New Lmna knock-in mice provide a molecular mechanism for the 'segmental aging' in Hutchinson-Gilford progeria syndrome.
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Nuclear lamins and neurobiology.Mice that express farnesylated versions of prelamin A in neurons develop achalasia.Longitudinal epigenetic and gene expression profiles analyzed by three-component analysis reveal down-regulation of genes involved in protein translation in human aging.Nuclear lamina remodelling and its implications for human disease.MicroRNAs in hereditary and sporadic premature aging syndromes and other laminopathies.Disrupting the LINC complex in smooth muscle cells reduces aortic disease in a mouse model of Hutchinson-Gilford progeria syndrome
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New Lmna knock-in mice provide a molecular mechanism for the 'segmental aging' in Hutchinson-Gilford progeria syndrome.
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New Lmna knock-in mice provide ...... son-Gilford progeria syndrome.
@en
New Lmna knock-in mice provide ...... son-Gilford progeria syndrome.
@nl
type
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New Lmna knock-in mice provide ...... son-Gilford progeria syndrome.
@en
New Lmna knock-in mice provide ...... son-Gilford progeria syndrome.
@nl
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New Lmna knock-in mice provide ...... son-Gilford progeria syndrome.
@en
New Lmna knock-in mice provide ...... son-Gilford progeria syndrome.
@nl
P2093
P2860
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New Lmna knock-in mice provide ...... son-Gilford progeria syndrome.
@en
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Angelica Tatar
Chika Nobumori
Hea-Jin Jung
Loren G Fong
Shao H Yang
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P304
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10.1093/HMG/DDT537
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2013-11-07T00:00:00Z