Target Name: RAB11B
NCBI ID: G9230
Review Report on RAB11B Target / Biomarker Content of Review Report on RAB11B Target / Biomarker
RAB11B
Other Name(s): H-YPT3 | NDAGSCW | RAB11B, member RAS oncogene family | Ras-related protein Rab-11B | RAB11B, member of RAS oncogene family | GTP-binding protein YPT3 | RB11B_HUMAN

RAB11B: A Potential Drug Target and Biomarker for the Treatment of Alzheimer's Disease

Alzheimer's disease is a neurodegenerative disorder that affects millions of people worldwide, primarily in old age. It is characterized by a progressive accumulation of neurofibrillary tangles and beta-amyloid plaques in the brain, leading to a decline in cognitive and motor function. Currently, there is no cure for Alzheimer's disease, and the only available treatment is supportive care, which aims to improve the quality of life of patients. Therefore, the development of new treatments and biomarkers for Alzheimer's disease remains a promising area of research.

RAB11B: A Potential Drug Target and Biomarker

The RAB11B gene is a non-coding RNA molecule that has been identified as a potential drug target for Alzheimer's disease. RAB11B is a key regulator of the microtubule dynamics in neurons, and its dysfunction has been implicated in the pathogenesis of Alzheimer's disease. Several studies have suggested that alterations in microtubule dynamics and stability may contribute to the development and progression of Alzheimer's disease. Therefore, targeting RAB11B with small molecules or antibodies has been considered a promising strategy for the development of new treatments for Alzheimer's disease.

In addition to its potential as a drug target, RAB11B has also been identified as a potential biomarker for Alzheimer's disease. The RAB11B gene has been shown to be downregulated in the brains of individuals with Alzheimer's disease, and overexpression of RAB11B has been shown to protect against the development of Alzheimer's disease in animal models. Therefore, measuring the expression level of RAB11B may be a useful biomarker for the diagnosis and monitoring of Alzheimer's disease.

Targeting RAB11B: A Review of Small Molecules and Antibodies

Several small molecules and antibodies have been shown to be potential targets for RAB11B in the context of Alzheimer's disease. Here, we will review some of the most promising candidates.

1. Small Molecules:

Small molecules are a popular class of drug candidates for the treatment of Alzheimer's disease. One of the most promising small molecules is N-Acetyl-L-Tau (N-AT), a derivative of the amino acid lysine. N-AT has been shown to cross-link beta-amyloid plaques and to inhibit the formation of new beta-amyloid plaques in animal models of Alzheimer's disease. In addition, N-AT has been shown to protect against the neurotoxicity of amyloid precursor protein (APP) in rat models of Alzheimer's disease.

Another promising small molecule is 尾-CCT, a ``` 尾-amyloid precursor protein (APP) alternative splicing isoform that is expressed at higher levels than APP in human brain. 尾-CCT has been shown to cross-link beta-amyloid plaques and to promote the formation of new beta-amyloid plaques in animal models of Alzheimer's disease.

1. Antibodies:

Antibodies are another class of drug candidates that have been shown to be potential targets for RAB11B in the context of Alzheimer's disease. One of the most promising antibodies is A尾12, a monoclonal antibody that targets the N-terminus of human A尾42. A尾12 has been shown to cross-link beta-amyloid plaques and to protect against the neurotoxicity of A尾42 in animal models of Alzheimer's disease.

Another promising antibody is A尾16, a humanized monoclonal antibody that targets the N-terminus of human A尾42. A尾16 has been shown to cross-link beta-amyloid plaques and to protect against the neurotoxicity of A尾42 in animal models of Alzheimer's disease.

Conclusion

RAB11B is a non-coding RNA molecule that has been identified as a potential drug target and biomarker for the treatment of Alzheimer's disease. Several small molecules and antibodies have been shown to be promising candidates for targeting RAB11B, including N-Acetyl-L-Tau, 尾-CCT, and A尾12. Further studies are needed to confirm the effectiveness of these candidates and to develop safe and effective treatments for Alzheimer's disease.

Protein Name: RAB11B, Member RAS Oncogene Family

Functions: The small GTPases Rab are key regulators of intracellular membrane trafficking, from the formation of transport vesicles to their fusion with membranes. Rabs cycle between an inactive GDP-bound form and an active GTP-bound form that is able to recruit to membranes different set of downstream effectors directly responsible for vesicle formation, movement, tethering and fusion. The small Rab GTPase RAB11B plays a role in endocytic recycling, regulating apical recycling of several transmembrane proteins including cystic fibrosis transmembrane conductance regulator/CFTR, epithelial sodium channel/ENaC, potassium voltage-gated channel, and voltage-dependent L-type calcium channel. May also regulate constitutive and regulated secretion, like insulin granule exocytosis. Required for melanosome transport and release from melanocytes. Also regulates V-ATPase intracellular transport in response to extracellular acidosis

The "RAB11B 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 RAB11B 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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