Results 51 to 60 of about 5,487 (200)

De HGP-write aux « super-cellules » [PDF]

open access: yesmédecine/sciences, 2018
The HGP-write project, announced in 2016 but not really implemented yet, comes back as a project aimed at constructing an “ultra-safe” human cell line fully resistant to virus infection and with other desirable characteristics. This involves introducing 400,000 changes in the genome and raises a number of technical and financial issues, but may become ...
openaire   +2 more sources

Vascular smooth muscle cell loss underpins the accelerated atherosclerosis in Hutchinson-Gilford progeria syndrome

open access: yesNucleus, 2019
Lamin A, a product of the LMNA gene, is an essential nuclear envelope component in most differentiated cells. Mutations in LMNA have been linked to premature aging disorders, including Hutchinson-Gilford progeria syndrome (HGPS).
Magda R. Hamczyk, Vicente Andrés
doaj   +1 more source

Epigenetic deregulation of lamina-associated domains in Hutchinson-Gilford progeria syndrome

open access: yesGenome Medicine, 2020
Background Hutchinson-Gilford progeria syndrome (HGPS) is a progeroid disease characterized by the early onset of age-related phenotypes including arthritis, loss of body fat and hair, and atherosclerosis. Cells from affected individuals express a mutant
Florian Köhler   +9 more
doaj   +1 more source

Defective lamin A-Rb signaling in Hutchinson-Gilford Progeria Syndrome and reversal by farnesyltransferase inhibition. [PDF]

open access: yesPLoS ONE, 2010
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare premature aging disorder caused by a de novo heterozygous point mutation G608G (GGC>GGT) within exon 11 of LMNA gene encoding A-type nuclear lamins.
Jackleen Marji   +8 more
doaj   +1 more source

Antisense-Based Progerin Downregulation in HGPS-Like Patients’ Cells [PDF]

open access: yesCells, 2016
Progeroid laminopathies, including Hutchinson-Gilford Progeria Syndrome (HGPS, OMIM #176670), are premature and accelerated aging diseases caused by defects in nuclear A-type Lamins. Most HGPS patients carry a de novo point mutation within exon 11 of the LMNA gene encoding A-type Lamins.
Harhouri, Karim   +9 more
openaire   +3 more sources

Direct reprogramming of human smooth muscle and vascular endothelial cells reveals defects associated with aging and Hutchinson-Gilford progeria syndrome

open access: yeseLife, 2020
Vascular dysfunctions are a common feature of multiple age-related diseases. However, modeling healthy and pathological aging of the human vasculature represents an unresolved experimental challenge. Here, we generated induced vascular endothelial cells (
Simone Bersini   +4 more
doaj   +1 more source

Inhibition of the NLRP3 inflammasome improves lifespan in animal murine model of Hutchinson–Gilford Progeria

open access: yesEMBO Molecular Medicine, 2021
Inflammation is a hallmark of aging and accelerated aging syndromes such as Hutchinson–Gilford progeria syndrome (HGPS). In this study, we present evidence of increased expression of the components of the NLRP3 inflammasome pathway in HGPS skin ...
Alvaro González‐Dominguez   +9 more
doaj   +1 more source

Targeting of NAT10 enhances healthspan in a mouse model of human accelerated aging syndrome. [PDF]

open access: yes, 2018
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, but devastating genetic disease characterized by segmental premature aging, with cardiovascular disease being the main cause of death.
Abrudan, Monica   +17 more
core   +2 more sources

Human Genome Project (HGP)

open access: yes, 2023
Human Genome Project by Genetic Manipulation   lecture for Agriculture, Biology, Botany, Zoology, Chemistry, Biotechnology, Microbiology, and Genetics Students by Salman Saeed Lecturer Botany University College of Management and Sciences Khanewal, Pakistan.
openaire   +1 more source

Organic Transistor‐Based Neuromorphic Electronics and Their Recent Applications

open access: yesSmall Methods, EarlyView.
This review highlights recent progress in organic neuromorphic electronics, showing how organic semiconductors enable synaptic and neuronal functions with low power, mechanical flexibility, and biocompatibility. By bridging materials, devices, and systems, organic platforms are accelerating brain‐inspired computing toward applications in artificial ...
Ziru Wang, Feng Yan
wiley   +1 more source

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