Results 71 to 80 of about 18,314 (233)

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

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

NEMO regulates a cell death switch in TNF signaling by inhibiting recruitment of RIPK3 to the cell death-inducing complex II [PDF]

open access: yes, 2016
Incontinentia Pigmenti (IP) is a rare X-linked disease characterized by early male lethality and multiple abnormalities in heterozygous females. IP is caused by NF-κB essential modulator (NEMO) mutations.
Draber, P   +4 more
core   +1 more source

Harnessing ferroptosis from multilayer defense networks to nanoplatforms for specific cancer therapy

open access: yesBMEMat, EarlyView.
Nanomaterials target metabolically‐regulated ferroptosis for cancer therapy. Iron‐based or alternative nanoplatforms integrate ferroptosis with chemotherapy, immunotherapy, or radiotherapy. They enable stimulus‐responsive therapies (photothermal, photodynamic, sonodynamic) activated by near‐infrared, light, or ultrasound, achieving potent synergistic ...
Xinyue Xu   +5 more
wiley   +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

Connexins : substrates and regulators of autophagy [PDF]

open access: yes, 2016
Connexins mediate intercellular communication by assembling into hexameric channel complexes that act as hemichannels and gap junction channels. Most connexins are characterized by a very rapid turn-over in a variety of cell systems.
Bultynck, Geert   +4 more
core   +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

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

SUMOylation regulates tumorigenesis and progression: Molecular mechanisms and therapeutic applications

open access: yesInterdisciplinary Medicine, EarlyView.
SUMOylation, a dynamic post‐translational modification, acts as a master regulator at the heart of tumor malignancy. Our work delineates how the SUMOylation cycle—mediated by E1/E2/E3 enzymes and reversed by SENPs—orchestrates multiple hallmarks of cancer. The central pathway converges on three critical pathological axes: 1.
Yimao Wu   +6 more
wiley   +1 more source

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