Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Machine learning for predicting lifespan-extending chemical compounds Nuclear envelopathies: a complex LINC between nuclear envelope and pathology.Emerging candidate treatment strategies for Hutchinson-Gilford progeria syndrome.Autophagic Removal of Farnesylated Carboxy-Terminal Lamin Peptides.

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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2016 nî lūn-bûn

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2016 թուականին հրատարակուած գիտական յօդուած

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2016 թվականին հրատարակված գիտական հոդված

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2016年の論文

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2016年論文

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2016年論文

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2016年論文

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2016年論文

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2016年論文

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2016年论文

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

@ast

Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

@en

P2093

Diana Gabriel

http://www.w3.org/2001/XMLSchema#string

Leslie B Gordon

http://www.w3.org/2001/XMLSchema#string

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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

Protein quality control during aging involves recruitment of the macroautophagy pathway by BAG3

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome

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.

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

A biomarker that identifies senescent human cells in culture and in aging skin in vivo

Lamin A-dependent nuclear defects in human aging

53BP1: pro choice in DNA repair

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e0168988

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scholarly article

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10.1371/JOURNAL.PONE.0168988

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English

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http://www.w3.org/2001/XMLSchema#string

P478

http://www.w3.org/2001/XMLSchema#string

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Karima Djabali

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2016-12-29T00:00:00Z

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P698

28033363

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5199099

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Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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P2860

P2860

Temsirolimus Partially Rescues the Hutchinson-Gilford Progeria Cellular Phenotype

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P1433

P1476

P2093

P2860

P304

P31

P356

P407

P433

P478

P50

P577

P698

P932

P356

P1433

P1476

P2093

P2860

P304

P31

P356

P407

P433

P478

P50

P577

P698

P932