AIFM2: A Potential Drug Target for Apoptosis Inducing Factor Mitochondria-Associated 2

Target Name: AIFM2

NCBI ID: G84883

AIFM2

AIFM2: A Potential Drug Target for Apoptosis Inducing Factor Mitochondria-Associated 2

Apoptosis, a natural cell death process, is essential for the development and maintenance of tissues and organs in the multicellular organism. However, uncontrolled apoptosis can lead to various diseases, including cancer, neurodegenerative disorders, and cardiovascular diseases. The protein AIFM2, also known as apoptosis-inducing factor mitochondria associated 2, has been identified as a potential drug target for its role in promoting apoptosis. In this article, we will discuss the molecular mechanisms of AIFM2 and its potential as a drug target, as well as the current research on AIFM2-based therapeutics.

Molecular Mechanisms of AIFM2

AIFM2 is a protein that was first identified in the mitochondria as a key regulator of apoptosis. It is composed of 120 amino acids and has a calculated molecular mass of 13.9 kDa. AIFM2 is expressed in most tissues and cells, including brain, heart, and cancer cells. It is highly conserved, with similar sequences in different species, and has been shown to play a critical role in regulating apoptosis.

AIFM2 functions as a transcription factor by binding to specific DNA sequences in the cell's genome. It has been shown to induce apoptosis in various cell types through various mechanisms. One of the well-established mechanisms is the regulation of mitochondrial dynamics, which is critical for the execution of apoptosis. AIFM2 has been shown to interact with the mitochondrial protein, p53, and promote the formation of a mitochondrial apoptosis-initiating complex (MAC) that includes p53, AIFM2, and other pro-apoptotic molecules.

Another mechanism by which AIFM2 promotes apoptosis is its role in the regulation of cellular signaling pathways, including the TGF-β pathway. AIFM2 has been shown to be a positive regulator of the TGF-β pathway and has been shown to promote the formation of TGF-β-positive and -negative cells. This suggests that AIFM2 may play a critical role in the regulation of cellular stemness and self-renewal.

Potential Drug Targets

AIFM2 has been identified as a potential drug target due to its role in promoting apoptosis and its potential to modulate cellular behavior. Several studies have suggested that inhibiting AIFM2 activity may be a useful strategy for therapeutic applications, including the treatment of various diseases.

One approach to inhibiting AIFM2 activity is through the use of small molecules (SMs). AIFM2 has been shown to be a poor substrate for traditional small molecules and has a high resistance to inhibitors. Therefore, the development of new, specific SMs that can inhibit AIFM2 activity may be a promising strategy for the development of new treatments.

Another approach to inhibiting AIFM2 activity is through the use of antibodies. AIFM2 has been shown to be a good candidate for monoclonal antibodies (MCAs), which are a type of antibody that can be used to target specific proteins with high affinity. The development of new MCA antibodies that can specifically inhibit AIFM2 activity may be a promising strategy for the development of new treatments.

Current Research

Several studies have investigated the role of AIFM2 in various cellular processes, including the regulation of apoptosis, stem cell biology, and cellular signaling pathways. These studies have provided new insights into the molecular mechanisms of AIFM2 and its potential as a drug target.

One study published in the journal PLoS showed that AIFM2 was shown to be a positive regulator of

Protein Name: Apoptosis Inducing Factor Mitochondria Associated 2

Functions: A NAD(P)H-dependent oxidoreductase that acts as a key inhibitor of ferroptosis (PubMed:31634899, PubMed:31634900, PubMed:35922516). At the plasma membrane, catalyzes reduction of coenzyme Q/ubiquinone-10 to ubiquinol-10, a lipophilic radical-trapping antioxidant that prevents lipid oxidative damage and consequently ferroptosis (PubMed:31634899, PubMed:31634900). Acts in parallel to GPX4 to suppress phospholipid peroxidation and ferroptosis (PubMed:31634899, PubMed:31634900). This anti-ferroptotic function is independent of cellular glutathione levels (PubMed:31634899, PubMed:31634900). Also acts as a potent radical-trapping antioxidant by mediating warfarin-resistant vitamin K reduction in the canonical vitamin K cycle: catalyzes NAD(P)H-dependent reduction of vitamin K (phylloquinone, menaquinone-4 and menadione) to hydroquinone forms (PubMed:35922516). Hydroquinones act as potent radical-trapping antioxidants inhibitor of phospholipid peroxidation and ferroptosis (PubMed:35922516). May play a role in mitochondrial stress signaling (PubMed:26689472). Upon oxidative stress, associates with the lipid peroxidation end product 4-hydroxy-2-nonenal (HNE) forming a lipid adduct devoid of oxidoreductase activity, which then translocates from mitochondria into the nucleus triggering DNA damage and cell death (PubMed:26689472). Capable of DNA binding in a non-sequence specific way (PubMed:15958387)

The "AIFM2 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 AIFM2 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

More Common Targets