Results 31 to 40 of about 2,950 (183)

Correction to "The Activation of cGAS-STING Pathway Causes Abnormal Uterine Receptivity in Aged Mice". [PDF]

Aging Cell
Aging Cell, Volume 25, Issue 5, May 2026.
europepmc   +2 more sources

Identification of differential protein interactors of lamin A and progerin [PDF]

Nucleus, 2010
The nuclear lamina is an interconnected meshwork of intermediate filament proteins underlying the nuclear envelope. The lamina is an important regulator of nuclear structural integrity as well as nuclear processes, including transcription, DNA replication and chromatin remodeling. The major components of the lamina are A- and B-type lamins.
Kubben, N, Voncken, JW, Demmers, Jeroen, Calis, C, van Almen, G, Pinto, Y, Misteli, T   +6 more
openaire   +3 more sources

Progerin-expressing endothelial cells are unable to adapt to shear stress [PDF]

Biophysical Journal, 2021
Abstract Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare premature aging disease caused by a single-point mutation in the lamin A gene, resulting in a truncated and farnesylated form of lamin A. This mutant lamin A protein, known as progerin, accumulates at the periphery of the nuclear lamina, resulting in both an abnormal nuclear
Brooke E. Danielsson, Hannah C. Peters, Kranthi Bathula, Lindsay M. Spear, Natalie A. Noll, Kris N. Dahl, Daniel E. Conway   +6 more
openaire   +2 more sources

Oxidative stress-induced premature senescence and aggravated denervated skeletal muscular atrophy by regulating progerin–p53 interaction

Skeletal Muscle, 2022
Background Progerin elevates atrophic gene expression and helps modify the nuclear membrane to cause severe muscle pathology, which is similar to muscle weakness in the elderly, to alter the development and function of the skeletal muscles.
Yaoxian Xiang, Zongqi You, Xinying Huang, Junxi Dai, Junpeng Zhang, Shuqi Nie, Lei Xu, Junjian Jiang, Jianguang Xu   +8 more
doaj   +1 more source

Cardiomyocyte-Restricted Expression of Progerin Confers Cardiac Hypertrophy. [PDF]

Circ Res
Subati T, Buehler DP, Zhong L, Miller FJ, Agrawal V, Brown JD.   +5 more
europepmc   +4 more sources

Expression of progerin does not result in an increased mutation rate [PDF]

Chromosome Research, 2017
In the premature ageing disease Hutchinson-Gilford progeria syndrome (HGPS), the underlying genetic defect in the lamin A gene leads to accumulation at the nuclear lamina of progerin-a mutant form of lamin A that cannot be correctly processed. This has been reported to result in defects in the DNA damage response and in DNA repair, leading to the ...
Deniaud, Emmanuelle, Lemaitre, Charlene, Boyle, Shelagh, Bickmore, Wendy; id_orcid 0000-0001-6660-7735   +3 more
openaire   +3 more sources

ESCRT-III controls nuclear envelope deformation induced by progerin [PDF]

Scientific Reports, 2020
AbstractHutchinson-Gilford progeria syndrome (HGPS) is a premature aging disorder, caused by mutation in the gene encoding lamin A/C, which produces a truncated protein called progerin. In cells from HGPS patients, progerin accumulates at the nuclear membrane (NM), where it causes NM deformations. In this study, we investigated whether progerin-induced
Arii, Jun, Maeda, Fumio, Maruzuru, Yuhei, Koyanagi, Naoto, Kato, Akihisa, Mori, Yasuko, Kawaguchi, Yasushi   +6 more
openaire   +2 more sources

The Impact of Progerin on Genome Maintenance in Mammalian Cells [PDF]

, 2023
Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare genetic condition characterized by accelerated aging. The cause of HGPS is a point mutation in the LMNA gene, which encodes lamins A and the splice variant lamin C.
Joudeh, Liza Alexandra
core   +1 more source

progerin overexpression in C3h10 cells RNAseq.xls

, 2023
we overexpressed progerin in the C3H10 cell line and performed RNA sequencing analysis. 106 genes were down-regulated and 254 genes were up-regulated in progerin expressed cells with fold change greater than 1.5 and P-value less than 0.05, compared with ...
jinlong suo (15151015)
core   +1 more source

Progerin guilty of size discrimination [PDF]

Journal of Cell Biology, 2013
![Figure][1] Tpr (red) accumulates in the nuclei of cells from a healthy person (left), but it remains in the cytoplasm of cells from an HGPS patient (right). A mutant protein responsible for Hutchinson-Gilford Progeria syndrome (HGPS) bars large proteins from entering the nucleus ...
openaire   +1 more source