GTPBP9 Blocking Peptide
- Known as:
- GTPBP9 Blocking Peptide
- Catalog number:
- 33r-3413
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- GTPBP9 Blocking Peptide
Related genes to: GTPBP9 Blocking Peptide
- Gene:
- OLA1 NIH gene
- Name:
- Obg like ATPase 1
- Previous symbol:
- GTPBP9
- Synonyms:
- PTD004
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 2006-08-08
- Date modifiied:
- 2016-08-11
Related products to: GTPBP9 Blocking Peptide
Related articles to: GTPBP9 Blocking Peptide
- The non-canonical translation factor OBG-like ATPase 1 (OLA1) is conserved across all domains of life. OLA1 has been studied for decades by many groups, often under different names such GBP45, GTBP9, DOC45, PTD004, EngD, YyaF, Ybr025c, and in bacteria, YchF. Studies have correlated OLA1 with iron metabolism, oxidative stress response, mediation of temperature stress, and virulence. OLA1 has gained attention for its implicated role in a wide range of health conditions and cellular processes including cancer, centrosome regulation/cell proliferation, heart disease, persistent pulmonary hypertension of the newborn, mitochondrial function, neuronal differentiation, protein degradation, atherosclerosis, Down's Syndrome, as well as ribosome-dependent protein synthesis. On the background of such a wide range of functional implications, insight into the molecular mechanism of the evolutionary ancient OLA1 will help to explain the breadth of phenotypic traits. Information about the different protein structural domains present in OLA1 and results fromOLA1 in vivo and in vitro studies suggest a role in ribosome dependent translation regulation based on molecular mimicry with the canonical translation factors. - Source: PubMed
Publication date: 2026/04/16
Semmelrock JessicaWieden Hans-Joachim - Cytoskeletal organization, cell adhesion, and cell motility are key to neuronal development and functional synapses. Obg-like ATPase 1 (OLA1) regulates cell-matrix adhesion by modulating focal adhesion kinase (FAK) levels, therefore regulating cytoskeletal dynamics and cell motility. To date, however, no Mendelian phenotypes in humans have been linked to OLA1. We identified fourteen individuals from nine families in whom hypermobility-neurodevelopmental disorder with distinct facies is linked to bi-allelic deleterious variants in OLA1. The hypermobility phenotype evoked a diagnosis of Ehlers-Danlos syndrome (EDS) in some affected individuals. The loss-of-function nature of these variants is confirmed in proband-derived fibroblasts, recapitulating the impaired migration and proliferation phenotype previously described in OLA1-deficient cells. To explore the pathogenesis of abnormal neurodevelopment in our probands, we investigated neurons derived from proband fibroblasts and identified impaired adhesion and cytoskeletal control. Modeling ola-1 deficiency in C. elegans revealed reduced neurite numbers compared to the wild type. Additionally, transcriptomic analysis of the ola-1-deficient worms suggested that dysregulation of key signaling pathways results in suppression of microtubule dynamics and axon regrowth, ultimately crippling the regenerative competence of mutant animals compared to wild-type controls. Our results support an autosomal-recessive OLA1-related hypermobility-neurodevelopmental disorder and suggest that dysregulation of key signaling pathways results in the suppression of microtubule dynamics as a potential underlying mechanism. - Source: PubMed
Publication date: 2026/03/25
AlAbdi LamaSezer AbdullahAlzahrani FatemaCevik SebihaDemir ZanyarAbdullah Nor LindaDurukan ÖzlemDallı EfeHashem Mais OAbuyousef OmarAljamal BayanHelaby RanaRadwan MonaJaafar AmalAlshidi TarfaSalem IsraaHamid HalimaAlhaddad BaderBakur KhadijahTaşdelen ElifcanKılıç MustafaAl-Owain MohammedAlhashem AmalBratland EirikPaulsen JulieHouge Douzgos GunnarPoliti Anya RevahUguen KevinMasson EmmanuelleAudebert SeverineAlAnzi TalalArold Stefan TErgin BoraIbrahim Leena AKaplan Oktay IAlkuraya Fowzan S - Premature ovarian failure (POF) is a serious reproductive disorder that deprives women of fertility and predisposes them to long-term metabolic, cardiovascular, and neuropsychological complications. Here we reveal that cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway driven ferroptosis is a key mechanism of granulosa-cell loss in POF. Mitochondrial stress releases cytosolic mtDNA, activating the cGAS-STING pathway. Activated STING was found to be a key upstream driver of ferroptosis by suppressing the Nrf2-mediated antioxidant defense system. Mechanistically, we identified Obg-like ATPase 1 (OLA1) as a novel STING-interacting protein. STING activation enhanced its binding to OLA1, disrupting the OLA1-Keap1 interactions, which in turn liberated Keap1 to promote Nrf2 degradation. Gene knockdown or pharmacologic inhibition of STING restored Nrf2 activity, limited ferroptosis in cellular models of POF and preserved follicular integrity in murine models of POF. Furthermore, we demonstrate that the natural flavonoid Icariin (ICA) binds directly to the His50/Asn131 pocket of STING, competitively displacing OLA1 and thereby enhancing OLA1-Keap1 interaction. This molecular realignment restores Nrf2 signaling, attenuates ferroptosis, and significantly preserves ovarian reserve in vivo. Collectively, our findings define the STING-OLA1-Keap1-Nrf2 axis as a pivotal driver of ferroptosis in POF and position ICA as a STING-targeting agent for this pathway. This mechanistic insight offers a substantial foundation for developing targeted ovarian-protective therapies, providing a mechanistic basis for exploring new therapeutic strategies for POF. - Source: PubMed
Publication date: 2025/12/04
Zhang NieLi JiaoyuZhang RuixinChen HongxuHe FangLi FangfangHe ZhuoyingLiu XiaoyingCheng LinghuiZhong FeiZhu Fengyu - Early detection of hepatocellular carcinoma (HCC) enhances survival outcomes. Tumor-associated autoantibodies demonstrate early emergence during carcinogenesis, offering potential as non-invasive diagnostic biomarkers. This multicenter study aims to evaluate the diagnostic value of anti-OLA1 autoantibody in HCC. - Source: PubMed
Publication date: 2025/10/30
Xiong WenzhuoDuan XuehuiDai LipingWang PengYe HuaShi JianxiangWang Keyan - Gastric cancer (GC) is a leading cause of cancer-related deaths due to late diagnosis. Altered glycolytic metabolism, notably the Warburg effect, plays a critical role in tumorigenesis, offering potential for early detection and targeted therapy. - Source: PubMed
Publication date: 2025/08/25
Xu YifanZhang ChonghuiWu JinpengQiu MingyangZhu MengWang ChaoFeng Yugong