Identification of the porcine homologous of human disease causing trinucleotide repeat sequences. (Q52840349)

8 May 2018

title

Identification of the porcine homologous of human disease causing trinucleotide repeat sequences. (English)

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8 May 2018

author

Merete Fredholm

5

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8 May 2018

Anders Nielsen

7

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8 May 2018

Bo Thomsen

object named as

Bo Thomsen

2

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Christian Bendixen

4

object named as

Christian Bendixen

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8 May 2018

Lone Bruhn Madsen

1

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8 May 2018

Christina Ane Elisabeth Sølvsten

3

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8 May 2018

Arne Lund Jørgensen

6

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8 May 2018

publication date

22 May 2007

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8 May 2018

published in

Neurogenetics

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8 May 2018

volume

8

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8 May 2018

issue

3

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8 May 2018

page(s)

207-218

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8 May 2018

https://scigraph.springernature.com/pub.10.1007/s10048-007-0088-y

exact match

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cites work

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A role for selection in regulating the evolutionary emergence of disease-causing and other coding CAG repeats in humans and mice.

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CAG repeat instability at SCA2 locus: anchoring CAA interruptions and linked single nucleotide polymorphisms

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Expansion of a novel CAG trinucleotide repeat in the 5' region of PPP2R2B is associated with SCA12.

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Genomic context drives SCA7 CAG repeat instability, while expressed SCA7 cDNAs are intergenerationally and somatically stable in transgenic mice

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Antisense transcription and heterochromatin at the DM1 CTG repeats are constrained by CTCF.

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Trinucleotide repeats (CGG)22TGG(CGG)43TGG(CGG)21 from the fragile X gene remain stable in transgenic mice.

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Expansion of an unstable trinucleotide CAG repeat in spinocerebellar ataxia type 1.

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Duplication of Atxn1l suppresses SCA1 neuropathology by decreasing incorporation of polyglutamine-expanded ataxin-1 into native complexes

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12 December 2020

Molecular architecture of CAG repeats in human disease related transcripts

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12 December 2020

10.1007/S10048-007-0088-Y

Identifiers

DOI

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8 May 2018

1 reference

8 May 2018