ArticleScientific reports2016
HIV-1 gp120 induces type-1 programmed cell death through ER stress employing IRE1α, JNK and AP-1 pathway.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 48 citations in OpenAlex.
- HIV-1 Tat and gp120 as key drivers of neurodegeneration in the central nervous system.Frontiers in microbiology · 2026Review
- Curcumin-enhanced elvitegravir therapy mitigates neuroinflammation and cognitive deficits in EcoHIV mice.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- HIV-1 and methamphetamine co-treatment in primary human astrocytes: TAARgeting ER/UPR dysfunction.NeuroImmune pharmacology and therapeutics · 2024Article
- Infectious Diseases.Advances in neurobiology · 2024Review
- The role of GRP78/ATF6/IRE1 and caspase-3/Bax/Bcl2 signaling pathways in the protective effects of gallic acid against cadmium-induced liver damage in rats.Iranian journal of basic medical sciences · 2023Article
- PKR-like ER kinase (PERK) Haplotypes Are Associated with Depressive Symptoms in People with HIV.Journal of neurology and psychology · 2023Article
- HIV-1 gp120 Protein Activates Cyclin-Dependent Kinase 1, a Possible Link to Central Nervous System Cell Death.Viruses · 2022Article
- Enhanced HIV SOSIP Envelope yields in plants through transient co-expression of peptidyl-prolyl isomerase B and calreticulin chaperones and ER targeting.Scientific reports · 2022Article
- Article
- Review
- A Non-Canonical Role for IRE1α Links ER and Mitochondria as Key Regulators of Astrocyte Dysfunction: Implications in Methamphetamine use and HIV-Associated Neurocognitive Disorders.Frontiers in neuroscience · 2022Article
- The molecular mechanism of GADD153 in apoptosis of keloid fibroblasts exposed to botulinum toxin type A.Journal of cellular and molecular medicine · 2021Article
- Review
- Cal'MAM'ity at the Endoplasmic Reticulum-Mitochondrial Interface: A Potential Therapeutic Target for Neurodegeneration and Human Immunodeficiency Virus-Associated Neurocognitive Disorders.Frontiers in neuroscience · 2021Review
- Endoplasmic reticulum stress and autophagy in HIV-1-associated neurocognitive disorders.Journal of neurovirology · 2020Review
- From Entry to Egress: Strategic Exploitation of the Cellular Processes by HIV-1.Frontiers in microbiology · 2020Review
- Update on the role of endoplasmic reticulum stress in asthma.American journal of translational research · 2020Review
- Type I interferons and endoplasmic reticulum stress in health and disease.International review of cell and molecular biology · 2020Review
- Friends Turn Foe-Astrocytes Contribute to Neuronal Damage in NeuroAIDS.Journal of molecular neuroscience : MN · 2019Review
- HIV-1 infection alters energy metabolism in the brain: Contributions to HIV-associated neurocognitive disorders.Progress in neurobiology · 2019Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The ER stress-mediated apoptosis has been implicated in several neurodegenerative diseases; however, its role in HIV/neuroAIDS remains largely unexplored. The present study was undertaken to assess the involvement and detailed mechanism of IRE1α pathway in HIV-1 gp120-mediated ER stress and its possible involvement in cell death. Various signaling molecules for IRE1α pathway were assessed using SVGA cells, primary astrocytes and gp120 transgenic mice, which demonstrated gp120-mediated increase in phosphorylated JNK, XBP-1 and AP-1 leading to upregulation of CHOP. Furthermore, HIV-1 gp120-mediated activation of IRE1α also increased XBP-1 splicing. The functional consequence of gp120-mediated ER stress was determined via assessment of gp120-mediated cell death using PI staining and MTT assay. The gp120-mediated cell death also involved caspase-9/caspase-3-mediated apoptosis. These findings were confirmed with the help of specific siRNA for IRE1α, JNK, AP-1, BiP and CHOP showing significant reduction in gp120-mediated CHOP expression. Additionally, silencing all the intermediates also reduced the gp120-mediated cell death and caspase-9/caspase-3 activation at differential levels. This study provides ER-stress as a novel therapeutic target in the management of gp120-mediated cell death and possibly in the treatment of neuroAIDS.
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Registered trials
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