Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice.
about
When lamins go bad: nuclear structure and diseaseMouse models of laminopathiesCardiomyocyte-specific expression of lamin a improves cardiac function in Lmna-/- miceRecent advances in animal and human pluripotent stem cell modeling of cardiac laminopathyImplications and Assessment of the Elastic Behavior of Lamins in LaminopathiesThe cardiac conduction systemNuclear lamin A/C deficiency induces defects in cell mechanics, polarization, and migrationLMNA E82K mutation activates FAS and mitochondrial pathways of apoptosis in heart tissue specific transgenic miceThe effect of the lamin A and its mutants on nuclear structure, cell proliferation, protein stability, and mobility in embryonic cellsActivation of MAPK pathways links LMNA mutations to cardiomyopathy in Emery-Dreifuss muscular dystrophy.Sex-dependent gene regulatory networks of the heart rhythm.Intermediate filaments take the heat as stress proteins.Attenuated hypertrophic response to pressure overload in a lamin A/C haploinsufficiency mouseAn accumulation of non-farnesylated prelamin A causes cardiomyopathy but not progeria.Lamin A/C and emerin regulate MKL1-SRF activity by modulating actin dynamicsLiver aging and pseudocapillarization in a Werner syndrome mouse model.Multistep ion channel remodeling and lethal arrhythmia precede heart failure in a mouse model of inherited dilated cardiomyopathy."Laminopathies": a wide spectrum of human diseases.Prelamin A and lamin A appear to be dispensable in the nuclear lamina.Lamin A/C haploinsufficiency causes dilated cardiomyopathy and apoptosis-triggered cardiac conduction system disease.Prelamin A, Zmpste24, misshapen cell nuclei, and progeria--new evidence suggesting that protein farnesylation could be important for disease pathogenesis.Activation of MAPK in hearts of EMD null mice: similarities between mouse models of X-linked and autosomal dominant Emery Dreifuss muscular dystrophy.Cellular mechanosensing: getting to the nucleus of it all.A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation.Investigating the purpose of prelamin A processingEmerin-lacking mice show minimal motor and cardiac dysfunctions with nuclear-associated vacuoles.Mice deleted for heart-type cytochrome c oxidase subunit 7a1 develop dilated cardiomyopathy.Nuclear lamins: key regulators of nuclear structure and activitiesMouse models of the laminopathies.Lamins at a glance.Nuclear mechanics in diseaseCAP2 in cardiac conduction, sudden cardiac death and eye development.Molecular genetics of autosomal-recessive axonal Charcot-Marie-Tooth neuropathies.Heuristic methods for finding pathogenic variants in gene coding sequences.Progerin elicits disease phenotypes of progeria in mice whether or not it is farnesylated.Targeting Mitogen-Activated Protein Kinase Signaling in Mouse Models of Cardiomyopathy Caused by Lamin A/C Gene MutationsMuscle development, regeneration and laminopathies: how lamins or lamina-associated proteins can contribute to muscle development, regeneration and disease.Adult stem cell maintenance and tissue regeneration in the ageing context: the role for A-type lamins as intrinsic modulators of ageing in adult stem cells and their niches.Disruption of nesprin-1 produces an Emery Dreifuss muscular dystrophy-like phenotype in mice.Epidermal expression of the truncated prelamin A causing Hutchinson-Gilford progeria syndrome: effects on keratinocytes, hair and skin
P2860
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P2860
Expression of an LMNA-N195K variant of A-type lamins results in cardiac conduction defects and death in mice.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh-hant
name
Expression of an LMNA-N195K va ...... ion defects and death in mice.
@en
Expression of an LMNA-N195K va ...... ion defects and death in mice.
@nl
type
label
Expression of an LMNA-N195K va ...... ion defects and death in mice.
@en
Expression of an LMNA-N195K va ...... ion defects and death in mice.
@nl
prefLabel
Expression of an LMNA-N195K va ...... ion defects and death in mice.
@en
Expression of an LMNA-N195K va ...... ion defects and death in mice.
@nl
P2093
P2860
P356
P1476
Expression of an LMNA-N195K va ...... ion defects and death in mice.
@en
P2093
Colin L Stewart
Jeffrey N Rottman
Leslie C Mounkes
Serguei V Kozlov
P2860
P304
P356
10.1093/HMG/DDI221
P577
2005-06-22T00:00:00Z