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1/74

Western blot analysis on HuvEc cell lysates using Nrf2 Antibody,The lane on the left was treated with the antigen-specific peptide.

AF0639 at 1/100 staining Mouse kidney tissue by IHC-P.

AF0639 at 1/100 staining human brain tissue sections by IHC-P.

AF0639 at 1/100 staining Mouse muscle tissue by IHC-P.

AF0639 at 1/100 staining Rat kidney tissue by IHC-P.

FIGURE 2|Byakangelicin alleviates liver injury in a carbon tetrachloride-induced model.

Fig.

$Fig. 5 Nrf2/HO-1 pathway mediates the protection of USP15 defciency against glutamate-induced cytotoxicity in HT22 cells. a Western blot analysis of Nrf2 and HO-1 protein level in the whole HT22 cell lysates. b Western blot analysis of Nrf2 protein in the nuclear and cytosolic fractions. The LaminB1 and GAPDH were used as markers for nucleus and cytoplasm, respectively. ImageJ software was used to quantify the bands. c Images of immunofuorescence staining showing Nrf2 nuclear presence in HT22 cells. Data are presented as mean±SEM; statistical analysis was performed using one-way ANOVA followed by Dunnett’ s tests (comparing each group with Con) for a and b (excluding the Glu+siUSP15 group), unpaired Student’s test for a and b (Glu group and Glu+siUSP15 group)$

Fig.

Figure 7 Bruguiera gymnorrhiza fruit (BGF) activated the Keap1/Nrf2 signaling pathway.

Fig.

Figure 6 AEPL increased Nrf2 expressions and translocated to nucleus.

Fig.

FIGURE 5 Effects of POL, ACT, and FTB on Keap1-Nrf2 and NF-κB p65 signaling pathways in TNF-α-induced cell injury in A549 cells (A,B) Western blot analyses of nucl-Nrf2, cyto-Nrf2, Keap1, nucl-p65, cyto-p65, and p-IκBα (C–F) Intensity of Keap1, cyto-Nrf2, p-IκBα, and cyto-p65 relative to β-actin.

Fig.

$Fig. 5 Ginsenoside Rg1 prevents senescence which is NRF2-dependent. a Evaluation of NRF2 and p-NRF2 (Ser 40) expression in Rg1-treated aging-MSCs by western blotting. Representative images are shown. b Expression of NRF2 in nuclear fraction of Rg1-treated aging-MSCs by western blotting. c Representative fluorescence images depicting NRF2 expression in MSCs induced by D gal (24 h) or Rg1 (24 h). d Representative immunofluorescence images of NRF2 of mouse thighbone from each group (normal, Rg1, D-gal, Rg1+D-gal). e Quantification of mRNA expression for GSTA1, NQO1, and SRX from Rg1-treated MSCs. f GCLC, GCLM, HO-1, and NQO1 expression levels in total protein from Rg1-treated aging-MSCs. g, h p21 and p16 expression levels in total protein from Rg1-treated aging-MSCs incubated in the absence or presence of ML385 (5μM) or Brusatol (0.2 μg/mL). i Quantification of SASP mRNA expression in each group (normal,D-gal, D-gal+Rg1, D-gal+Rg1+ML385). j, k Representative images and analysis of SA-β-gal staining in MSCs from different groups (normal, D-gal, D-gal+Rg1, D-gal+Rg1+ML385). l, m Representative fluorescence images and analysis of ROS in MSCs from each group. Bars represent 50 μm (c), 200 μm (d, j, l). Data in e, i, k, m represent mean ± SD (n=3, *P < 0.05; one-way ANOVA)$

Fig.

Figure 5 Effects of Y-1 and Y-2 on oxidative stress of NRK-52e cells stimulated by sodium oleate with/without CD36 silences.

Fig.

Figure 6 Photomicrographs (A) and histogram (B) show SOD1 expressions in the CA1 and CA3 region of the hippocampus based on immunohistochemistry results.

Figure 3 ROSI inhibited renal oxidative stress in the mouse model.

Fig.

Figure 6 |The effect of sevoflurane on the protein expression of p53 and Nrf2 in liver tissue induced by IR.

Figure 3 Zinc had a protective effect on mitochondria of PC12 neurons.

Figure 5 Effects of PAL and Col (1 µM) on NF-κB/NLRP3 and Nrf2 signaling pathways in LPS plus MSU-activated THP-1 cells.

Figure 4.

$FIGURE 5 BFB’s role in cellular P62-Keap1-Nrf2 pathway-related factors protein expression level. 400 μM H2O2 treatment in PC12 cells with/without BFB (1, 5, 10 μm) or NBP (15 μm) for a 3-h period (A) p62, keap1, HO-1 and total Nrf2 protein levels were examined by WB (B) Nuclear and cytoplasmic Nrf2 protein fractions were analyzed through WB (C–H) Quantification of relative band intensities of p62, keap1, total Nrf2, HO-1, nuclear Nrf2 and cytoplasmic Nrf2, and β-actin or Histone H3 served as loading control. Nrf2 suppression mitigated BFB’s inhibition on oxidative stress. 5 μm ML385 was added to pretreat PC12 cells for a 0.5-h period, followed by stimulation using H2O2 (400 μm) with/without BFB (30 μm) or NBP (30 μm) (I) Total Nrf2 and HO-1 protein expression determined through WB assay (J) Nuclear and cytoplasmic Nrf2 protein determined by Western Blot (K–N) Quantification of relative band intensities of total Nrf2, HO-1, nuclear Nrf2 and cytoplasmic Nrf2, with β-actin or Histone H3 being the endogenous reference. The values were represented by mean ± SD from 3 separate assays. *p < 0.05, **p < 0.01, versus Control, # p < 0.05, ## p < 0.01, versus H2O2 group. ▲ p < 0.05, ▲▲ p < 0.01, versus NBP group. △ p < 0.05, △△ p < 0.01, versus ML385 group.$

FIGURE 5 BFB’s role in cellular P62-Keap1-Nrf2 pathway-related factors protein expression level.

$FIGURE 6 BFB promoted Nrf2 nuclear translocation. Nrf2 protein localization was detected via immunofluorescence staining (A) Representative immunofluorescence images showing BFB promoted distribution of Nrf2 in nuclear fraction (B) Nrf2 inhibition blocked cellular Nrf2 distribution induced by BFB in nuclear fraction.$

FIGURE 6 BFB promoted Nrf2 nuclear translocation.

Figure 7 Trehalose inhibits ferroptosis by activating the NRF2/HO-1 signaling pathway.

Figure 6 Effects of GA on Keap1-Nrf2 signaling.

Fig.

FIGURE 6 Effect of MLG on NF-κB/Nrf2/HO-1 signaling pathway in ethanol-induced gastric lesions mice.

Fig.

Figure 6 WFA upregulates nuclear factor E2-related factor 2 (Nrf2) expression and promotes nuclear translocation of Nrf2 after ICH in vivo and in vitro.

Figure 6.

Figure 7.

Fig.

Figure 7 Effects of increased BMAL1 on the Nrf2 signaling pathway after ICH.

Figure 5 TsI inhibits oxidative stress and activates the Nrf2 signaling pathway in the MPS-induced SIONFH rat model.

Fig.

$Figure 4 AST IV promotes Nrf2 activation in CIRI. (a) Western blot assay showing the Nrf2 levels in the nuclear and total protein fractions. (b, c) Quantitative analysis of Nrf2 levels in the nuclear, normalized to Lamin B1 and total protein fractions, normalized to β-actin. Values are mean ± SD, n = 3. ∗∗P < 0.01 vs. the sham group; #P < 0.01, ##P < 0.01 vs. the MCAO/R group. (d) Immunofluorescence imaging of Nrf2 nuclear colocalization. SH-SY5Y cells were randomly assigned to the following groups: the sham group (complete medium), the OGD/R group (complete medium), the OGD/R + AST IV group (20 μg/ml AST IV was administered 24 h before OGD, OGD was performed for 2 h, and 20 μg/ml AST IV was administered at 24 h just after OGD to achieve reperfusion), and the OGD/R +20 μg/ml AST IV+20 μM ML385 group (20 μg/ml AST IV+20 μM ML385) was administered 24 h before OGD, OGD was performed for 2 h, and 20 μg/ml AST IV+20 μM ML385 was administered at 24 h just after OGD to achieve reperfusion. (e) Intracellular ROS stained via DCFH-DA. (f) Quantitative analysis of Nrf2 nuclear immunofluorescence intensity. Values are mean ± SD, n = 3. ∗∗P < 0.01 vs. the sham group; ##P < 0.01 vs. the OGD/R group; &&P < 0.01 vs. the AST IV group. (g) Representative quantification of cellular ROS contents. Values are mean ± SD, n = 3. ∗∗P < 0.01 vs. the sham group; ##P < 0.01 vs. the OGD/R group; &&P < 0.01 vs. the AST IV group.$

Figure 4 AST IV promotes Nrf2 activation in CIRI.

Figure 4 Effect of DOFE on Nrf2/HO-1-mediated antioxidant response.

Figure 3 Gla ameliorated liver oxidative stress caused by ethanol via the Nrf2 pathway in vivo.

Figure 8.

Figure 4 TNIK binds to the ECD domain to phosphorylate EGFR and regulate ferroptosis resistance (A) Immunoprecipitation of TNIK in C4-2 cells followed by immunoblot analysis of EGFR or TNIK.

Figure 5 BA suppresses pyroptosis and promotes anti-oxidation in the spinal cord of SCI rats.

FIGURE 8 BZP regulated VD-like pathology by regulating Nrf2/TLR4/NF-κB p65 pathway in rat brain.

产品:	Nrf2 抗体
货号:	AF0639
描述:	Rabbit polyclonal antibody to Nrf2
应用:	WB IHC IF/ICC
反应:	Human, Mouse, Rat
预测:	Pig, Bovine, Horse, Rabbit, Dog, Chicken
分子量:	100～120kD; 68kD(Calculated).
蛋白号:	Q16236
RRID:	AB_2833793

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阻断肽(封闭肽)是特异性结合目标抗体和阻断抗体结合的多肽。这些多肽包含抗体识别的抗原表位。与阻断肽结合的抗体不再与靶蛋白上的表位结合。例如，在免疫印迹(WB)和免疫组化(IHC)中，通过比较被阻断抗体和未阻断抗体的染色，可以看到哪种染色是特异性的。

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来源:

Rabbit

应用:

WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:

Human,Mouse,Rat

预测:

Pig(100%), Bovine(100%), Horse(88%), Rabbit(88%), Dog(100%), Chicken(100%)

克隆:

Polyclonal

特异性:

Nrf2 Antibody detects endogenous levels of total Nrf2.

RRID:

AB_2833793
引用格式: Affinity Biosciences Cat# AF0639, RRID:AB_2833793.

偶联:

Unconjugated.

纯化:

The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).

保存:

Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.

别名:

展开/折叠

erythroid derived 2; HEBP1; like 2; NF E2 related factor 2; NF-E2-related factor 2; NF2L2_HUMAN; NFE2 related factor 2; NFE2-related factor 2; Nfe2l2; Nrf 2; NRF2; Nuclear factor (erythroid derived 2) like 2; Nuclear factor; nuclear factor erythroid 2 like 2; Nuclear factor erythroid 2 related factor 2; Nuclear factor erythroid 2-related factor 2; Nuclear factor erythroid derived 2 like 2;

抗原和靶标

免疫原:

Uniprot:

Q16236(NF2L2_HUMAN) >>Visit HPA database.

基因/基因ID:

NFE2L2(4780)

表达:

Q16236 NF2L2_HUMAN:

Widely expressed. Highest expression in adult muscle, kidney, lung, liver and in fetal muscle.

描述:

GABPA Transcription factor capable of interacting with purine rich repeats (GA repeats). Necessary for the expression of the Adenovirus E4 gene. Belongs to the ETS family. Heterotetramer of two alpha and two beta subunits.

序列:

Q16236 NF2L2_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

MMDLELPPPGLPSQQDMDLIDILWRQDIDLGVSREVFDFSQRRKEYELEKQKKLEKERQEQLQKEQEKAFFAQLQLDEETGEFLPIQPAQHIQSETSGSANYSQVAHIPKSDALYFDDCMQLLAQTFPFVDDNEVSSATFQSLVPDIPGHIESPVFIATNQAQSPETSVAQVAPVDLDGMQQDIEQVWEELLSIPELQCLNIENDKLVETTMVPSPEAKLTEVDNYHFYSSIPSMEKEVGNCSPHFLNAFEDSFSSILSTEDPNQLTVNSLNSDATVNTDFGDEFYSAFIAEPSISNSMPSPATLSHSLSELLNGPIDVSDLSLCKAFNQNHPESTAEFNDSDSGISLNTSPSVASPEHSVESSSYGDTLLGLSDSEVEELDSAPGSVKQNGPKTPVHSSGDMVQPLSPSQGQSTHVHDAQCENTPEKELPVSPGHRKTPFTKDKHSSRLEAHLTRDELRAKALHIPFPVEKIINLPVVDFNEMMSKEQFNEAQLALIRDIRRRGKNKVAAQNCRKRKLENIVELEQDLDHLKDEKEKLLKEKGENDKSLHLLKKQLSTLYLEVFSMLRDEDGKPYSPSEYSLQQTRDGNVFLVPKSKKPDVKKN

种属预测

种属预测:

score>80的预测可信度较高，可尝试用于WB检测。*预测模型主要基于免疫原序列比对，结果仅作参考，不作为质保凭据。

Species

Results

Score

Pig

100

Bovine

100

Dog

100

Chicken

100

Horse

Rabbit

Xenopus

Sheep

Zebrafish

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - Q16236 作为底物

Q16236

Site	PTM Type	Enzyme	Source
S40	Phosphorylation	P05771 (PRKCB) , P17252 (PRKCA)	Uniprot
K44	Ubiquitination		Uniprot
K64	Ubiquitination		Uniprot
T80	Phosphorylation		Uniprot
S215	Phosphorylation		Uniprot
S301	Phosphorylation		Uniprot
S344	Phosphorylation	P49841 (GSK3B)	Uniprot
S347	Phosphorylation	P49841 (GSK3B)	Uniprot
S351	Phosphorylation		Uniprot
S356	Phosphorylation		Uniprot
T395	Phosphorylation	Q00535 (CDK5)	Uniprot
S408	Phosphorylation		Uniprot
S433	Phosphorylation	Q00535 (CDK5)	Uniprot
R437	Methylation		Uniprot
K438	Acetylation		Uniprot
T439	Phosphorylation	Q00535 (CDK5)	Uniprot
K443	Acetylation		Uniprot
K445	Acetylation		Uniprot
S447	Phosphorylation		Uniprot
K462	Acetylation		Uniprot
K462	Ubiquitination		Uniprot
K472	Acetylation		Uniprot
K487	Acetylation		Uniprot
K506	Acetylation		Uniprot
K508	Acetylation		Uniprot
K516	Acetylation		Uniprot
K516	Ubiquitination		Uniprot
K518	Acetylation		Uniprot
K518	Sumoylation		Uniprot
K518	Ubiquitination		Uniprot
K533	Acetylation		Uniprot
K536	Acetylation		Uniprot
K538	Acetylation		Uniprot
K541	Acetylation		Uniprot
K543	Acetylation		Uniprot
K548	Acetylation		Uniprot
K548	Ubiquitination		Uniprot
K554	Acetylation		Uniprot
K554	Ubiquitination		Uniprot
K555	Acetylation		Uniprot
S558	Phosphorylation		Uniprot
T559	Phosphorylation		Uniprot
Y561	Phosphorylation		Uniprot
K574	Ubiquitination		Uniprot
Y576	Phosphorylation	P06241 (FYN)	Uniprot
S577	Phosphorylation		Uniprot
K596	Acetylation		Uniprot
K599	Acetylation		Uniprot

研究背景

Q16236_NF2L2_HUMAN

功能:

Transcription factor that plays a key role in the response to oxidative stress: binds to antioxidant response (ARE) elements present in the promoter region of many cytoprotective genes, such as phase 2 detoxifying enzymes, and promotes their expression, thereby neutralizing reactive electrophiles. In normal conditions, ubiquitinated and degraded in the cytoplasm by the BCR(KEAP1) complex. In response to oxidative stress, electrophile metabolites inhibit activity of the BCR(KEAP1) complex, promoting nuclear accumulation of NFE2L2/NRF2, heterodimerization with one of the small Maf proteins and binding to ARE elements of cytoprotective target genes. The NFE2L2/NRF2 pathway is also activated in response to selective autophagy: autophagy promotes interaction between KEAP1 and SQSTM1/p62 and subsequent inactivation of the BCR(KEAP1) complex, leading to NFE2L2/NRF2 nuclear accumulation and expression of cytoprotective genes. May also be involved in the transcriptional activation of genes of the beta-globin cluster by mediating enhancer activity of hypersensitive site 2 of the beta-globin locus control region.

翻译修饰:

Ubiquitinated in the cytoplasm by the BCR(KEAP1) E3 ubiquitin ligase complex leading to its degradation. In response to oxidative stress, electrophile metabolites, such as sulforaphane, modify KEAP1, leading to inhibit activity of the BCR(KEAP1) complex, promoting NFE2L2/NRF2 nuclear accumulation and activity. In response to autophagy, the BCR(KEAP1) complex is inactivated (By similarity).

Phosphorylation of Ser-40 by PKC in response to oxidative stress dissociates NFE2L2 from its cytoplasmic inhibitor KEAP1, promoting its translocation into the nucleus.

Acetylation at Lys-596 and Lys-599 increases nuclear localization whereas deacetylation by SIRT1 enhances cytoplasmic presence.

Glycation impairs transcription factor activity by preventing heterodimerization with small Maf proteins. Deglycation by FN3K restores activity.

细胞定位:

Cytoplasm>Cytosol. Nucleus.
Note: Cytosolic under unstressed conditions: ubiquitinated and degraded by the BCR(KEAP1) E3 ubiquitin ligase complex (PubMed:15601839, PubMed:21196497). Translocates into the nucleus upon induction by electrophilic agents that inactivate the BCR(KEAP1) E3 ubiquitin ligase complex (PubMed:21196497).

组织特异性:

Widely expressed. Highest expression in adult muscle, kidney, lung, liver and in fetal muscle.

亚基结构:

Heterodimer; heterodimerizes with small Maf proteins (By similarity). Interacts (via the bZIP domain) with MAFG and MAFK; required for binding to antioxidant response elements (AREs) on DNA (By similarity). Interacts with KEAP1; the interaction is direct and promotes ubiquitination by the BCR(KEAP1) E3 ubiquitin ligase complex. Forms a ternary complex with PGAM5 and KEAP1. Interacts with EEF1D at heat shock promoter elements (HSE). Interacts via its leucine-zipper domain with the coiled-coil domain of PMF1. Interacts with CHD6; involved in activation of the transcription (By similarity). Interacts with ESRRB; represses NFE2L2 transcriptional activity (By similarity).

(Microbial infection) Interacts with herpes virus 8 protein LANA1.

蛋白家族:

The ETGE motif, and to a lower extent the DLG motif, mediate interaction with KEAP1.

Belongs to the bZIP family. CNC subfamily.

研究领域

· Genetic Information Processing > Folding, sorting and degradation > Protein processing in endoplasmic reticulum. (View pathway)

· Human Diseases > Cancers: Overview > Pathways in cancer. (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma. (View pathway)

文献引用

1). Diamond-Like Carbon Depositing on the Surface of Polylactide Membrane for Prevention of Adhesion Formation During Tendon Repair. Nano-micro letters, 2024 (PubMed: 38687411) [IF=26.6]

Application: WB Species: Rat Sample:

Fig. 2 DLC suppress ROS production and oxidative stress both in vitro and in vivo. a Detection of cell ROS level on different membranes using ROS probes and b statistical analysis. c Diagram of animal experiment. d, f Content of MDA, 8-OHdG, and 3-NT in peritendinous tissues after 7 days of injury was examined by assay kit respectively. g Representative bands of Nrf2, HO-1, p-NF-κB were measured by Western blotting. h Nrf2 and HO-1 expression normalized to β-actin expression. i p-NF-κB expression normalized to NF-κB expression. Data represent independent experiments, and all data are presented as mean ± SD; NS non-significant,

2). Oral Metal-Free Melanin Nanozymes for Natural and Durable Targeted Treatment of Inflammatory Bowel Disease (IBD). Small (Weinheim an der Bergstrasse, Germany), 2023 (PubMed: 36760016) [IF=13.3]

3). Ultrasmall PtAu2 nanoclusters activate endogenous anti-inflammatory and anti-oxidative systems to prevent inflammatory osteolysis. Theranostics, 2023 (PubMed: 36793859) [IF=12.4]

4). Mitochondria-targeted supramolecular coordination container encapsulated with exogenous itaconate for synergistic therapy of joint inflammation. Theranostics, 2023 (PubMed: 35547753) [IF=12.4]

5). Breaking the vicious loop between inflammation, oxidative stress and coagulation, a novel anti-thrombus insight of nattokinase by inhibiting LPS-induced inflammation and oxidative stress. Redox Biology, 2020 (PubMed: 32193146) [IF=11.4]

Application: WB Species: Mice Sample: RAW264.7 cells

Fig. 4. NK suppressed the LPS-induced ROS generation and NOX2 activation in RAW264.7 cells. (A) Effect of NK on LPS-induced ROS generation in RAW 264.7 cells. Cells were pretreated with NK (0.30 FU/ml) for 1 h and then exposed to LPS (0.1 μg/mL) for 24 h. Intracellular ROS appeared green under a confocal microscopy (Scale bar is 40 μm), and the green fluorescent intensity was quantified by Image Pro Plus. Data represent the mean ± SD from three independent experiments. The mean fluorescence intensity were standardized to LPS treatment cells. **P < 0.01, vs. control; ##P < 0.01, ###P < 0.001, vs. LPS-stimulated cells. (B) Effect of NK on LPS-induced Nrf2 and AKT activation in RAW264.7 cells. Cells were pretreated with NK (0.08, 0.15, 0.30 FU/mL) for 1 h and then were stimulated with LPS (0.1 μg/mL) for 6 h. Equal amounts of total cell lysates were loaded and subjected to immunoblot analysis. β-actin was used as the control for equal protein loading and protein integrity. Data represent the mean ± SD from three independent experiments. *P < 0.01, vs. control; #P < 0.05, ##P < 0.05, vs. LPS-stimulated cells. (C) Effect of NK on LPS-induced P47 translocation via immunofluorescence assay. Cells were pretreated with NK (0.30 FU/ml) for 1 h before LPS (0.1 μg/mL) stimulation for 2 h. Double immunostainings were performed with anti-NOX2 (in green) and anti-p47phox (in red); nuclei were stained with Hochest (blue). Scale bars: 40 μm. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

6). iNOS contributes to heart failure with preserved ejection fraction through mitochondrial dysfunction and Akt S-nitrosylation. Journal of Advanced Research, 2023 (PubMed: 36585107) [IF=10.7]

Application: WB Species: Mouse Sample: heart tissue

Fig. 6. iNOS inhibition alleviated oxidative stress in the heart of HFpEF mice. (A-C) Representative immunostaining and semi-quantification of NOX4 and SOD2 in heart tissue samples. (D) Myocardial malondialdehyde levels. (E) GSH-Px activity. (F-H) Representative immunostaining and semi-quantification of p-Nrf2/Nrf2 as well as HO-1 in the heart tissue samples from mice in different experimental groups. n = 6. The data are shown as mean ± SEM and were analyzed using one-way ANOVA followed by Tukey’s post hoc test. *, P < 0.05. **, P < 0.01. ***, P < 0.0005. ****, P < 0.0001. ns, no significant.

7). Total flavonoids of Inula japonica alleviated the inflammatory response and oxidative stress in LPS-induced acute lung injury via inhibiting the sEH activity: Insights from lipid metabolomics. PHYTOMEDICINE, 2022 (PubMed: 36150346) [IF=7.9]

8). Agrimoniin sensitizes pancreatic cancer to apoptosis through ROS-mediated energy metabolism dysfunction. Phytomedicine, 2022 (PubMed: 34785107) [IF=7.9]

9). Oleanolic acid alleviates ANIT-induced cholestatic liver injury by activating Fxr and Nrf2 pathways to ameliorate disordered bile acids homeostasis. PHYTOMEDICINE, 2022 (PubMed: 35605478) [IF=7.9]

10). NRF2 and FXR dual signaling pathways cooperatively regulate the effects of oleanolic acid on cholestatic liver injury. Phytomedicine, 2023 (PubMed: 36343550) [IF=7.9]

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Nrf2 Antibody - #AF0639

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实验方案

WB Handbook

IHC Protocol

IF/ICC Protocol

产品描述

抗原和靶标

种属预测

翻译修饰 - Q16236 作为底物

研究背景

研究领域

文献引用

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