A protein which aggravates Alzheimer's Disease
In mice, over-expression of ITPKB protein leads to exacerbation of Alzheimer's disease. Moreover, inhibition of ITPKB in cultured mouse neurons limits the production of amyloid peptides responsible for the formation of senile plaques.
From the immune system to the nervous system
In 2003, Stéphane Schurmans and his team obtained the first knock-out mouse for the ITPKB gene (inositol 1, 4, 5 triphosphate 3-kinase B). 'We then discovered that these mice presented a particular phenotype because they did not have peripheral T lymphocytes , i.e. in the lymph nodes and the spleen', continues Professor Schurmans. Additional studies showed that other cells in the immune system, such as B lymphocytes, neutrophils, myeloid cells, and mast cells were also altered in ITPKB knock-out mice. 'These results show the importance of the role of the ITPKB enzyme in the haematopoietic system and the immune system', says the researcher. Thus, the ITPKB knock-out mice logically could be useful for the study of the ITPKB enzyme function within these biological systems.