ABCB8: A Drug Target and Potential Biomarker for Mitochondrial Disorders

Target Name: ABCB8

NCBI ID: G11194

ABCB8

ABCB8: A Drug Target and Potential Biomarker for Mitochondrial Disorders

Mitochondrial disorders are a group of genetic and metabolic disorders that affect the powerhouses of cells, the mitochondria. They are characterized by a range of symptoms, including muscle weakness, cognitive impairments, and a variety of systemic issues. One of the main underlying mechanisms behind these disorders is the dysfunction of the ATP-binding cassette (ABC) proteins, which are responsible for transporting molecules across the mitochondrial membrane. In this article, we will focus on ABCB8, a protein that has been identified as a potential drug target and biomarker for mitochondrial disorders.

Synonyms and Acronyms

The full name of the ABCB8 protein is mitochondrial ATP-binding cassette subfamily B member 8. It is also sometimes referred to as Mammalian ATP-binding protein 8 (MABP-8) or simply as ABCB8. The gene for ABCB8 is located on chromosome 13q21 and has a protein length of 174 amino acids.

Function and Importance

ABCB8 is a member of the ABCB family of proteins, which are known for their ability to form ATP-binding sites on the outer membrane of mitochondria. These proteins are involved in a variety of cellular processes, including the transport of molecules across the membrane and the regulation of mitochondrial function.

ABCB8 is specifically involved in the regulation of mitochondrial ATP homeostasis, which is critical for maintaining the integrity of the mitochondrial membrane and the delivery of oxygen to the body's cells. ABCB8 helps to maintain the proper balance of ATP to ADP and Pi, which are the active forms of ATP that are used by the cell to power its various processes.

Dysfunction of ABCB8 in Mitochondrial Disorders

Mitochondrial disorders are a range of genetic and metabolic disorders that are characterized by dysfunction of the mitochondria. One of the main underlying mechanisms behind these disorders is the dysfunction of the ABCB8 protein.

Studies have shown that ABCB8 dysfunction is associated with a variety of mitochondrial disorders, including mutations in the ABCB8 gene, as well as disruptions in the ABCB8 protein's normal function. For example, studies have shown that individuals with certain mitochondrial disorders have lower levels of ABCB8 in their mitochondria, which is thought to contribute to the dysfunction of these disorders.

In addition, research has also shown that ABCB8 dysfunction is associated with a variety of cellular processes that are important for maintaining the integrity of the mitochondrial membrane. For example, studies have shown that ABCB8 helps to regulate the delivery of oxygen to the body's cells, which is critical for maintaining cellular health and function.

Potential Therapeutic Use

The dysfunction of the ABCB8 protein is an attractive target for therapeutic intervention, given the importance of ABCB8 in maintaining the integrity of the mitochondrial membrane and the delivery of oxygen to the body's cells. Several studies have shown that drugs that can modulate ABCB8 function have the potential to treat a variety of mitochondrial disorders.

For example, studies have shown that inhibitors of the ABCB8 protein have the potential to treat a variety of mitochondrial disorders, including those caused by mutations in the ABCB8 gene. These drugs work by binding to the ABCB8 protein and preventing it from forming ATP-binding sites on the outer membrane of the mitochondria.

In addition, studies have also shown that modulators of ABC

Protein Name: ATP Binding Cassette Subfamily B Member 8

Functions: ATP-binding subunit of the mitochondrial potassium channel located in the mitochondrial inner membrane (PubMed:31435016). Together with CCDC51/MITOK, forms a protein complex localized in the mitochondria that mediates ATP-dependent potassium currents across the inner membrane (that is, mitoK(ATP) channel) (PubMed:31435016). Plays a role in mitochondrial iron transport (PubMed:30623799). Required for maintenance of normal cardiac function, possibly by influencing mitochondrial iron export and regulating the maturation of cytosolic iron sulfur cluster-containing enzymes (By similarity)

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