TCEAL1: A Potential Drug Target and Biomarker for ALS-Like Diseases

Target Name: TCEAL1

NCBI ID: G9338

TCEAL1

TCEAL1: A Potential Drug Target and Biomarker for ALS-Like Diseases

Ammonia-induced neurotoxicity, or TCEAL1-mediated neurotoxicity, is a phenomenon that has been observed in various organisms, including humans. TCEAL1, a gene encoding a protein involved in ammonia detoxification, has been identified as a potential drug target and biomarker for ammonia-toxicity-related diseases, including amyotrophic lateral sclerosis (ALS). This article will discuss the TCEAL1 protein, its function, and its potential as a drug target and biomarker.

Function of TCEAL1

TCEAL1 is a 21-kDa protein that is expressed in various tissues, including brain, heart, and liver. It is composed of two distinct domains: an N-terminal transmembrane domain and a C-terminal cytoplasmic domain. The N-terminal domain contains a putative cytoplasmic acidophilic loop, which is involved in the detoxification of ammonia. The C-terminal domain contains a putative G-protein-coupled receptor (GPCR) domain, which is involved in signaling.

TCEAL1 functions as a cytoplasmic protein that is involved in the detoxification of ammonia, which is a toxic compound that can cause a variety of neurotoxicity-related diseases, including ALS. Ammonia has been shown to cross the blood-brain barrier and to cause neurotoxicity by reacting with various cellular components, including neurotransmitters, ion channels, and neuroproteins. TCEAL1 is involved in the detoxification of ammonia by forming a covalent complex with glutamyl-glutamyl transferase (GGT), which is an enzyme involved in the detoxification of ammonia.

Potential Drug Target

TCEAL1 has been identified as a potential drug target for ALS-like diseases due to its involvement in the detoxification of ammonia, which is a known risk factor for ALS. Studies have shown that individuals with the genetic variation in the TCEAL1 gene are at increased risk for developing ALS-like diseases. Additionally, TCEAL1 has been shown to be overexpressed in ALS patients, which may contribute to the neurotoxicity associated with ALS.

TCEAL1 has also been shown to interact with various drug targets that are involved in ALS, including the neurotransmitter GABA, which is known to have neuroprotective properties. TCEAL1 has been shown to modulate GABA release and to affect the activity of GABA receptors, suggesting that it may play a role in the treatment of ALS-like diseases.

Biomarker

TCEAL1 has also been identified as a potential biomarker for ALS-like diseases due to its increased expression in individuals with the genetic variation in the TCEAL1 gene. Additionally, TCEAL1 has been shown to be expressed in various tissues and cells that are affected by ALS, including brain and spinal cord cells. This suggests that TCEAL1 may be a useful biomarker for the diagnosis and monitoring of ALS-like diseases.

Conclusion

TCEAL1 is a protein that is involved in the detoxification of ammonia and has been identified as a potential drug target and biomarker for ALS-like diseases. Its function in the detoxification of ammonia and its interaction with various drug targets, including GABA, make it a promising target for the development of neuroprotective agents for ALS-like diseases. Further research is needed to fully understand the role of TCEAL1 in ALS-like diseases and to develop effective treatments.

Protein Name: Transcription Elongation Factor A Like 1

Functions: May be involved in transcriptional regulation. Modulates various viral and cellular promoters in a promoter context-dependent manner. For example, transcription from the FOS promoter is increased, while Rous sarcoma virus (RSV) long terminal repeat (LTR) promoter activity is repressed. Does not bind DNA directly

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