Anti-UBXD8 antibody

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.

Activity summary

UBXD8 also known as UBX domain-containing protein 8 or FAF2 is an essential player in cellular regulation. This protein weighs approximately 64 kDa and is expressed in various tissues with prominent activity in the liver and adipose tissue. Mechanically UBXD8 functions as part of the Endoplasmic Reticulum-Associated Degradation (ERAD) pathway where it interacts with other proteins to facilitate the extraction and turnover of misfolded proteins. UBXD8 being part of the p97/VCP protein complex plays an important role in maintaining protein homeostasis within cells.

Biological function summary

UBXD8 regulates lipid metabolism and transport. It ensures lipid droplets' stability and controls lipid efflux from the liver contributing to systemic lipid homeostasis. The protein acts as a bridge in the process of tethering lipid droplets to the ER membrane thereby participating in lipid droplet biogenesis and turnover. As part of a larger complex with p97/VCP UBXD8 supervises the transfer and processing of lipid-related components linking it dynamically to cellular lipid management.

Pathways

The biogenesis of lipid droplets and the pathway of protein degradation heavily involve UBXD8. It interacts with pathways such as the unfolded protein response (UPR) ensuring the ER handles protein misfolding effectively. Collaborating closely with proteins like p97/VCP and E4B UBXD8 supports the ubiquitin-proteasome system which leads to efficient degradation of defective proteins. These interactions highlight UBXD8’s participation in cellular stress responses and maintenance of cellular equilibrium.

Associated diseases and disorders

Aberrations in UBXD8 function link it to metabolic and neurodegenerative diseases. In conditions like non-alcoholic fatty liver disease (NAFLD) UBXD8's dysfunction can disrupt normal lipid storage and cause excessive fat accumulation in the liver. Also improper activity connects UBXD8 to neurodegenerative disorders such as Alzheimer's disease where it might influence protein aggregation and clearance. Here its interaction with p97/VCP becomes significant suggesting potential therapeutic targets in correcting or mitigating these pathological conditions.