ArticleThe Journal of biological chemistry2011
Enhanced lysosomal activity is involved in Bax inhibitor-1-induced regulation of the endoplasmic reticulum (ER) stress response and cell death against ER stress: involvement of vacuolar H+-ATPase (V-ATPase).
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Endoplasmic reticulum stress induced autophagy alters cellular processing of cationic lipid delivered siRNAs.Drug delivery and translational research · 2026Article
- The Emerging Roles of Vacuolar-Type ATPase-Dependent Lysosomal Acidification in Cardiovascular Disease.Biomolecules · 2025Review
- Article
- Innate immune and endoplasmic reticulum unfolded protein response pathways protectJournal of biosciences · 2025Article
- Resistance to Chemotherapeutic 5-Fluorouracil Conferred by Modulation of Heterochromatic Integrity through Ino80 Function in Fission Yeast.International journal of molecular sciences · 2023Article
- The V-ATPases in cancer and cell death.Cancer gene therapy · 2022Review
- Overexpression of V-ATPase B2 attenuates lung injury/fibrosis by stabilizing lysosomal membrane permeabilization and increasing collagen degradation.Experimental & molecular medicine · 2022Article
- Control of lysosomal-mediated cell death by the pH-dependent calcium channel RECS1.Science advances · 2021Article
- Breast Cancer Treatments: Updates and New Challenges.Journal of personalized medicine · 2021Review
- TMBIM6 (transmembrane BAX inhibitor motif containing 6) enhances autophagy through regulation of lysosomal calcium.Autophagy · 2021Article
- TMBIM6/BI-1 contributes to cancer progression through assembly with mTORC2 and AKT activation.Nature communications · 2020Article
- BAX inhibitor-1: between stress and survival.The FEBS journal · 2020Review
- The Function of V-ATPases in Cancer.Physiological reviews · 2016Review
- Bafilomycin A1 inhibits the growth and metastatic potential of the BEL-7402 liver cancer and HO-8910 ovarian cancer cell lines and induces alterations in their microRNA expression.Experimental and therapeutic medicine · 2015Article
- Obesity-Induced Inflammation Is Associated with Alterations in Subcellular Zinc Pools and Premature Mammary Gland Involution in Lactating Mice.The Journal of nutrition · 2015Article
- TMBIM protein family: ancestral regulators of cell death.Oncogene · 2015Review
- Article
- Article
- Bax inhibitor-1-mediated inhibition of mitochondrial Ca2+ intake regulates mitochondrial permeability transition pore opening and cell death.Scientific reports · 2014Article
- BAX inhibitor-1-associated V-ATPase glycosylation enhances collagen degradation in pulmonary fibrosis.Cell death & disease · 2014Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bax inhibitor-1 (BI-1) is an evolutionarily conserved protein that protects cells against endoplasmic reticulum (ER) stress while also affecting the ER stress response. In this study, we examined BI-1-induced regulation of the ER stress response as well as the control of the protein over cell death under ER stress. In BI-1-overexpressing cells (BI-1 cells), proteasome activity was similar to that of control cells; however, the lysosomal fraction of BI-1 cells showed sensitivity to degradation of BSA. In addition, areas and polygonal lengths of lysosomes were greater in BI-1 cells than in control cells, as assessed by fluorescence and electron microscopy. In BI-1 cells, lysosomal pH was lower than in control cells and lysosomal vacuolar H(+)-ATPase(V-ATPase), a proton pump, was activated, suggesting high H(+) uptake into lysosomes. Even when exposed to ER stress, BI-1 cells maintained high levels of lysosomal activities, including V-ATPase activity. Bafilomycin, a V-ATPase inhibitor, leads to the reversal of BI-1-induced regulation of ER stress response and cell death due to ER stress. In BI-1 knock-out mouse embryo fibroblasts, lysosomal activity and number per cell were relatively lower than in BI-1 wild-type cells. This study suggests that highly maintained lysosomal activity may be one of the mechanisms by which BI-1 exerts its regulatory effects on the ER stress response and cell death.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.