CBR3 Antibody
- Known as:
- CBR3 Antibody
- Catalog number:
- csb-pa004587esr1hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- CBR3 Antibody
Ask about this productRelated genes to: CBR3 Antibody
- Gene:
- CBR3 NIH gene
- Name:
- carbonyl reductase 3
- Previous symbol:
- -
- Synonyms:
- SDR21C2
- Chromosome:
- 21q22.12
- Locus Type:
- gene with protein product
- Date approved:
- 1998-01-16
- Date modifiied:
- 2016-10-05
Related products to: CBR3 Antibody
Related articles to: CBR3 Antibody
- Severe pneumonia (SP) is a life-threatening pulmonary infection characterized by high morbidity, frequent complications, and elevated mortality, with rising global incidence in recent years. This study investigated the prognostic value and molecular mechanisms of lncRNA CBR3-AS1 (CBR3-AS1) in patients with SP. - Source: PubMed
Liu ChaoLi MeieYang JunfaLong Pan - Doxorubicin (Dox) is a cornerstone in the treatment of pediatric acute lymphoblastic leukemia (ALL), but its use is limited by dose-dependent cardiotoxicity. Oxidative stress, arising from mitochondrial dysfunction, enzymatic generation of reactive oxygen species, and cardiotoxic metabolites, has been implicated as a central mechanism, with interindividual variability partly influenced by genetic factors. This study evaluated oxidative DNA damage 8-hydroxy-2'-deoxyguanosine (8-OHdG) as an integrative marker of redox-related pathways in Dox-induced cardiotoxicity. In a prospective case-control study, 93 pediatric patients with ALL treated with Dox and 63 controls were included. Cardiotoxicity was assessed by serial echocardiography, and 8-OHdG levels were measured by ELISA. Genotyping of rs3743527, rs1883112, and rs1056892 was performed, and multivariable analyses were conducted. Dox-treated patients showed higher 8-OHdG levels than controls, and patients with cardiotoxicity ( = 11) had higher levels than those without. A higher frequency and severity of cardiotoxicity was observed in female patients, although this finding should be interpreted cautiously. Although allele frequencies did not reach statistical significance, distinct distribution patterns were observed between groups. These findings suggest that 8-OHdG may function as an integrative marker of redox dysfunction associated with Dox-induced cardiotoxicity. - Source: PubMed
Publication date: 2026/06/01
Gándara-Mireles Jesús AlonsoReyes Espinoza Elio AarónLoera-Castañeda VerónicaCórdova Hurtado Lourdes PatriciaGonzález Font Antonio EmilioGrijalva Ávila Julio CesarVillanueva Fierro IgnacioLares-Asseff IsmaelMuñoz Cynthia MoraVelasco Villa GabrielaPayán Gándara HugoPatrón-Romero LeslieAlmanza-Reyes Horacio - Syrup (ABS) is a commonly used traditional Chinese patent medicine for insomnia and amnesia, and also has the potential to anti-aging but lacks scientific support of pharmacological and mechanism research. This study aims to investigate the anti-aging effect of ABS and its underlying mechanism. - Source: PubMed
Publication date: 2026/03/10
Sun YuanfangXia QiWu RuolanLiu GangWang YongkuanYan ShikaiJin HuiziZhang XiuyunXiao XueLi Shasha - Aberrant proliferation of mesangial cells (MCs) is a central driver of glomerular injury in IgA nephropathy (IgAN) and lupus nephritis (LN), the two most common mesangioproliferative glomerulopathies. Emerging evidence implicates dysregulated arginine-proline metabolism in this process; however, the key regulatory genes and underlying mechanisms remain incompletely defined. Here, we performed integrative bulk RNA sequencing of glomerular datasets and applied machine learning algorithms (LASSO and SVM-RFE) to identify disease-specific differentially expressed genes (DEGs) linked to the arginine-proline metabolic pathway. We identified 34 LN-specific and 18 IgAN-specific DEGs, among which ASS1, PCK1, and CBR3 emerged as core hub genes through feature selection and network analyses. A nomogram-based diagnostic model incorporating these genes demonstrated strong predictive performance, with AUC values exceeding 0.75 in internal cohorts and robust validation across external datasets. Single-cell RNA sequencing of mouse models delineated seven MC subclusters, highlighting Rasl12 and Col3a1 subpopulations with pronounced proliferative-inflammatory phenotypes, characterized by downregulated ASS1 and PCK1 and upregulated CBR3. These transcriptional patterns were corroborated in vivo in anti-Thy1 nephritis rats, BAFF-transgenic IgAN mice, and MRL/lpr LN mice, where altered gene expression correlated with mesangial hyperplasia, macrophage infiltration, and elevated inflammatory cytokines. Functional assays in PDGF-BB-stimulated human MCs further demonstrated that overexpression of ASS1 or PCK1, or knockdown of CBR3, attenuated MC activation, proliferation, and proinflammatory crosstalk with macrophages. Collectively, our results position ASS1, PCK1, and CBR3 as pivotal regulators of arginine-proline metabolism in mesangial proliferation, establishing them as innovative diagnostic biomarkers and therapeutic targets for precise management of IgAN and LN. - Source: PubMed
Publication date: 2025/12/04
He JiayiPeng FeiQu YilunZhao YinghuaLi YueyangZhou YueranGuo ChangLi XingangSong MansuChen XiangmeiHong QuanWang Wei - The global demand for processed foods has increased reliance on synthetic phenolic antioxidants (SPAs), including tert-butylhydroquinone (TBHQ), a widely used additive to prevent lipid oxidation and extend shelf life. TBHQ is considered safe at present regulated levels; however, studies suggest potential adverse effects, including oxidative stress, genotoxicity, and impacts on immune function, raising concerns about human health and ecological risks. Herein, we investigated the immunomodulatory effects of TBHQ on RAW 264.7 murine macrophages pre-exposed to 0.1, 1, and 5 µM TBHQ and then stimulated with lipopolysaccharide (LPS) or polyinosinic-polycytidylic acid (poly I:C, PIC) to model bacterial and viral immune challenges. We then used functional assays and transcriptomic profiling to assess inflammatory responses and oxidative stress signaling. TBHQ reduced nitric oxide production and IL-10 secretion at the highest non-cytotoxic dose, and enhanced phagocytosis and IL-6 secretion at the lowest concentrations. Overall, transcriptomics revealed significant downregulation of proinflammatory pathways and induction of glutathione and xenobiotic metabolism. Pre-treatment with TBHQ increased gene transcript counts of key metabolic genes/transporters such as , , , , and . Following treatment with LPS or PIC several genes for classical proinflammatory chemokines and cytokines such as , , , , , , and were downregulated. Genes involved in NF-κB signaling, such as , , and were also downregulated. Our study suggests that the induction of Nrf2-related antioxidant pathways by TBHQ is the main driver for reduced inflammatory signaling in macrophages. - Source: PubMed
Publication date: 2025/10/16
Whisel Alyssa MRice Charles D