Alexa Fluor® 594 Anti-CD68 antibody [EPR20545]

Supplementary info

Activity summary

CD68 is a glycoprotein that functions as a scavenger receptor. It plays an important role in the regulation of cellular debris and apoptotic cell clearance. Researchers often refer to it as KP1 or macrosialin in the literature. CD68 with a molecular weight of approximately 110 kDa is highly expressed in macrophages and monocytes. The mucin-like structure of CD68 allows it to be heavily glycosylated which aids in its function. Researchers detect CD68 in tissues through methods like immunohistochemistry (IHC) immunofluorescence and CD68 staining and it is widely used as a macrophage marker in research.

Biological function summary

CD68 facilitates functions associated with the innate immune response. It serves as an important part of macrophages which contribute to immune surveillance and tissue homeostasis. Though it primarily operates on its own in some contexts CD68 might assist in forming complexes with other receptors to modulate phagocytic activity. This target is significant in atherosclerotic plaque stability as macrophages engulf lipids and cell debris through processes facilitated by CD68.

Pathways

CD68 is involved in pathways connected to inflammation and phagocytosis. The CD68 protein works closely with other scavenger receptors like CD36 to mediate uptake of oxidized low-density lipoproteins (oxLDL) in the lipid metabolism pathway. Additionally CD68 engagement can influence the toll-like receptor (TLR) signaling pathways thereby linking innate immunity and inflammatory responses critical for host defense and disease progression.

Associated diseases and disorders

CD68 is associated with atherosclerosis and multiple sclerosis. In atherosclerosis its role becomes evident as it accumulates in macrophages within the plaques making it a marker of disease severity. In multiple sclerosis CD68 expression in macrophages and microglia indicates active demyelination and inflammation. It also relates to proteins such as CD36 in atherosclerosis where both mediate the uptake of modified LDL contributing to foam cell formation in plaques.