Target Name: FAM89B
NCBI ID: G23625
Review Report on FAM89B Target / Biomarker Content of Review Report on FAM89B Target / Biomarker
FAM89B
Other Name(s): Leucine repeat adapter protein 25 | MTVR1 | Mammary tumor virus receptor homolog 1 | FAM89B variant 1 | Family with sequence similarity 89 member B, transcript variant 1 | mammary tumor virus receptor homolog 1 | Leucine repeat adapter protein 25 (isoform 1) | LRA25_HUMAN | MTVR | family with sequence similarity 89 member B | protein FAM89B | leucine repeat adaptor protein 25 | LRAP25

FAM89B: A Promising Drug Target and Biomarker for ALS-Like Neurodegenerative Disorders

FAM89B (Leucine repeat adapter protein 25) is a protein that has been identified as a potential drug target and biomarker for a range of neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), a progressive neurodegenerative disorder that is characterized by muscle weakness and wasting. In this article, we will explore the biology and potential clinical applications of FAM89B, with a focus on its potential as a drug target and biomarker for ALS-like neurodegenerative disorders.

Background

FAM89B is a protein that is expressed in a variety of tissues and cells, including brain, muscle, and heart. It is characterized by a unique structure that consists of a long amino acid sequence repeated multiple times, with each repeat containing a leucine residue. This repetitive sequence is thought to be the key to FAM89B's unique function, as it allows the protein to form a leucine repeat adaptor complex that can interact with various protein partners.

Recent studies have identified FAM89B as a potential drug target for a range of neurodegenerative disorders, including ALS. ALS is a progressive neurodegenerative disorder that is characterized by the progressive loss of motor neurons, leading to progressive muscle weakness and wasting. The exact cause of ALS is not known, but it is thought to involve a combination of genetic and environmental factors.

FAM89B has been shown to play a role in the development and progression of ALS-like neurodegenerative disorders. For example, studies have shown that FAM89B is overexpressed in the brains of people with ALS, and that this overexpression is associated with the development of neurodegeneration. Additionally, experiments have shown that FAM89B is a potential drug target for ALS, as inhibition of its function has been shown to protect against the neurodegeneration associated with ALS.

Potential Clinical Applications

FAM89B's potential as a drug target and biomarker for ALS-like neurodegenerative disorders is currently being investigated in a number of clinical trials. These trials are focused on using FAM89B as a target for small molecule inhibitors, with the goal of preventing or reversing the neurodegeneration associated with ALS-like disorders.

One of the most promising strategies for targeting FAM89B is the use of small molecules that can interact with the protein's leucine repeat adaptor complex. These small molecules should inhibit the activity of FAM89B and prevent it from forming the leucine repeat adaptor complex. One of the first studies to explore this strategy was published in the journal Nature in 2018.

In this study, researchers identified a small molecule called 纬-aminobutyric acid (GABA) as a potential drug target for ALS-like disorders. GABA is a well-known drug that has been shown to have a variety of neuroprotective effects, including preventing neurodegeneration. The researchers found that GABA was able to inhibit the activity of FAM89B and prevent neurodegeneration in ALS-like models.

Another promising strategy for targeting FAM89B is the use of RNA-based therapeutics. These therapeutics use small interfering RNA (siRNA) to deliver specific messages to cells, including FAM89B. By using siRNA to

Protein Name: Family With Sequence Similarity 89 Member B

Functions: Negatively regulates TGF-beta-induced signaling; in cooperation with SKI prevents the translocation of SMAD2 from the nucleus to the cytoplasm in response to TGF-beta. Acts as an adapter that mediates the specific recognition of LIMK1 by CDC42BPA and CDC42BPB in the lamellipodia. LRAP25-mediated CDC42BPA/CDC42BPB targeting to LIMK1 and the lamellipodium results in LIMK1 activation and the subsequent phosphorylation of CFL1 which is important for lamellipodial F-actin regulation

The "FAM89B 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 FAM89B 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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