ArticleThe Journal of biological chemistry2012
The C terminus of Bax inhibitor-1 forms a Ca2+-permeable channel pore.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 91 citations in OpenAlex.
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- TMBIM-2 orchestrates systemic mitochondrial stress response via facilitating Ca2+ oscillations.The Journal of cell biology · 2025Article
- The BCL2 family: from apoptosis mechanisms to new advances in targeted therapy.Signal transduction and targeted therapy · 2025Review
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- Bax Inhibitor-1 preserves pancreatic β-cell proteostasis by limiting proinsulin misfolding and programmed cell death.Cell death & disease · 2024Article
- New Insights into the Regulation of mTOR Signaling via CaInternational journal of molecular sciences · 2023Review
- The regulatory mechanism and therapeutic potential of transcription factor EB in neurodegenerative diseases.CNS neuroscience & therapeutics · 2023Review
- TMBIM5 loss of function alters mitochondrial matrix ion homeostasis and causes a skeletal myopathy.Life science alliance · 2022Article
- Bcl-xL acts as an inhibitor of IPCell death and differentiation · 2022Article
- Ion Channels and Transporters in Autophagy.Autophagy · 2022Article
- Control of lysosomal-mediated cell death by the pH-dependent calcium channel RECS1.Science advances · 2021Article
- TMBIM6 (transmembrane BAX inhibitor motif containing 6) enhances autophagy through regulation of lysosomal calcium.Autophagy · 2021Article
- The Evolutionary Conserved Transmembrane BAX Inhibitor Motif (TMBIM) Containing Protein Family Members 5 and 6 Are Essential for the Development and Survival ofFrontiers in cell and developmental biology · 2021Article
- Integrated Proteomic and Transcriptomic Analyses Reveal the Roles ofFrontiers in microbiology · 2021Article
- The ER Stress/UPR Axis in Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis.Life (Basel, Switzerland) · 2020Review
- Structure and regulation of the BsYetJ calcium channel in lipid nanodiscs.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- TMBIM6/BI-1 contributes to cancer progression through assembly with mTORC2 and AKT activation.Nature communications · 2020Article
- Lessons from the Endoplasmic Reticulum CaCells · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bax inhibitor-1 (BI-1) is a multitransmembrane domain-spanning endoplasmic reticulum (ER)-located protein that is evolutionarily conserved and protects against apoptosis and ER stress. Furthermore, BI-1 is proposed to modulate ER Ca(2+) homeostasis by acting as a Ca(2+)-leak channel. Based on experimental determination of the BI-1 topology, we propose that its C terminus forms a Ca(2+) pore responsible for its Ca(2+)-leak properties. We utilized a set of C-terminal peptides to screen for Ca(2+) leak activity in unidirectional (45)Ca(2+)-flux experiments and identified an α-helical 20-amino acid peptide causing Ca(2+) leak from the ER. The Ca(2+) leak was independent of endogenous ER Ca(2+)-release channels or other Ca(2+)-leak mechanisms, namely translocons and presenilins. The Ca(2+)-permeating property of the peptide was confirmed in lipid-bilayer experiments. Using mutant peptides, we identified critical residues responsible for the Ca(2+)-leak properties of this BI-1 peptide, including a series of critical negatively charged aspartate residues. Using peptides corresponding to the equivalent BI-1 domain from various organisms, we found that the Ca(2+)-leak properties were conserved among animal, but not plant and yeast orthologs. By mutating one of the critical aspartate residues in the proposed Ca(2+)-channel pore in full-length BI-1, we found that Asp-213 was essential for BI-1-dependent ER Ca(2+) leak. Thus, we elucidated residues critically important for BI-1-mediated Ca(2+) leak and its potential channel pore. Remarkably, one of these residues was not conserved among plant and yeast BI-1 orthologs, indicating that the ER Ca(2+)-leak properties of BI-1 are an added function during evolution.
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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.