Advances in Down Syndrome Research by Y. Kazuki, T. C. Schulz, T. Shinohara, M. Kadota (auth.),

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 study in different parts of Down Syndrome (DS). a brand new promising animal version of DS is suggested and this opens new possibilities to check pathomechanisms and pharmacological ways because it is greater than tough to hold out reports in people and the scientific positive factors are hugely variable. when it comes to biology, phone cycle and stem mobile reports and by way of biochemistry, relevance of reviews on a particular protein kinase, channels, transporters, superoxide dismutase, antioxidant process, chromosome meeting issue and different very important organic buildings 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 number of particular chromosome 21 encoded constructions together with transcription elements are certainly overexpressed even supposing findings in fetal DS are varied from these in grownup DS mind whilst Alzheimer-like neuropathology supervenes.

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Advances in Down Syndrome Research

"Advances in Down Syndrome study” represents up to date examine in numerous components of Down Syndrome (DS). a brand new promising animal version of DS is stated and this opens new possibilities to review pathomechanisms and pharmacological techniques because it is greater than tough to hold out reports in people and the medical positive factors are hugely variable.

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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.

1) '"0 ~ ~ '"0 (JQ S· ~ ('1) 26 K. Gardiner only inferred, such functional annotations are nevertheless usefui. Genes have been grouped in general categories, clearly representing a broad range of cellular processes, protein complexes and pathways. If expression levels of chromosome 21 genes are increased by 50% in DS, as much but not all data in the literature suggest, and depending upon mechanism, it is possible that many of these processes will be perturbed. Table 2 reorganizes subsets of the orthologous gene pairs according to location within chromosome 21 relative to homologous regions of mouse chromosomes 16, 17 and 10, and, importantly, relative to the trisomic regions of the mouse chromosome 16 segmental trisomy models of DS, Ts65Dn and Ts1Cje.

A series of transcription factors (TF) are encoded on chromosome 21 and are considered to play a pathogenetic role in DS. We therefore decided to study brain expression of TF encoded on chromosome 21 in patients with DS and AD compared to controls: Frontal cortex of 6 male DS patients, 6 male patients with AD and 6 male controls were used for the experiments. Immunoblotting was used to determine protein levels of TF BACH1, ERG, SIM2 and RUNX1. SIM2 and RUNX1 were comparable between groups, while BACH1 was significantly reduced in DS, and ERG was increased in DS and AD as compared to controls.

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