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Developmental defects in trisomy 21 and mouse models.

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TLDR
The main phenotypic alterations occurring during the development of patients with T21 and the developmental abnormalities observed in mouse models are described, and phenotypes common to both species are investigated.
Abstract
Aneuploidies have diverse phenotypic consequences, ranging from mental retardation and developmental abnormalities to susceptibility to common phenotypes and various neoplasms. This review focuses on the developmental defects of murine models of a prototype human aneuploidy: trisomy 21 (Down syndrome, DS, T21). Murine models are clearly the best tool for dissecting the phenotypic consequences of imbalances that affect single genes or chromosome segments. Embryos can be studied freely in mice, making murine models particularly useful for the characterization of developmental abnormalities. This review describes the main phenotypic alterations occurring during the development of patients with T21 and the developmental abnormalities observed in mouse models, and investigates phenotypes common to both species.

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Journal ArticleDOI

DYRK1A and DYRK3 Promote Cell Survival through Phosphorylation and Activation of SIRT1

TL;DR: These findings provide a novel mechanism by which two anti-apoptotic DYRK members promote cell survival through direct modification of SIRT1, an NAD+-dependent protein deacetylase that is essential in a variety of physiological processes including stress response and energy metabolism.
Journal ArticleDOI

Communication breaks-Down: From neurodevelopment defects to cognitive disabilities in Down syndrome

TL;DR: The potential mechanisms by which defects in neurogenesis and neurodegenerative processes lead to altered formation of neural circuits and impair cognitive function are discussed, in connection with findings on pharmacological treatments of potential benefit for DS.
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Aneuploidy: From a Physiological Mechanism of Variance to Down Syndrome

TL;DR: This review focuses on Down syndrome as the prototype of "genomic disorder" induced by copy number change and the role of genome-altering processes in the generation of diversity in DS neural phenotypes, focusing on the impact of trisomy on brain structure and mental retardation.
Journal ArticleDOI

The Protein Kinase DYRK1A Regulates Caspase-9-Mediated Apoptosis during Retina Development

TL;DR: The data suggest a model in which dysregulation of the apoptotic response in differentiating neurons participates in the neuropathology of diseases that display DYRK1A gene-dosage imbalance effects, such as Down's syndrome.
References
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Book Chapter

A Quantitative Analysis

Journal ArticleDOI

Down syndrome phenotypes: the consequences of chromosomal imbalance

TL;DR: Evidence is provided for a significant contribution of genes outside the D21S55 region to the DS phenotypes, including the facies, microcephaly, short stature, hypotonia, abnormal dermatoglyphics, and mental retardation, which strongly suggests DS is a contiguous gene syndrome and augurs against a single DS chromosomal region responsible for most of the phenotypic features.
Journal ArticleDOI

NFAT dysregulation by increased dosage of DSCR1 and DYRK1A on chromosome 21

TL;DR: It is suggested that the 1.5-fold increase in dosage of DSCR1 and DYRK1A cooperatively destabilizes a regulatory circuit, leading to reduced NFATc activity and many of the features of Down's syndrome, and the destabilization of regulatory circuits can underlie human disease.
Journal ArticleDOI

Chromosome 21 and down syndrome: from genomics to pathophysiology.

TL;DR: Comparative genomics is beginning to identify the functional components of the chromosome and that in turn will set the stage for the functional characterization of the sequences.
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