We have demonstrated that red blood cell (RBC) membranes in membranopathies
are targets for inducible Hsp70 family members. A similar phenomenon was o
bserved in several types of hereditary haemolytic anaemias. One common feat
ure of the inherited haemolytic anaemias is that the mutations are manifest
ed in the form of an altered RBC membrane structure resulting in premature
cell destruction. Hence, we propose that malfolded (and mutated) RBC membra
ne proteins are recognised by Hsp70 protein. Although the function of Hsp70
family members as a 'quality control system' is well known, this is the fi
rst report of their presence in human anaemias.