Postnatal lethality and cardiac anomalies in the Ts65Dn Down syndrome mouse model (Q46340910)

21 December 2017

title

Postnatal lethality and cardiac anomalies in the Ts65Dn Down syndrome mouse model (English)

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21 December 2017

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Clara S Moore

1

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21 December 2017

publication date

3 October 2006

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21 December 2017

number of pages

8

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inferred from page(s)

published in

Mammalian Genome

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21 December 2017

volume

17

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21 December 2017

page(s)

1005-1012

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21 December 2017

issue

10

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21 December 2017

https://scigraph.springernature.com/pub.10.1007/s00335-006-0032-8

exact match

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cites work

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Mice containing a human chromosome 21 model behavioral impairment and cardiac anomalies of Down's syndrome.

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A chromosome 21 critical region does not cause specific Down syndrome phenotypes.

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H2-haplotype-dependent unequal transmission of the 17(16) translocation chromosome from Ts65Dn females

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Longevity and mortality in Down's syndrome

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Poor outcome in Down syndrome fetuses with cardiac anomalies or growth retardation

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Cardiac morphology at late fetal stages in the mouse with trisomy 16: consequences for different formation of the atrioventricular junction when compared to humans with trisomy 21

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Aberrant right subclavian artery as a new cardiac sign in second- and third-trimester fetuses with Down syndrome.

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Mortality associated with Down's syndrome in the USA from 1983 to 1997: a population-based study

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An aneuploid mouse strain carrying human chromosome 21 with Down syndrome phenotypes

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Ts1Cje, a partial trisomy 16 mouse model for Down syndrome, exhibits learning and behavioral abnormalities

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12 December 2020

10.1007/S00335-006-0032-8

Identifiers

DOI

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21 December 2017

PubMed ID

17019652

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21 December 2017