PMID- 19747464 OWN - NLM STAT- MEDLINE DCOM- 20100105 LR - 20220129 IS - 1872-6240 (Electronic) IS - 0006-8993 (Print) IS - 0006-8993 (Linking) VI - 1301 DP - 2009 Dec 8 TI - Expression of kinase interacting with stathmin (KIS, UHMK1) in human brain and lymphoblasts: Effects of schizophrenia and genotype. PG - 197-206 LID - 10.1016/j.brainres.2009.08.090 [doi] AB - Single nucleotide polymorphisms (SNPs) within the gene encoding the serine/threonine kinase KIS (Kinase Interacting with Stathmin, also known as UHMK1) have recently been associated with schizophrenia. As none of the disease associated SNPs are coding, they may confer susceptibility by altering some facet of KIS expression. Here we have characterised the cellular distribution of KIS in human brain using in situ hybridisation and immunohistochemistry, and quantified KIS protein and mRNA in two large brain series to determine if KIS expression is altered in schizophrenia or bipolar disorder or in relation to a schizophrenia-associated SNP (rs7513662). Post-mortem tissue from the superior temporal gyrus of schizophrenia and control subjects, and also dorsolateral prefrontal cortex, anterior cingulate cortex, and cerebellum from schizophrenia, bipolar disorder, and control subjects were used. KIS expression was measured by quantitative PCR (mRNA) and immunoautoradiography (protein), and was also quantified by immunoblot in lymphoblast cell lines derived from schizophrenia and control subjects. Our results demonstrate that KIS is expressed in neurons, and its encoded protein is localised to the nucleus and cytoplasm. No difference in KIS expression was found between diagnostic groups, or in the lymphoblast cell lines, and no effect of rs7513662 genotype on KIS expression was found. Hence, these data do not provide support for the hypothesis that altered expression is the mechanism by which genetic variation of KIS may increase susceptibility to schizophrenia, nor evidence that KIS expression is altered in the disease itself, at least in terms of the parameters studied here. FAU - Bristow, Greg C AU - Bristow GC AD - University Department of Psychiatry, Warneford Hospital, Oxford, UK. FAU - Lane, Tracy A AU - Lane TA FAU - Walker, Mary AU - Walker M FAU - Chen, Li AU - Chen L FAU - Sei, Yoshi AU - Sei Y FAU - Hyde, Thomas M AU - Hyde TM FAU - Kleinman, Joel E AU - Kleinman JE FAU - Harrison, Paul J AU - Harrison PJ FAU - Eastwood, Sharon L AU - Eastwood SL LA - eng GR - G0500180/MRC_/Medical Research Council/United Kingdom GR - Z01 MH002903-01/ImNIH/Intramural NIH HHS/United States PT - Journal Article PT - Research Support, N.I.H., Intramural PT - Research Support, Non-U.S. Gov't DEP - 20090909 PL - Netherlands TA - Brain Res JT - Brain research JID - 0045503 RN - 0 (Intracellular Signaling Peptides and Proteins) RN - 0 (RNA, Messenger) RN - EC 2.7.11.1 (Protein Serine-Threonine Kinases) RN - EC 2.7.11.1 (UHMK1 protein, human) SB - IM MH - Adult MH - Aged MH - Analysis of Variance MH - Autoradiography MH - Blotting, Western MH - Brain/*metabolism MH - Cell Line, Tumor MH - Female MH - Gene Expression/*genetics MH - *Genotype MH - Humans MH - Immunohistochemistry MH - In Situ Hybridization MH - Intracellular Signaling Peptides and Proteins/*genetics/metabolism MH - Male MH - Middle Aged MH - Neurons/metabolism MH - Polymorphism, Single Nucleotide/genetics MH - Protein Serine-Threonine Kinases/*genetics/metabolism MH - RNA, Messenger/genetics/metabolism MH - Reverse Transcriptase Polymerase Chain Reaction MH - Schizophrenia/*genetics/metabolism PMC - PMC2783906 MID - NIHMS144750 EDAT- 2009/09/15 06:00 MHDA- 2010/01/06 06:00 PMCR- 2010/12/08 CRDT- 2009/09/15 06:00 PHST- 2009/06/19 00:00 [received] PHST- 2009/08/25 00:00 [revised] PHST- 2009/08/26 00:00 [accepted] PHST- 2009/09/15 06:00 [entrez] PHST- 2009/09/15 06:00 [pubmed] PHST- 2010/01/06 06:00 [medline] PHST- 2010/12/08 00:00 [pmc-release] AID - S0006-8993(09)01867-8 [pii] AID - 10.1016/j.brainres.2009.08.090 [doi] PST - ppublish SO - Brain Res. 2009 Dec 8;1301:197-206. doi: 10.1016/j.brainres.2009.08.090. Epub 2009 Sep 9.