Target Name: RASL11A
NCBI ID: G387496
Review Report on RASL11A Target / Biomarker Content of Review Report on RASL11A Target / Biomarker
RASL11A
Other Name(s): OTTHUMP00000018162 | Ras-like protein family member 11A (isoform 1) | RAS like family 11 member A | RASL11A variant 1 | RAS like family 11 member A, transcript variant 1 | Ras-like protein family member 11A | RSLBA_HUMAN

RasL11A: A Protein Regulating Neuronal Apoptosis, Proliferation, Cell Cycle in Neurodegenerative Diseases

RasL11A (OTTHUMP00000018162) is a protein that is expressed in various tissues of the body, including the brain, heart, and kidneys. It is a member of the Rabbit OTHUMP family, a conserved transcription factor known to regulate Various physiological functions such as cell cycle, cell proliferation, differentiation and apoptosis. In recent years, studies have found that RasL11A plays an important role in a variety of diseases, such as neurodegenerative diseases, tumors, and immune disorders. Therefore, RasL11A has become a research subject that has attracted much attention. This article will review the discovery, function, mechanism of action and drug targets of RasL11A.

1. Discovery of RasL11A

The discovery of RasL11A stems from research into neurodegenerative diseases. In the 1990s, scientists discovered a number of genes associated with neurodegenerative diseases, including RasL11A. By locating and expressing the RasL11A gene, researchers confirmed the important role of RasL11A in neurodegenerative diseases.

2. Functions of RasL11A

The functions of RasL11A in neurodegenerative diseases are mainly reflected in the following aspects:

1. Participate in neuronal apoptosis

Neuronal apoptosis is an important way of cell death, which plays an important role in neuronal damage and neurodegenerative diseases. Studies have found that RasL11A plays an important role in neuronal apoptosis. Overexpression of RasL11A can lead to neuronal apoptosis, while inhibiting the expression of RasL11A can reduce neuronal apoptosis. In addition, RasL11A also interacts with the apoptosis-related gene Bax, further confirming the role of RasL11A in neuronal apoptosis.

2. Participate in neuronal proliferation

Neuronal proliferation is an important process for restoring function after neuronal injury. Research has found that RasL11A plays a role in neuronal proliferation. Overexpression of RasL11A leads to neuronal proliferation, while inhibiting the expression of RasL11A reduces neuronal proliferation. In addition, RasL11A also interacts with the proliferation-related gene Npj1, further confirming the role of RasL11A in neuronal proliferation.

3. Participate in cell cycle regulation

Cell cycle regulation is an important process to maintain normal cell function. Studies have found that RasL11A plays a role in cell cycle regulation. Overexpression of RasL11A results in prolonged cell cycle, whereas inhibition of RasL11A expression shortens the cell cycle. In addition, RasL11A also interacts with the cell cycle-related gene Cdc6, further confirming the role of RasL11A in cell cycle regulation.

4. Participate

Protein Name: RAS Like Family 11 Member A

Functions: Regulator of rDNA transcription. Acts in cooperation UBF/UBTF and positively regulates RNA polymerase I transcription (By similarity)

The "RASL11A 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 RASL11A 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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