Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence. - Wikidata - awgldk - TriplyDB

Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence.

Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence.

http://www.wikidata.org/entity/Q53542805

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Role of endoplasmic reticulum stress in drug-induced toxicity New look at the role of progerin in skin aging Nuclear lamins and oxidative stress in cell proliferation and longevity Monoclonal antibodies specific for disease-associated point-mutants: lamin A/C R453W and R482W A pathway linking oxidative stress and the Ran GTPase system in progeria.Defective nuclear import of Tpr in Progeria reflects the Ran sensitivity of large cargo transport.Mitochondria, bioenergetics, and the epigenome in eukaryotic and human evolution Dynamics of lamin-A processing following precursor accumulation.Prelamin A accumulation and stress conditions induce impaired Oct-1 activity and autophagy in prematurely aged human mesenchymal stem cell Intermediate filaments take the heat as stress proteins.The posttranslational processing of prelamin A and disease.Oxidative stress accumulates in adipose tissue during aging and inhibits adipogenesis.Requirements for efficient proteolytic cleavage of prelamin A by ZMPSTE24.Inner nuclear membrane proteins: impact on human disease.HIV protease inhibitors elicit volume-sensitive Cl- current in cardiac myocytes via mitochondrial ROS.DNA repair defects and genome instability in Hutchinson-Gilford Progeria Syndrome.HIV protease inhibitors do not cause the accumulation of prelamin A in PBMCs from patients receiving first line therapy: the ANRS EP45 "aging" study Human lipodystrophies: genetic and acquired diseases of adipose tissue.Nuclear lamins: major factors in the structural organization and function of the nucleus and chromatin Mutations in LMNA modulate the lamin A--Nesprin-2 interaction and cause LINC complex alterations LMNA mutations induce a non-inflammatory fibrosis and a brown fat-like dystrophy of enlarged cervical adipose tissue.Familial partial lipodystrophy, Dunnigan variety - challenges for patient care during pregnancy: a case report.Proteomic profiling of adipose tissue from Zmpste24-/- mice, a model of lipodystrophy and premature aging, reveals major changes in mitochondrial function and vimentin processing.Energetics, epigenetics, mitochondrial genetics.Perturbation of nuclear lamin A causes cell death in chondrocytes.HIV protease inhibitors and nuclear lamin processing: getting the right bells and whistles.Sustained accumulation of prelamin A and depletion of lamin A/C both cause oxidative stress and mitochondrial dysfunction but induce different cell fates A Novel Lamin A Mutant Responsible for Congenital Muscular Dystrophy Causes Distinct Abnormalities of the Cell Nucleus.A potent HIV protease inhibitor, darunavir, does not inhibit ZMPSTE24 or lead to an accumulation of farnesyl-prelamin A in cells.Sp1 transcription factor interaction with accumulated prelamin a impairs adipose lineage differentiation in human mesenchymal stem cells: essential role of sp1 in the integrity of lipid vesicles.Till disassembly do us part: a happy marriage of nuclear envelope and chromatin.Prelamin A processing, accumulation and distribution in normal cells and laminopathy disorders.Antiretroviral-related adipocyte dysfunction and lipodystrophy in HIV-infected patients: Alteration of the PPARγ-dependent pathways Partial lipodystrophy with severe insulin resistance and adult progeria Werner syndrome.A Heterozygous ZMPSTE24 Mutation Associated with Severe Metabolic Syndrome, Ectopic Fat Accumulation, and Dilated Cardiomyopathy Detection of mesenchymal stem cells senescence by prelamin A accumulation at the nuclear level.Lipodystrophies: disorders of adipose tissue biology.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.Keratins Are Altered in Intestinal Disease-Related Stress Responses.The R439C mutation in LMNA causes lamin oligomerization and susceptibility to oxidative stress

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P2860

Human lipodystrophies linked to mutations in A-type lamins and to HIV protease inhibitor therapy are both associated with prelamin A accumulation, oxidative stress and premature cellular senescence.

http://www.wikidata.org/entity/Q53542805

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2007 nî lūn-bûn

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Human lipodystrophies linked t ...... premature cellular senescence.

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Human lipodystrophies linked t ...... premature cellular senescence.

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Human lipodystrophies linked t ...... premature cellular senescence.

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Human lipodystrophies linked t ...... premature cellular senescence.

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Auclair M

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10.1038/SJ.CDD.4402197

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