SLC26A9-AS1: A Potential Drug Target and Biomarker (G103021296)

Target Name: SLC26A9-AS1

NCBI ID: G103021296

SLC26A9-AS1

Other Name(s): SLC26A9-AS1 variant 1 | SLC26A9 and RAB7B antisense RNA 1, transcript variant 1 | SLC26A9 and RAB7B antisense RNA 1

SLC26A9-AS1: A Potential Drug Target and Biomarker

Sodium channels play a crucial role in the regulation of various physiological processes in the body. Mammalian sodium channels are involved in neurotransmitter signaling, muscle contractions, and homeostasis. The SLC26A9 gene family is a key gene family that encodes for the sodium channel subfamily A9. SLC26A9-AS1 is a variant of the SLC26A9 gene that has been shown to be expressed in various tissues and cells.

The SLC26A9-AS1 gene has four exons, and its corresponding protein has 11 transmembrane segments and 1 voltage-dependent sodium channel that can conduct a rapid and long-lasting increase in the membrane potential. SLC26A9-AS1 is a potential drug target and biomarker due to its unique genetic variation and its expression in various tissues and cells.

Potential Drug Target

SLC26A9-AS1 is a voltage-dependent sodium channel that can conduct a rapid and long-lasting increase in the membrane potential. This property makes it an attractive drug target for the treatment of various neurological and psychiatric disorders.

One of the leading causes of epilepsy is the disruption of the normal electrical activity in the brain, which is often caused by a failure to regulate the sodium channels. SLC26A9-AS1 is involved in the regulation of sodium channels, and its dysfunction has been implicated in the development of epilepsy.

In addition to its role in epilepsy, SLC26A9-AS1 may also be a potential drug target for other neurological disorders such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. These disorders are characterized by the progressive loss of brain cells and the presence of neurofibrillary tangles, which are thought to be caused by the dysfunction of sodium channels.

Biomarker

SLC26A9-AS1 has also been shown to be a potential biomarker for various diseases. For example, SLC26A9-AS1 has been shown to be upregulated in various tissues and cells under conditions of stress, such as stress, exercise, and infection. This increase in expression may indicate that SLC26A9-AS1 is involved in the regulation of stress responses and may serve as a potential biomarker for stress-induced diseases.

In addition, SLC26A9-AS1 has also been shown to be downregulated in various diseases, such as Alzheimer's disease and Parkinson's disease. This downregulation may indicate that SLC26A9-AS1 is involved in the regulation of neurodegenerative diseases and may serve as a potential biomarker for these disorders.

Conclusion

SLC26A9-AS1 is a voltage-dependent sodium channel that has been shown to be involved in the regulation of various physiological processes in the body. Its unique genetic variation and expression in various tissues and cells make it an attractive drug target and biomarker for the treatment of neurological and psychiatric disorders.

Further research is needed to fully understand the role of SLC26A9-AS1 in the regulation of sodium channels and its potential as a drug target and biomarker. However, its potential as a drug target and biomarker is an exciting area of research that may have significant implications for the treatment of various neurological and psychiatric disorders.

Protein Name: SLC26A9 And RAB7B Antisense RNA 1

The "SLC26A9-AS1 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 SLC26A9-AS1 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;
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•   related combination drugs;
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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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