Results 71 to 80 of about 18,020 (210)

The Autophagy-Initiating Kinase ULK1 Controls RIPK1-Mediated Cell Death

open access: yesCell Reports, 2020
Summary: Autophagy, apoptosis, and necroptosis are stress responses governing the ultimate fate of a cell. However, the crosstalk between these cellular stress responses is not entirely understood.
Wenxian Wu   +17 more
doaj   +1 more source

Safety, pharmacokinetics and target engagement of novel RIPK1 inhibitor SAR443060 (DNL747) for neurodegenerative disorders: Randomized, placebo‐controlled, double‐blind phase I/Ib studies in healthy subjects and patients

open access: yesClinical and Translational Science, 2022
RIPK1 is a master regulator of inflammatory signaling and cell death and increased RIPK1 activity is observed in human diseases, including Alzheimer’s disease (AD) and amyotrophic lateral sclerosis (ALS).
Maurits F. J. M. Vissers   +24 more
doaj   +1 more source

Akt and mTOR mediate programmed necrosis in neurons [PDF]

open access: yes, 2014
Necroptosis is a newly described form of regulated necrosis that contributes to neuronal death in experimental models of stroke and brain trauma. Although much work has been done elucidating initiating mechanisms, signaling events governing necroptosis ...
Degterev, A   +9 more
core   +1 more source

Targeting neutrophil extracellular traps in metabolic and immune niche: Nanomaterials for diabetes tissue regeneration

open access: yesBMEMat, EarlyView.
The effects of NETs on regeneration of various diabetic tissues, and strategies targeting NETs for diabetes tissue regeneration. In the diabetic environment, NETs undergo complex metabolic and immune reprogramming, leading to dynamic changes in antibacterial and proinflammatory functions, and affecting regeneration of multiple systemic tissues.
Xinyi Jiang   +6 more
wiley   +1 more source

RIPK1-dependent mitophagy: A novel mechanism to eliminate cells detached from the extracellular matrix

open access: yesMolecular & Cellular Oncology, 2018
For cancer cells to survive during extracellular matrix (ECM)-detachment, they must inhibit anoikis and rectify metabolic deficiencies that lead to the induction of non-apoptotic cell death.
Mark A. Hawk, Zachary T. Schafer
doaj   +1 more source

Poly-ubiquitination in TNFR1-mediated necroptosis [PDF]

open access: yes, 2016
Tumor necrosis factor (TNF) is a master pro-inflammatory cytokine, and inappropriate TNF signaling is implicated in the pathology of many inflammatory diseases.
Henning Walczak   +3 more
core   +3 more sources

TRAF6 regulates the abundance of RIPK1 and inhibits the RIPK1/RIPK3/MLKL necroptosis signaling pathway and affects the progression of colorectal cancer

open access: yesCell Death and Disease, 2023
Colorectal cancer cannot be completely cured at present, and it is still an important clinical medical problem. TRAF6 is highly expressed in many malignant tumors. However, the role of TRAF6 in colorectal cancer is still controversial, mainly because the
Penghang Lin   +9 more
doaj   +1 more source

The Impact of RIPK1 Kinase Inhibition on Atherogenesis: A Genetic and a Pharmacological Approach

open access: yesBiomedicines, 2022
RIPK1 (receptor-interacting serine/threonine-protein kinase 1) enzymatic activity drives both apoptosis and necroptosis, a regulated form of necrosis.
Pauline Puylaert   +8 more
doaj   +1 more source

The protein arginine methyltransferase PRMT1 ameliorates cerebral ischemia–reperfusion injury by suppressing RIPK1-mediated necroptosis and apoptosis

open access: yesActa Pharmaceutica Sinica B
Receptor-interacting protein kinase 1 (RIPK1) plays an essential role in regulating the necroptosis and apoptosis in cerebral ischemia-reperfusion (I/R) injury.
Tengfei Liu   +15 more
doaj   +1 more source

METTL14 Regulates Myocardial Infarction Progression via m6A‐Dependent Modulation of OTUD1‐Mediated Deubiquitination of DUSP6

open access: yesThe Kaohsiung Journal of Medical Sciences, EarlyView.
ABSTRACT Myocardial infarction (MI) is the most severe clinical manifestation of coronary artery diseases (CVD) and serves as a critical driver of sudden cardiac death and heart failure (HF). Its pathophysiology begins with the abrupt cessation of coronary blood flow, leading to severe ischemia and subsequent cardiomyocyte necrosis. This study aimed to
Cheng‐Cheng Wei   +2 more
wiley   +1 more source

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