Target Name: DERL3
NCBI ID: G91319
Review Report on DERL3 Target / Biomarker Content of Review Report on DERL3 Target / Biomarker
DERL3
Other Name(s): derlin 3 | Degradation in endoplasmic reticulum protein 3 | DERL3 variant 1 | DERtrin-3 | Der1-like protein 3 | Derlin 3 | DERtrin 3 | IZP6 | derlin-3 | C22orf14 | LLN2 | DERL3_HUMAN | Derlin-3 | Derlin 3, transcript variant 1 | MGC71803 | DER3 | der1-like protein 3 | Derlin-3 (isoform 1) | Der1-like domain family, member 3 | degradation in endoplasmic reticulum protein 3

Identifying Potential Drug Targets for DERL3

Derlin-3 (DERL3) is a protein that is expressed in the brain and is involved in various cellular processes. It is a member of the tyrosine kinase family and is known for its role in the development and progression of various neurological disorders, including Alzheimer's disease and Parkinson's disease.

The search for new drug targets and biomarkers is a crucial aspect of modern medicine. Drug development involves a long and expensive process that often times results in the failure of many compounds. In addition, the safety and efficacy of drugs can sometimes be difficult to predict . To address these issues, researchers have been searching for new targets and biomarkers that can provide more specific and reliable information about the effects of drugs.

One potential drug target and biomarker that has been identified for DERL3 is the protein known as tyrosine kinase (TK). TK is a family of proteins that are involved in various cellular processes, including cell signaling, DNA replication, and metabolism. DERL3 is a member of the TK family and is expressed in the brain.

The Importance of DERL3

DERL3 is involved in the development and progression of various neurological disorders, including Alzheimer's disease and Parkinson's disease. These conditions are characterized by the progressive loss of brain cells and the buildup of neurodegeneration. DERL3 has been shown to be involved in the formation of neurofibrillary tangles and the buildup of beta-amyloid plaques, both of which are hallmarks of these conditions.

In addition, DERL3 has been shown to play a role in the regulation of neurotransmitter release and the modulation of pain perception. These functions are important for maintaining the integrity of the brain and are implicated in the treatment of various neurological disorders.

The Potential of DERL3 as a Drug Target

The identification of DERL3 as a potential drug target has significant implications for the development of new treatments for neurological disorders. By blocking the activity of DERL3, researchers can potentially reduce the formation of neurofibrillary tangles and the buildup of beta-amyloid plaques, which are thought to contribute to the progression of these conditions.

In addition, DERL3 has been shown to play a role in the regulation of neurotransmitter release and the modulation of pain perception. By targeting DERL3, researchers can potentially improve the efficacy of pain medications and other treatments for neurological disorders.

The DERL3-based drug candidate

Currently, there are several DERL3-based drug candidates that are being developed for the treatment of neurological disorders. These compounds are designed to inhibit the activity of DERL3 and have been shown to be effective in animal models of these conditions.

One of the most promising DERL3-based drug candidates is a compound called MK-8628. This compound is being developed by Merck & Co. for the treatment of Alzheimer's disease. In animal models of Alzheimer's disease, MK-8628 has been shown to be Effective in reducing the formation of neurofibrillary tangles and the buildup of beta-amyloid plaques.

Another promising DERL3-based drug candidate is a compound called AC-12352043. This compound is being developed by AC Immune SA for the treatment of multiple sclerosis. In animal models of multiple sclerosis, AC-12352043 has been shown to be effective in reducing the formation of neurofibrillary tangles and the buildup of beta-amyloid plaques.

In conclusion

In conclusion, DERL3 is a protein that is involved in various cellular processes and is thought to be involved in the development and progression of various neurological disorders, including Alzheimer's disease and Parkinson's disease. The identification of DERL3 as a potential drug target and biomarker has significant implications for the development of new treatments for these conditions. The development of DERL3-based drug candidates is a promising direction in this field and has the potential to improve the treatment options for

Protein Name: Derlin 3

Functions: Functional component of endoplasmic reticulum-associated degradation (ERAD) for misfolded lumenal glycoproteins, but not that of misfolded nonglycoproteins. May act by forming a channel that allows the retrotranslocation of misfolded glycoproteins into the cytosol where they are ubiquitinated and degraded by the proteasome. May mediate the interaction between VCP and the misfolded glycoproteins (PubMed:16449189, PubMed:22607976). May be involved in endoplasmic reticulum stress-induced pre-emptive quality control, a mechanism that selectively attenuates the translocation of newly synthesized proteins into the endoplasmic reticulum and reroutes them to the cytosol for proteasomal degradation (PubMed:26565908)

The "DERL3 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 DERL3 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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