| 2011 |
miR-101 directly binds to the 3'UTR of ATP5B mRNA and negatively regulates ATP5B expression; knockdown of ATP5B significantly inhibited HSV-1 replication, and ectopic overexpression of ATP5B lacking the 3'UTR rescued viral replication suppressed by miR-101, establishing ATP5B as a pro-viral factor regulated by miR-101. |
Luciferase reporter assay (3'UTR binding), RNAi knockdown, plaque assay, ectopic overexpression rescue experiment |
Antiviral research |
Medium |
21291913
|
| 2011 |
ATP5B (ectopically localized at the plasma membrane) physically interacts with the calcium channel α2/δ1 subunit in developing myotubes, forming a functional signaling complex at the plasma membrane that accelerates the rate of decline of calcium transients, particularly during repetitive stimulation. |
Co-immunoprecipitation, FRET, functional calcium transient measurements in myotubes |
American journal of physiology. Cell physiology |
Medium |
21490313
|
| 2012 |
The mRNA-binding export protein REF undergoes deimination (arginine-to-citrulline conversion), and deiminated REF has higher ATP5B mRNA binding strength than non-deiminated REF; impaired deimination of REF in ND4 transgenic mice leads to defective ATP5B mRNA transport to mitochondria and reduced mitochondrial ATP synthase activity. |
mRNA binding assays, inhibition of deimination in PC12 cells, transgenic mouse model, mitochondrial ATP synthase activity assay |
EMBO reports |
Medium |
22261716
|
| 2019 |
ATP5B binds with high affinity to the conserved 3'UTR consensus sequences of rotavirus (RV) RNA; during infection, ATP5B co-localizes with viral RNA and viroplasm; siRNA depletion of ATP5B reduces production of infectious viral progeny without altering intracellular viral RNA levels or translation, indicating ATP5B supports late-stage RV maturation/assembly. |
RaPID proteomics-based RNA-protein interaction screen, siRNA knockdown, plaque assay, co-localization imaging, human intestinal enteroids with chemical ATP synthase inhibition |
The Journal of biological chemistry |
High |
30770472
|
| 2021 |
ATP5B overexpression in gastric cancer cells elevates intracellular and extracellular ATP levels, activates the FAK/AKT/MMP2 signaling pathway via the plasma membrane P2X7 receptor, and promotes cell migration, invasion, and proliferation; inhibitors of P2X7, FAK, AKT, or MMP2 suppressed these effects. |
Overexpression and knockdown experiments, ATP measurement, phospho-protein Western blot, inhibitor treatments, migration/invasion assays |
FASEB journal |
Medium |
33715234
|
| 2021 |
Inhibition of ATP5B in bone marrow macrophage-derived osteoclasts reduces expression of osteoclast differentiation genes, impairs F-actin formation, decreases adhesion-associated proteins, impairs vacuolar proton secretion and MMP9 secretion, causes mitochondrial dysfunction, and suppresses bone resorption; local ATP5B knockdown in arthritic mice protected joints from destruction. |
siRNA/lentiviral knockdown in primary osteoclasts, gene/protein expression, bone resorption assay, F-actin staining, in vivo collagen-induced arthritis model |
Pharmacological research |
Medium |
33515708
|
| 2021 |
Ectopic ATP5B at the plasma membrane of MDA-MB-231 breast cancer cells physically co-localizes and co-immunoprecipitates with Caveolin-1 (Cav-1) in caveolar lipid rafts; Cav-1 knockdown reduces migration and invasion, and cholesterol-loading increases ectopic ATP5B levels and promotes invasion, effects blocked by the ATP5B-specific peptide B04. |
Co-immunoprecipitation, double immunofluorescence, Cav-1 knockdown, cholesterol loading, peptide inhibition (B04), migration/invasion assays |
Medical oncology |
Medium |
34009483
|
| 2022 |
ATP5B is expressed on the cell surface of hepatocellular carcinoma cell lines and binds myristoylated (but not non-myristoylated) HBV preS1 peptide (residues 2-47); ATP5B knockdown in NTCP-expressing HepG2 cells reduces HBV infectivity and cccDNA formation, establishing ATP5B as an essential factor for HBV cell entry. |
Cell surface expression analysis, peptide binding assay (myristoylated vs. non-myristoylated preS1), siRNA knockdown, cccDNA quantification, infectivity assay |
International journal of molecular sciences |
Medium |
36076968 36976868
|
| 2023 |
Two ATP5F1B missense variants (p.Thr334Pro and p.Val482Ala) segregate with autosomal dominant early-onset isolated dystonia; functional studies in patient fibroblasts show no decrease in ATP5F1B protein levels but severe reduction in complex V (ATP synthase) activity and impaired mitochondrial membrane potential, consistent with a dominant-negative mechanism. |
Genetic segregation analysis, fibroblast functional studies (complex V activity assay, mitochondrial membrane potential measurement) |
Brain |
Medium |
36860166
|
| 2023 |
ATP5B is identified as a direct binding protein of adamantaniline derivative HI-101 (via affinity-based protein profiling); mechanistically, HI-101 promotes the binding of HIF-1α mRNA to ATP5B, thereby inhibiting HIF-1α translation and transcriptional activity, with anti-tumor activity in a xenograft model. |
Affinity-based protein profiling (probe HI-102), high-throughput screening, RNA-protein binding assay (HIF-1α mRNA to ATP5B), reporter assays, xenograft mouse model |
Advanced science |
Medium |
37401167
|
| 2023 |
Under PFOS exposure, ATP5B translocates from the plasma membrane to mitochondria and physically interacts with TFR2 (transferrin receptor 2); this cooperative translocation drives mitochondrial iron overload, which triggers hepatic insulin resistance. Stabilizing ATP5B on the plasma membrane or ATP5B knockdown prevented TFR2 translocation and reversed mitochondrial iron overload and insulin resistance. |
Co-immunoprecipitation, subcellular fractionation, knockdown, pharmacological stabilization of plasma membrane ATP synthase, mitochondrial iron measurement, insulin resistance assays in hepatocytes and mouse liver |
Ecotoxicology and environmental safety |
Medium |
36801541
|
| 2023 |
Flagellar hook protein FlgE from Pseudomonas aeruginosa directly interacts with ATP5B (identified by pull-down assay); blocking ATP5B attenuates FlgE-induced NF-κB/MAPK signaling, lipid uptake, foam cell formation, and inflammatory responses in macrophages. |
Pull-down assay, Western blotting, ATP5B blocking experiments, macrophage functional assays |
Atherosclerosis |
Low |
38278062
|
| 2024 |
Mitochondria-localized lysine acetyltransferase MOF acetylates ATP5B at lysine 201 (K201); SIRT3 deacetylates this site; hyperacetylation of ATP5B at K201 impairs mitochondrial respiration and energy metabolism both in vitro and in vivo, contributing to cardiac dysfunction and heart failure. |
Quantitative lysine acetylome analysis, MOF overexpression and SIRT3 knockout mouse models, mitochondrial respiration assays, site-specific mutagenesis (K201 acetylation) |
Cell reports |
High |
39392752
|
| 2024 |
Under PFOS exposure, ATP5B interacts with both TRPML1 (lysosomal calcium output channel) and VDAC1 (mitochondrial calcium intake channel); ATP5B inhibition or plasma membrane stabilization disrupts the TRPML1-VDAC1 interaction and reverses PFOS-induced mitochondrial calcium overload, worsening lysosomal calcium accumulation, demonstrating ATP5B as a regulator of lysosome-to-mitochondria calcium transmission. |
Co-immunoprecipitation, ATP5B knockdown, pharmacological plasma membrane stabilization, calcium measurements in hepatocytes and mouse liver |
Ecotoxicology and environmental safety |
Medium |
38626609
|
| 2024 |
Under PFOS exposure, VDAC1 interacts with ATP5B and undergoes increased oligomerization primarily at mitochondria; ATP5B knockdown or plasma membrane stabilization of ATP5B reduces VDAC1 oligomerization and NLRP3 inflammasome activation, indicating ATP5B facilitates VDAC1 transfer from plasma membrane to mitochondria where it undergoes pro-inflammatory oligomerization. |
Co-immunoprecipitation, ATP5B knockdown, pharmacological plasma membrane stabilization, VDAC1 oligomerization assay, NLRP3 inflammasome activation assay |
Ecotoxicology and environmental safety |
Medium |
38944014
|
| 2024 |
ATP5B (as TGEV Nsp2 binding partner identified by Co-IP/LC-MS/MS) interacts with TGEV Nsp2 as confirmed by Co-IP and indirect immunofluorescence; downregulation of ATP5B expression promotes TGEV replication, indicating ATP5B functions as a negative regulator of TGEV replication. |
Immunoprecipitation/LC-MS/MS, Co-IP, indirect immunofluorescence, ATP5B knockdown with viral replication readout |
Virulence |
Low |
39239724
|
| 2020 |
The bovine ATP5B promoter contains functional binding sites for transcription factors MyoD and GATA1; site-directed mutation of these sites and chromatin immunoprecipitation (ChIP) demonstrated that MyoD and GATA1 binding drives basal ATP5B transcription; the proximal minimal promoter was mapped to the region -539/220 relative to the transcriptional start site. |
5'-RACE, luciferase reporter assay with 5'-deletion constructs, site-directed mutagenesis, chromatin immunoprecipitation (ChIP) |
Animal biotechnology |
Medium |
33124493
|
| 2025 |
Cend1 protein physically interacts with Atp5f1b (ATP5F1B) in mitochondria; Cend1 forms dimers via conserved GXXXA motifs in its transmembrane domain to enhance ATP synthesis, and disruption of Cend1 dimerization (G130P mutation) destabilizes Cend1 and abolishes its ATP-enhancing effects; Cend1 KO mice show reduced Complex V activity and worsened ischemia/reperfusion injury. |
Co-IP (Cend1-Atp5f1b interaction), Cend1 KO mouse model, site-directed mutagenesis (G130P), mitochondrial membrane potential, mPTP opening, Complex I and V activity assays, infarct volume measurement |
Communications biology |
Medium |
41469760
|