Results 101 to 110 of about 2,950 (183)

Autophagic Removal of Farnesylated Carboxy-Terminal Lamin Peptides

open access: yesCells, 2018
The mammalian nuclear lamina proteins—prelamin A- and B-type lamins—are post-translationally modified by farnesylation, endoproteolysis, and carboxymethylation at a carboxy-terminal CAAX (C, cysteine; a, aliphatic amino acid; X, any amino ...
Xiang Lu, Karima Djabali
doaj   +1 more source

Progerin accumulation in human elderly skin biopsy sections.

open access: yes, 2013
A, Forehead skin section from a 69-year-old individual probed with anti-progerin antibody and counterstained with dapi. Bars correspond to 100 and 50 µm, respectively. B, Forehead skin section from a 93-year-old donor.
Desiree Ratner (82177)   +6 more
core   +1 more source

Healing of chromosomal breaks is impeded in cells expressing progerin

open access: yes
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare genetic condition characterized by features of accelerated aging, with a life expectancy of less than two decades. HGPS is commonly caused by a point mutation in the LMNA gene which codes for lamin A,
Alannah J. DiCintio   +4 more
core   +1 more source

Progerin expression disrupts critical adult stem cell functions involved in tissue repair

open access: yes, 2014
Vascular disease is one of the leading causes of death worldwide. Vascular repair, essential for tissue maintenance, is critically reduced during vascular disease and aging.
Gomez, Lourdes Adriana   +5 more
core   +1 more source

Endothelial progerin expression causes cardiovascular pathology through an impaired mechanoresponse

open access: yesJournal of Clinical Investigation, 2018
Hutchinson-Gilford progeria syndrome (HGPS) is a premature aging disorder characterized by accelerated cardiovascular disease with extensive fibrosis. It is caused by a mutation in LMNA leading to expression of truncated prelamin A (progerin) in the nucleus.
Osmanagic-Myers, Selma   +10 more
openaire   +3 more sources

Mechanotransduction of the vasculature in Hutchinson-Gilford Progeria Syndrome

open access: yesFrontiers in Physiology
Hutchinson-Gilford Progeria Syndrome (HGPS) is a premature aging disorder that causes severe cardiovascular disease, resulting in the death of patients in their teenage years.
Kevin L. Shores, George A. Truskey
doaj   +1 more source

Proximity-Labeling of Near Neighbors of Lamin A and Lamin A-Δ50 (PROGERIN). [PDF]

open access: yes, 2013
In an attempt to isolate and identify proteins that differentially interact with or locate near lamin A and progerin, we used a previously described method named BioID (proximity-dependent biotin identification).
Sabri, Mohammad
core   +1 more source

Hutchinson-Gilford Progeria Syndrome—Current Status and Prospects for Gene Therapy Treatment

open access: yesCells, 2019
Hutchinson-Gilford progeria syndrome (HGPS) is one of the most severe disorders among laminopathies—a heterogeneous group of genetic diseases with a molecular background based on mutations in the LMNA gene and genes coding for interacting proteins.
Katarzyna Piekarowicz   +3 more
doaj   +1 more source

Progerin accelerates atherosclerosis by inducing endoplasmic reticulum stress in vascular smooth muscle cells

open access: yesEMBO Molecular Medicine, 2019
Hutchinson–Gilford progeria syndrome (HGPS) is a rare genetic disorder caused by progerin, a mutant lamin A variant. HGPS patients display accelerated aging and die prematurely, typically from atherosclerosis complications. Recently, we demonstrated that
Magda R Hamczyk   +9 more
doaj   +1 more source

Progerin-Targeted Antisense Oligonucleotide Therapy

open access: yes
IPFS: QmW94cPPzxLcPj3qycSaBeJ673f2Jc7AMWCX8dcDHm2de1. TX: 0x331dbfaa95d67502fbc04ecac99feb026f1c466afddc12b78bb6be973e58e8ae. CC0.
openaire   +1 more source

Home - About - Disclaimer - Privacy