Results 71 to 80 of about 336,159 (263)
Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang +3 more
wiley +1 more source
Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley +1 more source
ABSTRACT Objective Super‐Refractory Status Epilepticus (SRSE) is a rare, life‐threatening neurological emergency with unclear etiology in many cases. Mitochondrial dysfunction, often due to disease‐causing genetic variants, is increasingly recognized as a cause, with each gene producing distinct pathophysiological mechanisms.
Pouria Mohammadi +2 more
wiley +1 more source
ALDOA Promotes Glycolysis and NLRP3/GSDMD Pyroptosis to Accelerate ALS Progression
ABSTRACT Objective Amyotrophic lateral sclerosis (ALS) is characterized by progressive motor neuron degeneration. Glycolytic dysregulation is implicated in disease progression, yet the underlying mechanisms remain unclear. This study investigates how Aldolase A (ALDOA) drives ALS progression through glycolysis‐mediated motor neuron pyroptosis.
Kaixin Yan +9 more
wiley +1 more source
Histopathological Evidence of Neurodegenerative Pathology in Epilepsy: A Systematic Review
ABSTRACT Epilepsy affects > 50 million people worldwide and is associated with a disproportionate burden of cognitive impairment. Emerging evidence suggests that neurodegenerative proteinopathies, particularly hyperphosphorylated tau (p‐tau) and amyloid‐β (Aβ), may contribute to cognitive dysfunction in people with epilepsy (PWE), even in the absence ...
Syeda Amrah Hashmi +7 more
wiley +1 more source
The molecular mechanism and evolutionary divergence of caspase 3/7-regulated gasdermin E activation
Caspase (CASP) is a family of proteases involved in cleavage and activation of gasdermin, the executor of pyroptosis. In humans, CASP3 and CASP7 recognize the same consensus motif DxxD, which is present in gasdermin E (GSDME).
Hang Xu +4 more
doaj +1 more source
A 3D Human Neuron‐on‐Chip Platform to Monitor Neuronal Injury Responses
This study presents a novel 3D Neuron‐on‐Chip model that can maintain human PSC‐derived excitatory prefrontal cortex neurons in 3D hydrogels and can be used to monitor neuronal injury responses over time. Results show injury‐induced acute neuronal excitotoxicity, declining neuronal connectivity, and the activation of a neurodegenerative, SASP‐like ...
Ruiping Tang +16 more
wiley +1 more source
Chen H, Dong Y, He X, Li J, Wang J. Drug Des Devel Ther. 2018;12:823–836. The authors have advised Figure 11D on page 833 is incorrect. Due to an error at the time of figure assembly Figure 10D and Figure 11D were duplicated.
Chen H, Dong Y, He X, Li J, Wang J
doaj
Caspase-9 swings both ways in the apoptosome
For nearly 2 decades, investigators have debated whether cysteinyl-aspartate-specific protease 9 (caspase-9) is activated within the apoptotic protease-activating factor 1 (Apaf-1) apoptosome through proximity-induced homodimerization or through ...
Chu-Chiao Wu, Shawn B. Bratton
doaj +1 more source
Caspase-9 Activation and Caspase Cleavage of tau in the Alzheimer's Disease Brain
Accumulating evidence supports a role for the activation of proteolytic enzymes, caspases, in the Alzheimer's disease (AD) brain. Neurons committed to apoptosis may do so through a mitochondrial pathway employing caspase-9 or through an alternative ...
Troy T. Rohn +5 more
doaj +1 more source

