Results 91 to 100 of about 2,216,606 (233)

Hyperviscous Diabetic Bone Marrow Niche Impairs BMSCs Osteogenesis via TRPV2‐Mediated Cytoskeletal‐Nuclear Mechanotransduction

open access: yesAdvanced Science, EarlyView.
Diabetic bone marrow exhibits pathological ECM hyperviscosity that activates TRPV2‐mediated Ca2⁺ influx, leading to perinuclear F‐actin disassembly, nuclear deformation, and chromatin condensation. This cytoskeletal‐nuclear decoupling suppresses osteogenic differentiation of BMSCs.
Yao Wen   +8 more
wiley   +1 more source

Heterozygous frameshift variants in HNRNPA2B1 cause early-onset oculopharyngeal muscular dystrophy

open access: yesNature Communications, 2022
Missense variants in RNA-binding proteins underlie many diseases. Here the authors report an oculopharyngeal muscular dystrophy caused by heterozygous frameshift mutations in HNRNPA2B1 that alter its nucleocytoplasmic transport dynamics and result in ...
Hong Joo Kim   +57 more
doaj   +1 more source

Nuclear inclusion of nontargeted and chromatin-targeted polystyrene beads and plasmid DNA containing nanoparticles [PDF]

open access: yes, 2011
The nuclear membrane is one of the major cellular barriers in the delivery of plasmid DNA (pDNA). Cell division has a positive influence on the expression efficiency since, at the end of mitosis, pDNA or pDNA containing complexes near the chromatin are ...
De Smedt, Stefaan   +5 more
core   +1 more source

Lactylation‐Driven YTHDC1 Alleviates MASLD by Suppressing PTPN22‐Mediated Dephosphorylation of NLRP3

open access: yesAdvanced Science, EarlyView.
In MASLD, YTHDC1 undergoes increased lactylation and ubiquitination, reducing its expression. AARS1 mediates lactylation at lysine 565, while disrupted binding to LDHA further promotes lactylation, suppressing YTHDC1. This downregulation enhances PTPN22 mRNA stability, leading to NLRP3 dephosphorylation and activation, which exacerbates inflammation ...
Feng Zhang   +16 more
wiley   +1 more source

Spatiotemporal dynamics of nucleocytoplasmic transport

open access: yesPhysical Review Research
Nucleocytoplasmic transport is essential for cellular function, presenting a canonical example of rapid molecular sorting inside cells. It consists of a coordinated interplay between import/export of molecules in/out the cell nucleus.
S. Alex Rautu   +2 more
doaj   +1 more source

Mechanism of metabolic control. Target of rapamycin signaling links nitrogen quality to the activity of the Rtg1 and Rtg3 transcription factors. [PDF]

open access: yes, 2000
De novo biosynthesis of amino acids uses intermediates provided by the TCA cycle that must be replenished by anaplerotic reactions to maintain the respiratory competency of the cell. Genome-wide expression analyses in Saccharomyces cerevisiae reveal that
Barbet   +63 more
core   +3 more sources

Metabolic Reprogramming Driven by Trophoblasts and Decidual XCR1+PMN‐MDSC Crosstalk Controls Adverse Outcomes Associated With Advanced Maternal Age

open access: yesAdvanced Science, EarlyView.
The interaction between trophoblasts and decidual polymorphonuclear myeloid‐derived suppressor cells (dPMN‐MDSCs) via the XCL1–XCR1 axis is crucial for fetal development during the third trimester. Disruption of this axis impairs FOXO1 activity and causes metabolic imbalance in dPMN‐MDSCs, contributing to adverse outcomes associated with advanced ...
Meiqi Chen   +12 more
wiley   +1 more source

TDP-43 pathology disrupts nuclear pore complexes and nucleocytoplasmic transport in ALS/FTD

open access: yesAlzheimer's & Dementia, 2017
The cytoplasmic mislocalization and aggregation of TAR DNA-binding protein-43 (TDP-43) is a common histopathological hallmark of the amyotrophic lateral sclerosis and frontotemporal dementia disease spectrum (ALS/FTD).
Ching-Chieh Chou   +24 more
semanticscholar   +1 more source

Comparative interactomics analysis of different ALS-associated proteins identifies converging molecular pathways [PDF]

open access: yes, 2016
Amyotrophic lateral sclerosis (ALS) is a devastating neurological disease with no effective treatment available. An increasing number of genetic causes of ALS are being identified, but how these genetic defects lead to motor neuron degeneration and ...
Anink, Jasper J.   +17 more
core   +3 more sources

Engineered GM1 Intersects Between Mitochondrial and Synaptic Pathways to Ameliorate ALS Pathology

open access: yesAdvanced Science, EarlyView.
Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease driven by genetic and molecular disruptions affecting energy balance, protein homeostasis, and stress responses in nerve cells. Studies using human and rodent models identified convergent defects in mitochondria and synaptic function.
Federica Pilotto   +11 more
wiley   +1 more source

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