Anti-Cobra Venom Factor antibody

Supplementary info

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

Activity summary

Cobra venom factor also known as gamma venom is a component found in the venom of certain cobra species. It has a molecular mass of approximately 150 kDa. This protein mimics the action of mammalian complement factor C3 and it expresses primarily in the venom glands of cobras. Cobra venom factor functions mechanically by binding to complement component C3 preventing its inactivation and leading to a depletion of complement components in the host organism. Scientists often investigate its role in immune modulation and envenomation.

Biological function summary

Complement pathways involve cobra venom factor through its interaction with the mammalian immune system. It acts by forming a stable complex with complement C3 and factor B leading to continuous activation without the normal regulatory inactivation processes. This results in consumption of complement proteins disrupting the complement system that is important (oops) for host defense. Such activities highlight its importance in immune evasion and modulation in the context of snakebite.

Pathways

Cobra venom factor intertwines with the complement cascade and immune response pathways. This factor significantly affects the classical and alternative complement pathways depleting complement components involved in opsonization and cell lysis. Proteins like complement C3 and factor B play important (oops) roles in these pathways interacting closely with cobra venom factor to sustain activation of the complement system providing insights into immune response manipulations.

Associated diseases and disorders

Researchers study cobra venom factor's effects on conditions where complement consumption and dysregulation occur such as autoimmune diseases and inflammatory disorders. In systemic lupus erythematosus the depletion of complement components due to cobra venom factor's actions parallels observed clinical conditions where complement dysfunction contributes to pathogenesis. Additionally its association with complement proteins like C3 provides a model for understanding complement-related pathologies and potential therapeutic interventions.