beta 2-Microglobulin modified with advanced glycation end products is a major component of hemodialysis-associated amyloidosis.

Eitemau Tebyg

• Involvement of beta 2-microglobulin modified with advanced glycation end products in the pathogenesis of hemodialysis-associated amyloidosis. Induction of human monocyte chemotaxis and macrophage secretion of tumor necrosis factor-alpha and interleukin-1.
  gan: Miyata, T, et al.
  Cyhoeddwyd: (1994)
• Identification of pentosidine as a native structure for advanced glycation end products in beta-2-microglobulin-containing amyloid fibrils in patients with dialysis-related amyloidosis.
  gan: Miyata, T, et al.
  Cyhoeddwyd: (1996)
• The receptor for advanced glycation end products (RAGE) is a central mediator of the interaction of AGE-beta2microglobulin with human mononuclear phagocytes via an oxidant-sensitive pathway. Implications for the pathogenesis of dialysis-related amyloidosis.
  gan: Miyata, T, et al.
  Cyhoeddwyd: (1996)
• Polymerization of intact beta 2-microglobulin in tissue causes amyloidosis in patients on chronic hemodialysis.
  gan: Gorevic, P D, et al.
  Cyhoeddwyd: (1986)
• Systemic amyloidosis of beta 2 microglobulin type.
  gan: Mazanec, K, et al.
  Cyhoeddwyd: (1992)