HO-1 Antibody (OASE00346)
- Known as:
- HO-1 Antibody (OASE00346)
- Catalog number:
- oase00346
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- HO-1 Antibody (OASE00346)
Related genes to: HO-1 Antibody (OASE00346)
- Gene:
- SARNP NIH gene
- Name:
- SAP domain containing ribonucleoprotein
- Previous symbol:
- -
- Synonyms:
- THO1, Hcc-1, CIP29
- Chromosome:
- 12q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2009-04-22
- Date modifiied:
- 2016-11-10
Related products to: HO-1 Antibody (OASE00346)
Related articles to: HO-1 Antibody (OASE00346)
- Gallbladder cancer (GBC) is a highly aggressive malignancy, and its robust antioxidant defense system frequently leads to profound therapeutic resistance. Targeted disruption of redox homeostasis offers a potential strategy to overcome such resistance. In this study, we developed ICFe@D, a supramolecular nanomedicine co-assembled from iso-liquiritigenin (ISL), Fe³⁺, and chlorin e6 (Ce6) within a DSPE-PEG matrix, to trigger combined ferroptosis and apoptosis. As a tumor microenvironment (TME)-responsive platform, ICFe@D systematically dismantles the antioxidant defenses of GBC cells through a "supply-and-exhaust" mechanism. Specifically, Fe-derived Fe and laser-activated Ce6 act as an efficient reactive oxygen species (ROS) generator via Fenton and photodynamic reactions, while ISL severely impairs the intracellular antioxidant capacity by downregulating GPX4 and activating the p62/Keap1/Nrf2/HMOX1 signaling pathway. We evaluated the therapeutic efficacy of this platform in patient-derived organoids (PDOs) and patient-derived organoid xenograft (PDOX) models. ICFe@D demonstrated potent and consistent tumor regression across heterogeneous patient-specific models with minimal systemic toxicity. This study presents a highly translatable and precise nanotherapeutic strategy that effectively sensitizes GBC to ferroptosis, providing a valuable preclinical framework for biliary tract cancer therapy. - Source: PubMed
Publication date: 2026/06/01
Zhao YuhaoZhang JingyunZhou ChenYang MaoZheng ZhigangGu YixiangZhang YangChen XingqiZhou ZhengjunGu JinZhao LijinWu WenguangLang MeidongLiu Yingbin - Diabetes mellitus exerts a deleterious effect on the male reproductive system, manifesting as a metabolic disease. Recent research has indicated that the ingestion of dietary supplements rich in natural antioxidants may reduce or prevent damage to the male reproductive system in cases of diabetes-induced infertility. This study investigated the effects of zingerone on diabetes-induced reproductive damage in male rats by analyzing the Sirt1/Nrf2/HO-1 signaling pathway, apoptosis, sperm quality, and histopathological changes. Seventy-five male Sprague Dawley rats, weighing between 250 and 300 g and aged 10 to 12 weeks, were divided into six groups. These included: control; zingerone (50 mg/kg); zingerone (100 mg/kg); diabetes; diabetes with zingerone (50 mg/kg); and diabetes with zingerone (100 mg/kg). Diabetes was induced via a single intraperitoneal injection of 55 mg/kg streptozotocin. Zingerone was given daily by oral gavage for a duration of 8 weeks. Results showed that zingerone significantly reduced glucose, MDA levels, and the Bax/Bcl-2 ratio, while markedly enhancing body weight, testosterone, GSH content, GSH-Px and CAT enzyme activity, and the expression of Sirt1, Nrf2, and HO-1. Additionally, it had a beneficial impact on spermatological parameters and histopathological findings in diabetic rats. The findings from this study, obtained from both healthy and diabetic rats, are consistent with each other, thereby providing a reliable basis for the conclusions drawn. Thus, incorporating zingerone into prophylactic regimens for healthy rats and therapeutic interventions for diabetic conditions may be advisable. Furthermore, combination drug therapies including zingerone may offer a viable approach to mitigating the toxic effects associated with certain drugs and to combating diabetes-related infertility. Consequently, it was concluded that zingerone ameliorates diabetes-induced damage to the male reproductive system, with 100 mg/kg zingerone demonstrating superior efficacy. - Source: PubMed
Ekmen Edanur GülerÇay MehmetGüngör İbrahim HalilÇeribaşı Ali Osman - Acute myeloid leukemia (AML) is an aggressive hematological malignancy with various molecular and cytogenetic subtypes. Treatment options for older adult patients are limited due to high toxicity of conventional chemotherapy. The B-cell leukemia/lymphoma 2 inhibitor venetoclax is effective in combination with hypomethylating agents or low-dose cytarabine, but ∼30% of patients do not respond to the initial combination treatment. Thus, alternative combinations are needed to sensitize AML cells to venetoclax and overcome resistance mechanisms. Here, we report that targeting histone lysine-specific demethylases induces a ferroptosis-like phenotype driven by oxidative stress in various AML subtypes. In both patient samples and cell lines, JIB-04 increases the level of reactive oxygen species, ferrous iron, and lipid peroxidation, all signs of ferroptosis. The combination of JIB-04 and venetoclax proved to be highly synergistic. Blocking the JIB-04-induced phenotype by using the antioxidant N-acetyl-l-cysteine reverses the synergistic killing. At the molecular level, the ferroptosis inducers HMOX1, SAT1, and PTGS2 were found to be upregulated by JIB-04. Collectively, these findings identify JIB-04 as a potential new ferroptosis inducer in AML and highlight the potential of oxidative stress induction as a valuable strategy in combination with venetoclax to treat AML. - Source: PubMed
Publication date: 2026/04/16
Wohlan KatharinaFan DandanGuzman Anna GQuezada AlexisPark HyunjiKhabusheva ElmiraSivandzade FarzaneWither MatthewAlcorn AmberThevarajah TamaraKornblau Steven MDiNardo Courtney DSu JianzhongGoodell Margaret ARau Rachel E - Malaria pathogenesis involves both parasite burden and host inflammatory and oxidative stress responses that contribute to haematological alterations. Full blood count (FBC)-derived indices have been explored as accessible surrogate biomarkers, reflecting systemic inflammatory changes; however, they provide limited mechanistic insight into underlying haem-driven oxidative stress pathways. Haem oxygenase-1 (HO-1) reflects cellular responses to free haem, while interleukin-6 (IL-6) mediates systemic inflammation. However, their combined role in relation to parasitaemia and haematological alterations in endemic populations remains insufficiently defined. This study evaluated plasma HO-1 and IL-6 as complementary host-response biomarkers in a hospital-based malaria-endemic population. - Source: PubMed
Publication date: 2026/05/15
Wakai TheophilusKintung IrrinusOgundimu TemitayoChinedu ShalomAfolabi Israel - Phototoxicity is a common adverse effect triggered by systemic or topical drug treatments. It is mainly caused by drug-induced sensitization to UVA radiation, arising from either the drug's inherent photosensitizing potential or its interference with the metabolism of endogenous photosensitizers. A potent endogenous UVA sensitizer is 6-formylindolo[3,2-b]carbazole (FICZ), a tryptophan photoproduct formed in UVB-irradiated epidermal cells. By sequentially activating the aryl hydrocarbon receptor signaling pathway and inducing cytochrome P450 (CYP) 1A1 expression, FICZ induces its own degradation. Recently, we reported that the BRAF inhibitor vemurafenib interferes with CYP1A1 activity and sensitizes keratinocytes to FICZ/UVA-induced phototoxicity. Herein, we screened 12 clinical drugs, known to exhibit phototoxicity in patients, for their potential to interfere with the metabolism of (exogenous) FICZ and sensitize HaCaT keratinocytes to UVA-induced phototoxicity. - Source: PubMed
Hartung FrederickDairou JulienRamamoorthy SamhitaRolfes Katharina MMeller StephanHaarmann-Stemmann Thomas