Results 111 to 120 of about 1,866,196 (278)

Macrophage Lamin A/C Regulates Inflammation and the Development of Obesity-Induced Insulin Resistance

open access: yesFrontiers in Immunology, 2018
Obesity-induced chronic low-grade inflammation, in particular in adipose tissue, contributes to the development of insulin resistance and type 2 diabetes. However, the mechanism by which obesity induces adipose tissue inflammation has not been completely
Youngjo Kim   +11 more
doaj   +1 more source

BCR::ABL1‐Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B‐ALL Cells to Enhancer‐Targeting Drugs

open access: yesAdvanced Science, EarlyView.
Ng et al. show that the BCR::ABL1 kinase that drives the lymphoid leukemia Ph+B‐ALL modulates enhancer function by coopting signaling‐inducible transcription factors such as MYC, STAT5, and ETV5. BCR::ABL1 thereby promotes the transcriptional program driving and defining this leukemia and renders Ph+B‐ALL cells hypersensitive to enhancer‐inhibiting ...
Han Leng Ng   +19 more
wiley   +1 more source

Ryanodine receptor remodeling in cardiomyopathy and muscular dystrophy caused by lamin A/C gene mutation.

open access: yesHuman Molecular Genetics, 2020
Mutations in the lamin A/C gene (LMNA), which encodes A-type lamins, cause several diseases called laminopathies, the most common of which is dilated cardiomyopathy with muscular dystrophy.
H. Dridi   +10 more
semanticscholar   +1 more source

Intracellular Aβ42 Sequestration by a Serine Protease Mitigates Neurotoxicity in a Drosophila Alzheimer's Disease Model

open access: yesAdvanced Science, EarlyView.
Emerging evidence suggests that intraneuronal Aβ accumulation represents an early pathogenic event in Alzheimer's disease (AD). Using Drosophila AD model, this study shows that a nonsecreted serine protease Yip7 physically interacts with Aβ. This causes intraneuronal Aβ accumulation but surprisingly reduces the associated neurotoxicity, arguing that ...
Jingyun Su   +4 more
wiley   +1 more source

Lamin Mutations Cause Increased YAP Nuclear Entry in Muscle Stem Cells

open access: yesCells, 2020
Mutations in the LMNA gene, encoding the nuclear envelope A-type lamins, are responsible for muscular dystrophies, the most severe form being the LMNA-related congenital muscular dystrophy (L-CMD), with severe defects in myonucleus integrity.
D. Owens   +6 more
semanticscholar   +1 more source

Context‐Dependent Role of GDF15: GDF15+ Tumor‐Associated Macrophages Suppress OSCC Progression by Enhancing Phagocytosis

open access: yesAdvanced Science, EarlyView.
This study identifies GDF15+ TAMs as a cell subset mediating tumor regression after immunotherapy. Macrophage‐intrinsic GDF15 enhances phagocytosis and antigen cross‐presentation to CD8+ T cells through the NF‐κB signaling pathway, thereby inhibiting tumor progression.
Xinyu Zhou   +9 more
wiley   +1 more source

In Vivo Assembly of a Dictyostelium Lamin Mutant Induced by Light, Mechanical Stress, and pH

open access: yesCells, 2020
We expressed Dictyostelium lamin (NE81) lacking both a functional nuclear localization signal and a CAAX-box for C-terminal lipid modification. This lamin mutant assembled into supramolecular, three-dimensional clusters in the cytosol that disassembled ...
Marianne Grafe   +4 more
doaj   +1 more source

Lamin A/C promotes DNA base excision repair.

open access: yesNucleic Acids Research, 2019
The A-type lamins (lamin A/C), encoded by the LMNA gene, are important structural components of the nuclear lamina. LMNA mutations lead to degenerative disorders known as laminopathies, including the premature aging disease Hutchinson-Gilford progeria ...
Scott Maynard   +9 more
semanticscholar   +1 more source

Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1–YAP Mechanotransduction

open access: yesAdvanced Science, EarlyView.
Progressive stiffening of the hepatic extracellular matrix and free fatty acid overload activate the mechanosensor Piezo1 in steatotic hepatocytes, inducing calcium influx and nuclear translocation of Yes‐associated protein. YAP‐dependent nuclear signaling further drives inflammatory and fibrotic gene programs, lipid metabolic reprogramming, and ...
Juan Ma   +15 more
wiley   +1 more source

NIBAN2/FLII/RREB1 Axis Drives Glioma Stem Cell Malignancy via TLR3 Pathway Activation

open access: yesAdvanced Science, EarlyView.
NIBAN2, highly expressed in glioma stem‐like cells (GSCs), assembles with FLII and transcription factor RREB1 to form a nuclear complex. This complex transcriptionally activates stemness‐associated genes (e.g., CD44, NANOG) and metabolic enzymes (e.g., LDHA), thereby sustaining both transcriptional and metabolic stemness programs.
Liang liang Shi   +14 more
wiley   +1 more source

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