GABRD: A GABA Receptor Delta Polypeptide in The Brain (G2563)

Target Name: GABRD

NCBI ID: G2563

GABRD

GABRD: A GABA Receptor Delta Polypeptide in The Brain

GABRD, or GABA-A receptor delta polypeptide, is a protein that is expressed in the brain and plays a crucial role in the function of the central nervous system (CNS). GABRD is a non-c coding RNA (ncRNA), which means that it is not a protein that is made by the body's cells, but rather a protein that is produced by the body's cells.

GABRD is a GABA (纬-aminobutyric acid) receptor, which is a well-known neurotransmitter that is involved in a wide range of physiological processes in the brain. The GABA receptor is a transmembrane protein that is composed of two main subunits: GABA- A and GABA-B. GABA-A is the primary receptor, and it is responsible for the majority of the effects of GABA.

GABRD is produced by the body's cells and is primarily located in the brain. It is a short protein that consists of four amino acids: GABA-A蔚2, GABA-A蔚1, GABA-A蔚3, and GABA-A蔚4. GABA-A蔚2 is the N -terminus, GABA-A蔚1 is the C-terminus, GABA-A蔚3 is the middle amino acid, and GABA-A蔚4 is the C-terminus.

GABRD is involved in a wide range of physiological processes in the brain, including the regulation of neurotransmitter release, the modulation of pain perception, and the control of muscle activity. It is well established that GABRD plays a key role in the regulation of pain perception and the modulation of neurotransmitter release.

One of the most promising aspects of GABRD is its potential as a drug target. GABRD has been shown to play a role in the regulation of pain perception and the modulation of neurotransmitter release, which makes it an attractive target for the development of new pain medications.

GABRD has been shown to play a role in the regulation of pain perception by modulating the release of neurotransmitters such as GABA and glutamate. GABA is a well-known neurotransmitter that is involved in the regulation of a wide range of physiological processes in the brain, including the modulation of pain perception. Glutamate is another neurotransmitter that is involved in pain perception and has been shown to play a role in the regulation of pain perception.

GABRD has also been shown to play a role in the regulation of neurotransmitter release by modulating the activity of GABA-A receptors. GABA-A receptors are involved in the regulation of a wide range of physiological processes in the brain, including the modulation of pain perception and the regulation of muscle activity.

In conclusion, GABRD is a non-c coding RNA that is expressed in the brain and plays a crucial role in the function of the central nervous system. It is involved in the regulation of pain perception and the modulation of neurotransmitter release, making it an attractive target for the development of new pain medications. Further research is needed to fully understand the role of GABRD in pain perception and the modulation of neurotransmitter release.

Protein Name: Gamma-aminobutyric Acid Type A Receptor Subunit Delta

Functions: GABA, the major inhibitory neurotransmitter in the vertebrate brain, mediates neuronal inhibition by binding to the GABA/benzodiazepine receptor and opening an integral chloride channel

The "GABRD 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 GABRD 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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