Understanding Rad9A: A Potential Drug Target (G5883)

Target Name: RAD9A

NCBI ID: G5883

RAD9A

Understanding Rad9A: A Potential Drug Target

Rad9A (RAD9A_HUMAN) is a protein that is expressed in various tissues of the human body, including the brain, spinal cord, and peripheral nerves. It is a key regulator of the cell cycle, and its dysfunction has been implicated in a number of neurological and psychiatric disorders. Despite its importance, little is known about Rad9A, and it has not been thoroughly studied. In this article, we will explore the biology of Rad9A and its potential as a drug target.

Structure and Expression

Rad9A is a 25 kDa protein that is expressed in the brain, spinal cord, and peripheral nerves. It is composed of a unique arrangement of 11 beta-strands and 12 alpha-helices. The protein has a molecular weight of 39.9 kDa and a calculated pI of 6.5.

Rad9A is predominantly expressed in the brain, with higher levels found in the prefrontal cortex, hippocampus, and cerebellum. It is also expressed in the spinal cord and peripheral nerves, but at much lower levels. The protein is synthesized using the cytosine deaminase gene (CAD) and is processed by the splicing machinery to generate a functional protein.

Function and Interactions

Rad9A is a key regulator of the cell cycle, and its dysfunction has been implicated in a number of neurological and psychiatric disorders. One of its most well-known functions is its role in the regulation of microtubules, which are important for the movement of cells and the transport of molecules within the cell.

Rad9A has been shown to play a role in the regulation of microtubule dynamics in various cell types. For example, studies have shown thatRad9A can interact with the protein T-tubulin, which is a key component of microtubules. This interaction between Rad9A and T-tubulin has been shown to play a role in the regulation of microtubule stability and dynamics.

Rad9A has also been shown to interact with the protein p16INK4a, which is a negative regulator of the cell cycle. This interaction between Rad9A and p16INK4a has been shown to play a role in the regulation of cell cycle progression and the maintenance of stem cell properties.

Drug Target Potential

The potential drug target for Rad9A is its role as a regulator of the cell cycle and its involvement in various neurological and psychiatric disorders. Its dysfunction has been implicated in a number of disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease.

One potential approach to targeting Rad9A is to use drugs that specifically interact with its functions as a regulator of the cell cycle. For example, drugs that inhibit the activity of T-tubulin or p16INK4a could potentially be effective in reducing the level of Rad9A and improving the function of the cell cycle.

Another approach to targeting Rad9A is to use drugs that specifically target its unique functions as a regulator of the cell cycle. For example, drugs that inhibit the activity of the splicing machinery could potentially be effective in reducing the level of Rad9A and improving the stability of the cell cycle.

Conclusion

Rad9A is a protein that is expressed in various tissues of the human body and is involved in the regulation of the cell cycle. Its dysfunction has been implicated in a number of neurological and psychiatric disorders. Despite its importance, little is known about Rad9A, and it has not been thoroughly studied. In this article, we have explored the biology of Rad9A and its potential as a drug target. Further research is needed to fully understand the role of Rad9A in the regulation of the cell cycle and its potential as a drug target.

Protein Name: RAD9 Checkpoint Clamp Component A

Functions: Component of the 9-1-1 cell-cycle checkpoint response complex that plays a major role in DNA repair. The 9-1-1 complex is recruited to DNA lesion upon damage by the RAD17-replication factor C (RFC) clamp loader complex. Acts then as a sliding clamp platform on DNA for several proteins involved in long-patch base excision repair (LP-BER). The 9-1-1 complex stimulates DNA polymerase beta (POLB) activity by increasing its affinity for the 3'-OH end of the primer-template and stabilizes POLB to those sites where LP-BER proceeds; endonuclease FEN1 cleavage activity on substrates with double, nick, or gap flaps of distinct sequences and lengths; and DNA ligase I (LIG1) on long-patch base excision repair substrates. The 9-1-1 complex is necessary for the recruitment of RHNO1 to sites of double-stranded breaks (DSB) occurring during the S phase. RAD9A possesses 3'->5' double stranded DNA exonuclease activity. Its phosphorylation by PRKCD may be required for the formation of the 9-1-1 complex

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