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Mammalian thioredoxin is a direct inhibitor of apoptosis signal‐regulating kinase (ASK) 1
TLDR
Evidence that Trx is a negative regulator of ASK1 suggests possible mechanisms for redox regulation of the apoptosis signal transduction pathway as well as the effects of antioxidants against cytokine‐ and stress‐induced apoptosis.
Induction of Apoptosis by ASK1, a Mammalian MAPKKK That Activates SAPK/JNK and p38 Signaling Pathways
TLDR
Overexpression of ASK1 induced apoptotic cell death, andASK1 was activated in cells treated with tumor necrosis factor-α, and TNF-α-induced apoptosis was inhibited by a catalytically inactive form of AsK1.
BCL-2 Is Phosphorylated and Inactivated by an ASK1/Jun N-Terminal Protein Kinase Pathway Normally Activated at G2/M
TLDR
Stress response kinases phosphorylate BCL-2 during cell cycle progression as a normal physiologic process to inactivate B CL-2 at G2/M.
ASK1 is essential for endoplasmic reticulum stress-induced neuronal cell death triggered by expanded polyglutamine repeats.
TLDR
It is suggested that ASK1 is a key element in ER stress-induced cell death that plays an important role in the neuropathological alterations in polyQ diseases.
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018
TLDR
An updated classification of cell death subroutines focusing on mechanistic and essential aspects of the process is proposed, and the utility of neologisms that refer to highly specialized instances of these processes are discussed.
Guidelines for the use and interpretation of assays for monitoring cell death in higher eukaryotes
TLDR
A nonexhaustive comparison of methods to detect cell death with apoptotic or nonapoptotic morphologies, their advantages and pitfalls is provided and the importance of performing multiple, methodologically unrelated assays to quantify dying and dead cells is emphasized.
Essential versus accessory aspects of cell death: recommendations of the NCCD 2015
TLDR
The Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death.
ROS-dependent activation of the TRAF6-ASK1-p38 pathway is selectively required for TLR4-mediated innate immunity
TLDR
It is shown that the reactive oxygen species–dependent TRAF6-ASK1-p38 axis is crucial for TLR4-mediated mammalian innate immunity and is resistant to lipopolysaccharide-induced septic shock.
Identification of type I receptors for osteogenic protein-1 and bone morphogenetic protein-4.
TLDR
Results suggest thatALK-3 and ALK-6 are type I receptors for OP-1 and BMP-4; in addition, ALk-2 is a type I receptor shared by activin and OP- 1, but not by B MP-4.
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