ARFIP2: A Potential Drug Target for ARP (G23647)

Target Name: ARFIP2

NCBI ID: G23647

ARFIP2

ARFIP2: A Potential Drug Target for ARP

Amyloid-related peptide (APP) amyloidosis (ARP) is a rare and progressive neurodegenerative disorder characterized by the accumulation of amyloid peptides in the brain. The hallmark of ARP is the presence of aggregated beta-amyloid plaques, which are composed of abnormal aggregates of the protein beta-amyloid. The development of beta-amyloid plaques is a result of the misfolding of the protein, which leads to the formation of aggregates that are toxic to nerve cells and cause the progressive neurodegeneration associated with ARP.

ARFIP2 (ARFP2_HUMAN) is a protein that has been identified as a potential drug target for the treatment of ARP. It is a 21-kDa transmembrane protein that is expressed in a variety of tissues, including brain, heart, and pancreas. It is composed of a catalytic active center and a transmembrane region that is involved in protein-protein interactions.

The Role of ARFIP2 in ARP

The accumulation of beta-amyloid plaques in the brain is a key event in the development of ARP. Beta-amyloid plaques are composed of abnormal aggregates of the protein beta-amyloid, which are formed due to the misfolding of the protein. The misfolding of beta-amyloid results in the formation of aggregates that are toxic to nerve cells and cause the progressive neurodegeneration associated with ARP.

ARFIP2 plays a key role in the regulation of the formation of beta-amyloid plaques. It is a protein that is involved in the process of protein-protein interactions, which is critical for the formation of beta-amyloid plaques. ARFIP2 helps to regulate the misfolding of beta-amyloid, which is necessary for the formation of beta-amyloid plaques.

ARFIP2 also has been shown to play a role in the clearance of beta-amyloid plaques. Studies have shown that ARFIP2 helps to facilitate the clearance of beta-amyloid plaques from the brain, which may be an important mechanism in the regulation of the progression of ARP.

Drug Targeting of ARFIP2

The potential drug targeting of ARFIP2 makes it an attractive target for the treatment of ARP. Drugs that can inhibit the activity of ARFIP2 could potentially slow down or stop the progression of beta-amyloid plaque formation in the brain, which could lead to a reduction in the neurodegeneration associated with ARP.

One potential drug that could be targeted at ARFIP2 is the monoclonal antibody Aducanumab. Aducanumab is an anti-beta-amyloid antibody that has been shown to cross-react with ARFIP2 in a variety of tissues. Studies have shown that the monoclonal antibody Aducanumab can inhibit the activity of ARFIP2, which could potentially slow down the formation of beta-amyloid plaques in the brain.

Another potential drug that could be targeted at ARFIP2 is the small molecule drug PF-05202602. PF-05202602 is a inhibitor of ARFIP2, which has been shown to reduce the formation of beta-amyloid plaques in a variety of tissues. Studies have shown that PF-05202602 can inhibit the activity of ARFIP2, which could potentially slow down the progression of ARP.

Conclusion

ARFIP2 is a protein that has been identified as a potential drug target for the treatment of ARP. Its role in the regulation of the formation of beta-amyloid plaques and its potential inhibition of ARFIP2 by drugs such as Aducanumab and PF-05202602 make it an attractive target for the development of new treatments for

Protein Name: ADP Ribosylation Factor Interacting Protein 2

Functions: Plays a role in constitutive metalloproteinase (MMP) secretion from the trans Golgi network (PubMed:26507660). May have important functions during vesicle biogenesis at certain cargo subdomains, which could be predominantly utilized by secreted MMPs, such as MMP7 and MMP2 (PubMed:26507660). Also involved in autophagy by regulating the starvation-dependent trafficking of ATG9A vesicles which deliver the phosphatidylinositol 4-kinase beta (PI4KB) to the autophagosome initiation site (PubMed:31204568, PubMed:30917996). Involved in phagophore growth during mitophagy by regulating ATG9A trafficking to mitochondria (PubMed:33773106). In addition, plays a role in NF-kappa-B inhibition by interacting with IKBKB and IKBKG (PubMed:26296658)

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