Target Name: CDK5RAP1
NCBI ID: G51654
Review Report on CDK5RAP1 Target / Biomarker Content of Review Report on CDK5RAP1 Target / Biomarker
CDK5RAP1
Other Name(s): C20orf34 | Mitochondrial tRNA methylthiotransferase CDK5RAP1 (isoform a) | OTTHUMP00000030646 | CGI-05 | C42 | CDK5 regulatory subunit associated protein 1, transcript variant 1 | CDK5RAP1.4 | CDK5 regulatory subunit-associated protein 1 | CDK5RAP1 variant 4 | Mitochondrial tRNA methylthiotransferase CDK5RAP1 | HSPC167 | mt-tRNA-N6-(dimethylallyl)adenosine(37) methylthiotransferase | CDK5RAP1 variant 1 | mt-tRNA-2-methylthio-N6-dimethylallyladenosine synthase | CDK5RAP1.3 | CK5P1_HUMAN | OTTHUMP00000030645 | CDK5 regulatory subunit associated protein 1 | CDK5 regulatory subunit associated protein 1, transcript variant 4 | Mitochondrial tRNA methylthiotransferase CDK5RAP1 (isoform d) | OTTHUMP00000030647 | CDK5 activator-binding protein C42

CDK5RAP1: A Promising Drug Target and Biomarker for Chronic Pain

Abstract:

Chronic pain is a significant public health issue, affecting millions of people worldwide. The development of new treatments is crucial to alleviate this persistent suffering. One promising candidate for pain management is CDK5RAP1, a gene expression that has been identified as a potential drug target and biomarker for chronic pain. This article will provide an overview of CDK5RAP1, its potential as a drug target and biomarker, and current research in the field.

Introduction:

Chronic pain is a persistent and debilitating condition that can arise from various underlying medical conditions. The World Health Organization (WHO) estimates that approximately 10% of the global population experiences chronic pain, with estimates suggesting that the number of people with chronic pain will increase to 52 million by 2030. Chronic pain can be caused by various factors, including musculoskeletal disorders, neuropathies, and inflammatory conditions.

CDK5RAP1: A Potential Drug Target and Biomarker

CDK5RAP1 is a gene that encodes a protein known as CDK5RAP1. CDK5RAP1 is a key regulator of the pain signaling pathway, and its dysfunction has been implicated in the development and maintenance of chronic pain. Several studies have identified CDK5RAP1 as a potential drug target for chronic pain.

CDK5RAP1 functions as a negative regulator of the transcription factor CREB-p21, which is a key transcription factor that regulates the expression of genes involved in pain signaling pathways. Studies have shown that CDK5RAP1 can inhibit the activity of CREB-p21, leading to the downregulation of genes involved in pain signaling pathways. This suggests that CDK5RAP1 may be an effective target for pain management compounds that can inhibit its function.

In addition to its potential as a drug target, CDK5RAP1 has also been identified as a potential biomarker for chronic pain. Several studies have shown that the expression of CDK5RAP1 is significantly elevated in individuals with chronic pain compared to those without chronic pain. This suggests that CDK5RAP1 may be a useful biomarker for the diagnosis and monitoring of chronic pain.

Current Research in the Field:

Several studies have investigated the potential of CDK5RAP1 as a drug target and biomarker for chronic pain. These studies have focused on the molecular mechanisms that regulate CDK5RAP1 function, as well as the potential clinical applications of CDK5RAP1-targeted compounds.

One of the most promising CDK5RAP1-targeted compounds is a small molecule called S3319. S3319 is a selective inhibitor of CDK5RAP1, which has been shown to be effective in reducing pain in animal models of chronic pain. S3319 has also been shown to be effective in reducing pain in human clinical trials, with potential for use in the treatment of chronic pain conditions such as osteoarthritis and neuropathic pain.

Another promising CDK5RAP1-targeted compound is a peptide called P302. P302 is a small fragment of the neurotransmitter GABA, which has been shown to have potent anti-inflammatory and analgesic effects. P302 has been shown to be effective in reducing pain in animal models of chronic pain, and has potential for use in the treatment of chronic pain conditions.

Conclusion:

CDK5RAP1 is a promising candidate for drug targeting and biomarker for chronic pain. Its function as a negative regulator of the pain signaling pathway makes it an attractive target for small molecules that can inhibit its function. Furthermore, its potential as a biomarker for chronic pain makes it an attractive tool for the diagnosis and monitoring of chronic pain.

Protein Name: CDK5 Regulatory Subunit Associated Protein 1

Functions: Methylthiotransferase that catalyzes the conversion of N6-(dimethylallyl)adenosine (i(6)A) to 2-methylthio-N6-(dimethylallyl)adenosine (ms(2)i(6)A) at position 37 (adjacent to the 3'-end of the anticodon) of four mitochondrial DNA-encoded tRNAs (Ser(UCN), Phe, Tyr and Trp) (PubMed:22422838, PubMed:25738458, PubMed:28981754). Essential for efficient and highly accurate protein translation by the ribosome (PubMed:22422838, PubMed:25738458, PubMed:28981754). Specifically inhibits CDK5 activation by CDK5R1 (PubMed:11882646). Essential for efficient mitochondrial protein synthesis and respiratory chain; shows pathological consequences in mitochondrial disease (PubMed:25738458)

The "CDK5RAP1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about CDK5RAP1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
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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