ArticleGenes & development2012
Endoplasmic reticulum protein BI-1 regulates Ca²⁺-mediated bioenergetics to promote autophagy.
Article in Genes & development, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
45 citing papers in PubMed, 86 citations in OpenAlex.
- P3/P3N-PIPO of PVY interacting with BI-1 inhibits the degradation of NIb by ATG6 to facilitate virus replication inFrontiers in plant science · 2023Article
- Transmembrane BAX inhibitor motif containing 6 suppresses presenilin-2 to preserve mitochondrial integrity after myocardial ischemia-reperfusion injury.International journal of biological sciences · 2023Article
- Canonical and Noncanonical ER Stress-Mediated Autophagy Is a Bite the Bullet in View of Cancer Therapy.Cells · 2022Review
- Pregnancy-associated plasma protein-aa regulates endoplasmic reticulum-mitochondria associations.eLife · 2021Article
- TMBIM6 (transmembrane BAX inhibitor motif containing 6) enhances autophagy through regulation of lysosomal calcium.Autophagy · 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
- Intersecting roles of ER stress, mitochondrial dysfunction, autophagy, and calcium homeostasis in HIV-associated neurocognitive disorder.Journal of neurovirology · 2020Review
- Linking Biochemical and Structural States of SERCA: Achievements, Challenges, and New Opportunities.International journal of molecular sciences · 2020Review
- BAX inhibitor-1: between stress and survival.The FEBS journal · 2020Review
- CACNA1H downregulation induces skeletal muscle atrophy involving endoplasmic reticulum stress activation and autophagy flux blockade.Cell death & disease · 2020Article
- Bax inhibitor 1 preserves mitochondrial homeostasis in acute kidney injury through promoting mitochondrial retention of PHB2.Theranostics · 2020Article
- Status of VEGF in preeclampsia and its effect on endoplasmic reticulum stress in placental trophoblast cells.European journal of obstetrics & gynecology and reproductive biology: X · 2019Article
- Ion and pH Sensitivity of a TMBIM CaStructure (London, England : 1993) · 2019Article
- The Best for the Most Important: Maintaining a Pristine Proteome in Stem and Progenitor Cells.Stem cells international · 2019Review
- Mitochondrial quality control mechanisms as molecular targets in cardiac ageing.Nature reviews. Cardiology · 2018Review
- Applications of Ruthenium Complex in Tumor Diagnosis and Therapy.Frontiers in pharmacology · 2018Review
- BCL-2 family: integrating stress responses at the ER to control cell demise.Cell death and differentiation · 2017Review
- Plant Bax Inhibitor-1 interacts with ATG6 to regulate autophagy and programmed cell death.Autophagy · 2017Article
- TMBIM-mediated CaBiochimica et biophysica acta. Molecular cell research · 2017Review
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 1 country.
Funding
Abstract
Autophagy is a lysosomal degradation pathway that converts macromolecules into substrates for energy production during nutrient-scarce conditions such as those encountered in tumor microenvironments. Constitutive mitochondrial uptake of endoplasmic reticulum (ER) Ca²⁺ mediated by inositol triphosphate receptors (IP₃Rs) maintains cellular bioenergetics, thus suppressing autophagy. We show that the ER membrane protein Bax inhibitor-1 (BI-1) promotes autophagy in an IP₃R-dependent manner. By reducing steady-state levels of ER Ca²⁺ via IP₃Rs, BI-1 influences mitochondrial bioenergetics, reducing oxygen consumption, impacting cellular ATP levels, and stimulating autophagy. Furthermore, BI-1-deficient mice show reduced basal autophagy, and experimentally reducing BI-1 expression impairs tumor xenograft growth in vivo. BI-1's ability to promote autophagy could be dissociated from its known function as a modulator of IRE1 signaling in the context of ER stress. The results reveal BI-1 as a novel autophagy regulator that bridges Ca²⁺ signaling between ER and mitochondria, reducing cellular oxygen consumption and contributing to cellular resilience in the face of metabolic stress.
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Registered trials
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.