Affinage

OLA1

Obg-like ATPase 1 · UniProt Q9NTK5

Length
396 aa
Mass
44.7 kDa
Annotated
2026-04-29
36 papers in source corpus 21 papers cited in narrative 21 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

OLA1 is a conserved Obg-family P-loop NTPase that functions as a multifunctional regulatory hub integrating translational control, centrosome homeostasis, redox signaling, and cytoskeletal dynamics. It preferentially hydrolyzes ATP over GTP (PMID:17430889), inhibits eIF2 ternary complex formation to suppress global protein synthesis and promote the integrated stress response — with Ola1 knockout mice accumulating p21 through enhanced eIF2-dependent translation (PMID:26283179, PMID:27481995) — and stabilizes HSP70 by competitively blocking CHIP-mediated ubiquitination, a mechanism also governing SOD2 turnover in pulmonary vascular disease (PMID:23412384, PMID:31476900). OLA1 localizes to centrosomes where BARD1 serves as its ATPase-activating protein, and Aurora A/NEK2-dependent phosphorylation and ubiquitination of OLA1 drive its degradation during G2 to permit centrosome maturation; phosphorylation-dependent nuclear translocation switches its NTPase specificity from ATPase to GTPase, coupling redox and stress signals to mitochondrial bioenergetic gene transcription (PMID:24289923, PMID:35134491, PMID:37481721, PMID:36481055). Bi-allelic loss-of-function OLA1 variants cause a neurodevelopmental disorder with joint hypermobility in humans (PMID:41887223).

Mechanistic history

Synthesis pass · year-by-year structured walk · 14 steps
  1. 2007 High

    Establishing that OLA1 is an ATPase rather than a canonical GTPase resolved its enzymatic identity and explained the divergent nucleotide specificity of the YchF/OLA1 subfamily through structural determination.

    Evidence Biochemical nucleotide hydrolysis assays and X-ray crystallography of hOLA1 with AMPPCP

    PMID:17430889

    Open questions at the time
    • No cellular substrate or downstream effector identified
    • Whether GTPase activity is biologically relevant was not addressed
  2. 2009 High

    Demonstrating that OLA1 negatively regulates the antioxidant response through a nontranscriptional mechanism positioned it as a post-translational modulator of cellular redox homeostasis and linked it to cancer cell migration via ROS.

    Evidence RNAi knockdown with ROS/glutathione measurements and cycloheximide block; migration/invasion assays with NAC rescue

    PMID:19706404 PMID:19882753

    Open questions at the time
    • Direct molecular target mediating ROS regulation was not identified
    • Whether ATPase activity is required for redox function was untested
  3. 2013 High

    Identifying OLA1 as an HSP70 stabilizer that blocks CHIP-mediated ubiquitination defined a chaperone-protection mechanism, while discovery of OLA1 at centrosomes in complex with BRCA1 and γ-tubulin revealed its role in restraining centriole duplication.

    Evidence Reciprocal co-IP, ubiquitination assays, heat-shock survival (HSP70 axis); mass spectrometry, co-IP, centrosome counting, cancer-associated mutant analysis (centrosome axis)

    PMID:23412384 PMID:24289923

    Open questions at the time
    • Whether HSP70 stabilization and centrosome regulation are linked through a common ATPase mechanism was unknown
    • The E168Q mutant's effect on ATPase activity was not measured
  4. 2015 High

    Showing that OLA1 inhibits eIF2 ternary complex formation via GTP hydrolysis established a direct translational control mechanism and explained how OLA1 promotes the integrated stress response and CHOP-mediated apoptosis.

    Evidence Co-IP with eIF2, GTPase assays, polysome profiling, ATF4/CHOP reporters, xenograft models

    PMID:26283179

    Open questions at the time
    • Whether ATP or GTP hydrolysis is the physiologically dominant activity in translational regulation was not resolved
    • Structural basis for eIF2 binding was not determined
  5. 2016 High

    Genetic epistasis in Ola1-knockout mice confirmed in vivo translational control: Ola1-/- MEFs accumulated p21 via eIF2-dependent translation, and p21 knockout partially rescued embryonic growth retardation, placing OLA1 upstream of translational p21 regulation.

    Evidence Ola1-/- and Ola1-/-;p21-/- double-knockout mouse models, polysome/translation assays

    PMID:27481995

    Open questions at the time
    • Whether additional mRNAs beyond p21 are selectively regulated was not catalogued
    • Tissue-specific requirements for OLA1 translational control were not fully mapped
  6. 2018 High

    Systematic mutagenesis demonstrated that OLA1–BARD1 interaction is essential for centrosome number control, with phosphomimetic OLA1 mutants restoring BARD1 binding and rescuing centrosome amplification, defining phosphorylation as a regulatory switch.

    Evidence Co-IP of five OLA1 missense mutants, BARD1 knockdown, cancer-derived BARD1 mutant analysis, centrosome counting

    PMID:29858377

    Open questions at the time
    • The kinase responsible for phosphorylation that promotes BARD1 binding was not identified at this stage
    • How the BRCA1/BARD1 E3 ligase activity integrates with OLA1 ATPase function was unclear
  7. 2019 High

    OLA1's role in HSP70-CHIP biology was extended to SOD2 regulation in pulmonary hypertension, showing that OLA1 deficiency enhances CHIP-mediated SOD2 ubiquitination, linking the chaperone-protection mechanism to vascular pathology in two animal models.

    Evidence Co-IP and ubiquitination assays in pulmonary artery cells, Ola1-/- mice and fetal lamb PPHN model

    PMID:31476900

    Open questions at the time
    • Whether OLA1 directly binds SOD2 or acts solely through HSP70 was not distinguished
    • Therapeutic reversibility of pulmonary phenotype by OLA1 restoration was not tested
  8. 2019 High

    Identification of OLA1 as a substrate of NTMT1 N-terminal methyltransferase established a new post-translational modification on OLA1, expanding its regulatory input layer.

    Evidence Activity-based Hey-SAM profiling, CRISPR NTMT1 KO validation, mass spectrometry in HEK293FT cells

    PMID:31857877

    Open questions at the time
    • Functional consequence of N-terminal methylation on OLA1 activity or localization was not determined
  9. 2022 High

    Structural and kinetic demonstration that BARD1 BRCT domain acts as an ATPase-activating protein for OLA1 via the conserved BUDR motif explained how BRCA1/BARD1 mechanistically controls OLA1 enzymatic output, with the cancer mutation V695L reducing activation.

    Evidence 1.88 Å crystal structure of BARD1 BRCT-OLA1 TGS complex, enzyme kinetics, mutagenesis

    PMID:35134491

    Open questions at the time
    • Whether ATPase activation by BARD1 is required in vivo for centrosome regulation was not directly tested with catalytic-dead mutants
    • Full-length complex structure is lacking
  10. 2023 High

    Discovery that Aurora A ubiquitinates OLA1 and NEK2 phosphorylates OLA1 at T124 to promote this degradation resolved how centrosomal OLA1 is removed during G2 to permit centrosome maturation, completing the regulatory circuit.

    Evidence In vitro and in vivo ubiquitination assays, kinase assays, phosphomutants, centrosome imaging

    PMID:37481721

    Open questions at the time
    • Whether other centrosomal substrates of Aurora A E3 ligase activity exist was not addressed
    • Temporal coordination between BARD1-mediated ATPase activation and Aurora A-mediated degradation at centrosomes is undefined
  11. 2023 Medium

    Phosphorylation-dependent nuclear translocation of OLA1 (Ser232/Tyr236) and a subsequent activity switch from ATPase to GTPase (Thr325) coupled stress/redox sensing to transcriptional control of mitochondrial bioenergetic genes, regulated by ERK1/2 and PP1A.

    Evidence Phosphomimetic/phosphoresistant mutants, subcellular fractionation, nuclear imaging, metabolic gene expression, ERK1/2 knockdown, Ola1-/- mice

    PMID:36481055

    Open questions at the time
    • Structural basis for the ATPase-to-GTPase switch is unknown
    • Nuclear binding partners or chromatin targets of GTPase-active OLA1 were not identified
    • Independent replication in a second laboratory is needed
  12. 2024 Medium

    OLA1 was shown to interact with STING and inhibit its translocation and phosphorylation, placing OLA1 in the cGAS-STING innate immune pathway; HIV-1 p17 disrupts this interaction to promote STING signaling.

    Evidence Co-IP, STING phosphorylation/translocation assays, cGAMP stimulation, species-specific p17 controls

    PMID:38132845

    Open questions at the time
    • Whether OLA1 ATPase or GTPase activity is required for STING inhibition was not determined
    • Physiological relevance outside HIV infection context is untested
  13. 2025 Medium

    OLA1 was found to sequester Keap1 away from Nrf2, promoting antioxidant defense; STING activation disrupts OLA1-Keap1 binding, freeing Keap1 to degrade Nrf2 and promote ferroptosis, linking OLA1's redox role to the Keap1-Nrf2 axis.

    Evidence Co-IP, Nrf2 activity assay, siRNA, in vivo mouse POF model

    PMID:41352507

    Open questions at the time
    • Direct binding domain on OLA1 for Keap1 is unmapped
    • Whether this mechanism accounts for the nontranscriptional antioxidant phenotype reported in 2009 remains unconnected
  14. 2026 High

    Bi-allelic OLA1 loss-of-function variants were identified as causal for a human neurodevelopmental disorder with joint hypermobility, validated by impaired migration and adhesion in proband fibroblasts/neurons and reduced neurite dynamics in C. elegans, establishing OLA1 as essential for nervous system development.

    Evidence Human genetics (biallelic variants in multiple families), proband-derived fibroblast and neuron assays, C. elegans ola-1 knockout with neurite imaging

    PMID:41887223

    Open questions at the time
    • Genotype-phenotype correlation across different variant types is limited
    • Whether translational, centrosomal, or cytoskeletal functions of OLA1 drive the neurodevelopmental phenotype is undetermined

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis for OLA1's phosphorylation-dependent ATPase-to-GTPase switch, how its multiple functions (translational control, centrosome regulation, redox modulation, STING inhibition) are coordinately regulated in different cellular contexts, and which specific OLA1 activity underlies the human neurodevelopmental phenotype.
  • No full-length OLA1 structure in complex with eIF2 or STING
  • Relative contributions of ATPase vs GTPase activity to distinct cellular functions are unresolved
  • Cell-type-specific regulation and substrate specificity of OLA1 remain poorly defined

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 4 GO:0140657 ATP-dependent activity 3 GO:0003924 GTPase activity 2 GO:0140313 molecular sequestering activity 1
Localization
GO:0005815 microtubule organizing center 3 GO:0005829 cytosol 2 GO:0005634 nucleus 1 GO:0005739 mitochondrion 1
Pathway
R-HSA-392499 Metabolism of proteins 5 R-HSA-1640170 Cell Cycle 4 R-HSA-1266738 Developmental Biology 2 R-HSA-8953854 Metabolism of RNA 2 R-HSA-8953897 Cellular responses to stimuli 2 R-HSA-168256 Immune System 1
Partners
AURKABARD1BRCA1EIF2S1HSPA1ANEK2STING1STUB1
Complex memberships
BRCA1/BARD1

Evidence

Reading pass · 21 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 Human OLA1 (hOLA1) is an ATPase that binds and hydrolyzes ATP more efficiently than GTP, distinguishing it from other Obg-family GTPases. X-ray crystal structure of hOLA1 bound to the non-hydrolyzable ATP analogue AMPPCP explains the altered nucleotide specificity of the YchF/OLA1 subfamily. Biochemical nucleotide hydrolysis assays, X-ray crystallography (structure with AMPPCP) The Journal of biological chemistry High 17430889
2009 OLA1 functions as a negative regulator of the cellular antioxidant response through nontranscriptional mechanisms. Knockdown of OLA1 increases resistance to oxidizing agents (tBH, diamide), decreases intracellular ROS, and reduces glutathione depletion, without changing mRNA levels of antioxidant genes or requiring de novo protein synthesis. RNAi knockdown, cell viability assays, ROS measurement, glutathione assay, cycloheximide block experiment 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, as treatment with the ROS scavenger N-acetylcysteine phenocopies OLA1 knockdown. siRNA knockdown, wound-healing assay, Transwell migration/invasion assay, ROS measurement, NAC treatment Journal of Zhejiang University. Science. B Medium 19882753
2013 OLA1 stabilizes HSP70 by binding to the HSP70 carboxyl-terminus variable domain, thereby preventing recruitment of the E3 ubiquitin ligase CHIP and blocking CHIP-mediated ubiquitination and degradation of HSP70. OLA1 knockdown reduces HSP70 levels and impairs thermotolerance; overexpression elevates HSP70 and improves heat-shock survival. RNAi knockdown, gene disruption, overexpression, co-immunoprecipitation, ubiquitination assay, heat-shock survival assay Cell death & disease High 23412384
2013 OLA1 localizes to centrosomes in interphase and spindle poles in mitosis, directly binds to BRCA1 (amino-terminal region) and γ-tubulin, and is required for centrosome number regulation. OLA1 knockdown causes centrosome amplification and microtubule aster formation. A cancer-associated OLA1 mutant (E168Q) fails to bind BRCA1 and cannot rescue centrosome amplification. BRCA1 variant I42V also abrogates BRCA1-OLA1 binding. Mass spectrometry, co-immunoprecipitation, immunofluorescence/confocal microscopy, siRNA knockdown, centrosome counting, mutagenesis Molecular cell High 24289923
2014 OLA1 negatively regulates cell adhesion and spreading. OLA1-deficient cells show elevated FAK protein levels and decreased Ser3 phosphorylation of cofilin; OLA1-overexpressing cells show the opposite. OLA1 thus regulates actin dynamics and cell-matrix adhesion through FAK and cofilin. RNAi knockdown, gene overexpression, cell adhesion/spreading assays, Western blot for FAK and phospho-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, and interfering with eIF2 ternary complex (TC) formation. OLA1 depletion causes hypoactive ISR and reduces CHOP-mediated apoptosis, while promoting tumor growth and metastasis in vivo. Co-immunoprecipitation, GTPase assay, polysome profiling, ATF4/CHOP reporter assays, siRNA knockdown, xenograft tumor models Scientific reports High 26283179
2016 OLA1 contributes to epithelial-mesenchymal transition (EMT) in lung cancer by interacting with GSK3β and inhibiting GSK3β activity via promotion of its Ser9 phosphorylation. This suppresses GSK3β-mediated degradation of Snail, which in turn downregulates E-cadherin. Co-immunoprecipitation, kinase activity assay, siRNA knockdown, Western blot, TGF-β-induced EMT assay Oncotarget Medium 26863455
2016 OLA1 is required for normal cell cycle progression and organismal development in mice. Ola1-/- MEFs accumulate p21 due to enhanced mRNA translation mediated through an eIF2-dependent mechanism. Knockout of p21 partially rescues growth retardation of Ola1-/- embryos, placing OLA1 upstream of translational p21 control. Knockout mouse model, primary MEF culture, cell cycle analysis, polysome/translation assays, double-knockout epistasis (p21-/- Ola1-/-), immunohistochemistry Molecular and cellular biology High 27481995
2018 OLA1 requires interaction with BARD1 for proper centrosome number regulation. Five OLA1 missense mutants deficient in centrosome regulation were identified; three failed to bind BARD1. Phosphomimetic mutations restored BARD1 binding and rescued centrosome amplification. BARD1 knockdown or cancer-derived BARD1 mutants that fail to bind OLA1 also caused centrosome amplification. Co-immunoprecipitation, overexpression of OLA1 mutants, centrosome counting, BARD1 knockdown 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 using the SAM analogue Hey-SAM and validated in NTMT1 knockout HEK293FT cells. Activity-based substrate profiling with Hey-SAM analogue, CRISPR-Cas9 NTMT1 KO cell validation, mass spectrometry Chemical science High 31857877
2019 Decreased OLA1 expression in pulmonary artery cells of PPHN enhances CHIP affinity for Hsp70-SOD2 complexes, facilitating SOD2 ubiquitination and proteasomal degradation, impairing mitochondrial H2O2 generation. OLA1-deficient lambs and ola1-/- mice show downregulated SOD2, pulmonary arterial remodeling, and right ventricular hypertrophy. Co-immunoprecipitation, ubiquitination assay, OLA1 knockout mouse model, fetal lamb PPHN model, echocardiography Hypertension (Dallas, Tex. : 1979) High 31476900
2020 OLA1 localizes to spindles in mouse oocyte meiosis and is required for normal spindle assembly and spindle assembly checkpoint (SAC) activation. OLA1 knockdown causes multipolar spindles, premature anaphase onset, and precocious SAC inactivation. Immunofluorescence/confocal microscopy, nocodazole treatment, siRNA microinjection into oocytes, chromosome spreading PeerJ Medium 31915569
2020 HIV p17 protein interacts with OLA1 and disrupts the OLA1-GSK3β complex, leading to GSK3β hyperactivation, suppression of autophagy, and enhanced T cell proliferation under nutrient starvation. Co-immunoprecipitation, GSK3β activity assay, autophagy flux assay, T cell proliferation assay Journal of medical virology Medium 32790080
2021 ZFAS1 lncRNA recognizes the OBG-type functional domain of OLA1, facilitates exposure of its ATP-binding sites (NVGKST, residues 32–37), enhances OLA1 ATPase activity, and accelerates ATP hydrolysis and the Warburg effect in colorectal cancer cells. This axis is stabilized by the m6A reader IMP2. RNA pull-down, RIP, ATP hydrolysis assay, ECAR/lactate assay, co-immunoprecipitation, Western blot Journal of hematology & oncology Medium 34743750
2022 BARD1 acts as an ATPase activating protein for OLA1 via its BRCT domain binding to the OLA1 TGS domain through a conserved BUDR motif, increasing OLA1 ATPase kcat. A cancer-related BARD1 mutation V695L reduces BARD1-mediated OLA1 activation by perturbing the OLA1 binding site, as shown in a 1.88 Å crystal structure. Enzyme kinetics (ATPase assay), X-ray crystallography (1.88 Å), co-immunoprecipitation, mutagenesis Biochimica et biophysica acta. General subjects High 35134491
2023 Aurora A binds to OLA1 and polyubiquitinates it, targeting it for proteasomal degradation. NEK2 phosphorylates OLA1 at T124, which increases OLA1 binding to Aurora A and Aurora A-mediated polyubiquitination. Reduction of centrosomal OLA1 in G2 phase promotes pericentriolar material protein recruitment and centrosome maturation. Aurora A's E3 ligase activity is required for centrosome amplification induced by its overexpression. Co-immunoprecipitation, in vitro and in vivo ubiquitination assays, kinase assay, mutagenesis, centrosome imaging Cell reports High 37481721
2023 OLA1 phosphorylation at Ser232/Tyr236 triggers translocation from cytoplasm/mitochondria to the nucleus, and subsequent phosphorylation at Thr325 switches its biochemical activity from ATPase to GTPase, promoting transcription of nuclear-encoded mitochondrial bioenergetic genes. This process is regulated by ERK1/2 and restrained by PP1A. A phosphoresistant T325A OLA1 mutant fails to translocate and leads to cellular energy depletion. Phosphomimetic/phosphoresistant mutants, subcellular fractionation, nuclear translocation imaging, metabolic gene expression assays, ERK1/2 knockdown, PP1A assay, OLA1 knockout mice American journal of respiratory cell and molecular biology Medium 36481055
2024 HIV-1 p17 promotes STING signaling by binding OLA1 and inhibiting OLA1's regulation of STING. OLA1 normally interacts with STING and inhibits STING translocation and phosphorylation upon cGAMP stimulation. HIV-1 p17 (but not HIV-2 or SIV p17) also specifically promotes the ATPase and GTPase activities of OLA1. Co-immunoprecipitation, STING phosphorylation/translocation assay, cGAMP stimulation, ATPase/GTPase assay Journal of cell science Medium 38132845
2025 OLA1 interacts with Keap1 and disrupts the Keap1-Nrf2 interaction; when STING is activated, STING binds OLA1 and disrupts OLA1-Keap1 interactions, freeing Keap1 to promote Nrf2 degradation and thereby suppressing antioxidant defense and promoting ferroptosis. Co-immunoprecipitation, siRNA knockdown, Nrf2 activity assay, in vivo mouse model of POF International journal of biological macromolecules Medium 41352507
2026 Bi-allelic loss-of-function variants in OLA1 in humans cause a neurodevelopmental disorder with joint hypermobility. Proband-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. Human genetics (biallelic variants), proband-derived fibroblast functional assays, neuron differentiation assays, C. elegans ola-1 knockout with neurite imaging and transcriptomics American journal of human genetics High 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 96 34743750
2007 Human OLA1 defines an ATPase subfamily in the Obg family of GTP-binding proteins. The Journal of biological chemistry 90 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 62 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 55 23412384
2015 OLA1 regulates protein synthesis and integrated stress response by inhibiting eIF2 ternary complex formation. Scientific reports 38 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 31 26863455
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) 28 31476900
2016 OLA1, a Translational Regulator of p21, Maintains Optimal Cell Proliferation Necessary for Developmental Progression. Molecular and cellular biology 28 27481995
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 17 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 6 36481055
2014 OLA1 in centrosome biology alongside the BRCA1/BARD1 complex: looking beyond centrosomes. Molecular cell 6 24411079
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 5 37856434
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
2022 BARD1 is an ATPase activating protein for OLA1. Biochimica et biophysica acta. General subjects 2 35134491
2025 The Obg-like ATPase Ola1 prevents excessive mitochondrial reactive oxygen species by inhibiting MAPK/Pmk1 signaling in fission yeast. Microbiological research 1 40543417
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