Journal: Foods

Article Title: Sea Buckthorn Pericarp Flavonoids Improve Diet-Induced Hyperlipidemia via Coordinated Modulation of Hepatic Lipid Metabolism and Gut Microbiota

doi: 10.3390/foods15061049

Figure Lengend Snippet: TFSP modulates the expression of ACC, FAS, CPT-1α, PPARα and ATGL proteins in the livers of HFD mice. n = 6 per group. Data are presented as mean ± SD. Different letters above bars indicate statistically significant differences ( p < 0.05) by one-way ANOVA followed by LSD post hoc test.

Article Snippet: Peroxisome proliferator-activated receptor alpha (PPARα) primary antibody (Cat. No. A00600-2), carnitine palmitoyltransferase-1 alpha (CPT-1α) primary antibody (Cat. No. A00917-3), acetyl-CoA carboxylase (ACC) primary antibody (Cat. No. M01802-2), fatty acid synthase (FAS) primary antibody (Cat. No. BA0484), adipose triglyceride lipase (ATGL) primary antibody (Cat. No. A01800-1), and GAPDH primary antibody (Cat. No. BM1623) were obtained from BOSTER Biological Technology Co., Ltd. (Wuhan, China).

Techniques: Expressing

Journal: Human & experimental toxicology

Article Title: Evaluation of the toxic effects of thimerosal and/or aluminum hydroxide in SH-SY5Y cell line.

doi: 10.1177/09603271221136206

Figure Lengend Snippet: Figure 6. Norepinephrine, dopamine, dopamine transporter protein and dopamine β-hydroxylase levels of study groups. a,b,c,d Bars that do not share same letters (superscripts) are significantly different from each other (p < 0.05). A: Norepinephrine levels; B: Dopamine levels; C: DAT levels; D: DBH levels DAT: Dopamine transporter; DBH: Dopamine β-hydroxlase.

Article Snippet: Human dopamine assay kit was obtained from Cusabio (Wuhan, China) and human dopamine transporter (DAT) assay kit was purchased from Elabscience (Houston, TX).

Techniques:

Journal: International Journal of Molecular Sciences

Article Title: SARS-CoV-2 Spike Protein Induces Time-Dependent and Brain-Region-Specific Alterations in Ferroptosis Markers: A Preliminary Study in K18-hACE2 Mice

doi: 10.3390/ijms27031526

Figure Lengend Snippet: Ferroptosis machinery is composed of three hallmarks: iron dysregulation, antioxidant failure, and lipid peroxidation. Iron dysregulation, a driver of ferroptosis, occurs through increased labile iron pool (LIP). This can happen by release of iron from its storage sites in ferritin by ferritinophagy, increased iron import through transferrin receptor 1 (TFR1) and divalent metal transporter 1 (DMT1), and decreased iron export from the cell through ferroportin 1 (FPN1). Antioxidant failure occurs through increased ROS production that is fostered by increased LIP (ferrous iron: Fe +2 ) through a Fenton-like reaction. On the other hand, depletion of antioxidant defenses occurs by decreased glutathione (GSH), glutathione peroxidase 4 (GPx4), the main brakes of ferroptosis, and a decrease in the antioxidant transcription factor Nuclear Factor Erythroid 2-Related Factor 2 (NrF2). Decreased NrF2 leads to a reduction in GSH production and inhibits the cystine/glutamate antiporter SLC7A11/xCT. Slc7a11 is needed for exporting glutamate and importing cystine that is needed to form GSH along with glycine and glutamate after conversion to cysteine. Acyl-CoA synthetase long-chain family member 4 (ACSL4) incorporates long polyunsaturated fatty acids (PUFAs) into the cell membrane and converts them to PUFA-COA, which is crucial for the process of lipid peroxidation. Both iron dysregulation (through a Fenton-like reaction) and the production of hydrogen peroxide (H 2 O 2 ) propagate the process of lipid peroxidation and the formation of more lipid peroxides (PUFAOOH . ), which execute ferroptosis that leads to membrane disruption. “Created in BioRender. Hatem, A. (2026) https://BioRender.com/qzdemai , accessed on 28 December 2025”.

Article Snippet: We used primary antibodies for transferrin receptor 1 (TFR1) (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 46222) (1:1000), ferroportin 1 (FPN1) (Proteintech, Chicago, IL, USA, Cat. no. 26601-1-AP) (1:2000), divalent metal transporter-1 (DMT-1) (Abcam, Washington, DC, USA, Cat. no. ab55735) (1:1000), MDA-conjugated proteins (Abcam, Washington, DC, USA, Cat. no. ab243066) (1:1000), Nuclear Factor Erythroid 2-Related Factor 2 (NrF2) (Abcam, Washington, DC, USA, Cat. no. ab62352) (1:2000), GPx4 (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 52455) (1:1000), and beta-actin (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 3700T) (1:1000).

Techniques: Membrane, Disruption

Journal: International Journal of Molecular Sciences

Article Title: SARS-CoV-2 Spike Protein Induces Time-Dependent and Brain-Region-Specific Alterations in Ferroptosis Markers: A Preliminary Study in K18-hACE2 Mice

doi: 10.3390/ijms27031526

Figure Lengend Snippet: Changes in expression of ferroptotic markers in the hippocampus. Representative Western blot bands of measured ferroptosis markers and beta-actin are shown in ( A ). Two-way ANOVA identified a significant time effect # on TFR1 (F 1.584,15.05 = 4.972, p = 0.028), but no statistically significant differences were observed in post hoc pairwise comparisons ( B ) or in FPN1 (time effect #: F 2,12 = 6.879, p = 0.0102). Šídák post hoc comparisons showed a significant increase in FPN1 in the spike group at 2 weeks (adjusted p = 0.0126) ( D ); NRF2 ( C ), DMT1 ( E ), MDA-conjugated proteins ( F ), and GPx4 ( G ) showed no significant main effects or interactions. Data are represented as mean ± SEM; * p < 0.05. ns: non-significant.

Article Snippet: We used primary antibodies for transferrin receptor 1 (TFR1) (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 46222) (1:1000), ferroportin 1 (FPN1) (Proteintech, Chicago, IL, USA, Cat. no. 26601-1-AP) (1:2000), divalent metal transporter-1 (DMT-1) (Abcam, Washington, DC, USA, Cat. no. ab55735) (1:1000), MDA-conjugated proteins (Abcam, Washington, DC, USA, Cat. no. ab243066) (1:1000), Nuclear Factor Erythroid 2-Related Factor 2 (NrF2) (Abcam, Washington, DC, USA, Cat. no. ab62352) (1:2000), GPx4 (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 52455) (1:1000), and beta-actin (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 3700T) (1:1000).

Techniques: Expressing, Western Blot

Journal: International Journal of Molecular Sciences

Article Title: SARS-CoV-2 Spike Protein Induces Time-Dependent and Brain-Region-Specific Alterations in Ferroptosis Markers: A Preliminary Study in K18-hACE2 Mice

doi: 10.3390/ijms27031526

Figure Lengend Snippet: Changes in expression of ferroptotic markers in the prefrontal cortex. All Western blot representative bands of measured ferroptosis markers and beta-actin are shown in ( A ). Two-way ANOVA showed no significant main effects or interactions for TFR1 ( B ), NRF2 ( C ), or FPN1 ( D ). For DMT1, two-way ANOVA identified significant main effects of time # (F 1.541,15.41 = 20.12, p = 0.0001) and treatment ## (F 1,20 = 12.61, p = 0.002). Šídák post hoc testing demonstrated a significant increase in the spike group at 2 weeks (adjusted p = 0.002), with no differences at 6 or 12 weeks ( E ). For MDA-conjugated proteins, two-way ANOVA revealed a significant time effect # (F 1.858,11.15 = 6.411, p = 0.015) ( F ). For GPx4, two-way ANOVA identified a significant main effect of treatment ## (F 1,20 = 13.60, p = 0.001), with no statistically significant difference observed at any time point ( G ). Šídák post hoc comparisons were not significant (at 6 weeks, adjusted p = 0.052). Data are represented as mean ± SEM; ** p < 0.01, ns = non-significant.

Article Snippet: We used primary antibodies for transferrin receptor 1 (TFR1) (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 46222) (1:1000), ferroportin 1 (FPN1) (Proteintech, Chicago, IL, USA, Cat. no. 26601-1-AP) (1:2000), divalent metal transporter-1 (DMT-1) (Abcam, Washington, DC, USA, Cat. no. ab55735) (1:1000), MDA-conjugated proteins (Abcam, Washington, DC, USA, Cat. no. ab243066) (1:1000), Nuclear Factor Erythroid 2-Related Factor 2 (NrF2) (Abcam, Washington, DC, USA, Cat. no. ab62352) (1:2000), GPx4 (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 52455) (1:1000), and beta-actin (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 3700T) (1:1000).

Techniques: Expressing, Western Blot

Journal: International Journal of Molecular Sciences

Article Title: SARS-CoV-2 Spike Protein Induces Time-Dependent and Brain-Region-Specific Alterations in Ferroptosis Markers: A Preliminary Study in K18-hACE2 Mice

doi: 10.3390/ijms27031526

Figure Lengend Snippet: Changes in expression of ferroptotic markers in cerebellum. All Western blot representative bands of measured ferroptosis markers and beta-actin are shown in ( A ). Two-way ANOVA identified significant main effects of time # (F 1.654,16.54 = 8.343, p = 0.0045) and treatment ## (F 1,20 = 11.44, p = 0.003) for TFR1. Šídák post hoc comparisons were not significant at individual time points (at 2 weeks, adjusted p = 0.054) ( B ). NRF2 showed no significant main effects or interaction ( C ). For FPN1, two-way ANOVA showed significant main effects of time # (F 1.829,18.29 = 4.339, p = 0.0315) and treatment ## (F 1,20 = 6.266, p = 0.0211). Šídák post hoc testing demonstrated a significant increase in the spike group at 2 weeks (adjusted p = 0.0219), with no differences at 6 or 12 weeks ( D ). For DMT1, a significant main effect of treatment ## was detected (F 1,8 = 6.296, p = 0.0364), with no significant time or interaction effects. Šídák comparisons were not significant (at 12 weeks, adjusted p = 0.0684) ( E ). For MDA-conjugated proteins, two-way ANOVA revealed a significant time effect # (F 1.830,10.98 = 9.883, p = 0.004. Šídák post hoc testing identified a significant increase in the spike group at 12 weeks (adjusted p = 0.043) ( F ). For GPx4, two-way ANOVA showed significant main effects of time # (F 1.842,11.05 = 15.17, p = 0.0008) and treatment ## (F 1,8 = 12.47, p = 0.0077). Šídák post hoc comparisons demonstrated a significant increase in the spike group at 2 weeks (adjusted p = 0.0033), with no differences at later time points. ( G ). Data are represented as mean ± SEM; * p < 0.05, ** p < 0.01, ns = non-significant.

Article Snippet: We used primary antibodies for transferrin receptor 1 (TFR1) (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 46222) (1:1000), ferroportin 1 (FPN1) (Proteintech, Chicago, IL, USA, Cat. no. 26601-1-AP) (1:2000), divalent metal transporter-1 (DMT-1) (Abcam, Washington, DC, USA, Cat. no. ab55735) (1:1000), MDA-conjugated proteins (Abcam, Washington, DC, USA, Cat. no. ab243066) (1:1000), Nuclear Factor Erythroid 2-Related Factor 2 (NrF2) (Abcam, Washington, DC, USA, Cat. no. ab62352) (1:2000), GPx4 (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 52455) (1:1000), and beta-actin (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 3700T) (1:1000).

Techniques: Expressing, Western Blot

Journal: International Journal of Molecular Sciences

Article Title: SARS-CoV-2 Spike Protein Induces Time-Dependent and Brain-Region-Specific Alterations in Ferroptosis Markers: A Preliminary Study in K18-hACE2 Mice

doi: 10.3390/ijms27031526

Figure Lengend Snippet: Changes in expression of ferroptotic markers in the olfactory bulb. All Western blot representative bands of measured ferroptosis markers and beta-actin are shown in ( A ). Two-way ANOVA identified a significant main effect of time # for TFR1 (F 1.998,11.99 = 11.93, p = 0.001), with no significant main effect of treatment. Šídák post hoc comparisons between saline and spike groups were not significant at 2, 6, or 12 weeks ( B ). For FPN1, two-way ANOVA showed a significant main effect of treatment ## (F 1,8 = 8.329, p = 0.02) with no significant time or interaction effects. Šídák post hoc testing identified a significant increase in the spike group at 12 weeks (adjusted p = 0.0006) ( D ). For DMT1, a significant main effect of treatment ## was detected (F 1,20 = 5.962, p = 0.024). Šídák comparisons were not significant at individual time points ( E ). NRF2 ( C ) and MDA-conjugated proteins ( F ) showed no significant main effects or interactions. For GPx4, two-way ANOVA revealed a significant main effect of treatment ## (F 1,8 = 8.051, p = 0.021) with no significant time or interaction effects. Šídák post hoc comparisons were not significant (at 2 weeks, adjusted p = 0.0799) ( G ). Data are represented as mean ± SEM; *** p < 0.001, ns = non-significant.

Article Snippet: We used primary antibodies for transferrin receptor 1 (TFR1) (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 46222) (1:1000), ferroportin 1 (FPN1) (Proteintech, Chicago, IL, USA, Cat. no. 26601-1-AP) (1:2000), divalent metal transporter-1 (DMT-1) (Abcam, Washington, DC, USA, Cat. no. ab55735) (1:1000), MDA-conjugated proteins (Abcam, Washington, DC, USA, Cat. no. ab243066) (1:1000), Nuclear Factor Erythroid 2-Related Factor 2 (NrF2) (Abcam, Washington, DC, USA, Cat. no. ab62352) (1:2000), GPx4 (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 52455) (1:1000), and beta-actin (Cell Signaling Technology, Danvers, MA, USA, Cat. no. 3700T) (1:1000).

Techniques: Expressing, Olfactory, Western Blot, Saline

Journal: Stem Cell Research & Therapy

Article Title: Curcumin pretreatment enhances the capacity of BMSC exosomes to attenuate renal ischemia-reperfusion injury by ferroptosis suppression via miR-16-5p/Smad3/Mb axis

doi: 10.1186/s13287-026-04931-8

Figure Lengend Snippet: Cur-exo exhibited enhanced anti-ferroptotic effect in TCMK-1 cells. A Flow cytometry analysis of TCMK-1 cellular uptake of exo and cur-exo. B Confocal microscopy visualization of exo/cur-exo internalization in TCMK-1 cells. Scale bars, 20 μm. C CCK8 assay determining the IC 50 of erastin-induced ferroptosis in TCMK-1 cells ( n = 5). D CCK-8 assay identifying the optimal concentration of exo/cur-exo for alleviating TCMK-1 cell death ( n = 5, ** P < 0.01 vs. exo). E Measurement of Fe 2+ content in TCMK-1 cells. F Assessment of MDA levels in TCMK-1 cells. G Quantification of GSH concentration in TCMK-1 cells. H qRT-PCR analysis of ACSL4, GPX4, and SLC7A11 mRNA expression levels. I Western blotting detection of ACSL4, GPX4, and SLC7A11 protein expression. J TEM visualization of mitochondrial morphology in erastin-treated TCMK-1 cells with exo/cur-exo intervention. Scale bars, 500 nm. K Flow cytometric quantification of ROS-positive cell percentage. L Inverted fluorescence microscopy imaging of intracellular ROS levels in TCMK-1 cells. Scale bars, 100 μm ( n = 3, # P < 0.05, ## P < 0.01 vs. Era + exo; * P < 0.05, ** P < 0.01 vs. Erastin)

Article Snippet: Proteins were separated on SDS-PAGE gels by electrophoresis at 150 V for 60 min, followed by wet transfer to PVDF membranes (#ISEQ00010, Millipore) at 400 mA for 30 min. Membranes were blocked with 5% skimmed milk in TBST for 1 h at room temperature, then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:1,000, #GB11001-100, Servicebio), ACSL4 (1:2,000, #22401-1-AP, Proteintech), GPX4 (1:1,000, #AF7020, Beyotime), SLC7A11 (1:2,000, #26864-1-AP, Proteintech), Mb (1:5,000, #16048-1-AP, Proteintech), Smad3 (1:1,000, #AF1501, Beyotime), CD63 (1:1,000, #ab134045, Abcam), CD9 (1:1,000, #ab236630, Abcam), TSG101 (1:1,000, #ab125011, Abcam), APOB (1:10,000, #ab157205, Abcam) and CYP1B1(1: 1000, # MA563709 , Thermo Fisher).

Techniques: Flow Cytometry, Confocal Microscopy, CCK-8 Assay, Concentration Assay, Quantitative RT-PCR, Expressing, Western Blot, Fluorescence, Microscopy, Imaging

Journal: Stem Cell Research & Therapy

Article Title: Curcumin pretreatment enhances the capacity of BMSC exosomes to attenuate renal ischemia-reperfusion injury by ferroptosis suppression via miR-16-5p/Smad3/Mb axis

doi: 10.1186/s13287-026-04931-8

Figure Lengend Snippet: Mb is the pivotal mediator through which cur-exo regulates ferroptosis. A , B RNA-Seq analysis of DEGs in TCMK-1 cells treated with Era + cur-exo versus Era + exo ( n = 3). C GO enrichment analysis (Top 10 terms). D qRT-PCR validation of Mb mRNA expression. E Western blotting validation of Mb protein expression in TCMK-1cells ( n = 3, * P < 0.05, ** P < 0.01 vs. Erastin; # P < 0.05 vs. Era + exo). F Western blotting validation of Mb protein expression in murine kidney tissue ( n = 3, ** P < 0.01 vs. IRI+Saline; ## P < 0.01 vs. IRI + exo). G Immunofluorescence analysis of Mb expression in murine kidney tissue. Scale bars, 100 μm. H qRT-PCR confirmation of transfection efficiency for Mb overexpression plasmid ( n = 3, ** P < 0.01 vs. NC). I , J Western blotting detection of Mb, ACSL4, GPX4, and SLC7A11 expression levels in TCMK-1 cells. K Measurement of Fe 2+ content in TCMK-1 cells. L Assessment of MDA levels in TCMK-1 cells. M Quantification of GSH concentration in TCMK-1 cells ( n = 3, ## P < 0.01 vs. Era + OE Mb; & P < 0.05, && P < 0.01 vs. Era + OE NC + cur-exo; * P < 0.05, ** P < 0.01 vs. Era + OE NC). N Mitochondrial morphology alterations in TCMK-1 cells post-Mb overexpression. Scale bars, 500 nm. O qRT-PCR verification of Mb siRNA transfection efficiency ( n = 3, ** P < 0.01 vs. NC). P , Q Western blotting analysis of Mb, ACSL4, GPX4, and SLC7A11 expression in TCMK-1 cells R Fe 2+ content analysis in TCMK-1 cells. S MDA level evaluation in TCMK-1 cells. T GSH concentration measurement in TCMK-1 cells ( n = 3, ## P < 0.01 vs. Era+siMb; && P < 0.01 vs. Era+siNC + cur-exo; * P < 0.05, ** P < 0.01 vs. Era+siNC). U Mitochondrial morphology alterations in TCMK-1 cells post-Mb knockdown. Scale bars, 500 nm

Article Snippet: Proteins were separated on SDS-PAGE gels by electrophoresis at 150 V for 60 min, followed by wet transfer to PVDF membranes (#ISEQ00010, Millipore) at 400 mA for 30 min. Membranes were blocked with 5% skimmed milk in TBST for 1 h at room temperature, then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:1,000, #GB11001-100, Servicebio), ACSL4 (1:2,000, #22401-1-AP, Proteintech), GPX4 (1:1,000, #AF7020, Beyotime), SLC7A11 (1:2,000, #26864-1-AP, Proteintech), Mb (1:5,000, #16048-1-AP, Proteintech), Smad3 (1:1,000, #AF1501, Beyotime), CD63 (1:1,000, #ab134045, Abcam), CD9 (1:1,000, #ab236630, Abcam), TSG101 (1:1,000, #ab125011, Abcam), APOB (1:10,000, #ab157205, Abcam) and CYP1B1(1: 1000, # MA563709 , Thermo Fisher).

Techniques: RNA Sequencing, Quantitative RT-PCR, Biomarker Discovery, Expressing, Western Blot, Saline, Immunofluorescence, Transfection, Over Expression, Plasmid Preparation, Concentration Assay, Knockdown

Journal: Stem Cell Research & Therapy

Article Title: Curcumin pretreatment enhances the capacity of BMSC exosomes to attenuate renal ischemia-reperfusion injury by ferroptosis suppression via miR-16-5p/Smad3/Mb axis

doi: 10.1186/s13287-026-04931-8

Figure Lengend Snippet: miR-16-5p downregulates Mb expression through post-transcriptional regulation of Smad3. A Bioinformatic prediction of miRs interacting with Smad3. B qRT-PCR analysis of differential miR expression between exo and cur-exo. C qRT-PCR assessment of miR expression in TCMK-1 cells following exo/cur-exo treatment ( n = 3, * P < 0.05, ** P < 0.01 vs. exo). D Measurement of Fe²⁺ content in TCMK-1 cells. E Assessment of MDA levels in TCMK-1 cells. F Quantification of GSH concentration in TCMK-1 cells. G Western blotting detection of ACSL4, GPX4, and SLC7A11 expression ( n = 3, ## P < 0.01 vs. Era + cur-exo; ** P < 0.01 vs. Erastin). H Measurement of Fe²⁺ content in TCMK-1 cells. I Assessment of MDA levels in TCMK-1 cells. J Quantification of GSH concentration in TCMK-1 cells. K Western blotting analysis of ACSL4, GPX4, and SLC7A11 expression ( n = 3, ** P < 0.01 vs. Erastin). L Flow cytometric quantification of ROS-positive cell percentage. M Immunofluorescence analysis of SLC7A11 expression. Scale bars, 100 µm. N qRT-PCR quantification of Smad3 mRNA levels. O Western blotting validation of Smad3 protein expression ( n = 3, ** P < 0.01 vs. NC). P Schematic representation of miR-16-5p binding to the 3’-UTR of Smad3. Q Dual-luciferase reporter assay confirmed that miR-16-5p binds to Smad3 ( n = 3, ** P < 0.01 vs. NC)

Article Snippet: Proteins were separated on SDS-PAGE gels by electrophoresis at 150 V for 60 min, followed by wet transfer to PVDF membranes (#ISEQ00010, Millipore) at 400 mA for 30 min. Membranes were blocked with 5% skimmed milk in TBST for 1 h at room temperature, then incubated overnight at 4 °C with the following primary antibodies: β-actin (1:1,000, #GB11001-100, Servicebio), ACSL4 (1:2,000, #22401-1-AP, Proteintech), GPX4 (1:1,000, #AF7020, Beyotime), SLC7A11 (1:2,000, #26864-1-AP, Proteintech), Mb (1:5,000, #16048-1-AP, Proteintech), Smad3 (1:1,000, #AF1501, Beyotime), CD63 (1:1,000, #ab134045, Abcam), CD9 (1:1,000, #ab236630, Abcam), TSG101 (1:1,000, #ab125011, Abcam), APOB (1:10,000, #ab157205, Abcam) and CYP1B1(1: 1000, # MA563709 , Thermo Fisher).

Techniques: Expressing, Quantitative RT-PCR, Concentration Assay, Western Blot, Immunofluorescence, Biomarker Discovery, Binding Assay, Luciferase, Reporter Assay

Journal: Inflammation

Article Title: Integrated Transcriptomic Analysis Identifies TAP1 as a Key Regulator of PANoptosis in Diabetic Kidney Disease Tubular Injury

doi: 10.1007/s10753-025-02400-7

Figure Lengend Snippet: Machine learning-based screening of candidate genes for DKD. ( A-B ) LASSO regression analysis identified 5 candidate genes. ( C-D ) Random forest analysis selected 10 top-ranked genes based on relative importance. ( E ) Venn diagram of the overlapping hub genes (CASP1, PRKX, TAP1) derived from LASSO regression and random forest analysis. (F) Protein-protein interaction network of hub genes generated by GeneMANIA

Article Snippet: Paraffin-embedded kidney sections were subjected to antigen retrieval, followed by overnight incubation at 4 °C with anti-TAP1 primary antibody (1:200, Proteintech).

Techniques: Derivative Assay, Generated

Journal: Inflammation

Article Title: Integrated Transcriptomic Analysis Identifies TAP1 as a Key Regulator of PANoptosis in Diabetic Kidney Disease Tubular Injury

doi: 10.1007/s10753-025-02400-7

Figure Lengend Snippet: Validation of hub gene (CASP1, PRKX, TAP1) expression patterns in DKD. ( A ) Scatter plots comparing expression levels between DKD patients and controls in the GSE30122 dataset. ( B ) Heatmap of normalized expression for the three hub genes across samples. ( C-E ) Independent validation in renal tubule tissues using Nephroseq v5 database: ( C ) CASP1, ( D ) PRKX, and ( E ) TAP1. ( F-H ) Correlation of hub gene expression with glomerular filtration rate: ( F ) CASP1, ( G ) PRKX, and ( H ) TAP1. Statistical analysis: t-tests for normally distributed data (Fig. 6A, C) and Wilcoxon rank-sum tests for non-normal data (Fig. 6D, E). * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns, no significance

Article Snippet: Paraffin-embedded kidney sections were subjected to antigen retrieval, followed by overnight incubation at 4 °C with anti-TAP1 primary antibody (1:200, Proteintech).

Techniques: Biomarker Discovery, Expressing, Gene Expression, Filtration

Journal: Inflammation

Article Title: Integrated Transcriptomic Analysis Identifies TAP1 as a Key Regulator of PANoptosis in Diabetic Kidney Disease Tubular Injury

doi: 10.1007/s10753-025-02400-7

Figure Lengend Snippet: GSEA of hub genes using GO and KEGG gene sets from MSigDB datasets. ( A-B ) GSEA results for CASP1: ( A ) GO and ( B ) KEGG analyses. ( C-D ) GSEA results for PRKX: ( C ) GO and ( D ) KEGG analyses. ( E-F ) GSEA results for TAP1: ( E ) GO and ( F ) KEGG analyses

Article Snippet: Paraffin-embedded kidney sections were subjected to antigen retrieval, followed by overnight incubation at 4 °C with anti-TAP1 primary antibody (1:200, Proteintech).

Techniques:

Journal: Inflammation

Article Title: Integrated Transcriptomic Analysis Identifies TAP1 as a Key Regulator of PANoptosis in Diabetic Kidney Disease Tubular Injury

doi: 10.1007/s10753-025-02400-7

Figure Lengend Snippet: Immune infiltration analysis in DKD. ( A ) Box plot showing the relative abundance of 22 immune cell types across different groups. ( B-D ) correlation analysis between the expression of hub genes and infiltrating immune cell proportions: ( B ) PRKX, ( C ) TAP1, and ( D ) CASP1. * P < 0.05, ** P < 0.01, *** P < 0.001; ns, no significance

Article Snippet: Paraffin-embedded kidney sections were subjected to antigen retrieval, followed by overnight incubation at 4 °C with anti-TAP1 primary antibody (1:200, Proteintech).

Techniques: Expressing

Journal: Inflammation

Article Title: Integrated Transcriptomic Analysis Identifies TAP1 as a Key Regulator of PANoptosis in Diabetic Kidney Disease Tubular Injury

doi: 10.1007/s10753-025-02400-7

Figure Lengend Snippet: Single-cell RNA sequencing profile of kidney tissues. ( A ) UMAP projection after Harmony batch correction, integrating datasets across samples. ( B ) 22 distinct clusters visualized by UMAP plotting. ( C ) Annotation of 10 major cell types based on marker genes. ( D ) Dot plot illustrating the expression of marker genes in different cell types. ( E-G ) Bubble plots comparing expression patterns of three hub genes in PT cells (DKD vs. controls). ( E ) CASP1, ( F ) TAP1, and ( G ) PRKX. Statistical significance was determined by Wilcoxon rank-sum tests (**** P < 0.0001). LOH, loop of Henle cells; PT, proximal tubule cells; DCT, distal convoluted tubule cells; ENDO, endothelial cells; FIB, fibroblasts; LEUK, leukocytes; ICA, type A intercalated cells; PODO, podocytes; PEC, parietal epithelial cells; ICB, type B intercalated cells

Article Snippet: Paraffin-embedded kidney sections were subjected to antigen retrieval, followed by overnight incubation at 4 °C with anti-TAP1 primary antibody (1:200, Proteintech).

Techniques: Single Cell, RNA Sequencing, Marker, Expressing

Journal: Inflammation

Article Title: Integrated Transcriptomic Analysis Identifies TAP1 as a Key Regulator of PANoptosis in Diabetic Kidney Disease Tubular Injury

doi: 10.1007/s10753-025-02400-7

Figure Lengend Snippet: Validation of hub genes in experimental and clinical DKD. ( A ) qRT-PCR analysis of TAP1, CASP1, and PRKX expression in HK-2 cells under low glucose (LG, 5.5 mmol/L glucose) or high glucose (HG, 25 mmol/L glucose) conditions. ( B ) Western blot analysis of TAP1 protein levels in LG or HG. ( C ) Representative kidney histology (H&E, PAS, and Masson trichrome staining) in db/m and db/db mice. Scale bar, 20 μm. ( D ) Western blot of TAP1 protein levels in kidney tissues from db/m and db/db mice ( n = 3 for each group). ( E ) Representative IHC staining of TAP1 in db/m ( n = 3) and db/db ( n = 3) mouse kidney tissue. Scale bar, 50 μm. ( F ) Representative IHC staining of TAP1 in human kidney tissues from DKD ( n = 3) and control ( n = 3) patients. Scale bar, 50 μm. * P < 0.05, ** P < 0.01; ns, no significance

Article Snippet: Paraffin-embedded kidney sections were subjected to antigen retrieval, followed by overnight incubation at 4 °C with anti-TAP1 primary antibody (1:200, Proteintech).

Techniques: Biomarker Discovery, Quantitative RT-PCR, Expressing, Western Blot, Staining, Immunohistochemistry, Control