RXR_
- Known as:
- RXR_
- Catalog number:
- RXR3001
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- RXR_
Related genes to: RXR_
- Gene:
- TXNRD2 NIH gene
- Name:
- thioredoxin reductase 2
- Previous symbol:
- -
- Synonyms:
- TR, TRXR2, TR3
- Chromosome:
- 22q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 2002-02-22
- Date modifiied:
- 2019-04-23
- Gene:
- TXNRD3 NIH gene
- Name:
- thioredoxin reductase 3
- Previous symbol:
- TXNRD3NB, TXNRD3IT1
- Synonyms:
- TR2, TRXR3, TGR, TR2IT1, TXNRD3NT1
- Chromosome:
- 3q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-11
- Date modifiied:
- 2019-03-28
Related products to: RXR_
alpha RXR antibodyalpha RXR antibodyalpha RXR antibody Polyclonal Antibodies Primary antibodiesalpha-RXRalpha-RXR anti-Retinoid X Receptor, Ligand Binding Domain rabbit, polyclonalalpha-RXR anti-Retinoid X Receptor, Ligand Binding Domainrabbit, polyclonalAntibodies: RXR alpha HOST: Goat Clonality: pAbAntibodies: RXR beta HOST: Goat Clonality: pAbAntibodies: RXR gamma HOST: Goat Clonality: pAbAntigens RXR-alpha( Retinoid x receptor;111-228aa, Human) Recombinant, expressed in E.coliBos taurus,Bovine,NR2B3,Nuclear receptor subfamily 2 group B member 3,Retinoic acid receptor RXR-gamma,Retinoid X receptor gamma,RXRGBovine Retinoic acid receptor RXR-gamma(RXRG) ELISA kitBovine Retinoic acid receptor RXR-gamma(RXRG) ELISA kitBovine Retinoic acid receptor RXR-gamma(RXRG) ELISA kit SpeciesBovineBovine Soluble Retinoid X Receptor ELISA, RXR Related articles to: RXR_
- Extensive application of lead (Pb) brought about environmental pollution and toxic reactions of organisms. Selenium (Se) has the effect of antagonizing Pb poisoning in humans and animals. However, it is still unclear how Pb causes brainstem toxicity. In the present study, we wanted to investigate whether Se can alleviate Pb toxicity in chicken brainstems by reducing apoptosis. One hundred and eighty chickens were randomly divided into four groups, namely the control group, the Se group, the Pb group, and the Se/Pb group. Morphological examination, ultrastructural observation, relative mRNA expressions of genes on heat shock proteins (HSPs); selenoproteins; inflammatory cytokines; and apoptosis-related factors were investigated. The results showed that Pb exposure led to tissue damage and apoptosis in chicken brainstems. Furthermore, an atypical expression of HSPs (HSP27, HSP40, HSP60, HSP70, and HSP90); selenoprotein family glutathione peroxidase (GPx) 1, GPx2, GPx3, and GPx4), thioredoxin reductases (Txnrd) (Txnrd1, Txnrd2, and Txnrd3), dio selenoprotein famliy (diodothyronine deiodinases (Dio)1, Dio2, and Dio3), as well as other selenoproteins (selenoprotein (Sel)T, SelK, SelS, SelH, SelM, SelU, SelI, SelO, Selpb, selenoprotein n1 (Sepn1), Sepp1, Sepx1, Sepw1, 15-kDa selenoprotein (Sep15), and selenophosphate synthetases 2 (SPS2)); inflammatory cytokines (Interleukin 2 (IL-2), IL-4, IL-6, IL-12β, IL-17, and Interferon-γ (IFN-γ)); and apoptosis-related genes (B-cell lymphoma-2 (Bcl-2), tumor protein 53 (p53), Bcl-2 Associated X (Bax), Cytochrome c (Cyt c), and Caspase-3) were identified. An inflammatory reaction and apoptosis were induced in chicken brainstems after exposure to Pb. Se alleviated the abnormal expression of HSPs, selenoproteins, inflammatory cytokines, and apoptosis in brainstem tissues of chickens treated with Pb. The results indicated that HSPs, selenoproteins, inflammatory, and apoptosis were involved in Se-resisted Pb poisoning. Overall, Se had resistance effect against Pb poisoning, and can be act as an antidote for Pb poisoning in animals. - Source: PubMed
Publication date: 2024/02/03
Chen DechunYu WeikangHao ZhiyuQiu MinnaCui JiawenTang YouTeng XiaohuaLiu YuhaoLiu Haifeng - Lead (Pb), a hazardous heavy metal, can damage the health of organisms. However, it is not clear whether Pb can damage chicken cerebellums and thalami. Selenium (Se), an essential nutrient for organisms, has a palliative effect on Pb poisoning in chickens. In our experiment, a model of chickens treated with Pb and Se alone and in combination was established to investigate the molecular mechanism of Se alleviating Pb-caused damage in both chicken cerebellums and thalami. Our morphological results indicated that Pb caused apoptotic lesions, such as mitochondrial and nuclear damage. Further, the anti-apoptotic gene Bcl-2 decreased; on the contrary, four pro-apoptotic genes (p53, Bax, Cyt c, and Caspase-3) increased under Pb treatment, meaning that Pb caused apoptosis via the p53-Cyt c-Caspase-3 pathway. Furthermore, we further demonstrated that Pb elevated four HSPs (HSP27, HSP40, HSP70, and HSP90), as well as HSP70 took part in the molecular mechanism of Pb-caused apoptosis. In addition, we found that Pb exposure led to oxidative stress via up-regulating the oxidant HO and down-regulating four antioxidants (CAT, SOD, GST, and GPx). Moreover, Pb decreased three Se-containing factors (Txnrd1, Txnrd2, and Txnrd3), further confirming that Pb caused oxidative stress. Interestingly, Se supplementation reversed the above changes caused by Pb and alleviated Pb-induced oxidative stress and apoptosis. A time dependency was demonstrated for Bcl-2, Bax, and Cyt c in the cerebellums, as well as CAT, GPx, and p53 in the thalami of Pb-exposed chickens. HSP70 in cerebellums and HSP27 in thalami were more sensitive than those in thalami and cerebellums, respectively, under Pb exposure. Pb-induced apoptosis of thalami was more severe than cerebellums. In conclusion, after Pb treatment, Txnrds mediated oxidative stress, oxidative stress up-regulated HSPs, and finally, HSP70 triggered apoptosis. Se supplementation antagonized Pb-induced oxidative stress and apoptosis via the mitochondrial pathway and selenoproteins in chicken cerebellums and thalami. This study provides new information for the mechanism of environmental pollutant poisoning and the detoxification of Se on abiotic stress. - Source: PubMed
Publication date: 2023/08/25
Hong WeichenLiu YuhaoLiang JiatianJiang ChunyuYu MeijinSun WeiHuang BinDong NaKang LuTang You - The trace element selenium (Se) plays a key role in development and various physiological processes, mainly through its transformation into selenoproteins. To investigate the developmental patterns of Se content and expression of selenoproteins, the liver and longissimus dorsi (LD) muscle of Duroc pigs were collected at 1, 21, 80, and 185 days of age (7 pigs each age) for the determination of Se content, mRNA expression of selenoproteins, and concentrations of glutathione peroxidase (GPX), thioredoxin reductase (TrxR or TXNRD), and selenoprotein P (SELP). The results showed that age significantly affected the expression of GPX1, GPX2, GPX3, TXNRD1, TXNRD2, TXNRD3, iodothyronine deiodinases 2 (DIO2), DIO3, SELF, SELH, SELM, SELP, SELS, SELW, and selenophosphate synthetase2 (SPS2) in the liver, as well as GPX3, GPX4, TXNRD1, TXNRD2, DIO2, DIO3, SELF, SELN, SELP, SELR, SELS, and SELW in the LD muscle of Duroc pigs. The concentrations of GPX, TrxR, and SELP showed an increasing trend with age, and they were positively correlated with Se content at 1, 21, and 185 days of age and negatively correlated at 80 days of age, both in the liver and LD muscle. The Se content decreased at the age of 80 days, especially in the LD muscle. In summary, our study revealed developmental changes in Se content and expression of selenoproteins in the liver and LD muscle of Duroc pigs at different growth stages, which provided a theoretical basis for further study of Se nutrition and functions of selenoproteins. - Source: PubMed
Publication date: 2023/04/24
He YiwenGuan PengZeng YanHuang LePeng CanKong XiangfengZhou Xihong - Effects of selenoproteins on many renal diseases have been reported. However, their role in renal ischemia-reperfusion (I/R) injury is unclear. The present study was performed to investigate the impact of ebselen and renal I/R injury on the expression of selenoproteins. Sprague-Dawley rats were pretreated with or without ebselen (10 mg/kg) through a daily single oral administration from 3 days before renal I/R surgery. RT-qPCR (real-time quantitative PCR) was performed to determine the mRNA expression of 25 selenoprotein genes in the renal tissues. The expression levels of two selenoproteins, including GPX3 (glutathione peroxidase 3) and DIO1 (iodothyronine deiodinase 1), were evaluated by Western blot or/and IHF (immunohistofluorescence) assays. Furthermore, renal function, renal damage, oxidative stress, and apoptosis were assessed. The results showed that in renal I/R injury, the mRNA levels of 15 selenoprotein genes (GPX1, GPX3, GPX4, DIO1, DIO2, TXNRD2, TXNRD3, SEPHS2, MSRB1, SELENOF, SELENOK, SELENOO, SELENOP, SELENOS, and SELENOT) were decreased, whereas those of eight selenoprotein genes (GPX2, GPX6, DIO3, TXNRD1, SELENOH, SELENOM, SELENOV, and SELENOW) were increased. I/R also induced a reduction in the expression levels of GPX3 and DIO1 proteins. In addition, our results indicated that ebselen reversed the changes in those selenoprotein genes, excluding SELENOH, SELENOM, SELENOP, and SELENOT, in renal I/R injury and alleviated I/R-induced renal dysfunction, tissue damage, oxidative stress, and apoptosis. To our knowledge, this is the first study to investigate the changes of 25 mammalian selenoprotein genes in renal I/R injury kidneys. The present study also provided more evidence for the roles of ebselen against renal I/R injury. - Source: PubMed
Publication date: 2022/05/12
Wu YikunShi HuaXu YuangaoWen RaoGong MaodiHong GuangyiXu Shuxiong - The aim of this study was to investigate the role of selenoproteins in Macranthoidin B (MB) with regard to the inhibition of hepa1-6 cell proliferation. The CCK8 method was used to detect the inhibition rate in hepa1-6 cell of proliferation. The production of ROS, MDA, GSH levels, and GSH-Px and SOD activities was detected according to corresponding reagent kits. We determined the mRNA expressions of 25 selenoproteins in hepa1-6 cells via real-time quantitative PCR (qRT-PCR); moreover, the heat map and principal component analysis were used for further bioinformatics analysis. The results revealed that with an increasing concentration of MB, the inhibitory effect on hepa1-6 cell proliferation intensified. Compared with the control group, the treatment group showed significantly increased ROS levels, elevated MDA contents, and decreased GSH level, GSH-Px activity, and SOD activity. Increasing MB concentration treatment induced remarkable degradation of Txnrd1, Txnrd2, Txnrd3, Gpx1, Gpx2, Gpx3, Gpx6, Dio1, Dio2, Selt, Selp, Selh, Selk, Selw, Seln, and Dio3. Principal component analysis revealed that Txnrd 3, Selk, Selo, Selw, Selt, Dio2, Txnrd1, Dio3, Gpx6, and Dio1 were highly correlated with MB. In conclusion, MB dose dependently inhibited hepa1-6 cell proliferation and induced oxidative stress. Based on bioinformatics analysis, with MB treatment, Txnrd 3, Selk, Selo, Selw, Selt, Dio2, Txnrd1, Dio3, Gpx6, and Dio1 exhibited critical role in the inhibition of hepa1-6 cells proliferation. The functions of these selenoproteins were associated with oxidative stress. - Source: PubMed
Publication date: 2022/01/26
Tan SiranLiu QiYang JieCai JingzengYu MiaoJi Yubin