BLVRA ELISA kit
- Known as:
- BLVRA Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- DL-BLVRA-Ra
- Product Quantity:
- 96T
- Category:
- Elisa Kits
- Supplier:
- WDSTD
- Gene target:
- BLVRA ELISA kit
Related genes to: BLVRA ELISA kit
- Gene:
- BLVRA NIH gene
- Name:
- biliverdin reductase A
- Previous symbol:
- BLVR
- Synonyms:
- -
- Chromosome:
- 7p13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2015-08-24
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- Osteomyelitis (OM) remains difficult to diagnose early due to its heterogeneous pathology and reliance on invasive biopsy. This study aimed to identify reliable diagnostic biomarkers and explore their roles in macrophage senescence during OM pathogenesis. - Source: PubMed
Publication date: 2026/05/14
Zhang JinyeMao XinyuanZheng HaonanYang KaifanYu Bin - Jaundice, a condition characterized by elevated circulating bilirubin generated by biliverdin reductase A (BVRA), is protective against malaria. Beyond its oxidoreductase activity, BVRA acts as a protein kinase and transcriptional regulator. To probe the protective effect of BVRA oxidoreductase activity, we generated mice harboring G17A and E97A missense mutations in its NAD(P)H-binding and reductase motifs, respectively. BVRA oxidoreductase activity was reduced by ∼95% and ∼80%-90% in and vs. wild-type ( ) mice, respectively. AS () infection was lethal in and , compared to the non-lethal outcome in control mice. Quantification of circulating unconjugated bilirubin in -infected mice revealed dose response effect whereby the mutant strains failed to reach a protective ∼20-30 μM (∼1-2 mg/dL) threshold. These findings establish the antimalarial effect of BVRA oxidoreductase activity and define a threshold of circulating bilirubin required for malaria protection, informing on therapeutic development and biomarker-guided strategies. - Source: PubMed
Publication date: 2026/04/30
Mesquita MiguelFigueiredo AnaRastogi Sonia TrikhaMartins RuiRamos SusanaPagnotta SaraCarlos Ana RitaCosta MartimCardoso SilviaNovoa AnaMallo MoisesPaul Bindu DJentho ElisaSoares Miguel P - Deferoxamine (DFX), a classic iron-chelating agent, has exhibited neuroprotective effects in preclinical studies of hemorrhagic stroke. However, its clinical translation remains limited, and its precise mechanisms of action in subarachnoid hemorrhage (SAH) have not been fully elucidated. This study aimed to investigate the therapeutic efficacy and underlying molecular mechanisms of DFX in a mouse model of SAH, with a particular focus on ferroptosis and astrocyte polarization. Our results demonstrated that DFX alleviated early brain injury (EBI) by reducing iron overload, oxidative stress, and ferroptosis induced by heme degradation. DFX treatment also inhibited the pathological activation of both pro-inflammatory A1 and anti-inflammatory A2 reactive astrocytes, but failed to fully suppress the overall neuroinflammatory response. Notably, biliverdin reductase A (BLVRA) was found to modulate inflammatory cytokine production via inducible nitric oxide synthase (NOS2) and TLR4 signaling, independent of astrocyte polarization. Consequently, combined treatment with DFX and siBLVRA exerted a synergistic therapeutic effect, resulting in significantly improved neurological outcomes relative to DFX monotherapy. In conclusion, DFX effectively mitigates iron-dependent ferroptosis and pathological astrocyte activation after SAH, but shows limited efficacy in controlling neuroinflammation. The enhanced anti-inflammatory effect achieved by BLVRA inhibition highlights a novel and promising therapeutic strategy that simultaneously targets iron overload and the BLVRA pathway for the treatment of SAH. - Source: PubMed
Publication date: 2026/04/22
Zheng YanningLang DongcenLi ZhengZhang JingNiu MengyuLi WenchaoHuang LiyongXue JiangyuLi LiChen Ying - : Long-term exposure to polychlorinated biphenyls (PCBs), including the mixture of PCBs in Aroclor1260 (Ar1260), results in metabolic dysfunction-associated steatotic liver disease (MASLD) in mice and humans. While the effects of PCBs on gene expression are well-documented using short-read RNA sequencing, the regulatory roles of alternative splicing (AS) and differential transcript usage (DTU) are uncharacterized. AS has been implicated in MASLD. Previously, we reported that chronic (34 wks.) exposure of normal, low-fat-diet (LFD)-fed male mice to Ar1260 resulted in 12 hepatic RNA modifications. Proteomic analysis of these same liver samples identified Ar1260 exposure-associated changes in selenoproteins: GPX4 and SELENBP2 were increased and SELENOS and SELENOF were reduced. : Here we used long-read isoform sequencing (IsoSeq) to identify DTU in four genes in the Ar1260-exposed livers: , , , and . : Network analysis of the corresponding proteins revealed a strong association with pathways relevant to MASLD including lipid metabolism, glycolysis, and oxidative stress. : These findings suggest that PCB exposure alters the transcript isoform landscape of key metabolic genes involved in MASLD. - Source: PubMed
Publication date: 2026/01/25
Petri Belinda JPiell Kellianne MWahlang BanridaChariker Julia HRouchka Eric CCave Matthew CKlinge Carolyn M - Biliverdin reductase A (BLVRA) is a key enzyme in bilirubin metabolism, where it reduces biliverdin to bilirubin. Bilirubin is a potent antioxidant that protects cells from oxidative stress. Therefore, reduced or deregulated BLVRA activity may contribute to increased oxidative DNA damage, which is one of the factors leading to the neoplastic transformation of cells. - Source: PubMed
Publication date: 2026/01/23
Solárová ZuzanaDanková KristínaHarvanik PavolBober PeterMajerová PetraMichalková RadkaBhide MangeshSolár Peter