Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome - sprookjes - yvandenbroek - TriplyDB

Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome

Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome

http://www.wikidata.org/entity/Q24562621

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The cell nucleus and aging: tantalizing clues and hopeful promises Three-dimensional maps of all chromosomes in human male fibroblast nuclei and prometaphase rosettes.The mutant form of lamin A that causes Hutchinson-Gilford progeria is a biomarker of cellular aging in human skin Dermal fibroblasts in Hutchinson-Gilford progeria syndrome with the lamin A G608G mutation have dysmorphic nuclei and are hypersensitive to heat stress The nuclear envelopathies and human diseases Emerin-prelamin A interplay in human fibroblasts Mammalian SUN protein interaction networks at the inner nuclear membrane and their role in laminopathy disease processes Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome Age-related changes of nuclear architecture in Caenorhabditis elegans Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome Hutchinson-Gilford progeria mutant lamin A primarily targets human vascular cells as detected by an anti-Lamin A G608G antibody.Phenotype and course of Hutchinson-Gilford progeria syndrome Exome sequencing and functional analysis identifies BANF1 mutation as the cause of a hereditary progeroid syndrome Blocking protein farnesylation improves nuclear shape abnormalities in keratinocytes of mice expressing the prelamin A variant in Hutchinson-Gilford progeria syndrome The epidemiology of premature aging and associated comorbidities Progerin and telomere dysfunction collaborate to trigger cellular senescence in normal human fibroblasts Model of human aging: recent findings on Werner's and Hutchinson-Gilford progeria syndromes A farnesyltransferase inhibitor prevents both the onset and late progression of cardiovascular disease in a progeria mouse model Lamin A-dependent nuclear defects in human aging Hallmarks of progeroid syndromes: lessons from mice and reprogrammed cells Epigenetics and aging Anchoring a Leviathan: How the Nuclear Membrane Tethers the Genome Molecular insights into the premature aging disease progeria Mouse models of laminopathies The nuclear envelope as a chromatin organizer Higher order chromatin organization in cancer Roles of endothelial A-type lamins in migration of T cells on and under endothelial layers.Nuclear pore proteins nup153 and megator define transcriptionally active regions in the Drosophila genome Lamina-associated polypeptide (LAP)2α and other LEM proteins in cancer biology Recent advances in understanding the role of lamins in health and disease Physiological and Pathological Aging Affects Chromatin Dynamics, Structure and Function at the Nuclear Edge New approaches for understanding the nuclear force balance in living, adherent cells Aging and radiation: bad companions Laminopathies and the long strange trip from basic cell biology to therapy Abnormal nuclear shape and impaired mechanotransduction in emerin-deficient cells Prelamin A farnesylation and progeroid syndromes Lamin A and ZMPSTE24 (FACE-1) defects cause nuclear disorganization and identify restrictive dermopathy as a lethal neonatal laminopathy Hutchinson-Gilford progeria syndrome: clinical findings in three patients carrying the G608G mutation in LMNA and review of the literature Potential therapeutic approaches for modulating expression and accumulation of defective lamin A in laminopathies and age-related diseases Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome

http://www.wikidata.org/entity/Q24562621

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Accumulation of mutant lamin A ...... nson-Gilford progeria syndrome

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Anne E Goldman

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Dale K Shumaker

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Leslie B Gordon

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Maria Eriksson

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Michael R Erdos

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Robert D Goldman

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Satya Khuon

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Yosef Gruenbaum

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P2860

Nuclear lamins: building blocks of nuclear architecture

Alteration of nuclear lamin organization inhibits RNA polymerase II-dependent transcription

Nuclear lamins A and B1: different pathways of assembly during nuclear envelope formation in living cells

Pathway of incorporation of microinjected lamin A into the nuclear envelope

An ectopic human XIST gene can induce chromosome inactivation in postdifferentiation human HT-1080 cells

Structural analysis of emerin, an inner nuclear membrane protein mutated in X-linked Emery-Dreifuss muscular dystrophy

The karyopherin Kap142p/Msn5p mediates nuclear import and nuclear export of different cargo proteins.

Recurrent de novo point mutations in lamin A cause Hutchinson-Gilford progeria syndrome

LMNA mutations in atypical Werner's syndrome

Protein kinase phosphorylation site sequences and consensus specificity motifs: tabulations

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