Results 71 to 80 of about 54,589 (273)

Lamin and the heart [PDF]

open access: yesHeart, 2017
Lamins A and C are intermediate filament nuclear envelope proteins encoded by the LMNA gene. Mutations in LMNA cause autosomal dominant severe heart disease, accounting for 10% of dilated cardiomyopathy (DCM). Characterised by progressive conduction system disease, arrhythmia and systolic impairment, lamin A/C heart disease is more malignant than other
Captur, Gabriella   +13 more
openaire   +4 more sources

USP4‐Dependent CHAF1B Stabilization Regulates Distinct SETDB1 Ubiquitin States Linked to AKT T308 Signaling and Lipogenic Remodeling in HCC

open access: yesAdvanced Science, EarlyView.
USP4 stabilizes CHAF1B by limiting K48‐linked ubiquitination. Stabilized CHAF1B supports UHRF1‐associated K63‐linked SETDB1 ubiquitination and cytoplasmic redistribution, whereas CHAF1B loss favors VHL‐dependent K11‐associated degradative ubiquitination and proteasomal loss of SETDB1.
Saiyan Bian   +9 more
wiley   +1 more source

PLOD1 Catalytic Activity Stabilizes ENO1 by Limiting FBXW7‐dependent Degradation to Promote Glycolysis and TMZ Resistance in Glioblastoma

open access: yesAdvanced Science, EarlyView.
PLOD1 interacts with ENO1 and limits its FBXW7‐dependent ubiquitination and proteasomal degradation through a mechanism requiring PLOD1 catalytic activity. ENO1 stabilization sustains glycolysis, promoting glioblastoma cell proliferation, migration, and temozolomide resistance.
Fen Xue   +4 more
wiley   +1 more source

The Putative Type III Secreted Chlamydia abortus Virulence-Associated Protein CAB063 Targets Lamin and Induces Apoptosis

open access: yesFrontiers in Microbiology, 2020
Since intracellular survival of all chlamydiae depends on the manipulation of the host cell through type III secreted effector proteins, their characterization is crucial for the understanding of chlamydial pathogenesis. We functionally characterized the
Miriam Theresia Marschall   +4 more
doaj   +1 more source

Ultrafast Micrometric Laser Structuring of Polymer Surfaces for Highly Organized Skeletal Muscle Tissue Modeling

open access: yesAdvanced Science, EarlyView.
Standard cell culture supports were functionalized by laser‐structuring to generate advanced topographies tailored to skeletal muscle tissue. The physicochemical modifications of the polymeric surfaces and their interactions with cells were thoroughly investigated, confirming both safety and effectiveness in guiding muscle cell organization.
Lucas Duvert   +10 more
wiley   +1 more source

Lamin A conformation modelling

open access: yes, 2019
Data in support of manuscript: "Lamin A molecular compression and sliding as mechanisms behind nucleoskeleton elasticity" Lamin A is a nuclear intermediate filament protein critical for nuclear architecture and mechanics and mutated in a wide range of ...
Rappsilber, Juri   +7 more
core   +1 more source

MPP8 Facilitates DNA DSB Repair via NHEJ to Promote Chemoresistance of TNBC Independent of Methyl‐H3K9 Binding

open access: yesAdvanced Science, EarlyView.
Chemoresistance is often linked to elevated DNA repair. MPP8 is found to promote breast cancer chemoresistance as a novel NHEJ accessory factor independent of its epigenetic functions. Through multiple protein interactions, MPP8 facilitates association of DNAPK and ligase complexes to promote DNA repair progression.
Rupa Kumari, Jia Fang
wiley   +1 more source

An investigation of emerin and nuclear lamins: : Interactions, distribution, and role in cell cycle regulation, in cells derived from EDMD patients. [PDF]

open access: yes, 2002
Emery Dreifuss muscular dystrophy (EDMD) is caused by mutations either in the gene encoding emerin or in the gene encoding A-type lamins (lamins A and C).
Maria, Choleza
core  

Aging of Hutchinson-Gilford progeria syndrome fibroblasts is characterised by hyperproliferation and increased apoptosis [PDF]

open access: yes, 2004
Hutchinson-Gilford progeria syndrome is a rare genetic disorder that mimics certain aspects of aging prematurely. Recent work has revealed that mutations in the lamin A gene are a cause of the disease.
Kill, IR   +3 more
core   +3 more sources

Age‐Related Lamin B1 Deficiency Activates SLC7A11‐Dependent Disulfidptosis to Impair Osteogenesis via Intercepting Mitochondrial Fission

open access: yesAdvanced Science, EarlyView.
This study reveals that age‐related LMNB1 deficiency in mesenchymal stem cells epigenetically upregulates SLC7A11, triggering actin disulfidptosis and mitochondrial dysfunction. This cascade impairs bone formation in senile osteoporosis. Furthermore, researchers identified the FDA‐approved drug naldemedine as a targeted SLC7A11 inhibitor to reverse ...
Wenhui Yu   +12 more
wiley   +1 more source

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