Spectrin

[2] Spectrin cleavage causes the membrane to form blebs and ultimately to be degraded, usually leading to the death of the cell.

[4] The convenience of using erythrocytes compared to other cell types means they have become the standard model for the investigation of the spectrin cytoskeleton.

Mutations in βH spectrin in C. elegans cause defects in morphogenesis resulting in a significantly shorter, but otherwise mostly normal, animal that moves and reproduces.

[7] A mutation in β spectrin in C. elegans results in an uncoordinated phenotype in which the worms are paralysed and much shorter than wild-type.

Knock-out of α or β spectrin in D. melanogaster results in neurons that are morphologically normal but have reduced neurotransmission at the neuromuscular junction.

In myocardial cells, aII spectrin distribution is coincident with Z-discs and the plasma membrane of myofibrils.

In humans, a mutation within the AnkB gene results in the long QT syndrome and sudden death, strengthening the evidence for a role for the spectrin cytoskeleton in excitable tissue.

A schematic diagram of spectrin and other cytoskeletal molecules
Localization of alpha-II spectrin in green under the plasma membrane of rat neurons in tissue culture as shown with confocal microscopy and immunofluorescence . The nuclei of the cells is revealed in blue by the DNA dye DAPI .