By Y. Kazuki, T. C. Schulz, T. Shinohara, M. Kadota (auth.), Prof. Dr. G. Lubec (eds.)

"Advances in Down Syndrome study” represents up-to-date learn in different components of Down Syndrome (DS). a brand new promising animal version of DS is pronounced and this opens new possibilities to check pathomechanisms and pharmacological ways because it is greater than tricky to hold out reviews in people and the medical gains are hugely variable. when it comes to biology, mobile cycle and stem mobile reviews and by way of biochemistry, relevance of experiences on a particular protein kinase, channels, transporters, superoxide dismutase, antioxidant approach, chromosome meeting issue and different vital organic constructions are supplied. And back, the gene dosage speculation is addressed and even supposing the majority of chromosome 21 gene items is unchanged in fetal DS mind, a couple of particular chromosome 21 encoded buildings together with transcription components are certainly overexpressed even if findings in fetal DS are diversified from these in grownup DS mind while Alzheimer-like neuropathology supervenes.

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Actin (43 kDa) ______to> - - - - - - - - - - _ _ _ _ _ - NSE (46 kDa) ______to> - ~~-----------~- Fig. 1. Western blot of four proteins (BACH1, ERG, SIM2, RUNX1) in frontal cortex of patients with DS, AD and controls. S% homogeneous gel and transferred onto PVDF membranes. The membranes were immunoreacted with primary and secondary antibody as described in "materials and methods", and specific immunoreactive band (BACH1, 81kDa; ERG, 80kDa; SIM2, 40kDa; RUNX1, SOkDa; Actin, 43kDa, NSE, 46kDa) were detected Aberrant protein expression of transcription factors BACH1 and ERG 43 Table 1.

Of the seven chromosome 21 encoded proteins evaluated here, five showed gene dosage-related increases in 4-6 (or 12) month mouse brain and two, Ets2 and, surprisingly, Sod1, showed no increases. , 2003a,b; see also Engidawok and Lubec, 2003, for some summaries). Indeed, a review of the literature shows that data on overexpression are frequently conflicting. Possible causes for differences among experiments include the use of RNA vs protein, mouse vs human samples, adult vs fetal brain, and whole brain vs different brain regions vs cell lines.

Together with the location on chromosome 21 of the MAPK-relevant genes listed in Table 2, these data support the hypothesis that perturbation of this pathway may contribute to the cognitive phenotype of DS. Ca1cineurin is a Ca2 +/calmodulin-dependent serine-threonine protein phosphatase. , 2001). , 1998). , 1999). , 2003). MAP Kinase and chromosome 21 genes MAPK pathways are activated by stimuli that include binding of growth factors to receptor tyrosine kinases followed by endocytosis. Initial MAPK Chr 17 Chr 10 Chr 16;Ts650Dn Chr 16; +Ts65Dn, -Ts1Cje Chr 16; + Ts65Dn, +Ts1Cje Mouse genomic region U2AF1 C21orf70 ADAR2 PCBP3 SFRS15 C21orf66 RBMll RNA Processing UBE2G2 SMT3H1 CBS DNMT3L SCL19A1 FrCD HRMT1L1 ITGB2 S100~ TRPC7 DSCR1 PCP4 C21orf25 APP, SOD1 APP TIAM1 GABPA SYNJ1, ITSN DYRK1A DSCR1, RUNX1, ETS2 USP16 N6AMT1 RIP140 RIP140 USP25 Methylation Cal CaN MAP kinase/ Endocytosis Ubiquitin Proteasome JAM2 CLDN17 CLDN8 CLDN14 CXADR Cell adhesionffight junctions Table 2.

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