Results 81 to 90 of about 5,892 (251)
Progeria: Translational insights from cell biology [PDF]
, 2012 Cell biologists love to think outside the box, pursuing many surprising twists and unexpected turns in their quest to unravel the mysteries of how cells work. But can cell biologists think outside the bench? We are certain that they can, and clearly some
Cao, Kan +2 more
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Advanced Science, EarlyView.Programmable hydration pathways enable reconfigurable ionic thermoelectrics in polyquaternium hydrogels. By coupling microscopic solvation, mesoscale water channels, and macroscopic boundary control, hydration‐gated protonics decouples thermopower, response speed, and stability.
Zehao Zhao, Yun Shen, Dongyan Xu
wiley +1 more source
Hutchinson–Gilford Progeria Syndrome: Clinical and Molecular Characterization
The Application of Clinical Genetics, 2020 Harry Pachajoa,1,2 Angelica Claros-Hulbert,3,4 Ximena García-Quintero,3,4 Lina Perafan,1 Andres Ramirez,5 Andres F Zea-Vera6 1Faculty of Health Sciences, Congenital Anomalies and Rare Diseases Investigation Center (CIACER), Universidad Icesi, Cali,
Pachajoa H +5 more
doaj
Defective lamin A-Rb signaling in Hutchinson-Gilford Progeria Syndrome and reversal by farnesyltransferase inhibition. [PDF]
PLoS 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
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PDE4D and PDE3B orchestrate distinct cAMP microdomains in 3T3‐L1 adipocytes
British Journal of Pharmacology, EarlyView.Basal conditions: •Ins/PDE3B lowers cytoplasmic cAMP (cyt‐cAMP) without affecting plasma membrane cAMP (pm‐cAMP). •Insulin decreases lipid droplet cAMP (LD‐cAMP) independent of PDE3B. •FGF1/PDE4D modestly reduces both cyt‐ and pm‐cAMP, while PDE4D alone can modulate LD‐cAMP. ISO stimulation: •Ins/PDE3B has minimal impact on cyt‐cAMP.
Johannes Krier +9 more
wiley +1 more source
EMBO 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
Proteostasis of organelles in aging and disease
The FEBS Journal, EarlyView.Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi +5 more
wiley +1 more source
Cell Reports, 2014 Summary: Advanced age and DNA damage accumulation are prominent risk factors for cancer. The premature aging disorder Hutchinson-Gilford progeria syndrome (HGPS) provides a unique opportunity for studying the interplay between DNA damage and aging ...
Patricia Fernandez +5 more
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Hutchinson Gilford Progeria Syndrome: A Therapeutic Approach via Adenoviral Delivery of CRISPR/cas Genome Editing System [PDF]
, 2014 Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare human genetic disease caused by mutations in the LMNA gene. LMNA codes for structural components of the nuclear lamina. Alterations of nuclear lamina lead to a very variable class of diseases known as
ARANCIO, Walter +3 more
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Behind the scenes of the HGP [PDF]
Nature Genetics, 2003 Future geneticists will probably reflect on the Human Genome Project (HGP) as a milestone in their field. Perhaps it will be recognized alongside the chromosome theory of inheritance, the transforming material as DNA, the double helical structure for the genetic material and the cracking of the genetic code.
openaire +1 more source