Results 81 to 90 of about 13,017 (220)

Macrophage PABPC4‐SPP1 Axis Orchestrates Immunosuppression in Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
In the CRC microenvironment, macrophage PABPC4 binds to the 3′UTR of SPP1 mRNA to stabilize its expression, thereby sustaining M2‐like immunosuppressive macrophage polarization. Concurrently, this axis suppresses CD8+ T cell effector functions via CD44 signaling, collectively fostering an immunosuppressive niche that drives tumor progression.
Meng Wang   +14 more
wiley   +1 more source

Increased MLKL mRNA level in the PBMCs is correlated with autoantibody production, renal involvement, and SLE disease activity

open access: yesArthritis Research & Therapy, 2020
Background Necroptosis is a form of regulated necrosis that is involved in various autoimmune diseases. Mixed lineage kinase domain-like pseudokinase (MLKL) has been identified as a key executor of necroptosis; however, the significance of MLKL in ...
Mingjiao Zhang   +14 more
doaj   +1 more source

Leveraging ZBP1 signaling for cancer immunotherapy

open access: yesFrontiers in Cell Death
Immune checkpoint inhibitors (ICIs) have transformed cancer care, yet durable responses remain limited in a majority of patients. This is particularly true of immunologically cold tumors, which are characterized by insufficient T-cell infiltration, low ...
Parth Desai   +2 more
doaj   +1 more source

Lactylation‐Driven PROS1‐TYRO3‐CARF Signaling Promotes Therapy‐Induced Senescence Escape and Radioresistance in Meningioma

open access: yesAdvanced Science, EarlyView.
A glycolysis‐driven epigenetic switch promotes therapy resistance in meningioma. Increased lactate production enhances histone H3K27 lactylation, which activates PROS1 secretion. Secreted PROS1 engages TYRO3 signaling to degrade the senescence regulator CARF, allowing cancer cells to escape growth arrest.
Zhuohang Wang   +12 more
wiley   +1 more source

MLKL ubiquitylation: more than a makeover [PDF]

open access: yesCell Death & Differentiation, 2022
Weihong Wang, Yi-Nan Gong
openaire   +2 more sources

Non-Hematopoietic MLKL Protects Against Salmonella Mucosal Infection by Enhancing Inflammasome Activation

open access: yesFrontiers in Immunology, 2018
The intestinal mucosal barrier is critical for host defense against pathogens infection. Here, we demonstrate that the mixed lineage kinase-like protein (MLKL), a necroptosis effector, promotes intestinal epithelial barrier function by enhancing ...
Shui-Xing Yu   +13 more
doaj   +1 more source

MLKL deficiency alleviates neuroinflammation and motor deficits in the α-synuclein transgenic mouse model of Parkinson’s disease

open access: yesMolecular Neurodegeneration, 2023
Parkinson’s disease (PD), one of the most devastating neurodegenerative brain disorders, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and deposits of α-synuclein aggregates.
Lu Geng   +22 more
doaj   +1 more source

A Rare RIPK3 Variant Enhances Necroptosis and Promotes Inflammation in a Still Disease–Like Autoinflammatory Syndrome

open access: yesArthritis &Rheumatology, EarlyView.
Objective Still disease represents a prototypical polygenic systemic autoinflammatory disease, characterized by recurrent systemic inflammation and dysregulation of innate immunity. Despite extensive clinical characterization, familial clustering Still disease remains unreported.
Longfang Chen   +23 more
wiley   +1 more source

Human Monocytic Models Reveal Genotype‐Dependent Inflammatory Programs in VEXAS Syndrome

open access: yesArthritis &Rheumatology, Accepted Article.
Objectives VEXAS syndrome is a severe X‐linked autoinflammatory disorder caused by somatic mutations in ubiquitin‐like modifier activating enzyme 1 (UBA1), with clinical outcomes that vary by UBA1 genotype. We aimed to elucidate genotype‐specific inflammatory programs and identify potential therapeutic targets.
Kana Higashitani   +10 more
wiley   +1 more source

Thioredoxin-1 actively maintains the pseudokinase MLKL in a reduced state to suppress disulfide bond-dependent MLKL polymer formation and necroptosis [PDF]

open access: yesJournal of Biological Chemistry, 2017
Necroptosis is an immunogenic cell death program that is associated with a host of human diseases, including inflammation, infections, and cancer. Receptor-interacting protein kinase 3 (RIPK3) and its substrate mixed lineage kinase domain-like protein (MLKL) are required for necroptosis activation.
Eduardo Reynoso   +5 more
openaire   +2 more sources

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