Affinage

OLA1

Obg-like ATPase 1 · UniProt Q9NTK5

Length
396 aa
Mass
44.7 kDa
Annotated
2026-06-10
36 papers in source corpus 24 papers cited in narrative 24 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 8/8 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

OLA1 is a universally conserved P-loop ATPase of the Obg/YchF subfamily that preferentially binds and hydrolyzes ATP over GTP, a specificity rationalized by its AMPPCP-bound crystal structure (PMID:17430889), and which acts as a multifunctional regulatory hub coupling nucleotide hydrolysis to translational, proteostatic, centrosomal, and redox control. In translation, OLA1 binds eIF2 and interferes with ternary complex (eIF2-GTP-tRNAi) formation, inhibiting protein synthesis and promoting the integrated stress response; loss of OLA1 yields a hypoactive ISR and enhanced translation of targets such as p21, and Ola1-knockout mice show growth retardation and cell-cycle defects (PMID:26283179, PMID:27481995). Through its chaperone-like activity, OLA1 binds the HSP70 C-terminal variable domain to block CHIP-mediated ubiquitination and degradation of HSP70, an interaction extended to protection of the Hsp70–SOD2 complex from CHIP-driven turnover (PMID:23412384, PMID:31476900). At centrosomes and spindle poles, OLA1 forms a complex with the N-terminus of BRCA1, with γ-tubulin, and with the BARD1 C-terminus; its loss causes centrosome amplification, and BARD1's BRCT domain binds the OLA1 TGS domain to allosterically increase ATPase turnover, while cancer-associated mutations (OLA1 E168Q; BARD1 V695L) disrupt binding and abolish centrosome-number rescue (PMID:24289923, PMID:29858377, PMID:35134491). Centrosomal OLA1 abundance is set by Aurora A-mediated polyubiquitination enhanced by NEK2 phosphorylation at T124, controlling pericentriolar material recruitment during centrosome maturation (PMID:37481721). OLA1 also negatively regulates the cellular antioxidant response and ROS through nontranscriptional mechanisms (PMID:19706404), binds and inhibits GSK3β via Ser9 phosphorylation to stabilize Snail and promote TGF-β-induced EMT and to modulate HIF1α/CA9 signaling (PMID:26863455, PMID:35440019), and undergoes ERK1/2-driven phosphorylation at Ser232/Tyr236 and Thr325 that triggers nuclear translocation and an ATPase-to-GTPase switch driving expression of nuclear-encoded mitochondrial bioenergetic genes (PMID:36481055). OLA1 interacts with STING to suppress its activation, and competing STING engagement liberates Keap1 to destabilize Nrf2, linking OLA1 to innate immune and ferroptosis regulation (PMID:38132845, PMID:41352507). Bi-allelic loss-of-function variants in OLA1 cause a human neurodevelopmental disorder with joint hypermobility, with patient cells and model organisms showing impaired migration, adhesion, and cytoskeletal/microtubule dynamics via FAK (PMID:41887223).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2007 High

    Established the fundamental biochemical identity of OLA1, resolving whether this Obg-family protein is a GTPase or an ATPase.

    Evidence Nucleotide-binding/hydrolysis assays and an AMPPCP-bound X-ray structure of human OLA1

    PMID:17430889

    Open questions at the time
    • Did not establish a cellular substrate or pathway for the ATPase activity
    • Functional consequence of nucleotide hydrolysis in vivo unaddressed
  2. 2009 High

    Defined OLA1 as a nontranscriptional negative regulator of the antioxidant response, distinguishing it from canonical transcription-driven redox control.

    Evidence Bidirectional RNAi/overexpression with ROS and viability assays plus cycloheximide block and qRT-PCR in human cells; migration/invasion link in breast cancer cells

    PMID:19706404 PMID:19882753

    Open questions at the time
    • Molecular target mediating ROS suppression not identified
    • Connection between ROS control and motility correlative
  3. 2013 High

    Placed OLA1 in two distinct protein complexes — a centrosomal BRCA1/BARD1/γ-tubulin module and an HSP70-stabilizing chaperone role — defining its first direct physical partners.

    Evidence Mass spectrometry, reciprocal Co-IP, direct binding, immunofluorescence, RNAi, and mutant rescue (E168Q); ubiquitination and thermotolerance assays for HSP70/CHIP

    PMID:23412384 PMID:24289923

    Open questions at the time
    • How ATPase activity couples to centrosome regulation unresolved
    • Whether HSP70 and centrosome roles are mechanistically related unknown
  4. 2015 High

    Demonstrated that OLA1 inhibits translation initiation and drives the integrated stress response by binding eIF2 and blocking ternary complex formation, with tumor-suppressive consequences in vivo.

    Evidence Co-IP, GTPase and ternary complex formation assays, polysome profiling, RNAi, and xenograft models

    PMID:26283179

    Open questions at the time
    • Stoichiometry and regulation of OLA1–eIF2 binding undefined
    • Relationship to the centrosomal pool of OLA1 unclear
  5. 2016 High

    Showed OLA1 is genetically required for mammalian development and connects translational control to cell-cycle progression via eIF2-dependent p21 translation, and separately identified GSK3β as a partner driving EMT.

    Evidence Ola1 knockout mice, primary MEFs, double-knockout epistasis, and eIF2α pharmacology; Co-IP and EMT assays for GSK3β/Snail

    PMID:26863455 PMID:27481995

    Open questions at the time
    • How OLA1 mechanistically restrains eIF2α-dependent p21 translation unresolved
    • Direct effect of OLA1 on GSK3β Ser9 phosphorylation mechanism unclear
  6. 2019 Medium

    Extended the OLA1–HSP70 chaperone axis to disease-relevant SOD2 protection and identified OLA1 as a substrate of N-terminal methyltransferase NTMT1.

    Evidence OLA1 KO mice and CHIP-Hsp70-SOD2 Co-IP/ubiquitination in a PPHN model; activity-based substrate profiling and NTMT1 CRISPR KO validation

    PMID:31476900 PMID:31857877

    Open questions at the time
    • Functional consequence of N-terminal methylation on OLA1 activity not established
    • Whether SOD2 protection is direct or via HSP70 stabilization not fully separated
  7. 2020 Medium

    Identified meiotic spindle functions for OLA1 and revealed that viral and host factors converge on the OLA1–GSK3β axis to control autophagy.

    Evidence Immunofluorescence, nocodazole, siRNA microinjection in mouse oocytes; Co-IP and autophagy/proliferation assays for HIV p17 disruption of OLA1–GSK3β

    PMID:31915569 PMID:32790080

    Open questions at the time
    • Mechanism linking OLA1 to SAC timing not defined
    • Single-lab ortholog/viral models without reciprocal validation
  8. 2021 Medium

    Demonstrated that a lncRNA (ZFAS1) can allosterically enhance OLA1 ATPase activity by exposing its ATP-binding motif, coupling OLA1 enzymatic output to cancer metabolism.

    Evidence RNA pulldown, RIP, ATP hydrolysis and glycolysis assays with ATP-site mutagenesis in colorectal cancer cells

    PMID:34743750

    Open questions at the time
    • Whether ZFAS1 regulation operates in non-cancer contexts unknown
    • Single lab
  9. 2022 High

    Resolved BARD1 as an allosteric ATPase-activating protein for OLA1 and connected OLA1 to the GSK3β–HIF1α/CA9 hypoxic axis.

    Evidence Enzyme kinetics, 1.88 Å crystal structure of BARD1 BRCT V695L, and mutagenesis; CRISPR KO with mRNA-seq and xenografts for HIF1α/CA9

    PMID:35134491 PMID:35440019

    Open questions at the time
    • How allosteric activation feeds into centrosome regulation mechanistically incomplete
    • No direct OLA1–HIF1α interaction shown
  10. 2023 High

    Defined the ubiquitin-mediated control of centrosomal OLA1 abundance and a phosphorylation-driven nuclear translocation that switches OLA1 between ATPase and GTPase activities to control mitochondrial gene expression.

    Evidence In vitro ubiquitination, T124 mutagenesis, proteasome inhibition, and centrosome imaging (Aurora A/NEK2); phospho-site mutagenesis, fractionation, activity assays, ERK/PP1A manipulation and KO mice (Ser232/Tyr236/Thr325)

    PMID:36481055 PMID:37481721

    Open questions at the time
    • Kinase(s) directly phosphorylating Ser232/Tyr236 not fully defined
    • How a single protein partitions between nuclear, mitochondrial and centrosomal roles unresolved
  11. 2024 Medium

    Established OLA1 as a suppressor of STING-mediated innate immune signaling and a target of HIV-1 p17 antagonism.

    Evidence Co-IP of OLA1–STING and p17–OLA1, cGAMP stimulation, STING translocation/phosphorylation, and comparative HIV-1 vs HIV-2/SIV p17 with activity assays

    PMID:38132845

    Open questions at the time
    • Whether ATPase/GTPase activity is required for STING suppression unclear
    • Single lab, no reciprocal in vivo validation
  12. 2025 Medium

    Connected OLA1 to redox and cell-death regulation through a STING–OLA1–Keap1–Nrf2 axis and via MAPK/mitochondrial ROS control in a yeast ortholog.

    Evidence Co-IP of STING–OLA1 and OLA1–Keap1 with Nrf2 stability/ferroptosis readouts in a murine POF model; Co-IP and mtROS assays for S. pombe Ola1–Pmk1/Pek1

    PMID:40543417 PMID:41352507

    Open questions at the time
    • Direct biochemical basis of OLA1–Keap1 competition with STING undefined
    • Conservation of yeast MAPK mechanism to mammals untested
  13. 2026 Medium

    Established OLA1 as a Mendelian disease gene, linking its loss of function to a neurodevelopmental disorder with joint hypermobility via cytoskeletal/FAK-dependent defects.

    Evidence Exome sequencing across 14 individuals/9 families, proband fibroblast and iPSC-neuron assays, and C. elegans ola-1 knockout with transcriptomics

    PMID:41887223

    Open questions at the time
    • Which of OLA1's many molecular activities underlies the disorder unresolved
    • Mechanistic link between OLA1 and FAK levels not biochemically established

Open questions

Synthesis pass · forward-looking unresolved questions
  • How a single conserved ATPase coordinates its many partner-specific roles — translation, chaperoning, centrosome regulation, redox, and mitochondrial gene expression — into a unified mechanism remains unresolved.
  • No integrated model explaining context-dependent partner selection
  • Whether nucleotide hydrolysis is required across all functional contexts unknown
  • Spatial/temporal partitioning between subcellular pools undefined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 5 GO:0140657 ATP-dependent activity 4 GO:0003924 GTPase activity 2 GO:0016787 hydrolase activity 2 GO:0044183 protein folding chaperone 2
Localization
GO:0005815 microtubule organizing center 2 GO:0005856 cytoskeleton 2 GO:0005634 nucleus 1 GO:0005739 mitochondrion 1 GO:0005829 cytosol 1
Pathway
R-HSA-162582 Signal Transduction 3 R-HSA-1640170 Cell Cycle 3 R-HSA-392499 Metabolism of proteins 3 R-HSA-8953897 Cellular responses to stimuli 2 R-HSA-168256 Immune System 1
Partners
BARD1BRCA1EIF2GSK3BHSPA1AKEAP1STING1TUBG1
Complex memberships
BRCA1/BARD1/γ-tubulin centrosomal complex

Evidence

Reading pass · 24 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 Human OLA1 (hOLA1) binds and hydrolyzes ATP more efficiently than GTP, establishing it as an ATPase rather than a GTPase within the Obg/YchF subfamily. X-ray crystal structure of hOLA1 bound to the non-hydrolyzable ATP analogue AMPPCP explained the altered nucleotide specificity compared to other Obg-family GTPases. Biochemical nucleotide-binding and hydrolysis assays; X-ray crystallography with AMPPCP-bound structure The Journal of biological chemistry High 17430889
2009 OLA1 functions as a negative regulator of the cellular antioxidant response through nontranscriptional mechanisms. Knockdown increased resistance to oxidizing agents (tBH, diamide) and reduced intracellular ROS and glutathione depletion without altering antioxidant gene mRNA levels or requiring de novo protein synthesis. RNAi knockdown; OLA1 overexpression; cell viability and ROS assays; cycloheximide block experiments; qRT-PCR of antioxidant genes Proceedings of the National Academy of Sciences of the United States of America High 19706404
2009 Knockdown of OLA1 inhibits breast cancer cell migration and invasion through modulation of intracellular ROS levels, linking OLA1's regulation of ROS to cytoskeletal motility. siRNA knockdown; wound-healing and transwell invasion assays; ROS measurement; N-acetylcysteine treatment Journal of Zhejiang University. Science. B Medium 19882753
2013 OLA1 directly binds to the amino-terminal region of BRCA1 and to γ-tubulin; it interacts with the carboxy-terminal region of BARD1. OLA1 localizes to centrosomes in interphase and to the spindle pole in mitosis. OLA1 knockdown causes centrosome amplification and activation of microtubule aster formation. A cancer-derived mutation E168Q abrogates BRCA1 binding and fails to rescue centrosome amplification. Mass spectrometry identification; co-immunoprecipitation; direct binding assays; immunofluorescence localization; RNAi knockdown; rescue with mutant constructs Molecular cell High 24289923
2013 OLA1 stabilizes HSP70 by binding to its carboxyl-terminus variable domain, thereby blocking recruitment of the E3 ubiquitin ligase CHIP and preventing CHIP-mediated ubiquitination and degradation of HSP70. OLA1 downregulation reduces steady-state HSP70 levels and impairs heat-shock-induced HSP70 induction, increasing cellular sensitivity to heat shock. RNAi knockdown; targeted gene disruption; OLA1 overexpression; protein-protein interaction (co-IP/pulldown); ubiquitination assay; thermal resistance assay Cell death & disease High 23412384
2014 OLA1 negatively regulates cell-matrix adhesion and spreading. OLA1-deficient cells have elevated FAK protein levels and decreased Ser3 phosphorylation of cofilin, while OLA1-overexpressing cells show opposite changes, indicating OLA1 modulates adhesion at least partly through FAK expression and cofilin phosphorylation. RNAi knockdown; OLA1 overexpression; cell adhesion/spreading assays; western blot for FAK and p-cofilin Biochemical and biophysical research communications Medium 24486488
2015 OLA1 inhibits protein synthesis and promotes the integrated stress response (ISR) by binding eIF2, hydrolyzing GTP in that context, and interfering with ternary complex (eIF2-GTP-tRNAi) formation. OLA1 depletion causes hypoactive ISR, reduces CHOP induction, and promotes tumor growth and metastasis in vivo. Co-immunoprecipitation (OLA1-eIF2 interaction); GTPase activity assay; ternary complex formation assay; polysome profiling; RNAi knockdown; xenograft tumor models Scientific reports High 26283179
2016 OLA1 is a GSK3β-interacting protein and inhibits GSK3β activity by mediating its Ser9 phosphorylation, thereby suppressing GSK3β-mediated degradation of Snail, which promotes E-cadherin downregulation and contributes to TGF-β-induced epithelial-mesenchymal transition (EMT). Co-immunoprecipitation (OLA1-GSK3β); western blot for GSK3β Ser9 phosphorylation, Snail, and E-cadherin; RNAi knockdown; EMT assays with TGF-β treatment Oncotarget Medium 26863455
2016 OLA1 is required for normal mammalian development. Ola1-knockout mouse embryos have growth retardation and developmental delay. Primary Ola1-/- MEFs show impaired proliferation due to defective cell-cycle progression, with reduced cyclins D1/E1, attenuated Rb phosphorylation, and elevated p21 protein. p21 accumulation is due to enhanced mRNA translation that is reversed by eIF2α dephosphorylation inhibitor, placing OLA1 upstream of eIF2-mediated p21 translational control. Ola1 knockout mice; primary MEF culture; BrdU/cell-cycle analysis; western blot; polysome/translation assays; eIF2α pharmacological manipulation; p21-/-/Ola1-/- double-knockout rescue Molecular and cellular biology High 27481995
2018 OLA1 requires its interaction with BARD1 to properly regulate centrosome number. Three OLA1 missense mutants that fail to bind BARD1 are deficient in centrosome number regulation. Phosphomimetic mutations at specific OLA1 residues restore BARD1 binding and rescue centrosome amplification. BARD1 mutant V695L (cancer-associated) fails to bind OLA1 and cannot rescue BARD1 knockdown-induced centrosome amplification. Co-immunoprecipitation; site-directed mutagenesis of OLA1 (phosphorylation, acetylation, ATP-binding residues); overexpression of mutant constructs; RNAi knockdown/rescue; centrosome counting by immunofluorescence Molecular cancer research : MCR High 29858377
2019 OLA1 is N-terminally methylated in vivo by the N-terminal methyltransferase NTMT1, as demonstrated by activity-based substrate profiling and validation in NTMT1 knockout cells. Activity-based substrate profiling with Hey-SAM analogue; CRISPR-Cas9 NTMT1 knockout HEK293FT cells; mass spectrometry validation Chemical science Medium 31857877
2019 Decreased OLA1 expression in PPHN enhances CHIP affinity for the Hsp70-SOD2 complex, facilitating SOD2 ubiquitination and proteasomal degradation. OLA1 acts as a molecular chaperone whose stress-induced activity prevents CHIP-mediated SOD2 degradation; ola1-/- mice recapitulate PPHN phenotypes including SOD2 downregulation and pulmonary vascular remodeling. Patient/fetal lamb tissue analysis; OLA1 KO mice; co-immunoprecipitation of CHIP-Hsp70-SOD2; ubiquitination assays; right ventricular pressure measurement Hypertension (Dallas, Tex. : 1979) Medium 31476900
2020 OLA1 localizes to meiotic spindles in mouse oocytes (co-localizing with spindle structures after GVBD, confirmed by nocodazole treatment). OLA1 knockdown results in abnormal/multipolar spindle assembly, premature anaphase onset due to precocious spindle assembly checkpoint (SAC) inactivation, and impaired germinal vesicle breakdown. Immunofluorescence/confocal microscopy; nocodazole treatment; siRNA microinjection; chromosome spreading; polar body extrusion assays PeerJ Medium 31915569
2020 HIV p17 interacts with OLA1 and disrupts the OLA1-GSK3β complex, leading to GSK3β hyperactivation, suppression of autophagy, and enhanced proliferation of HIV-infected T cells under glucose starvation conditions. Co-immunoprecipitation (p17-OLA1, OLA1-GSK3β); autophagy flux assays; T cell proliferation assays under glucose starvation Journal of medical virology Medium 32790080
2021 ZFAS1 lncRNA recognizes the OBG-type functional domain of OLA1, facilitating exposure of its ATP-binding site (NVGKST, residues 32–37), enhancing OLA1 protein ATPase activity, and accelerating ATP hydrolysis and the Warburg effect in colorectal cancer cells. RNA pulldown; RIP assay; ATP hydrolysis assay; ECAR/glycolysis assay; mutagenesis of OLA1 ATP-binding site Journal of hematology & oncology Medium 34743750
2022 BARD1 acts as an ATPase activating protein (AAP) for OLA1. The BARD1 BRCT domain binds the OLA1 TGS domain via a conserved BUDR motif and allosterically increases OLA1 ATPase turnover number (kcat). Cancer-associated BARD1 mutation V695L reduces OLA1 binding and activation, as revealed by a 1.88 Å crystal structure of the V695L BRCT mutant. Enzyme kinetics assays; X-ray crystallography (BRCT V695L mutant at 1.88 Å); biophysical/biochemical binding assays; mutagenesis Biochimica et biophysica acta. General subjects High 35134491
2022 OLA1 knockout in colorectal cancer cells activates GSK3β and downregulates HIF1α and its target CA9 at the mRNA/protein level, linking OLA1 to the HIF1α/CA9 hypoxic signaling axis through GSK3β. CRISPR-Cas9 OLA1 knockout; mRNA sequencing; western blot for GSK3β, HIF1α, CA9; xenograft tumor models BMC cancer Medium 35440019
2023 Aurora A binds OLA1 and polyubiquitinates it, targeting OLA1 for proteasomal degradation. NEK2 phosphorylates OLA1 at T124, which increases OLA1 binding to Aurora A and enhances Aurora A-mediated polyubiquitination. The kinase activity of Aurora A suppresses its own E3 ligase activity toward OLA1. Reduction of centrosomal OLA1 by this mechanism promotes pericentriolar material protein recruitment in G2 phase, required for centrosome maturation. Co-immunoprecipitation; in vitro ubiquitination assay; mutagenesis (T124 phosphorylation site); proteasome inhibitor experiments; immunofluorescence of centrosomal OLA1; overexpression rescue Cell reports High 37481721
2023 OLA1 phosphorylation at Ser232/Tyr236 triggers its translocation from cytoplasm/mitochondria into the nucleus. Subsequent phosphorylation at Thr325 switches its biochemical activity from ATPase to GTPase and promotes expression of nuclear-encoded mitochondrial bioenergetic genes. ERK1/2 drives this process and is restrained by PP1A. OLA1 T325A (phosphoresistant) mutant blocks nuclear translocation and compromises mitochondrial gene expression. OLA1 knockout mice have fewer mitochondria, lower ATP, and higher lactate. Phospho-site mutagenesis; subcellular fractionation; immunofluorescence; ATPase/GTPase activity assays with phosphomimetic mutants; ERK inhibition; PP1A manipulation; OLA1 KO mice; metabolite measurements American journal of respiratory cell and molecular biology High 36481055
2024 HIV-1 p17 (but not HIV-2 or SIV p17) binds OLA1 and inhibits OLA1's interaction with STING, thereby blocking OLA1-mediated suppression of STING translocation and phosphorylation. OLA1 normally interacts with STING and inhibits STING activation upon cGAMP stimulation. HIV-1 p17 also specifically promotes OLA1 ATPase and GTPase activities. Co-immunoprecipitation (OLA1-STING, p17-OLA1); cGAMP stimulation assays; STING translocation/phosphorylation assays; comparative HIV-1 vs HIV-2/SIV p17 experiments; ATPase/GTPase activity assays Journal of cell science Medium 38132845
2025 In fission yeast (S. pombe), Ola1 physically interacts with MAPK/Pmk1 and its upstream kinase Pek1 (MAPKK), inhibiting MAPK/Pmk1 signaling to prevent excessive mitochondrial ROS accumulation. Absence of Ola1 increases mtROS, promotes nuclear localization of Hsf1, and upregulates Ssa1 (Hsp70 homolog). Co-immunoprecipitation (Ola1-Pmk1, Ola1-Pek1); mitochondrial ROS measurements; ola1 deletion; Hsf1 localization assay; western blot Microbiological research Medium 40543417
2025 OLA1 interacts with Keap1 and, when STING is activated, enhanced STING-OLA1 interaction disrupts the OLA1-Keap1 complex, liberating Keap1 to promote Nrf2 degradation and ferroptosis in granulosa cells. This STING-OLA1-Keap1-Nrf2 axis is mechanistically linked to premature ovarian failure. Co-immunoprecipitation (STING-OLA1, OLA1-Keap1); siRNA knockdown; Nrf2 protein stability assays; ferroptosis markers; murine POF model; molecular docking (Icariin-STING) International journal of biological macromolecules Medium 41352507
2023 Vitexin binds OLA1 (identified by tissue thermal proteome profiling and molecular docking) and the OLA1-vitexin complex interacts with Keap1, disrupting the Keap1-Nrf2 interaction and activating Nrf2. siRNA knockdown of OLA1 in Caco-2 cells confirmed OLA1's role in mediating Nrf2 protein expression and anti-inflammatory effects. Tissue thermal proteome profiling; molecular docking; siRNA knockdown; Nrf2 protein level assays; inflammatory cytokine measurements Journal of agricultural and food chemistry Low 37856434
2026 Bi-allelic loss-of-function variants in OLA1 cause a human neurodevelopmental disorder with joint hypermobility. Patient-derived fibroblasts recapitulate impaired migration and proliferation. Neurons derived from proband fibroblasts show impaired adhesion and cytoskeletal control. In C. elegans, ola-1 deficiency reduces neurite numbers and suppresses microtubule dynamics and axon regrowth, placing OLA1 in a pathway regulating cytoskeletal dynamics through FAK levels. Sanger/exome sequencing in 14 individuals from 9 families; proband-derived fibroblast migration/proliferation assays; iPSC-derived neuron adhesion/cytoskeletal assays; C. elegans ola-1 knockout; transcriptomics American journal of human genetics Medium 41887223

Source papers

Stage 0 corpus · 36 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2021 N6-methyladenosine reader IMP2 stabilizes the ZFAS1/OLA1 axis and activates the Warburg effect: implication in colorectal cancer. Journal of hematology & oncology 97 34743750
2007 Human OLA1 defines an ATPase subfamily in the Obg family of GTP-binding proteins. The Journal of biological chemistry 92 17430889
2009 OLA1, an Obg-like ATPase, suppresses antioxidant response via nontranscriptional mechanisms. Proceedings of the National Academy of Sciences of the United States of America 63 19706404
2013 The BRCA1/BARD1-interacting protein OLA1 functions in centrosome regulation. Molecular cell 61 24289923
2013 OLA1 protects cells in heat shock by stabilizing HSP70. Cell death & disease 57 23412384
2015 OLA1 regulates protein synthesis and integrated stress response by inhibiting eIF2 ternary complex formation. Scientific reports 39 26283179
2009 Knockdown of OLA1, a regulator of oxidative stress response, inhibits motility and invasion of breast cancer cells. Journal of Zhejiang University. Science. B 35 19882753
2016 OLA1 contributes to epithelial-mesenchymal transition in lung cancer by modulating the GSK3β/snail/E-cadherin signaling. Oncotarget 32 26863455
2016 OLA1, a Translational Regulator of p21, Maintains Optimal Cell Proliferation Necessary for Developmental Progression. Molecular and cellular biology 30 27481995
2019 Decreased OLA1 (Obg-Like ATPase-1) Expression Drives Ubiquitin-Proteasome Pathways to Downregulate Mitochondrial SOD2 (Superoxide Dismutase) in Persistent Pulmonary Hypertension of the Newborn. Hypertension (Dallas, Tex. : 1979) 29 31476900
2018 BRCA1-Interacting Protein OLA1 Requires Interaction with BARD1 to Regulate Centrosome Number. Molecular cancer research : MCR 23 29858377
2014 Regulation of cell-matrix adhesion by OLA1, the Obg-like ATPase 1. Biochemical and biophysical research communications 18 24486488
2022 OLA1 promotes colorectal cancer tumorigenesis by activation of HIF1α/CA9 axis. BMC cancer 12 35440019
2019 In vivo methylation of OLA1 revealed by activity-based target profiling of NTMT1. Chemical science 12 31857877
2021 The Role of the Universally Conserved ATPase YchF/Ola1 in Translation Regulation during Cellular Stress. Microorganisms 11 35056463
2020 The Function of BARD1 in Centrosome Regulation in Cooperation with BRCA1/OLA1/RACK1. Genes 11 32722046
2023 Aurora A polyubiquitinates the BRCA1-interacting protein OLA1 to promote centrosome maturation. Cell reports 10 37481721
2016 OLA1 gene sequencing in patients with BRCA1/2 mutation-negative suspected hereditary breast and ovarian cancer. Breast cancer (Tokyo, Japan) 8 27271530
2023 OLA1 Phosphorylation Governs the Mitochondrial Bioenergetic Function of Pulmonary Vascular Cells. American journal of respiratory cell and molecular biology 7 36481055
2023 Identification of OLA1 as a Novel Protein Target of Vitexin to Ameliorate Dextran Sulfate Sodium-Induced Colitis with Tissue Thermal Proteome Profiling. Journal of agricultural and food chemistry 6 37856434
2014 OLA1 in centrosome biology alongside the BRCA1/BARD1 complex: looking beyond centrosomes. Molecular cell 6 24411079
2020 HIV p17 enhances T cell proliferation by suppressing autophagy through the p17-OLA1-GSK3β axis under nutrient starvation. Journal of medical virology 5 32790080
2016 Metal mixture (As-Cd-Pb)-induced cell transformation is modulated by OLA1. Mutagenesis 5 26984302
2020 OLA1 is responsible for normal spindle assembly and SAC activation in mouse oocytes. PeerJ 4 31915569
2024 HIV-1 p17 matrix protein enhances type I interferon responses through the p17-OLA1-STING axis. Journal of cell science 3 38132845
2024 Identification and development of Tetra-ARMS PCR-based screening test for a genetic variant of OLA1 (Tyr254Cys) in the human failing heart. PloS one 3 38889130
2022 Association of Common Variants in OLA1 Gene with Preclinical Atherosclerosis. International journal of molecular sciences 3 36232807
2025 The Obg-like ATPase Ola1 prevents excessive mitochondrial reactive oxygen species by inhibiting MAPK/Pmk1 signaling in fission yeast. Microbiological research 2 40543417
2022 BARD1 is an ATPase activating protein for OLA1. Biochimica et biophysica acta. General subjects 2 35134491
2023 Identification and development of Tetra-ARMS PCR-based screening test for a genetic variant of OLA1 (Tyr254Cys) in the human failing heart. medRxiv : the preprint server for health sciences 1 37905026
2026 Bi-allelic variants in OLA1 cause a neurodevelopmental disorder with joint hypermobility. American journal of human genetics 0 41887223
2026 The universally conserved NTPase OLA1. Biochemistry and cell biology = Biochimie et biologie cellulaire 0 41992399
2025 Anti-OLA1 autoantibody is a potential early diagnostic marker for hepatocellular carcinoma. Frontiers in immunology 0 41246329
2025 The STING-OLA1-Keap1-Nrf2 axis regulates ferroptosis in premature ovarian failure. International journal of biological macromolecules 0 41352507
2024 Knockout of Brca1-interacting factor Ola1 in female mice induces tumors with estrogen suppressible centrosome amplification. Biochimica et biophysica acta. Molecular basis of disease 0 38537683
2024 Protocol to detect OLA1 polyubiquitination by Aurora A in vivo and in vitro. STAR protocols 0 38602870

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