid doses that are much higher than those provided by a normal diet. Mediates nicotinic acid-induced apoptosis in mature neutrophils. Receptor activation by nicotinic acid results in reduced cAMP levels which may affect activity of cAMP-dependent protein kinase A and phosphorylation of target proteins, leading to neutrophil apoptosis. The rank order of potency for the displacement of nicotinic acid binding is 5-methyl pyrazole-3-carboxylic acid = pyridine-3-acetic acid > acifran > 5-methyl nicotinic acid = acipimox >> nicotinuric acid = nicotinamide

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