HRP Anti-MGEA5/OGA antibody [EPR7154(B)]

Supplementary info

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

Activity summary

MGEA5 also referred to as OGA or O-GlcNAcase serves an important mechanical role in cellular metabolism. This enzyme with a molecular mass of around 103 kDa is primarily involved in the removal of O-GlcNAc modifications from serine/threonine residues on nuclear and cytoplasmic proteins. It is expressed in various tissues but exhibits predominant activity in the brain liver and pancreas. Alternative names like "OGA stains" or "OGA b" may also be encountered in literature or research contexts.

Biological function summary

MGEA5 acts as an important modulator of protein function and regulation by cycling O-GlcNAc modifications thereby influencing processes like transcription signal transduction and apoptosis. While not part of a well-defined complex it frequently interacts with other proteins involved in glucose metabolism and the cellular stress response. Its activity works in concert with OGT (O-GlcNAc transferase) which adds O-GlcNAc maintaining a balance important for cellular function.

Pathways

MGEA5 involvement centers largely around glucose homeostasis and the insulin signaling pathway. It modulates the function of proteins like insulin receptor substrate (IRS) and other key regulators in this pathway affecting metabolic regulation and energy homeostasis. It shows a direct relationship with OGT as they reciprocate in action effects highlighting their collaborative role in cellular pathways that affect cellular signaling and survival.

Associated diseases and disorders

MGEA5 has been implicated in neurodegenerative diseases and diabetes. In Alzheimer's disease altered O-GlcNAc cycling affects tau protein homeostasis which is significant in disease pathogenesis. Likewise in diabetes MGEA5 influences insulin resistance by regulating O-GlcNAc levels on insulin signaling molecules. Dysregulation of these processes may also involve proteins such as beta-amyloid further linking MGEA5 to these pathological states.