Annexins as disease modifiers
Lux Fatimathas and Stephen E. Moss
Department of Cell Biology, UCL Institute of Ophthalmology, London, UK.
Offprint requests to: Prof. Stephen E. Moss, Department of Cell Biology, UCL Institute of Ophthalmology, 11-43 Bath Street, London EC1V 9EL, UK. e-mail: firstname.lastname@example.org
Summary. The annexins are a family of calcium-dependent phospholipid binding proteins which are present in all eukaryotes. There are currently 12 identified human annexins all of which contain unique calcium binding sites, encoded in the highly conserved annexin repeat motifs within the C terminal core. In addition to the C terminal core the annexins contain a significantly more variable N terminal head. It is this domain which endows each annexin with unique functions in a diverse range of cellular processes including; endo- and exocytosis, cytoskeletal regulation and membrane conductance and organisation. Given their involvement in such a variety of processes it is not surprising that the annexins have also been implicated in a range of disease pathologies. Although there is no singular disease state directly attributed to a dysregulation in annexin function, several pathological conditions are suggested to be modified by the annexins. In this review we shall focus on the growing evidence for the role of the annexins in the progression of cancer, diabetes and the autoimmune disorder anti-phospholipid syndrome. Histol Histopathol 25, 527-532 (2010)
Key words: Cancer, Diabetes, Lipocortin, Calpactin, Synexin