Target Name: CACNA2D3
NCBI ID: G55799
Review Report on CACNA2D3 Target / Biomarker Content of Review Report on CACNA2D3 Target / Biomarker
CACNA2D3
Other Name(s): voltage-gated calcium channel subunit alpha-2/delta-3 | Calcium channel alpha2-delta3 subunit | Voltage-dependent calcium channel subunit delta-3 | Voltage-dependent calcium channel subunit alpha-2-3 | calcium channel, voltage-dependent, alpha 2/delta subunit 3 | Voltage-gated calcium channel subunit alpha-2/delta-3 | Calcium voltage-gated channel auxiliary subunit alpha2delta 3 | HSA272268 | calcium channel, voltage-dependent, alpha 2/delta 3 subunit | calcium channel alpha2-delta3 subunit | calcium voltage-gated channel auxiliary subunit alpha2delta 3 | Voltage-dependent calcium channel subunit alpha-2/delta-3 | CA2D3_HUMAN | alpha2delta-3

CACNA2D3: A Voltage-Gated Calcium Channel Subunit Alpha-2/Delta-3 as a Drug Target and Biomarker

Abstract:

CACNA2D3, the voltage-gated calcium channel subunit alpha-2/delta-3, has been identified as a potential drug target and biomarker for various neurological and psychiatric disorders. This protein plays a crucial role in neuronal communication, and its dysfunction has been implicated in a wide range of neuropsychiatric diseases. Understanding the molecular mechanisms underlying its function and potential therapeutic interventions may have significant implications for the treatment of such conditions.

Introduction:

CACNA2D3, also known as voltage-gated calcium channel subunit alpha-2/delta-3, is a transmembrane protein that is expressed in many different tissues, including neurons, muscle cells, and blood vessels. It is a key component of the voltage-gated calcium channel, which is a critical channel that regulates the flow of calcium ions into cells in response to changes in membrane potential. The alpha-2/delta-3 subunit is responsible for the channel's voltage-gated properties, as it is the region that is most involved in the regulation of channel opening and closing.

CACNA2D3 dysfunction has been implicated in a wide range of neuropsychiatric and neurological disorders, including Alzheimer's disease, Parkinson's disease, anxiety, and depression. Studies have shown that individuals with certain genetic variants, such as those in the CACNA2D3 gene, are at increased risk for developing these disorders. Additionally, alterations in CACNA2D3 expression have also been observed in various neurological conditions, such as epilepsy and schizophrenia.

Despite the growing body of evidence, the precise mechanisms underlying CACNA2D3 dysfunction are not well understood. However, several studies have identified alterations in the structure and function of CACNA2D3 that are involved in its neurotoxicity and neuroprotective properties.

Alterations in CACNA2D3 structure and function have been observed due to various factors, including genetic mutations, oxidative stress, and neurotoxins. For example, studies have shown that individuals with certain genetic variants, such as those in the CACNA2D3 gene, are at increased risk for developing neurodegenerative disorders due to changes in CACNA2D3 function. Additionally, research has suggested that CACNA2D3 dysfunction may be a neurotoxin, as it has been shown to be involved in the development of neurotoxicity in various organisms.

In addition to its potential role in neurodegenerative disorders, CACNA2D3 has also been implicated in the development of various psychiatric disorders. Studies have shown that individuals with certain genetic variants, such as those in the CACNA2D3 gene, are at increased risk for developing anxiety and depression, as well as other psychiatric disorders. Additionally, research has suggested that CACNA2D3 dysfunction may play a role in the development of certain psychiatric disorders, such as schizophrenia and Bipolar disorder.

Despite the growing body of evidence, the precise mechanisms underlying CACNA2D3 dysfunction are not well understood. However, several studies have identified alterations in the structure and function of CACNA2D3 that are involved in its neurotoxicity and neuroprotective properties. Further research is needed to fully understand the role of CACNA2D3 in neuropsychiatric and neurological disorders, as well as its potential as a drug target or biomarker.

Conclusion:

CACNA2D3, the voltage-gated calcium channel subunit alpha-2/delta-3, has been identified as a potential drug target and biomarker for various neurological and psychiatric disorders. Its dysfunction has been implicated in a wide range of neuropsychiatric and neurological diseases, including Alzheimer's disease, Parkinson's disease, anxiety, and depression. Additionally, alterations in CACNA2D3 expression have also been observed in various neurological conditions, such as epilepsy and schizophrenia. Further research is needed to fully understand the role of CACNA2D3 in neuropsychiatric and neurological disorders, as well as its potential as a drug target or biomarker.

Protein Name: Calcium Voltage-gated Channel Auxiliary Subunit Alpha2delta 3

Functions: The alpha-2/delta subunit of voltage-dependent calcium channels regulates calcium current density and activation/inactivation kinetics of the calcium channel. Acts as a regulatory subunit for P/Q-type calcium channel (CACNA1A), N-type (CACNA1B), L-type (CACNA1C OR CACNA1D) but not T-type (CACNA1G) (By similarity)

The "CACNA2D3 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 CACNA2D3 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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