ArticleCell death & disease2022
Anti-apoptotic HAX-1 suppresses cell apoptosis by promoting c-Abl kinase-involved ROS clearance.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025Pooled it
- HAX1 Promotes Hepatocellular Carcinoma Progression by Inhibiting Ferroptosis Through Modulation of Iron Homeostasis and the GSH/GPX4 Pathway.International journal of molecular sciences · 2026Article
- The pro-apoptotic GZMB and anti-apoptotic HAX-1 and DAD-1 genes and gene proteins in human right auricular tissue affected by coronary heart disease and aortic valve stenosis: a pilot study.Journal of molecular histology · 2026Article
- A multifunctional mitochondria-targeted nanoparticle for the effective treatment of dry eye disease via reactive oxygen species scavenging.Materials today. Bio · 2026Article
- Mechanically-adaptive, resveratrol-eluting neural probes for improved intracortical recording performance and stability.Npj flexible electronics · 2025Article
- HAX1-Overexpression Augments Cardioprotective Efficacy of Stem Cell-Based Therapy Through Mediating Hippo-Yap Signaling.Stem cell reviews and reports · 2024Article
- Article
- Myeloid leukemia factor 1: A "double-edged sword" in health and disease.Frontiers in oncology · 2023Review
- Brain-protective mechanisms of autophagy associated circRNAs: Kick starting self-cleaning mode in brain cellsFrontiers in molecular neuroscience · 2022Review
- DHCR24 in Tumor Diagnosis and Treatment: A Comprehensive Review.Technology in cancer research & treatmentReview
Corrections and comments
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Authors and funding
22 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-apoptotic protein HAX-1 has been proposed to modulate mitochondrial membrane potential, calcium signaling and actin remodeling. HAX-1 mutation or deficiency results in severe congenital neutropenia (SCN), loss of lymphocytes and neurological impairments by largely unknown mechanisms. Here, we demonstrate that the activation of c-Abl kinase in response to oxidative or genotoxic stress is dependent on HAX-1 association. Cellular reactive oxygen species (ROS) accumulation is inhibited by HAX-1-dependent c-Abl activation, which greatly contributes to the antiapoptotic role of HAX-1 in stress. HAX-1 (Q190X), a loss-of-function mutant responsible for SCN, fails to bind with and activate c-Abl, leading to dysregulated cellular ROS levels, damaged mitochondrial membrane potential and eventually apoptosis. The extensive apoptosis of lymphocytes and neurons in Hax-1-deficient mice could also be remarkably suppressed by c-Abl activation. These findings underline the important roles of ROS clearance in HAX-1-mediated anti-apoptosis by c-Abl kinase activation, providing new insight into the pathology and treatment of HAX-1-related hereditary disease or tumorigenesis.
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