| 1994 |
Crystal structure of bovine mitochondrial F1-ATPase at 2.8 Å resolution revealed that the three catalytic β-subunits (ATP5F1B orthologs) differ in conformation and bound nucleotide, supporting a rotary catalytic mechanism in which the three catalytic subunits are in different states of the catalytic cycle at any instant, with interconversion achieved by rotation of the α3β3 subassembly relative to the γ-subunit. |
X-ray crystallography at 2.8 Å resolution |
Nature |
High |
8065448
|
| 1999 |
The β-subunit of ATP synthase (ATP5F1B) is present on the surface of human endothelial cells and functions as a binding protein for angiostatin; angiostatin binding to cell-surface ATP synthase α/β-subunits mediates its antiproliferative and antiangiogenic effects on endothelial cells. |
Ligand blot analysis, amino-terminal sequencing, peptide mass fingerprinting, immunologic analysis, flow cytometry, immunofluorescence, anti-subunit antibody inhibition of angiostatin antiproliferative effect |
Proceedings of the National Academy of Sciences of the United States of America |
High |
10077593
|
| 2003 |
The β-chain of ATP synthase (ATP5F1B) is ectopically expressed on the surface of hepatocytes and functions as a high-affinity receptor for apolipoprotein A-I (apoA-I), mediating HDL endocytosis; receptor stimulation by apoA-I triggers holo-HDL endocytosis via a mechanism strictly dependent on ADP generation by cell-surface ATP hydrolase activity. |
Biochemical receptor isolation, immunologic confirmation of ectopic localization, cell-surface ATP hydrolase activity assay, endocytosis assay with ATP synthase inhibitor in perfused rat liver ex vivo |
Nature |
High |
12511957
|
| 2011 |
miR-101 directly binds to the 3'UTR of ATP5F1B (ATP5B) mRNA and negatively regulates ATP5B protein expression; knockdown of ATP5B significantly inhibits HSV-1 replication, demonstrating that ATP5B functions as a pro-viral host factor for HSV-1. |
Luciferase 3'UTR reporter assay, siRNA knockdown, plaque assay, real-time PCR |
Antiviral research |
Medium |
21291913
|
| 2011 |
ATP5F1B (ATP5B) interacts with the calcium channel α2/δ1 subunit at the plasma membrane of developing myotubes, forming a functional signaling complex that accelerates the rate of decline of calcium transients, particularly during trains of stimulation pulses. |
FRET, coimmunoprecipitation, fluorescence imaging, calcium transient measurements in myotubes |
American journal of physiology. Cell physiology |
Medium |
21490313
|
| 2012 |
In a mouse model of multiple sclerosis (ND4 mice), the mRNA export factor REF undergoes loss of deimination (arginine-to-citrulline conversion), which impairs its binding strength to ATP5F1B mRNA and reduces ATP5B mRNA transport to mitochondria; pharmacological inhibition of deimination in PC12 cells reduced mitochondrial ATP synthase activity. |
mRNA binding assay, mRNA transport assay, ATP synthase activity assay after deimination inhibition |
EMBO reports |
Medium |
22261716
|
| 2016 |
Knockdown of Atp5b in mouse spermatocytes (GC2 cells) decreased mitochondrial membrane potential and induced apoptosis, demonstrating that Atp5b is required for maintaining mitochondrial integrity in spermatocytes. |
siRNA knockdown, flow cytometry (mitochondrial membrane potential, apoptosis assay) |
Environmental toxicology and pharmacology |
Medium |
27525561
|
| 2019 |
ATP5F1B (ATP5B) binds to the 3'UTR consensus sequences of rotavirus (RV) RNA with high affinity; during RV infection, ATP5B co-localizes with viral RNA and viroplasm; siRNA-mediated depletion of ATP5B (or other ATP synthase subunits) reduces production of infectious viral progeny without altering intracellular viral RNA levels or translation, placing ATP5B as a positive regulator of late-stage RV maturation/particle formation. |
RaPID proteomics-based RNA-protein interaction screen, siRNA knockdown, viral plaque assay, chemical inhibition in human intestinal enteroids |
The Journal of biological chemistry |
High |
30770472
|
| 2021 |
ATP5F1B (ATP5B) overexpression in gastric cancer cells elevates intracellular ATP content, increases extracellular ATP secretion, activates the P2X7 purinergic receptor, and thereby activates the FAK/AKT/MMP2 signaling pathway to promote cell migration, invasion, and proliferation; inhibitors of P2X7, FAK, AKT, and MMP2 suppress these effects. |
Overexpression and knockdown in gastric cancer cell lines, ATP content assay, migration/invasion assays, Western blotting for pathway components, pharmacological inhibitor experiments |
FASEB journal |
Medium |
33715234
|
| 2021 |
Inhibition of ATP5F1B (ATP5B) by siRNA lentivirus impairs osteoclast differentiation, suppresses osteoclast-related gene and protein expression, significantly impairs F-actin ring formation, decreases adhesion-associated proteins, causes mitochondrial dysfunction, and impairs vacuolar proton secretion and MMP9 secretion, thereby protecting arthritic mouse joints from bone erosion. |
Lentiviral siRNA delivery in vitro and intra-articular in vivo, gene/protein expression analysis, F-actin staining, bone resorption pit assay, mitochondrial function assay |
Pharmacological research |
Medium |
33515708
|
| 2021 |
Ectopic ATP5F1B (ATP5B) at the plasma membrane co-localizes and physically interacts with caveolin-1 (Cav-1) in MDA-MB-231 breast cancer cells; Cav-1 knockdown reduces migration and invasion abilities and is required for the pro-migratory/invasive function of ectopic ATP5B. |
Coimmunoprecipitation, double immunofluorescence staining, siRNA knockdown, migration/invasion assays |
Medical oncology |
Medium |
34009483
|
| 2022 |
Cell-surface ATP5F1B (ATP5B) on hepatocellular carcinoma cells binds the myristoylated (but not non-myristoylated) preS1 2-47 peptide of hepatitis B virus; knockdown of ATP5B in NTCP-expressing HepG2 cells reduces HBV infectivity with less cccDNA formation, establishing ATP5B as an essential factor for HBV cell entry. |
Flow cytometry (cell surface expression), binding assay with myristoylated preS1 peptide, siRNA knockdown, HBV infection assay (cccDNA quantification) |
International journal of molecular sciences |
Medium |
36076968
|
| 2023 |
Two heterozygous missense variants in ATP5F1B (p.Thr334Pro and p.Val482Ala) segregate with autosomal dominant early-onset isolated dystonia with incomplete penetrance; functional studies in patient fibroblasts showed preserved ATP5F1B protein levels but severe reduction of complex V (ATP synthase) activity and impaired mitochondrial membrane potential, consistent with a dominant-negative mechanism. |
Genetic segregation analysis, protein quantification, complex V enzymatic activity assay, mitochondrial membrane potential measurement in patient fibroblasts |
Brain |
High |
36860166
|
| 2023 |
ATP5F1B (ATP5B) binds HIF-1α mRNA; small molecules (HI-derivatives containing an adamantaniline moiety) promote this binding and thereby inhibit HIF-1α translation without affecting mRNA levels; target identification was achieved via affinity-based protein profiling of the probe HI-102. |
Affinity-based protein profiling (chemoproteomic target ID), mRNA-binding assay, HIF-1α protein expression and translation assay, in vivo xenograft model |
Advanced science |
Medium |
37401167
|
| 2023 |
Under PFOS exposure, ATP5F1B (ATP5B) redistributes from the plasma membrane to mitochondria and interacts with transferrin receptor 2 (TFR2), facilitating TFR2 translocation to mitochondria, leading to mitochondrial iron overload that precedes and causes insulin resistance; stabilizing ATP5B on the plasma membrane or knockdown of ATP5B blocked TFR2 translocation and prevented insulin resistance. |
Subcellular fractionation, Co-IP, pharmacological inhibition of ectopic ATP synthase, ATP5B knockdown, mitochondrial iron measurement, insulin resistance assays in hepatocytes and mouse liver |
Ecotoxicology and environmental safety |
Medium |
36801541
|
| 2024 |
Mitochondria-localized acetyltransferase MOF directly acetylates ATP5F1B (ATP5B) at lysine K201; this acetylation, co-regulated by the deacetylase SIRT3, impairs mitochondrial respiration and energy metabolism; overexpression of mitochondria-targeted MOF in mice causes mitochondrial dysfunction, cardiac remodeling, and heart failure, and SIRT3 knockout aggravates these effects. |
Quantitative lysine acetylome mass spectrometry, mitochondria-targeted MOF overexpression mouse model, SIRT3 knockout, mitochondrial respiration assay, cardiac phenotyping |
Cell reports |
High |
39392752
|
| 2024 |
Under PFOS exposure, ATP5F1B (ATP5B) interacts with TRPML1 (lysosomal calcium channel) and VDAC1 (mitochondrial calcium channel), facilitating calcium transmission from lysosomes to mitochondria; inhibiting ATP5B expression or retaining ATP5B on the plasma membrane disrupts TRPML1-VDAC1 interaction and reverses mitochondrial calcium overload and insulin resistance. |
Co-IP, subcellular fractionation, siRNA knockdown, calcium imaging, pharmacological inhibition, mouse liver experiments |
Ecotoxicology and environmental safety |
Medium |
38626609
|
| 2024 |
Under PFOS exposure, ATP5F1B (ATP5B) interacts with VDAC1 and promotes VDAC1 translocation from the plasma membrane to mitochondria, where it undergoes oligomerization; this VDAC1 oligomerization activates the NLRP3 inflammasome; knockdown of ATP5B or immobilization of ATP5B on the plasma membrane prevents VDAC1 oligomerization and NLRP3 activation. |
Co-IP, VDAC1 oligomerization assay, siRNA knockdown, plasma membrane ATP5B stabilization, NLRP3 inflammasome activation assay in hepatocytes and mouse liver |
Ecotoxicology and environmental safety |
Medium |
38944014
|
| 2024 |
ATP5F1B (ATP5B) interacts with TGEV (transmissible gastroenteritis coronavirus) nonstructural protein Nsp2; downregulation of ATP5B promotes TGEV replication, indicating that ATP5B functions as a negative regulator of TGEV replication. |
Immunoprecipitation/LC-MS/MS, Co-IP, indirect immunofluorescence, siRNA knockdown with viral replication assay |
Virulence |
Medium |
39239724
|
| 2025 |
ATP5F1B (Atp5f1b) interacts with the mitochondrial protein Cend1; Cend1 deficiency in knockout mice exacerbates cerebral ischemia/reperfusion injury with impaired mitochondrial membrane potential, mPTP opening, ATP content reduction, and decreased Complex V activity; Cend1 dimerization via GXXXA motifs is required for ATP synthesis enhancement; the small molecule Tianeptine stabilizes Cend1 dimers, elevates ATP, and confers neuroprotection in a Cend1-dependent manner. |
Cend1 knockout mouse model, Co-IP (Atp5f1b-Cend1 interaction), mitochondrial function assays, mutagenesis (G130P), small molecule treatment, neurological phenotyping |
Communications biology |
Medium |
41469760
|
| 2023 |
The Pseudomonas aeruginosa flagellar hook protein FlgE directly interacts with cell-surface ATP5F1B (ATP5B) on macrophages, and blocking ATP5B attenuates FlgE-induced NF-κB/MAPK signaling, inflammatory responses, SR-A1 upregulation, and foam cell formation, indicating ATP5B mediates pathogen-induced pro-atherogenic macrophage activation. |
Pull-down assay, Western blotting, blocking experiments with anti-ATP5B, in vitro macrophage assays, ApoE-/- mouse atherosclerosis model |
Atherosclerosis |
Low |
38278062
|
| 2020 |
The bovine ATP5F1B (ATP5B) promoter contains two transcriptional start sites; the transcription factors MyoD and GATA1 bind to specific sites in the proximal promoter region (-539/+220 relative to TSS) and drive ATP5B basal transcription, as demonstrated by 5'-RACE, deletion analysis, site-directed mutagenesis, and ChIP assays. |
5'-RACE, luciferase reporter deletion assay, site-directed mutagenesis, chromatin immunoprecipitation (ChIP) |
Animal biotechnology |
Medium |
33124493
|