Establishing genomic/transcriptomic links between Alzheimer's disease and type 2 diabetes mellitus by meta-analysis approach.
Jiddah, Saudi Arabia. In Cns Neurol Disord Drug Targets, 2014
Significantly changed expression of "myeloid leukemia cell differentiation protein 1; RAS guanyl releasing protein 1; S100 calcium-binding protein A8; prostaglandin- endoperoxide synthase 2; parvalbumin; endoplasmic reticulum aminopeptidase 1; phosphoglycerate kinase 1; Eukaryotic translation initiation factor 3 subunit F; Interleukin-1 beta; tubulin, beta 2A; glycine receptor alpha 1 and ribosomal protein S24" genes were highly associated with T2DM, whereas "neuronal differentiation 6; G-protein coupled receptor 83; phosphoserine phosphatase; bobby sox homolog or HMG box -containing protein 2; Glutathione S-transferase theta 1; alpha-2-glycoprotein 1 zinc-binding; Heat shock 70kDa protein 1B; transportin 1, Acidic leucine-rich nuclear phosphoprotein 32 family member B; Nuclear factor of activated T-cells 5; inositol 1,4,5-trisphosphate 3-kinase B; prenylcysteine oxidase 1 like" were found to be strongly related with AD.
New therapeutic targets in immune disorders: ItpkB, Orai1 and UNC93B.
Los Angeles, United States. In Expert Opin Ther Targets, 2008
METHODS: We evaluate the potentials of inositol (1,4,5)trisphosphate 3-kinase B (ItpkB), Orai1 and UNC93B, three particularly interesting proteins that were recently identified through functional genomics, as targets in immune disorders.
Production of Ins(1,3,4,5)P4 mediated by the kinase Itpkb inhibits store-operated calcium channels and regulates B cell selection and activation.
San Diego, United States. In Nat Immunol, 2007
Here we report that mice lacking Ins(1,4,5)P3 3-kinase B (Itpkb), which converts Ins(1,4,5)P3 to inositol-1,3,4,5-tetrakisphosphate (Ins(1,3,4,5)P4), had impaired B lymphocyte development and defective immunoglobulin G3 antibody responses to a T lymphocyte-independent antigen.