ARL17A: A promising drug target and biomarker for ALZHEIMER'S DISEASE

Target Name: ARL17A

NCBI ID: G51326

ARL17A

ARL17A: A promising drug target and biomarker for ALZHEIMER'S DISEASE

Alzheimer's disease (AD) is a progressive neurological disorder that affects millions of people worldwide, primarily as a result of the accumulation of neurofibrillary tangles and beta-amyloid plaques in the brain. The underlying cause of AD is still not fully understood, but research has identified several genetic and molecular mechanisms involved in its development. One of these mechanisms is the role of ARL17A, a pseudogene that encodes a protein involved in the transfer of ADP-ribose to the ubiquitin system. In this article, we will explore the potential implications of ARL17A as a drug target and biomarker for AD.

The Story of ARL17A

ARL17A is a gene that encodes a protein with 17 amino acid residues. The protein has several unique features that make it an interesting candidate for drug targeting. Firstly, ARL17A is highly conserved across various species, which indicates that it has evolved under selective pressure and may have functions in different organisms. Secondly, ARL17A has a predicted hydrophobicity of 1.0, which suggests that it is likely to be soluble in aqueous environments and may be able to interact with other proteins in the cell. Finally, ARL17A has a unique post-translational modification (PTM) at its C-terminus, which involves the addition of a ubiquitin tag. This modification is known to play a role in protein stability and may be a target for small molecules that can modulate protein function.

Despite its unique features, ARL17A has not yet been studied in depth. Initial studies have focused on its expression and localization in various organisms, as well as its potential as a drug target.

ARL17A as a Drug Target

The potential drug target for ARL17A is its unique PTM, which involves the addition of a ubiquitin tag. This modification has been shown to play a role in protein stability and may be a target for small molecules that can modulate protein function. There is a growing interest in developing small molecules that can interact with this PTM and modulate the activity of ARL17A.

One approach to targeting ARL17A is to use small molecules that can modify the ubiquitin tag. This can lead to a decrease in the stability of the ARL17A protein and potentially disrupt its function. One example of a small molecule that can interact with the ubiquitin tag is 2-methoxyethanesulfonic acid (2-MES), which has been shown to reduce the stability of various proteins, including ARL17A.

Another approach to targeting ARL17A is to use small molecules that can modify the activity of the protein. This can be done by introducing small molecules that can interact with the various functions of the ARL17A protein, such as its catalytic activity or its ability to interact with other proteins. One example of a small molecule that can interact with the catalytic activity of ARL17A is known as 1-fluoro-2,4-dinitrophenyl-5-L-alanine aminotransferase (FL-ALAD), which has been shown to inhibit the catalytic activity of ARL17A while also modulating its stability.

ARL17A as a Biomarker

In addition to its potential as a drug target, ARL17A may also be a valuable biomarker for AD. The accumulation of neurofibrillary tangles and beta-amyloid plaques in the brain is a hallmark of AD, and the dysfunction of ARL17A has been implicated in the development

Protein Name: ADP Ribosylation Factor Like GTPase 17A

Functions: GTP-binding protein that functions as an allosteric activator of the cholera toxin catalytic subunit, an ADP-ribosyltransferase. Involved in protein trafficking; may modulate vesicle budding and uncoating within the Golgi apparatus (By similarity)

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•   general information;
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•   the target screening and validation;
•   expression level;
•   disease relevance;
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•   related combination drugs;
•   pharmacochemistry experiments;
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•   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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