Target Name: GJA4
NCBI ID: G2701
Review Report on GJA4 Target / Biomarker Content of Review Report on GJA4 Target / Biomarker
GJA4
Other Name(s): Gap junction alpha-4 protein | gap junction protein, alpha 4, 37kDa | connexin-37 | CXA4_HUMAN | Connexin-37 | Gap junction protein alpha 4 | gap junction protein alpha 4 | Gap junction protein, alpha 4, 37kD | Connexin 37 | OTTHUMP00000004181 | Cx37 | CX37 | OTTHUMP00000004182

GJA4: A Potential Drug Target and Biomarker for ALS

Gap junction alpha-4 (GJA4) is a protein that is expressed in the central nervous system (CNS) and is involved in the formation of the blood-brain barrier (BBB) and the regulation of neurotransmitter release. It has been identified as a potential drug target and biomarker for the progressive neurodegenerative disease amyotrophic lateral sclerosis (ALS). In this article, we will review the current state of research on GJA4 and its potential as a drug target and biomarker for ALS.

GJA4 is a transmembrane protein that is composed of four intracellular domains: an N-terminus, a transmembrane domain, a cytoplasmic domain, and an C-terminus. It is expressed in a variety of tissues, including the brain, and is involved in the formation of the BBB and the regulation of neurotransmitter release.

GJA4 is a key regulator of the neurotransmitter synapse, which is the site where neurotransmitters are released from the axon terminal of neurons and received by dendrites. GJA4 is involved in the formation of the synapse by regulating the trafficking of synaptic vesicles and the formation of the postsynaptic density (PSD), which is the matrix of synaptic vesicles that surrounds the axon terminal of each neuron.

In addition to its role in neurotransmission, GJA4 is also involved in the regulation of inflammation and immune cell function. It has been shown to be involved in the regulation of immune cell migration and the production of inflammatory cytokines.

GJA4 has also been identified as a potential drug target for ALS, a progressive neurodegenerative disease that is characterized by the progressive loss of motor neurons. There is evidence to suggest that GJA4 may be involved in the development and progression of ALS by regulating the formation of the BBB and by modulating the release of neurotransmitters that are involved in the pathophysiology of the disease.

One of the main challenges in researching GJA4 as a potential drug target for ALS is the lack of information about its specific role in the disease. While there is evidence to suggest that GJA4 may be involved in the pathophysiology of ALS, it is not clear how it contributes to the development and progression of the disease.

In conclusion, GJA4 is a protein that is expressed in the CNS and is involved in the formation of the BBB and the regulation of neurotransmission. It has also been identified as a potential drug target and biomarker for ALS. Further research is needed to determine its specific role in the disease and to develop effective treatments.

Protein Name: Gap Junction Protein Alpha 4

Functions: One gap junction consists of a cluster of closely packed pairs of transmembrane channels, the connexons, through which materials of low MW diffuse from one cell to a neighboring cell

The "GJA4 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 GJA4 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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