| Study (first author, year) | Publication date/month | Type | System (cells/tissues/animal) | Main finding relevant to OLA1 function/localization/pathway | Key quantitative stats | URL/DOI |
|---|---|---|---|---|---|---|
| Sidlowski 2023 | Apr 2023 | Primary mechanistic study | Human pulmonary vascular cells; mouse endothelial/lung models | OLA1 localizes to cytoplasm and mitochondria and stress-inducibly translocates to the nucleus. ERK1 phosphorylation at S232/Y236 promotes nuclear import, and ERK2 phosphorylation at T325 shifts OLA1 toward GTPase and DNA-binding activity to regulate nuclear-encoded mitochondrial bioenergetic genes. (pqac-00000008, pqac-00000024, pqac-00000025, pqac-00000027, pqac-00000044, pqac-00000045, pqac-00000046, pqac-00000049, pqac-00000050) | Enzyme/phosphorylation effects reported as highly significant with *P < 0.00001; vimentin/importin perturbation reduced nuclear phospho-OLA1 with *P < 0.001; OLA1 depletion lowered ATP and raised lactate and ADP:ATP with *P < 0.0001 in figure summary. (pqac-00000045, pqac-00000047, pqac-00000050) | https://doi.org/10.1165/rcmb.2022-0186oc |
| Lin 2023 | Apr 2023 | Review | Cross-species synthesis with human OLA1 emphasis | Reviews YchF/OLA1 as a conserved TRAFAC/Obg-like NTPase that hydrolyzes ATP and GTP, with human OLA1 biased toward ATP. Summarizes roles in eIF2 ternary-complex inhibition, oxidative-stress biology, and HSP70/CHIP-SOD2 proteostasis. (pqac-00000002, pqac-00000003, pqac-00000004, pqac-00000015, pqac-00000019) | No original cohort statistics; summarizes human OLA1 as a ~45 kDa cytoplasmic protein and reviews knockdown/overexpression phenotypes qualitatively. (pqac-00000003, pqac-00000019) | https://doi.org/10.3390/life13041058 |
| Wang 2023 | Jan 2023 | Clinical pathology study | Gastric cancer patient tissues; qRT-PCR on 30 paired tissues; IHC on 334 cases | OLA1 is elevated in gastric cancer and associated with aggressive clinicopathologic features. OLA1 expression positively correlates with Snail, linking OLA1 to EMT-related prognostic biology. (pqac-00000036, pqac-00000051, pqac-00000052, pqac-00000062, pqac-00000064) | Shorter overall survival with high OLA1, p = 0.002. Multivariate Cox: OLA1 HR 0.573, 95% CI 0.376-0.872, p = 0.009; lymph-node metastasis p = 0.0037; TNM stage p < 0.0001; OLA1-Snail correlation r = 0.334, p < 0.001. (pqac-00000051, pqac-00000064) | https://doi.org/10.5114/pjp.2023.127265 |
| Chen 2024 | Apr 2024 | Clinical translational study | HCC cohorts from TCGA and ICGC; Huh7 cells and gemcitabine-resistant Huh7 | Defines OLA1/CLEC3B as a prognostic HCC signature. High-risk OLA1-related tumors show stronger cell-cycle programs and worse prognosis, and OLA1 knockdown suppresses proliferation, increases apoptosis, prolongs S phase, and increases gemcitabine sensitivity. (pqac-00000034, pqac-00000037, pqac-00000053, pqac-00000054, pqac-00000063, pqac-00000065, pqac-00000070) | Cohorts: TCGA 370 HCC and 50 adjacent tissues; ICGC 231 HCC and 199 adjacent tissues. AUCs for OLA1/CLEC3B: TCGA 0.735 at 1 year, 0.720 at 2 years, 0.713 at 3 years; ICGC 0.722, 0.728, 0.737. Cell-cycle correlations P < 0.05. (pqac-00000054, pqac-00000063, pqac-00000065) | https://doi.org/10.1177/15330338241241935 |
| Dubey 2024 medRxiv | Oct 2024 preprint | Preprint cardiovascular genetics study | Human failing and non-failing heart tissue; AC16 cardiomyocytes; REGARDS cross-reference | Reports OLA1 downregulation in failing human hearts and predominantly cytoplasmic localization in cardiomyocytes. Also describes a Tetra-ARMS PCR assay for an OLA1 coding variant as a potential genotyping tool in cardiomyopathy research. (pqac-00000031, pqac-00000032, pqac-00000035, pqac-00000055, pqac-00000069) | REGARDS cohort referenced: 30239 participants. OLA1 CDS 1191 bp encoding 396 aa; gene has 11 exons and intronic span >100 kb. Significant downregulation in failing heart reported, but no HR or AUC values in cited pages. (pqac-00000035, pqac-00000055, pqac-00000069) | https://doi.org/10.1101/2023.10.16.23296746 |
| Dubey 2024 bioRxiv | Jun 2024 | Preprint functional animal study | Cardiomyocyte-specific mouse Ola1 deletion; Drosophila heart RNAi | Loss of Ola1 causes dilated cardiomyopathy and cardiac structural and functional defects, supporting a conserved role in cardiac homeostasis. (pqac-00000033, pqac-00000038) | Fly heart-specific knockdown caused 58% pupal lethality, about 25% smaller pupae, and reduced heart rate from 157 bpm in controls to 127 +/- 7 bpm, P = 0.007. Mouse haploinsufficiency caused about 10% decrease in ejection fraction and fractional shortening with age-dependent dilation. (pqac-00000038) | https://doi.org/10.1101/2024.05.28.596265 |
| Koller-Eichhorn 2007 | 2007 | Foundational biochemical study | Human OLA1 biochemical characterization | Established human OLA1 as an ATPase subfamily within the Obg family of nucleotide-binding proteins, foundational for later work on atypical ATP/GTP handling. (pqac-00000052) | Foundational study; no recent clinical performance metrics reported here. (pqac-00000052) | https://doi.org/10.1074/jbc.M700541200 |
| Chen 2015 | 2015 | Foundational mechanistic study | Human cell systems | Demonstrated that OLA1 regulates protein synthesis and the integrated stress response by inhibiting eIF2 ternary-complex formation, a core mechanism for OLA1 in translation control. (pqac-00000018, pqac-00000052) | Mechanistic result centered on inhibition of eIF2 ternary-complex formation rather than cohort-level HR or AUC metrics. (pqac-00000018, pqac-00000052) | https://doi.org/10.1038/srep13241 |
| Zhang 2009 | Sep 2009 | Foundational mechanistic study | Human cell systems | Identified OLA1 as an Obg-like ATPase that suppresses antioxidant responses via nontranscriptional mechanisms, establishing the oxidative-stress link in later OLA1 literature. (pqac-00000014, pqac-00000062) | Foundational mechanistic study; no AUC or HR values reported here. (pqac-00000014, pqac-00000062) | https://doi.org/10.1073/pnas.0907334106 |


*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.*