Inhibitor-of-differentiation 2 (Id2) is a recently identified protein that antagonizes differentiation mediated by the retinoblastoma protein, probably by scavenging downstream E-box basic helix-loop-helix proteins. Rapidly gaining attention as an immune modulator, Id2 as been shown to be obligatory for the maturation of B cells, facilitating antigen responsiveness and immune system participation; and for thymic NK cell development. Id2 is over-expressed in a number of cancers including human colorectal adenocarcinomas, and pancreatic cancers. In the latter, inhibition of Id2 expression prevented cell growth. Id2 is also implicated in various neurological tumors. Expression of Id2 is strongly predictive of poor outcome neuroblastoma, relating to its ability to maintain the malignant behavior of neuroblastoma cells. About half as frequent as cancer, ischemic stroke affects about 600,000 Americans each year, 8% of whom die within 30 days. A further 15-30% are permanently disabled and 20% require institutional care. Direct and indirect costs of stroke are therefore immense. The treatment of ischemic stroke remains one of the most challenging areas of medicine today. At present, only thrombolysis is approved as a treatment strategy, and for only a brief window of time. Since many patients present far beyond this three-hour window, not surprisingly most patients receive only palliative care. In order to open the window of therapeutic opportunity the pharmaceutical industry is currently focusing on the development of new opportunities including the identification of molecules able to stimulate angiogenesis or block apoptosis. University of Tubingen researchers have recently shown that neurons from Id2 knock-out mice are protected from apoptosis. Further, overexpression of Id2 induces neuronal cell death both in high potassium and low potassium conditions. These data suggest that blocking Id2 function may be beneficial to two major conditions, cancer and stroke

Link to journal abstract:

Adapted from Schulz et al, J Neurochem 2002 Mar;80(5):755-62

Interested in collaborating with this group? Contact leaddiscovery@bioportfolio.co.uk