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Histone H3 Antibody - Western blot analysis of extracts from various samples, using Histone H3 Antibody.

Histone H3 Antibody - Western blot analysis of extracts from various samples,using Histone H3 Antibody.

Histone H3 Antibody - AF0863 at 1/50 staining human breast cancer tissue sections by IHC-P.

Histone H3 Antibody - AF0863 at 1/50 staining human colon tissue sections by IHC-P.

Histone H3 Antibody - AF0863 at 1/200 staining human breast cancer tissue sections by IHC-P.

Histone H3 Antibody - AF0863 at 1/200 staining human colon tissue sections by IHC-P.

Histone H3 Antibody - AF0863 staining MCF-7 cells by ICC/IF.

Histone H3 Antibody - AF0863 staining Hela cells by IF/ICC.

Histone H3 Antibody - AF0863 staining A549 cells(UV treatment) by IF/ICC.

Histone H3 Antibody - .

Histone H3 Antibody - Figure 5.

Histone H3 Antibody - Fig.

Histone H3 Antibody - Figure 7 Subcellular locations of the truncated forms of PADI3 in HCT116 cells.

Histone H3 Antibody - Figure 4.

$Fig. 5 RIP3 impeded the nuclear translocation of TFEB in septic AKI mice and LPS-treated cultured PTECs. A Immunofluorescence staining for TFEB (green) and DAPI (blue) in the kidneys from C57BL/6 mice treated with sterilized saline (con), LPS, or LPS plus GSK’872 (GSK) for 24 h. GSK partially restored the decreased nuclear staining of TFEB in the renal tubular cells of LPS-induced mice. Scale bar = 20 μm. B Cultured PTECs treated with LPS, LPS plus GSK, LPS plus DMSO, LPS plus RIP3 siRNA, or LPS plus scrambled siRNA (Scramble) for 12 h. The nuclear protein fractions were immunoblotted for TFEB. Histone was used as the nuclear marker. TFEB expression against Histone was decreased by LPS treatment, which was restored by GSK or RIP3 siRNA (n = 3). C Immunofluorescence staining for TFEB (green) and DAPI (blue) in cultured PTECs treated as indicated. The nuclear translocation of TFEB was inhibited by LPS, which was rescued by GSK or RIP3 siRNA. Scale bar = 20 μm. D, E Lysates from cultured PTECs treated with LPS or DMSO (con) for 12 h were subjected to immunoprecipitation using an anti-RIP3 antibody (D) or anti-TFEB antibody (E), and IgG antibody followed by immunoblot for TFEB and RIP3. Input proteins were detected with anti-RIP3 and anti-TFEB antibodies. RIP3 interacted with TFEB in LPS-treated PTECs compared to the control group. F Lysates from cultured PTECs treated with LPS or DMSO (con) for 12 h were subjected to immunoprecipitation using anti-TFEB antibody and IgG antibody followed by immunoblot for p-RIP3. Input proteins were detected with anti-p-RIP3 and anti-TFEB antibodies. p-RIP3 interacted with TFEB in LPS-treated PTECs compared to the control group. *P < 0.05.$

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Histone H3 Antibody - Figure 7.

$Fig. 11. |Effect of XJEK treatment on the nuclear translocation of Nrf2 and HO-1 expression in renal tissues of MI rats. The expression levels of nuclear factor erythroid 2‐related factor (Nrf2) and heme oxygenase‐1 (HO-1) in renal cortical tissues were examined by Western blot analysis. (A, B and C) Nrf2 content in nuclear fraction of renal cortical tissues of rats for 2, 4 and 6wk post-MI by western blot, respectively (mean ± SEM, n = 4 in each group)$

Histone H3 Antibody - Fig.

Histone H3 Antibody - Figure 7.

Histone H3 Antibody - Fig.

$Figure 3 Effects of TP53INP2 knockdown on EMT and β-catenin. Notes: (A, B) The negative control or siTP53INP2 were transfected into the BIU87 and EJ cells. The cells were incubated for 48 h, and the changes in the expressions of EMT molecular markers and β-catenin were detected by Western blot. β-actin was used as an internal control. (C, D) The cellular location of active β-catenin and Snail1 in EJ cells after interference in TP53INP2. Scale bar, 50 μm. (E) The abundance of the active forms of β-catenin and Snail1 in nuclear and cytosolic fractions were detected by Western blot. GAPDH and H3 were used as cytosolic or nuclear controls. Abbreviations: EMT, epithelial-to-mesenchymal transition; GAPDH, glyceraldehyde 3-phosphate dehydrogenase.$

Histone H3 Antibody - Figure 3 Effects of TP53INP2 knockdown on EMT and β-catenin.

Histone H3 Antibody - FIGURE 4 Oxidative stress played a crucial role in crizotinib- and sunitinib-induced hepatotoxicity in vitro and in vivo.

Histone H3 Antibody - Fig.

Histone H3 Antibody - Figure 10.

Histone H3 Antibody - FIGURE 8 Effects of OCOP and COP on the NF-κB pathway in DSS-induced mice (A) Representative Western blotting images of pIκBα, IκBα, cytoplasmic p65 and nuclear p65 (B–E) The protein expression levels of pIκBα, IκBα, cytoplasmic p65 and nuclear p65 in the NF-κB pathway.

Histone H3 Antibody - Fig.

Histone H3 Antibody - Figure S3: | A: IHC staining of lung cancer tissues TTF-1, CEA and P63 (n=3).

Histone H3 Antibody - Fig.

Histone H3 Antibody - 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.

Histone H3 Antibody - FIGURE 9 Effects of SAL on the NF-κB signaling pathway.

Histone H3 Antibody - FIGURE 3 Effect of DPSC-Exos on the expression of TLR4, MyD88, NF-κB p65 and HMGB1 on day 7 after cerebral I/R damage.

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Histone H3 Antibody - FIGURE 7 | Involvement of the Nrf2 pathway in crizotinib- or sunitinib-mediated hepatotoxicity in vitro and in vivo.

Histone H3 Antibody - Figure 4.

Histone H3 Antibody - Figure 4 Calcitriol inhibited MI-induced cardiac myocyte apoptosis and death, as well as inflammation by modulating VDR signaling.

Histone H3 Antibody - Figure 2 Mito-TEMPO diminishes liver inflammation in LPS-induced sepsis.

Histone H3 Antibody - "FIGURE 4 XBJ alleviated the NETs formation in the lungs of septic mice (A–D).

XBJ alleviated the NETs formation in the lungs of septic mice (A–D). Immunofluorescent staining was performed on lung sections from CLP mice (n = 3) and analyzed by confocal microscopy. DAPI (blue), NE (Neutrophil elastase, red) and CitH3 (Citrulline histone 3, green) (A,C). The expression of CitH3 in lung tissues of indicated groups of mice. The expression of NE in lung tissues of different groups of mice was shown in (B,D–G). The expression of NETs formation markers, CitH3 and NE, were determined by immunohistochemistry in the lung sections of different groups of mice (F,G). The quantifications of CitH3 (F) and NE (G) expression levels in immunohistochemistry assays (n = 3) (H,I). Western blot was performed to determine the expression of CitH3 in the lung tissue of indicated groups of mice. I showed the quantification of CitH3 expression. N = 4/per group. The values were indicated as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, compared with the CLP group."" title=""FIGURE 4 XBJ alleviated the NETs formation in the lungs of septic mice (A–D). Immunofluorescent staining was performed on lung sections from CLP mice (n = 3) and analyzed by confocal microscopy. DAPI (blue), NE (Neutrophil elastase, red) and CitH3 (Citrulline histone 3, green) (A,C). The expression of CitH3 in lung tissues of indicated groups of mice. The expression of NE in lung tissues of different groups of mice was shown in (B,D–G). The expression of NETs formation markers, CitH3 and NE, were determined by immunohistochemistry in the lung sections of different groups of mice (F,G). The quantifications of CitH3 (F) and NE (G) expression levels in immunohistochemistry assays (n = 3) (H,I). Western blot was performed to determine the expression of CitH3 in the lung tissue of indicated groups of mice. I showed the quantification of CitH3 expression. N = 4/per group. The values were indicated as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, compared with the CLP group."" alt="Histone H3 Antibody - "FIGURE 4 XBJ alleviated the NETs formation in the lungs of septic mice (A–D).">

Histone H3 Antibody - "FIGURE 4 XBJ alleviated the NETs formation in the lungs of septic mice (A–D).

Histone H3 Antibody - Fig.

$Fig. 5. Effects of stigmasterol treatment on inflammatory pathways in Aβ42 oligomers induced BV2 cells when treated with AMPK inhibitor. Cells were pretreated with Compound C (10 μM) for 4 h, and then treated with Aβ42 oligomers (1 μM) for 24 h, followed by treatment with stigmasterol (20 μM) for 4 h. (A,B) Representative western blot analysis of AMPK signaling. GAPDH immunoreactivity was used as a loading control. (C-E) Representative western blot analysis of NF-κB signaling. The cytosolic and nuclear fractions were prepared and analyzed with total NF-κB p65. α-Tubulin immunoreactivity was used as a loading control in the cytosolic fraction, Histone H3 was used as the loading control in the nuclear fraction. (F-H) Representative western blot analysis of NLRP3 signaling, including NLRP3 and Caspase-1, p20. GAPDH immunoreactivity was used as a loading control (I, J) Concentration of TNFα and IL-1β. Data were presented as the mean ± SEM from three independent experiments. One-way ANOVA with Tukey’s multiple comparison test revealed a difference between groups.$

Histone H3 Antibody - Fig.

Histone H3 Antibody - FIGURE 5 Cinacalcet inhibits the translocation of P65 from the cytoplasm to the nucleus.

Histone H3 Antibody - 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.

$Figure 3 MBL limited AhR expression and its nuclear translocation in CD4+ T lymphocytes. (A and C) Naïve CD4+ T cells were cultured under Th17 differentiation conditions with or without MBL protein (5μg/mL). (A) The expression of AhR in CD4+ T cells was determined by FCM analysis. (B) The protein levels of AhR were determined by Western blot. (C) The level of phosphorylated STAT3 was assessed by FCM analysis. (D–E) Naïve CD4+ T cells were pretreated with 10μM Sc144 for 2h, then cultured under Th17 differentiation conditions with or without MBL protein (5μg/mL). (D) The mRNA expression of AhR in CD4+ T cells was determined by RT-qPCR analysis. (E) The protein level of AhR was assessed by Western blot analysis. (F–H) CD4+ T cells were treated with 200nM FICZ for 6h in the presence or absence of 5μg/mL MBL. (F) The fraction of cytoplasm and nucleus protein were separated, and the expression of AhR was determined by Western blot. (G) The mRNA levels of CYP1A1, CYP1A2, and CYP1B1 were detected by RT-qPCR analysis. (H) The mRNA levels of RORγt and IL-17 were detected by RT-qPCR analysis. *p < 0.05, **p < 0.01. The data represent three independent experiments with similar results.$

Histone H3 Antibody - Figure 3 MBL limited AhR expression and its nuclear translocation in CD4+ T lymphocytes.

Histone H3 Antibody - Figure 2.

$Fig. 8 11R-VIVIT attenuates TGFβ‑induced apoptosis in HK-2 cells. a TGFβ treatment increased total NFAT2 expression in HK-2 cells. b TGFβ treatment decreased p-NFAT2 (Ser172) expression and 11R-VIVIT could increase the protein expression of p-NFAT2 (Ser172). c Quantification of NFAT2 expression normalized to GAPDH. d Quantification of p-NFAT2 (Ser172) expression normalized to GAPDH. e–f TGFβ treatment increased nuclear NFAT2 expression in HK-2 cells, and 11R-VIVIT inhibited the nuclear localization of NFAT2. g Quantification of NFAT2 expression in the cytoplasmic fraction HK-2 cells; The results were normalized to GAPDH. h Quantification of NFAT2 expression in the nuclear fraction of HK-2 cells; The results were normalized to Histone H3. i The protein expression of α-SMA and fibronectin in HK-2 cells. j–k The quantitative results of α-SMA and fibronectin were normalized to GAPDH. l Apoptosis was examined by flow cytometry. m Quantification of RTEC apoptosis by flow cytometry. n Western blot analysis of the expression of caspase-3 and C‑caspase-3 in HK-2 cells. o The quantitative results of caspase-3 and C‑caspase-3 were normalized to β-actin. p Western blot analysis of the expression of Bax in HK-2 cells. q The quantitative results of Bax were normalized to β-actin. r TUNEL staining of HK-2 cells in the CON, TGFβ and 11R-VIVIT + TGFβ group. s Quantification of TUNEL‑positive tubular epithelial cells. Scale bars = 20 μm. *P$

Histone H3 Antibody - Fig.

Histone H3 Antibody - Figure 4 Effect of DOFE on Nrf2/HO-1-mediated antioxidant response.

Histone H3 Antibody - Figure 3 Expression and phosphorylation of MAPKs in PPD-treated NCI-H1299 cells.

Histone H3 Antibody - Fig.

Histone H3 Antibody - FIGURE 8 BZP regulated VD-like pathology by regulating Nrf2/TLR4/NF-κB p65 pathway in rat brain.

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Histone H3 Antibody - FIGURE 1.

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Histone H3 Antibody - Figure 4.

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Histone H3 Antibody - FIGURE 2 Effect of sevoflurane on hnRNPA2/B1 in hippocampal neurons under hypoxia.

Histone H3 Antibody - Fig.

$Fig. 2. ((Farrerol inhibits ferroptosis and apoptosis in R28 cells by activating the Nrf2 signaling pathway. A: Fluorescence microscopy was used to observe the nuclear translocation of Nrf2 in R28 cells under different conditions. Red fluorescence indicates Nrf2, and blue fluorescence indicates the nucleus. Bar = 100 μm. B: WB was used to detect Nrf2 expression in cytoplasmic and nuclear fractions, with ImageJ for quantification. C, D: Confocal microscopy was used to observe ACSL4 and GPX4 expression. Red fluorescence indicates ACSL4 and GPX4, green indicates actin, and blue indicates the nucleus. Bar = 10 μm. E, F: WB was used to detect ACSL4 and GPX4 protein levels, with ImageJ for relative quantification. At least three independent experiments were performed. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, ns not significant.)). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)$

Histone H3 Antibody - Fig.

产品:	Histone H3 抗体
货号:	AF0863
描述:	Rabbit polyclonal antibody to Histone H3
应用:	WB IHC IF/ICC
文献验证:	WB, IHC, IF/ICC
反应:	Human, Mouse, Rat, Fish
预测:	Bovine
蛋白ID:	P68431 \| Q71DI3 \| P84243
RRID:	AB_2810277

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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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50ul	RMB¥ 900	现货
100ul	RMB¥ 1500	现货
200ul	RMB¥ 2000	现货

货期: 当天发货

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实验方案

WB Handbook

IHC Protocol

IF/ICC Protocol

产品描述

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. For optimal experimental results, antibody reuse is not recommended.
*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, Fish

克隆:

Polyclonal

特异性:

Histone H3 Antibody detects endogenous levels of Histone H3.

RRID:

AB_2810277
引用格式: Affinity Biosciences Cat# AF0863, RRID:AB_2810277.

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

H3 histone family, member A; H3/A; H31_HUMAN; H3FA; Hist1h3a; HIST1H3B; HIST1H3C; HIST1H3D; HIST1H3E; HIST1H3F; HIST1H3G; HIST1H3H; HIST1H3I; HIST1H3J; histone 1, H3a; Histone cluster 1, H3a; Histone H3.1; Histone H3/a; Histone H3/b; Histone H3/c; Histone H3/d; Histone H3/f; Histone H3/h; Histone H3/i; Histone H3/j; Histone H3/k; Histone H3/l; ;H3.3A; HIST1 cluster, H3E; H3 histone family, member A; H3.1; H3/l; H3F3; H3FF; H3FJ; H3FL; Histone gene cluster 1, H3 histone family, member E; histone H3.1t; Histone H3/o; FLJ92264; H 3; H3; H3 histone family, member B; H3 histone family, member C; H3 histone family, member D; H3 histone family, member F; H3 histone family, member H; H3 histone family, member I; H3 histone family, member J; H3 histone family, member K; H3 histone family, member L; H3 histone family, member T; H3 histone, family 3A; H3/A; H3/b; H3/c; H3/d; h3/f; H3/h; H3/i; H3/j; H3/k; H3/t; H31_HUMAN; H3F1K; H3F3A; H3FA; H3FB; H3FC; H3FD; H3FH; H3FI; H3FK; HIST1 cluster, H3A; HIST1 cluster, H3B; HIST1 cluster, H3C; HIST1 cluster, H3D; HIST1 cluster, H3F; HIST1 cluster, H3G; HIST1 cluster, H3H; HIST1 cluster, H3I; HIST1 cluster, H3J; HIST1H3A; HIST1H3B; HIST1H3C; HIST1H3D; HIST1H3E; HIST1H3F; HIST1H3G; HIST1H3H; HIST1H3I; HIST1H3J; HIST3H3; Histone 1, H3a; Histone 1, H3b; Histone 1, H3c; Histone 1, H3d; Histone 1, H3e; Histone 1, H3f; Histone 1, H3g; Histone 1, H3h; Histone 1, H3i; Histone 3, H3; histone cluster 1 H3 family member a; histone cluster 1 H3 family member b; histone cluster 1 H3 family member c; histone cluster 1 H3 family member d; histone cluster 1 H3 family member e; histone cluster 1 H3 family member f; histone cluster 1 H3 family member g; histone cluster 1 H3 family member h; histone cluster 1 H3 family member i; histone cluster 1 H3 family member j; Histone cluster 1, H3a; Histone cluster 1, H3b; Histone cluster 1, H3c; Histone cluster 1, H3d; Histone cluster 1, H3e; Histone cluster 1, H3f; Histone cluster 1, H3g; Histone cluster 1, H3i; Histone cluster 1, H3j; Histone gene cluster 1, H3 histone family, member A; Histone gene cluster 1, H3 histone family, member B; Histone gene cluster 1, H3 histone family, member C; Histone gene cluster 1, H3 histone family, member D; Histone gene cluster 1, H3 histone family, member F; Histone gene cluster 1, H3 histone family, member G; Histone gene cluster 1, H3 histone family, member H; Histone gene cluster 1, H3 histone family, member I; Histone gene cluster 1, H3 histone family, member J; Histone gene cluster 1, H3A; Histone gene cluster 1, H3B; Histone gene cluster 1, H3C; Histone gene cluster 1, H3D; Histone gene cluster 1, H3E; Histone gene cluster 1, H3F; Histone gene cluster 1, H3G; Histone gene cluster 1, H3H; Histone gene cluster 1, H3I; Histone gene cluster 1, H3J; Histone H 3; Histone H3.1; Histone H3.2; Histone H3.3; Histone H3/a; Histone H3/b; Histone H3/c; Histone H3/d; Histone H3/f; Histone H3/h; Histone H3/i; Histone H3/j; Histone H3/k; Histone H3/l; Histone H3/m; H3 histone family 3A; H3 histone family 3B; H3 histone, family 3B (H3.3B); H3.3; H3.3A; H3.3B; H33_HUMAN; H3F3; H3F3A; H3f3b; Histone H3.3; Histone H3.3Q; Histone H3.A; Histone H3.B; MGC87782; MGC87783;

抗原和靶标

免疫原:

A synthesized peptide derived from human Histone H3.

基因/基因ID:

HIST2H3A; HIST2H3C; HIST2H3D(126961) | HIST1H3A; HIST1H3B; HIST1H3C; HIST1H3D; HIST1H3E; HIST1H3F; HIST1H3G; HIST1H3H; HIST1H3I; HIST1H3J(333932) | H3F3A; H3F3B(653604)

描述:

H3 Core component of nucleosome. Nucleosomes wrap and compact DNA into chromatin, limiting DNA accessibility to the cellular machineries which require DNA as a template. Histones thereby play a central role in transcription regulation, DNA repair, DNA replication and chromosomal stability. DNA accessibility is regulated via a complex set of post-translational modifications of histones, also called histone code, and nucleosome remodeling. The nucleosome is a histone octamer containing two molecules each of H2A, H2B, H3 and H4 assembled in one H3-H4 heterotetramer and two H2A-H2B heterodimers.

研究领域

· Human Diseases > Substance dependence > Alcoholism.

· Human Diseases > Cancers: Overview > Transcriptional misregulation in cancer.

· Human Diseases > Immune diseases > Systemic lupus erythematosus.

文献引用

1). ETV2 regulating PHD2-HIF-1α axis controls metabolism reprogramming promotes vascularized bone regeneration. Bioactive materials, 2024 (PubMed: 38549772) [IF=18.9]

2). Psychologic Stress Drives Progression of Malignant Tumors via DRD2/HIF1α Signaling. CANCER RESEARCH, 2021 (PubMed: 34321238) [IF=12.5]

Application: WB Species: mouse Sample: B16F10 and 4T1 tumor

Fig. 1 |DRD2 may promote the malignant progression of melanoma and breast cancer under psychologic stress condition. J, Western blot analysis of DRD2 expression levels in the nuclei of B16F10 and 4T1 tumor tissues with or without stress stimulation.

3). Salidroside can target both P4HB-mediated inflammation and melanogenesis of the skin. Theranostics, 2020 (PubMed: 33042273) [IF=12.4]

Application: WB Species: human Sample: A375 cells

Figure 4. P4HB regulates the ubiquitination degradation of IRF1. A. Changes in TYR activity in P4HB overexpression or knockdown A375 cells. B. Changes in TYR mRNA expression in Sal treated, P4HB overexpression, and P4HB knockdown A375 cells. C. Western blot analysis of TYR expression in P4HB overexpression or knockdown A375 cells. D. Proteins have interactions with P4HB and USF1 analyzed by FpClass. E. Interaction of P4HB and IRF1 in A375 cells detected by PLA. F. Western blot analysis of the expression of IRF1 and P4HB in P4HB overexpression or knockdown A375 cells. G. Western blot analysis of IRF1 expression in the nucleus of A375 cells after P4HB overexpression or knockdown. H. Effect of SAL on the ubiquitination of IRF1 as determined by Western blot. I. Western blot analysis of IRF1 expression in whole cells and nucleus of SAL-treated A375 cells. Data are expressed as mean ± SD (*P < 0.05, **P < 0.01).

4). Lactate drives epithelial-mesenchymal transition in diabetic kidney disease via the H3K14la/KLF5 pathway. Redox biology, 2024 (PubMed: 38925041) [IF=10.7]

Application: WB Species: Mouse Sample:

Fig. 5. Histone lactylaction is increased in db/db mice and AGEs-induced mTEC. (A) Immunoblot analysis of Pan kla expression in db/db mice. (B) The Pan kla immunoblots in AGE-induced mTEC. (C) The Pan kla and Pan kac immunoblots in AGE-induced mTEC at 0, 4, 8, 12, 24, and 48 h. (D–E) Immunoblot analysis demonstrating the expression of Pan kla, H3K14la, H3K18la, H3K9la, H3K23la, H3K27la and H3K14ac in AGEs-induced mTEC. (F) Immunofluorescent staining of Pan kla (red) and DAPI (blue). Scale bars, 50 μm. (G–H) Immunofluorescent staining of H3K14la (red) and DAPI (blue). Scale bars, 50 μm. (I–K) Immunoblot analysis of Pan kla and H3K14la in AGEs-induced mTEC. All statistic data were presented as mean ± SEM. Unpaired two tailed t-test. Data are expressed as Mean ± SEM, #P < 0.05, ##P < 0.01; *P < 0.05, **P < 0.01. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

5). Bilirubin-polymer nanocarriers enable targeted farrerol delivery for glaucoma neuroprotection via Nrf2-mediated ferroptosis/apoptosis inhibition. Materials Today Bio, 2025 [IF=10.2]

Application: WB Species: Rat Sample: R28 cells

Fig. 2. ((Farrerol inhibits ferroptosis and apoptosis in R28 cells by activating the Nrf2 signaling pathway. A: Fluorescence microscopy was used to observe the nuclear translocation of Nrf2 in R28 cells under different conditions. Red fluorescence indicates Nrf2, and blue fluorescence indicates the nucleus. Bar = 100 μm. B: WB was used to detect Nrf2 expression in cytoplasmic and nuclear fractions, with ImageJ for quantification. C, D: Confocal microscopy was used to observe ACSL4 and GPX4 expression. Red fluorescence indicates ACSL4 and GPX4, green indicates actin, and blue indicates the nucleus. Bar = 10 μm. E, F: WB was used to detect ACSL4 and GPX4 protein levels, with ImageJ for relative quantification. At least three independent experiments were performed. ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001, ns not significant.)). (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

6). Oxyberberine, a novel gut microbiota-mediated metabolite of berberine, possesses superior anti-colitis effect: impact on intestinal epithelial barrier, gut microbiota profile and TLR4-MyD88-NF-κB pathway. PHARMACOLOGICAL RESEARCH, 2020 (PubMed: 31863867) [IF=9.1]

Application: WB Species: Mice Sample: colonic tissues

Fig. 6. Effect of OBB on the activation of TLR4-MyD88-NF-κB signaling pathway in DSS-induced colonic tissues. (A) Representative Western blotting images of TLR4, MyD88, cytoplasmic p65, nuclear p65, p-IκBα and IκBα. Changes in the relative protein expression levels of TLR4 (B), MyD88 (C), nuclear p65 (D), cytoplasmic p65 (E), and p-IκBα/IκBα ratio (F) were measured. Data are shown as the mean ± SEM (n = 3). # P < 0.05, ## P < 0.01 vs. Control group, * P < 0.05, ** P < 0.01 vs. DSS group.

7). Sophora japonica flowers and their main phytochemical, rutin, regulate chemically induced murine colitis in association with targeting the NF-κB signaling pathway and gut microbiota. Food Chemistry, 2022 (PubMed: 35691061) [IF=8.5]

8). Targeting Macrophage-to-Myofibroblast Transition Mitigates Progression from Inflammation to Fibrosis in Rosacea. International journal of biological sciences, 2026 (PubMed: 41800255) [IF=8.2]

9). H3K79 methylation promotes rapid growth of Alexandrium pacificum under high light intensity via increased photosynthesis. Science of The Total Environment, 2023 (PubMed: 37311522) [IF=8.2]

10). RIP3 impedes transcription factor EB to suppress autophagic degradation in septic acute kidney injury. Cell Death & Disease, 2021 (PubMed: 34103472) [IF=8.1]

Application: WB Species: Mice Sample: kidney tissue

Fig. 5 RIP3 impeded the nuclear translocation of TFEB in septic AKI mice and LPS-treated cultured PTECs. A Immunofluorescence staining for TFEB (green) and DAPI (blue) in the kidneys from C57BL/6 mice treated with sterilized saline (con), LPS, or LPS plus GSK’872 (GSK) for 24 h. GSK partially restored the decreased nuclear staining of TFEB in the renal tubular cells of LPS-induced mice. Scale bar = 20 μm. B Cultured PTECs treated with LPS, LPS plus GSK, LPS plus DMSO, LPS plus RIP3 siRNA, or LPS plus scrambled siRNA (Scramble) for 12 h. The nuclear protein fractions were immunoblotted for TFEB. Histone was used as the nuclear marker. TFEB expression against Histone was decreased by LPS treatment, which was restored by GSK or RIP3 siRNA (n = 3). C Immunofluorescence staining for TFEB (green) and DAPI (blue) in cultured PTECs treated as indicated. The nuclear translocation of TFEB was inhibited by LPS, which was rescued by GSK or RIP3 siRNA. Scale bar = 20 μm. D, E Lysates from cultured PTECs treated with LPS or DMSO (con) for 12 h were subjected to immunoprecipitation using an anti-RIP3 antibody (D) or anti-TFEB antibody (E), and IgG antibody followed by immunoblot for TFEB and RIP3. Input proteins were detected with anti-RIP3 and anti-TFEB antibodies. RIP3 interacted with TFEB in LPS-treated PTECs compared to the control group. F Lysates from cultured PTECs treated with LPS or DMSO (con) for 12 h were subjected to immunoprecipitation using anti-TFEB antibody and IgG antibody followed by immunoblot for p-RIP3. Input proteins were detected with anti-p-RIP3 and anti-TFEB antibodies. p-RIP3 interacted with TFEB in LPS-treated PTECs compared to the control group. *P < 0.05.

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