The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

Research Report: Human OLA1 (UniProt Q9NTK5) — Functional Annotation and Translational Relevance

Executive summary

Obg-like ATPase 1 (OLA1; also called GTPBP9/DOC45) is the human eukaryotic homolog of the universally conserved YchF/Ola1 family of TRAFAC/Obg-like P-loop NTPases. It is an atypical NTPase that can bind/hydrolyze ATP and GTP but shows structural features favoring ATP, and it integrates stress signaling with translation initiation control, proteostasis, and mitochondria–nucleus (retrograde) communication. Recent 2023 work provides a mechanistic framework in which ERK1/2-dependent phosphorylation controls OLA1’s subcellular localization and switches its biochemical activity, thereby enabling OLA1 to act as a stress-responsive regulator of nuclear-encoded mitochondrial bioenergetic programs. Clinical/translational studies in 2023–2024 support OLA1 as a prognostic biomarker in several cancers and as a component of multi-gene prognostic signatures, with emerging interest in cardiovascular genetics and heart failure. (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 7-8, chen2024combinedola1and pages 6-7, wang2023clinicopathologicalsignificanceof pages 6-8)

1) Identity verification, key concepts, and definitions

1.1 Correct target protein and nomenclature

The requested target is human OLA1 (UniProt Q9NTK5), described as an Obg-like ATPase 1 in the TRAFAC class OBG-HflX-like GTPase superfamily and commonly discussed as the eukaryotic ortholog of bacterial YchF. Reviews explicitly treat “YchF/Ola1” as a conserved protein family and note ~45% identity (62% similarity) between human OLA1 and E. coli YchF. (jiang2025thefunctionof pages 69-71, jiang2025thefunctionof pages 67-69)

1.2 Protein family, domain architecture, and nucleotide specificity

Family/class: OLA1 belongs to the TRAFAC class and Obg-like family of P-loop NTPases/G proteins. (lin2023theuniversallyconserved pages 1-2, jiang2025thefunctionof pages 67-69)

Domain architecture: The YchF/Ola1 proteins are described as conserved three-domain proteins comprising an N-terminal G (NTPase) domain, a helical/coiled-coil domain, and a C-terminal TGS domain (often associated with RNA-binding functions). (jiang2025thefunctionof pages 69-71, jiang2025thefunctionofa pages 69-71)

Atypical G4 motif and ATP preference: A defining feature is a non-canonical G4 motif (often NxxE rather than the canonical NKxD), which is proposed to underlie altered nucleotide specificity and ATP preference relative to typical GTPases. (jiang2025thefunctionof pages 69-71, jiang2025thefunctionofa pages 69-71, lin2023theuniversallyconserved pages 2-4)

Dual ATP/GTP binding/hydrolysis: Reviews and primary work indicate OLA1/YchF can bind and hydrolyze both ATP and GTP, although multiple structural determinants bias human OLA1 toward ATP. For example, in the Lin 2023 review, residue-level interactions in hOLA1 (e.g., Asn230 in the G4 motif; Leu231 and Ser310 supporting adenine recognition) are discussed as supporting ATP preference. (lin2023theuniversallyconserved pages 2-4)

1.3 Conceptual roles: “unconventional G protein” and translation/proteostasis coupling

A current conceptual framing is that YchF/OLA1 family proteins are unconventional G proteins that can couple NTP hydrolysis to translation and proteostasis (ribosome/proteasome associations), with sensitivity to oxidative stress. (lin2023theuniversallyconserved pages 1-2)

2) Molecular function: biochemical activities, substrates, and mechanisms

2.1 What reaction does OLA1 catalyze?

At the most direct biochemical level, OLA1 is an NTPase that catalyzes nucleoside triphosphate hydrolysis (ATP→ADP+Pi; and in some contexts GTP→GDP+Pi). Its active-site architecture is atypical for canonical Ras-like GTPases and is associated with an ATP bias. (lin2023theuniversallyconserved pages 2-4)

2.2 Regulation by phosphorylation: activity switching and mechanistic consequences (major 2023 advance)

A key recent development is a phosphorylation-controlled model from Sidlowski et al. (peer-reviewed, Apr 2023):

• ERK1 phosphorylation at Ser232/Tyr236 triggers OLA1 translocation from cytoplasm/mitochondria to nucleus. (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 7-8)
• ERK2 phosphorylation at Thr325 alters OLA1 biochemical behavior and DNA binding, with evidence that T325 phosphorylation increases GTPase activity and suppresses ATPase activity and potentiates DNA binding. (sidlowski2023ola1phosphorylationgoverns pages 9-10, sidlowski2023ola1phosphorylationgoverns pages 7-8)

This phosphorylation-dependent biochemical “switch” provides a mechanistic explanation for how OLA1 can act as a stress-responsive effector linking kinase signaling to mitochondrial gene regulation. (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 9-10)

2.3 Protein and macromolecular interactions (mechanistic and regulatory)

Translation initiation machinery: OLA1 is reported to bind eIF2 and to inhibit translation initiation by preventing formation of the eIF2•GTP•Met-tRNAi ternary complex, thereby modulating pathways central to the integrated stress response (ISR). (jiang2025thefunctionofa pages 74-76, lin2023theuniversallyconserved pages 6-8)

Proteostasis / chaperone axis: OLA1 has been linked to heat-shock resilience via HSP70 stabilization and to oxidative stress control through effects on the CHIP/HSP70/SOD2 axis. (lin2023theuniversallyconserved pages 6-8)

Mitochondria-to-nucleus signaling complex: In pulmonary vascular cells, OLA1 is described as residing on mitochondria anchored by vimentin, then relocating to the nucleus via interaction with importin-α1 (KPNA2); disrupting importin-α1 blocks nuclear translocation of phosphorylated OLA1. (sidlowski2023ola1phosphorylationgoverns pages 7-8, sidlowski2023ola1phosphorylationgoverns pages 8-9, sidlowski2023ola1phosphorylationgoverns pages 9-10)

Regulatory partners: ERK1/2 and PP1A are implicated as key regulators; PP1A is described as restraining ERK-driven signaling when stress abates and is also reported among interactors in the ubiquitination/regulation framework. (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 9-10)

3) Biological processes, pathways, and localization

3.1 Subcellular localization (baseline and stress-induced)

Baseline localization: OLA1 is described as primarily cytoplasmic in the Lin 2023 review, and in cardiomyocytes it is mainly cytoplasmic with lower nuclear levels. (lin2023theuniversallyconserved pages 6-8, dubey2024identificationanddevelopment pages 8-12)

Mitochondrial localization: In pulmonary vascular cells, OLA1 shows a strong mitochondrial pool and is reported to localize to the outer mitochondrial membrane (supported by biochemical fractionation/protease protection and marker co-staining). (sidlowski2023ola1phosphorylationgoverns pages 4-5)

Stress-induced nuclear translocation: Cellular stresses (hypoxia, H2O2, mitochondrial uncoupling) induce nuclear accumulation of OLA1, with mechanistic dependence on ERK phosphorylation and nuclear import machinery (importin-α1) and the cytoskeletal intermediate filament vimentin. (sidlowski2023ola1phosphorylationgoverns pages 4-5, sidlowski2023ola1phosphorylationgoverns pages 7-8, sidlowski2023ola1phosphorylationgoverns pages 8-9)

Visual evidence: Cropped figure/table regions from Sidlowski et al. 2023 show (i) OLA1 cytoplasm/mitochondria localization, (ii) stress-induced nuclear translocation, and (iii) phosphorylation sites and ERK-dependence. (sidlowski2023ola1phosphorylationgoverns media 66b79221, sidlowski2023ola1phosphorylationgoverns media d67ed0b1, sidlowski2023ola1phosphorylationgoverns media 96be911f, sidlowski2023ola1phosphorylationgoverns media 2945524d, sidlowski2023ola1phosphorylationgoverns media 0b0b8e08)

3.2 Translation regulation and the integrated stress response (ISR)

A mechanistic theme across the literature is that OLA1 modulates translation initiation by acting on the eIF2 step:

• OLA1 binds eIF2 and stabilizes eIF2 in its GDP-bound state, inhibiting ternary complex formation and thereby decreasing canonical cap-dependent initiation while favoring stress-adaptive alternative initiation. (jiang2025thefunctionofa pages 74-76, jiang2025thefunctionof pages 74-76)
• The Lin 2023 review summarizes that hOLA1 blocks ternary complex formation and thereby prevents eIF2 from delivering initiator tRNA to the 40S ribosome. (lin2023theuniversallyconserved pages 6-8)

3.3 Oxidative stress and antioxidant response

OLA1 has long-standing links to oxidative stress regulation, including suppressing antioxidant responses via nontranscriptional mechanisms and influencing mitochondrial antioxidant enzyme status (SOD2), with downstream implications for cellular stress tolerance. (jiang2025thefunctionof pages 67-69, jiang2025thefunctionof pages 80-82, sidlowski2023ola1phosphorylationgoverns pages 11-11)

3.4 Mitochondrial bioenergetics and mitonuclear retrograde signaling (major 2023 advance)

Sidlowski et al. 2023 propose and experimentally support a model where OLA1 couples stress/redox cues to nuclear transcription programs regulating mitochondrial bioenergetics:

• Stress → ERK1/2 phosphorylation → OLA1 nuclear relocalization → altered DNA binding and transcriptional activation of nuclear-encoded mitochondrial genes. (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 9-10, sidlowski2023ola1phosphorylationgoverns pages 7-8)
• OLA1 depletion downregulates nuclear genes involved in oxidative phosphorylation and mitochondrial assembly/structure; phosphomimetic nuclear OLA1 (T325D) rescues mitochondrial gene expression better than phosphoresistant T325A. (sidlowski2023ola1phosphorylationgoverns pages 9-10)
• Functional metabolic outcomes include lower cellular ATP, higher lactate, and increased ADP:ATP ratio in OLA1-deficient endothelial cells. (sidlowski2023ola1phosphorylationgoverns pages 9-10, sidlowski2023ola1phosphorylationgoverns pages 8-9)

3.5 Cancer-associated pathways (EMT, cell cycle, centrosome regulation)

Multiple sources connect OLA1 to tumor-relevant pathways:

• EMT: OLA1 has been reported to contribute to EMT via the GSK3β/Snail/E-cadherin axis (noting that effects may be context dependent across cancer types). (jiang2025thefunctionofa pages 80-82, wang2023clinicopathologicalsignificanceof pages 6-8)
• Cell cycle and proliferation: OLA1 is described as a translational regulator of p21, and clinical/translational studies link OLA1 to P21/CDK2-related tumor progression models. (jiang2025thefunctionof pages 79-80, sidlowski2023ola1phosphorylationgoverns pages 11-11)
• DNA damage/centrosome regulation: OLA1 is described as DNA-damage regulated (DOC45) and a BRCA1/BARD1-interacting factor implicated in centrosome regulation, providing a mechanistic bridge between stress responses and genome stability phenotypes. (jiang2025thefunctionofa pages 80-82, wang2023clinicopathologicalsignificanceof pages 6-8)

4) Recent developments (prioritizing 2023–2024)

4.1 2023: Phosphorylation-controlled localization and NTPase switching model

The strongest 2023 mechanistic advance is the ERK/PP1A-centered phosphorylation framework linking OLA1 localization and enzymatic state to mitochondrial gene regulation and bioenergetic phenotypes. (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 9-10, sidlowski2023ola1phosphorylationgoverns pages 7-8)

4.2 2023: Clinical pathology evidence in gastric cancer

A 2023 gastric cancer tissue microarray study (334 patients) linked high OLA1 protein expression to more aggressive clinicopathological features and poorer survival, and reported correlation with Snail (EMT regulator). (wang2023clinicopathologicalsignificanceof pages 6-8)

4.3 2024: HCC prognostic signature and drug-sensitivity linkage

A 2024 HCC study proposed an OLA1|CLEC3B ratio-based prognostic signature validated across TCGA/ICGC, and provided experimental evidence that OLA1 knockdown reduces proliferation and increases gemcitabine sensitivity in Huh7 cells. (chen2024combinedola1and pages 6-7, chen2024combinedola1and pages 2-3)

4.4 2024: Cardiovascular genetics and functional models

2024 preprints report (i) a proposed PCR-based screen for a coding OLA1 variant in heart failure cohorts and (ii) cardiac-specific genetic deletion phenotypes consistent with cardiomyopathy in animal models. (dubey2024identificationanddevelopment pages 8-12, dubey2024obglikeatpase1 pages 14-18)

5) Current applications and real-world implementations

5.1 Prognostic biomarker use in cancer (clinical pathology implementation)

In gastric cancer, OLA1 IHC stratification was associated with survival differences and remained an independent prognostic factor in multivariate analysis. (wang2023clinicopathologicalsignificanceof pages 6-8)

5.2 Multi-gene prognostic signatures in HCC

The OLA1|CLEC3B ratio-based risk score provides time-dependent ROC performance in two independent cohorts, supporting its potential for clinical risk stratification workflows, and was incorporated into nomogram modeling. (chen2024combinedola1and pages 6-7, chen2024combinedola1and pages 2-3)

5.3 Emerging cardiovascular implementation: genotyping assay development

A 2024 medRxiv report describes development of a cost-effective Tetra-ARMS PCR assay for a putative OLA1 coding variant in failing heart contexts and highlights OLA1 downregulation in failing human hearts, representing an early translational step toward genetic screening/stratification in cardiomyopathy research settings. (dubey2024identificationanddevelopment pages 8-12)

6) Quantitative statistics and data from recent studies

6.1 Gastric cancer prognosis (2023)

In a 334-patient gastric cancer cohort, high OLA1 expression associated with worse overall survival (p = 0.002) and showed associations with tumor size, lymph node metastasis, and advanced stage. Multivariate Cox regression reported OLA1 expression HR = 0.573 (95% CI 0.376–0.872), p = 0.009, and OLA1-Snail correlation r = 0.334, p < 0.001. (wang2023clinicopathologicalsignificanceof pages 6-8)

6.2 HCC prognostic signature ROC performance (2024)

For the OLA1|CLEC3B signature, time-dependent AUCs were:

• TCGA: 1-year 0.735; 2-year 0.720; 3-year 0.713
• ICGC: 1-year 0.722; 2-year 0.728; 3-year 0.737

(chen2024combinedola1and pages 6-7)

6.3 Functional and metabolic phenotypes (2023 mechanistic study)

In endothelial OLA1 deficiency models, OLA1 loss is associated with decreased ATP and increased lactate and ADP:ATP ratio (figures summarized as statistically significant; *P < 0.0001). (sidlowski2023ola1phosphorylationgoverns pages 9-10, sidlowski2023ola1phosphorylationgoverns pages 8-9)

6.4 Cardiovascular functional models (2024)

A 2024 bioRxiv study reports that heart-specific Ola1 knockdown in Drosophila reduces heart rate (157 bpm control vs 127±7 bpm knockdown, P = 0.007) and causes developmental lethality, and that mouse cardiac deletion produces dilation and reduced function (e.g., ~10% decrease in EF/FS with age). (dubey2024obglikeatpase1 pages 14-18)

7) Expert synthesis and analysis (authoritative interpretations)

7.1 Unifying functional model

Across reviews and 2023 primary work, OLA1 can be interpreted as a stress-responsive NTPase “hub” operating at the interface of:

1. Translation initiation control (eIF2 ternary-complex inhibition; ISR-adjacent regulation) (jiang2025thefunctionofa pages 74-76, lin2023theuniversallyconserved pages 6-8)
2. Proteostasis/chaperone networks (HSP70/CHIP; mitochondrial antioxidant enzyme stability) (lin2023theuniversallyconserved pages 6-8)
3. Mitonuclear communication and metabolic adaptation (ERK-dependent phosphorylation triggers nuclear relocation and transcriptional regulation of mitochondrial bioenergetic programs) (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 9-10)

A notable 2023 conceptual advance is that OLA1 is not merely a cytosolic translational regulator but can become a phosphorylation-controlled, nucleus-localized regulator of mitochondrial gene programs under stress. (sidlowski2023ola1phosphorylationgoverns pages 1-2, sidlowski2023ola1phosphorylationgoverns pages 9-10)

7.2 Important caveats and open questions

• Context dependence in cancer: Clinical correlations (e.g., prognosis, EMT association) appear to vary across tumor types, and some reports suggest bidirectional effects depending on cellular context and in vitro vs in vivo setting. (wang2023clinicopathologicalsignificanceof pages 6-8)
• Direct catalytic “substrate specificity”: While OLA1’s immediate substrates are NTPs (ATP/GTP), many downstream phenotypes may be mediated through binding interactions and localization rather than classical enzyme–substrate turnover on a unique small-molecule substrate. (lin2023theuniversallyconserved pages 2-4, sidlowski2023ola1phosphorylationgoverns pages 7-8)

8) Summary table of key sources (2023–2024 prioritized)

Table: This table summarizes major recent and foundational studies on human OLA1, emphasizing function, localization, pathways, and any available quantitative clinical or experimental metrics. It is useful as a quick reference for both mechanistic biology and translational relevance.

Selected key references with URLs (publication dates)

• Sidlowski et al. “OLA1 Phosphorylation Governs the Mitochondrial Bioenergetic Function of Pulmonary Vascular Cells.” Apr 2023. https://doi.org/10.1165/rcmb.2022-0186oc (sidlowski2023ola1phosphorylationgoverns pages 1-2)
• Lin et al. “The Universally Conserved Unconventional G Protein YchF Is Critical for Growth and Stress Response.” Apr 2023. https://doi.org/10.3390/life13041058 (lin2023theuniversallyconserved pages 1-2)
• Wang et al. “Clinicopathological significance of Obg-like ATPase 1 and its association with Snail in gastric cancer.” Jan 2023. https://doi.org/10.5114/pjp.2023.127265 (wang2023clinicopathologicalsignificanceof pages 6-8)
• Chen et al. “Combined OLA1 and CLEC3B Gene Is a Prognostic Signature for Hepatocellular Carcinoma…” Apr 2024. https://doi.org/10.1177/15330338241241935 (chen2024combinedola1and pages 6-7)
• Dubey et al. “Identification and development of Tetra-ARMS PCR-based screening test for a genetic variant of OLA1…” Oct 2024 (posted). https://doi.org/10.1101/2023.10.16.23296746 (dubey2024identificationanddevelopment pages 8-12)

References

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3. (chen2024combinedola1and pages 6-7): Zhoufeng Chen, Liuwei Zeng, Zhuoyan Chen, Jun Xu, Xiangting Zhang, Huiya Ying, Yuan Zeng, and Fujun Yu. Combined ola1 and clec3b gene is a prognostic signature for hepatocellular carcinoma and impact tumor progression. Technology in Cancer Research & Treatment, Apr 2024. URL: https://doi.org/10.1177/15330338241241935, doi:10.1177/15330338241241935. This article has 1 citations and is from a peer-reviewed journal.

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13. (sidlowski2023ola1phosphorylationgoverns pages 8-9): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

14. (dubey2024identificationanddevelopment pages 8-12): Praveen K Dubey, Shubham Dubey, Sarojini Singh, Purnima Devaki Bhat, Steven Pogwizd, and Prasanna Krishnamurthy. Identification and development of tetra-arms pcr-based screening test for a genetic variant of ola1 (tyr254cys) in the human failing heart. medRxiv, Oct 2024. URL: https://doi.org/10.1101/2023.10.16.23296746, doi:10.1101/2023.10.16.23296746. This article has 7 citations.

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16. (sidlowski2023ola1phosphorylationgoverns media 66b79221): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

17. (sidlowski2023ola1phosphorylationgoverns media d67ed0b1): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

18. (sidlowski2023ola1phosphorylationgoverns media 96be911f): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

19. (sidlowski2023ola1phosphorylationgoverns media 2945524d): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

20. (sidlowski2023ola1phosphorylationgoverns media 0b0b8e08): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

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22. (jiang2025thefunctionof pages 80-82): H Jiang. The function of ychf in bacterial stress resistance. Unknown journal, 2025.

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24. (jiang2025thefunctionofa pages 80-82): H Jiang. The function of ychf in bacterial stress resistance. Unknown journal, 2025.

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26. (chen2024combinedola1and pages 2-3): Zhoufeng Chen, Liuwei Zeng, Zhuoyan Chen, Jun Xu, Xiangting Zhang, Huiya Ying, Yuan Zeng, and Fujun Yu. Combined ola1 and clec3b gene is a prognostic signature for hepatocellular carcinoma and impact tumor progression. Technology in Cancer Research & Treatment, Apr 2024. URL: https://doi.org/10.1177/15330338241241935, doi:10.1177/15330338241241935. This article has 1 citations and is from a peer-reviewed journal.

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28. (sidlowski2023ola1phosphorylationgoverns pages 5-6): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

29. (sidlowski2023ola1phosphorylationgoverns pages 6-7): Paul Sidlowski, Amanda Czerwinski, Yong Liu, Pengyuan Liu, Ru-Jeng Teng, Suresh Kumar, Clive Wells, Kirkwood Pritchard, Girija G. Konduri, and Adeleye J. Afolayan. Ola1 phosphorylation governs the mitochondrial bioenergetic function of pulmonary vascular cells. American Journal of Respiratory Cell and Molecular Biology, 68:395-405, Apr 2023. URL: https://doi.org/10.1165/rcmb.2022-0186oc, doi:10.1165/rcmb.2022-0186oc. This article has 11 citations and is from a peer-reviewed journal.

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32. (chen2024combinedola1and pages 1-2): Zhoufeng Chen, Liuwei Zeng, Zhuoyan Chen, Jun Xu, Xiangting Zhang, Huiya Ying, Yuan Zeng, and Fujun Yu. Combined ola1 and clec3b gene is a prognostic signature for hepatocellular carcinoma and impact tumor progression. Technology in Cancer Research & Treatment, Apr 2024. URL: https://doi.org/10.1177/15330338241241935, doi:10.1177/15330338241241935. This article has 1 citations and is from a peer-reviewed journal.

33. (chen2024combinedola1and pages 7-10): Zhoufeng Chen, Liuwei Zeng, Zhuoyan Chen, Jun Xu, Xiangting Zhang, Huiya Ying, Yuan Zeng, and Fujun Yu. Combined ola1 and clec3b gene is a prognostic signature for hepatocellular carcinoma and impact tumor progression. Technology in Cancer Research & Treatment, Apr 2024. URL: https://doi.org/10.1177/15330338241241935, doi:10.1177/15330338241241935. This article has 1 citations and is from a peer-reviewed journal.

34. (dubey2024identificationanddevelopment pages 15-19): Praveen K Dubey, Shubham Dubey, Sarojini Singh, Purnima Devaki Bhat, Steven Pogwizd, and Prasanna Krishnamurthy. Identification and development of tetra-arms pcr-based screening test for a genetic variant of ola1 (tyr254cys) in the human failing heart. medRxiv, Oct 2024. URL: https://doi.org/10.1101/2023.10.16.23296746, doi:10.1101/2023.10.16.23296746. This article has 7 citations.

35. (dubey2024obglikeatpase1 pages 23-27): Praveen K Dubey, Sarojini Singh, Hussain Khalil, Goutham K Kommini, Krishna Moorthi Bhat, and Prasanna Krishnamurthy. Obg-like atpase 1 genetic deletion leads to dilated cardiomyopathy in mice and structural changes in drosophila heart. bioRxiv, Jun 2024. URL: https://doi.org/10.1101/2024.05.28.596265, doi:10.1101/2024.05.28.596265. This article has 1 citations.

Artifacts

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Citations

1. lin2023theuniversallyconserved pages 2-4
2. lin2023theuniversallyconserved pages 1-2
3. lin2023theuniversallyconserved pages 6-8
4. wang2023clinicopathologicalsignificanceof pages 6-8
5. dubey2024identificationanddevelopment pages 8-12
6. wang2023clinicopathologicalsignificanceof pages 8-9
7. jiang2025thefunctionof pages 69-71
8. jiang2025thefunctionof pages 67-69
9. jiang2025thefunctionofa pages 69-71
10. jiang2025thefunctionofa pages 74-76
11. jiang2025thefunctionof pages 74-76
12. jiang2025thefunctionof pages 80-82
13. jiang2025thefunctionofa pages 80-82
14. jiang2025thefunctionof pages 79-80
15. wang2023clinicopathologicalsignificanceof pages 1-2
16. dubey2024identificationanddevelopment pages 15-19
17. https://doi.org/10.1165/rcmb.2022-0186oc
18. https://doi.org/10.3390/life13041058
19. https://doi.org/10.5114/pjp.2023.127265
20. https://doi.org/10.1177/15330338241241935
21. https://doi.org/10.1101/2023.10.16.23296746
22. https://doi.org/10.1101/2024.05.28.596265
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25. https://doi.org/10.1073/pnas.0907334106
26. https://doi.org/10.1165/rcmb.2022-0186oc,
27. https://doi.org/10.1177/15330338241241935,
28. https://doi.org/10.5114/pjp.2023.127265,
29. https://doi.org/10.3390/life13041058,
30. https://doi.org/10.1101/2023.10.16.23296746,
31. https://doi.org/10.1101/2024.05.28.596265,