ArticleThe Journal of biological chemistry2014
Competition through dimerization between antiapoptotic and proapoptotic HS-1-associated protein X-1 (Hax-1).
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Homologous expression and purification of human HAX-1 for structural studies.FEBS open bio · 2026Article
- HAX1 inhibits apoptosis and promotes maturation of neutrophils.Cell communication and signaling : CCS · 2025Article
- The type III secretion system effector EspO of enterohaemorrhagic Escherichia coli inhibits apoptosis through an interaction with HAX-1.Cellular microbiology · 2021Article
- Lamprey PHB2 maintains mitochondrial stability by tanslocation to the mitochondria under oxidative stress.Fish & shellfish immunology · 2020Article
- Synthesis and Antimicrobial Evaluation of 1,4-Naphthoquinone Derivatives as Potential Antibacterial Agents.ChemistryOpen · 2019Article
- 1,4-Naphthoquinone Analogues: Potent Antibacterial Agents and Mode of Action Evaluation.Molecules (Basel, Switzerland) · 2019Article
- Highly Flexible Electrospun Hybrid (Polyurethane/Dextran/Pyocyanin) Membrane for Antibacterial Activity via Generation of Oxidative Stress.ACS omega · 2018Article
- Epstein-Barr virus nuclear antigen EBNA-LP is essential for transforming naïve B cells, and facilitates recruitment of transcription factors to the viral genome.PLoS pathogens · 2018Article
- Abnormal expression of HAX‑1 is associated with cellular proliferation and migration in human hypopharyngeal squamous cell carcinoma.Molecular medicine reports · 2017Article
- Kostmann's Disease and HCLS1-Associated Protein X-1 (HAX1).Journal of clinical immunology · 2017Review
- Cardiac Specific Overexpression of Mitochondrial Omi/HtrA2 Induces Myocardial Apoptosis and Cardiac Dysfunction.Scientific reports · 2016Article
- Endoplasmic reticulum (ER) stress triggers Hax1-dependent mitochondrial apoptotic events in cardiac cells.Apoptosis : an international journal on programmed cell death · 2016Article
- Giant obscurins regulate the PI3K cascade in breast epithelial cells via direct binding to the PI3K/p85 regulatory subunit.Oncotarget · 2016Article
- Grb7 and Hax1 may colocalize partially to mitochondria in EGF-treated SKBR3 cells and their interaction can affect Caspase3 cleavage of Hax1.Journal of molecular recognition : JMR · 2016Article
- HAX1 deletion impairs BCR internalization and leads to delayed BCR-mediated apoptosis.Cellular & molecular immunology · 2016Article
- HAX1 regulates E3 ubiquitin ligase activity of cIAPs by promoting their dimerization.Oncotarget · 2014Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Studies on Hax-1 have mainly focused on variant (v) 1, demonstrating its antiapoptotic properties. However, HAX1 is heavily spliced, generating structurally distinct isoforms. We sought to characterize the Hax-1 isoforms expressed in rat heart before and after insult. We confirmed the presence of at least four Hax-1 transcripts in healthy rat cardiac muscle. These exhibited differential expression before and after induction of myocardial infarction, with v2 being up-regulated 12-fold at the transcript level and 1.5-fold at the protein level post-insult. Contrary to antiapoptotic rat and human v1, overexpression of rat v2 or human v4 (the human homologue of rat v2) in epithelial cells exacerbated cell death by 30% following H2O2 treatment compared with control vector. Coexpression of rat v1 and v2 or human v1 and v4 neutralized the protective effects of rat and human v1 and the proapoptotic effects of rat v2 and human v4 by modulating cytochrome c release. This is, at least partly, mediated by the ability of Hax-1 proteins to form homotypic and heterotypic dimers with binding affinities ranging from ~3.8 nm for v1 dimers to ~97 nm for v1/v2 dimers. The minimal binding region supporting these interactions lies between amino acids 97-278, which are shared by nearly all Hax-1 proteins, indicating that additional factors regulate the preferential formation of Hax-1 homo- or heterodimers. Our studies are the first to show that Hax-1 is a family of anti- and proapoptotic regulators that may modulate cell survival and death through homo- or heterodimerization.
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