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 components of Down Syndrome (DS). a brand new promising animal version of DS is said and this opens new possibilities to review pathomechanisms and pharmacological ways because it is greater than tough to hold out reports in people and the medical good points are hugely variable. when it comes to biology, mobilephone cycle and stem mobilephone stories and by way of biochemistry, relevance of stories on a particular protein kinase, channels, transporters, superoxide dismutase, antioxidant process, chromosome meeting issue and different vital organic buildings are supplied. And back, the gene dosage speculation is addressed and even if the majority of chromosome 21 gene items is unchanged in fetal DS mind, a number of particular chromosome 21 encoded buildings 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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Extra resources for Advances in Down Syndrome Research
Acad Sci USA 98: 10439-10444 Costa RM, Federov NB, Kogan JH, Murphy GG, Stern J, Ohno M, Kucherlapati R, Jacks T, Silva AJ (2002) Mechanism for the learning deficits in a mouse model of neurofibromatosis type 1. Nature 415: 526-530 Cousin MA, Tan TC, Robinson PJ (2001) Protein phosphorylation is required for endocytosis in nerve terminals: potential role for the dephosphins dynamin I and synaptojanin, but not AP180 or amphiphysin. J Neurochem 76: 105116 Predicting pathway perturbations in Down syndrome 35 Crnic LS, Pennington BF (2000) Down syndrome: neuropsychology and animal models.
2002). These do not bind DNA directly but stimulate transcription by acetylating histones and/or recruiting 46 K. S. Shim et al. the RNA polymerase II transcription initiation complex. , 2001). , 1996). , 2002), suggesting a yet-unrecognized role for this TF in the mammalian nervous system. RUNX1 as well as SIM2 were also comparable to controls in brain of the fetal period of DS. g. , 1998; Sawa, 1999; Mazzola and Sirover, 2002). In our study results for DS were identical for DS frontal cortex but statistical significance disappeared for ERG in AD.
BACH1 in fetal DS brain, however, was overexpressed during the early second trimester of gestation and may be therefore involved in the development of AD like neuropathology later in life (Ferrando-Miguel and Lubec, 2003). ERG belongs to the ets gene family acting as a regulator of genes required for maintenance and/or differentiation of early hematopoietic and nonhematopoietic cells (Trojanowska, 2000). During development in the mouse, ERG expression has been detected in cells derived from mesoderm and in neuroectoderm by northern analysis (Maroulakaou and Bowe, 2000).
Advances in Down Syndrome Research by Y. Kazuki, T. C. Schulz, T. Shinohara, M. Kadota (auth.), Prof. Dr. G. Lubec (eds.)