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anti nubp iron sulfur cluster assembly factor  (Boster Bio)


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    Boster Bio anti nubp iron sulfur cluster assembly factor
    Anti Nubp Iron Sulfur Cluster Assembly Factor, supplied by Boster Bio, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+nubpl+antibody/Anti-NUBPL+Antibody+Picoband/pm39805370-123-98-106
    Average 94 stars, based on 1 article reviews
    anti nubp iron sulfur cluster assembly factor - by Bioz Stars, 2026-09
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    Incubation:

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.
    Article Snippet: .. The paraffin sections were incubated with the first primary antibodies (overnight, 4 ◦C) which were as follows: anti-SLC7A11 antibody (Abcam, ab307601, dilution: 1:500), antiLRPPRC antibody (Abcam, ab259927, dilution: 1:200), anti-NDUFA11 antibody (Abclonal, A16239, dilution: 1:100), anti-NUBPL antibody (Boster, A10634–1, dilution: 1:100). .. After they were washed with PBS, the neurons were incubated with the red second antibodies (CST, #8889, dilution: 1:1000) (45 min, 37 ◦C).

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.
    Article Snippet: Subsequently, paraffin sections were blocked with 10 % goat serum (Sigma-Aldrich, G9023). .. The paraffin sections were incubated with the primary antibodies (overnight, 4 ◦C): anti-GYS1 antibody (Sangon Biotech, D122431, dilution: 1:100), anti-NDUFS1 antibody (Abcam, ab185733, dilution: 1:100), anti-OXSM antibody (Boster, A12866–1, dilution: 1:100), anti-LRPPRC antibody (Abcam, ab259927, dilution: 1:200), anti-NDUFA11 antibody (Abclonal, A16239, dilution: 1:100) (Yang et al., 2022), anti-NUBPL antibody (Boster, A10634–1, dilution: 1:100), anti-NCKAP1 antibody (Bioworld Technology, BS71703, dilution: 1:50), anti-SLC3A2 antibody (Santa, sc-390,154, dilution: 1:50), anti-SLC7A11 antibody (Abcam, ab307601. dilution: 1:500). .. The paraffin sections were washed with (PBS) and incubated with red fluorescent secondary antibody (CST, #8889, dilution: 1:1000; CST,#4408, dilution: 1:1000) (45 min, 37 ◦C).

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.
    Article Snippet: The protein samples (20 μg protein/lane) were separated by SDS-PAGE gel electrophoresis and transferred to a nitrocellulose (NC) membrane (Merck Millipore Ltd) by wet transfer for western blot analysis. .. The NC membranes were blocked with 5 % BSA and incubated at 4 ◦C overnight with primary antibodies: anti-GYS1 antibody (Sangon Biotech, D122431, dilution: 1:1000), anti-NDUFS1 antibody (abcam, ab185733, dilution: 1:1000), anti-OXSM antibody (Boster, A12866–1, dilution: 1:1000), anti-LRPPRC antibody (abcam, ab259927, dilution: 1:1000), anti-NDUFA11 antibody (Abclonal, A16239, dilution: 1:1000) (Yang et al., 2022), anti-NUBPL antibody (Boster, A10634–1, dilution: 1:1000), anti-NCKAP1 antibody (Bioworld Technology, BS71703, dilution: 1:1000), anti-SLC3A2 antibody (santa, sc-390,154, dilution: 1:500), and anti-SLC7A11 antibody (abcam, ab307601. dilution: 1:1000). .. The primary antibodies of loading control protein were anti-GAPDH antibody (abcam, ab8245, dilution: 1:10000) and anti-alpha Tubulin1 antibody (abcam, ab7291, dilution: 1:10000).



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    Identification of potential biomarkers in ATC/PDTC. A , volcano plot of DEPs in ATC/PDTC versus PTC with |log 2 FC| ≥ 1 and p < 0.05. B , correlation analysis of FCGR2A with NET formation markers PADI4 across groups. C , single-cell RNA-seq data ( GSE232237 ) showing FCGR2A expression predominantly in macrophages, with the highest expression in ATC. D , correlation analysis of FCGR2A expression with M0 macrophages, NK cells, and B cells examined by Spearman analysis. E , representative figures of IHC analysis validation of FCGR2A, UBE2C, and <t>NUBPL</t> expression in ATC (n = 11), PDTC (n = 7), and PTC (n = 10) tissues. The numbers at the upper left corner of each IHC image (0–3) indicate the immunoreactivity score for the representative case. The IHC scores were fully plotted in the bar plots assessed by pairwise student’s t tests. ns, not significant; ∗ p < 0.05; ∗∗∗ p < 0.001; and ∗∗∗∗ p < 0.0001. ATC, anaplastic thyroid carcinoma; FCGR2A, Fc fragment of IgG receptor IIa; IHC, immunohistochemistry; log 2 FC, log 2 fold change; NK, natural killer; PDTC, poorly differentiated thyroid carcinoma; PTC, papillary thyroid carcinoma; PADI4, peptidyl arginine deiminase 4; NUBPL, nucleotide-binding protein-like; UBE2C, ubiquitin-conjugating <t>enzyme</t> <t>E2</t> C.
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    Identification of potential biomarkers in ATC/PDTC. A , volcano plot of DEPs in ATC/PDTC versus PTC with |log 2 FC| ≥ 1 and p < 0.05. B , correlation analysis of FCGR2A with NET formation markers PADI4 across groups. C , single-cell RNA-seq data ( GSE232237 ) showing FCGR2A expression predominantly in macrophages, with the highest expression in ATC. D , correlation analysis of FCGR2A expression with M0 macrophages, NK cells, and B cells examined by Spearman analysis. E , representative figures of IHC analysis validation of FCGR2A, UBE2C, and <t>NUBPL</t> expression in ATC (n = 11), PDTC (n = 7), and PTC (n = 10) tissues. The numbers at the upper left corner of each IHC image (0–3) indicate the immunoreactivity score for the representative case. The IHC scores were fully plotted in the bar plots assessed by pairwise student’s t tests. ns, not significant; ∗ p < 0.05; ∗∗∗ p < 0.001; and ∗∗∗∗ p < 0.0001. ATC, anaplastic thyroid carcinoma; FCGR2A, Fc fragment of IgG receptor IIa; IHC, immunohistochemistry; log 2 FC, log 2 fold change; NK, natural killer; PDTC, poorly differentiated thyroid carcinoma; PTC, papillary thyroid carcinoma; PADI4, peptidyl arginine deiminase 4; NUBPL, nucleotide-binding protein-like; UBE2C, ubiquitin-conjugating <t>enzyme</t> <t>E2</t> C.
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    Identification of potential biomarkers in ATC/PDTC. A , volcano plot of DEPs in ATC/PDTC versus PTC with |log 2 FC| ≥ 1 and p < 0.05. B , correlation analysis of FCGR2A with NET formation markers PADI4 across groups. C , single-cell RNA-seq data ( GSE232237 ) showing FCGR2A expression predominantly in macrophages, with the highest expression in ATC. D , correlation analysis of FCGR2A expression with M0 macrophages, NK cells, and B cells examined by Spearman analysis. E , representative figures of IHC analysis validation of FCGR2A, UBE2C, and <t>NUBPL</t> expression in ATC (n = 11), PDTC (n = 7), and PTC (n = 10) tissues. The numbers at the upper left corner of each IHC image (0–3) indicate the immunoreactivity score for the representative case. The IHC scores were fully plotted in the bar plots assessed by pairwise student’s t tests. ns, not significant; ∗ p < 0.05; ∗∗∗ p < 0.001; and ∗∗∗∗ p < 0.0001. ATC, anaplastic thyroid carcinoma; FCGR2A, Fc fragment of IgG receptor IIa; IHC, immunohistochemistry; log 2 FC, log 2 fold change; NK, natural killer; PDTC, poorly differentiated thyroid carcinoma; PTC, papillary thyroid carcinoma; PADI4, peptidyl arginine deiminase 4; NUBPL, nucleotide-binding protein-like; UBE2C, ubiquitin-conjugating <t>enzyme</t> <t>E2</t> C.
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    Identification of potential biomarkers in ATC/PDTC. A , volcano plot of DEPs in ATC/PDTC versus PTC with |log 2 FC| ≥ 1 and p < 0.05. B , correlation analysis of FCGR2A with NET formation markers PADI4 across groups. C , single-cell RNA-seq data ( GSE232237 ) showing FCGR2A expression predominantly in macrophages, with the highest expression in ATC. D , correlation analysis of FCGR2A expression with M0 macrophages, NK cells, and B cells examined by Spearman analysis. E , representative figures of IHC analysis validation of FCGR2A, UBE2C, and <t>NUBPL</t> expression in ATC (n = 11), PDTC (n = 7), and PTC (n = 10) tissues. The numbers at the upper left corner of each IHC image (0–3) indicate the immunoreactivity score for the representative case. The IHC scores were fully plotted in the bar plots assessed by pairwise student’s t tests. ns, not significant; ∗ p < 0.05; ∗∗∗ p < 0.001; and ∗∗∗∗ p < 0.0001. ATC, anaplastic thyroid carcinoma; FCGR2A, Fc fragment of IgG receptor IIa; IHC, immunohistochemistry; log 2 FC, log 2 fold change; NK, natural killer; PDTC, poorly differentiated thyroid carcinoma; PTC, papillary thyroid carcinoma; PADI4, peptidyl arginine deiminase 4; NUBPL, nucleotide-binding protein-like; UBE2C, ubiquitin-conjugating <t>enzyme</t> <t>E2</t> C.
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    FIGURE 8 | Male mouse data for myocardial injury in the IC model. (A) Changes in body weight between the Control and IC groups of mice (n = 8). (B) Changes in serum LDH levels between the control and IC groups (n = 8). (C) Representative haematoxylin and eosin (HE) staining of myo- cardial tissue showing histological changes in the control and IC groups. Scale bar = 100 μm. (D) Masson's trichrome staining depicting the myocar- dial infarction area. Scale bar = 500 μm. (E) Echocardiography results showing heart rate, left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) (n = 8). (E) Relative mRNA expression levels of <t>NUBPL,</t> NCKAP1, <t>MYL6,</t> <t>MYH9</t> and MYH10 in male mice myocardial tissue (n = 6). Data are presented as mean ± SEM. (*p < 0.05, **p < 0.01.)
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    FIGURE 8 | Male mouse data for myocardial injury in the IC model. (A) Changes in body weight between the Control and IC groups of mice (n = 8). (B) Changes in serum LDH levels between the control and IC groups (n = 8). (C) Representative haematoxylin and eosin (HE) staining of myo- cardial tissue showing histological changes in the control and IC groups. Scale bar = 100 μm. (D) Masson's trichrome staining depicting the myocar- dial infarction area. Scale bar = 500 μm. (E) Echocardiography results showing heart rate, left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) (n = 8). (E) Relative mRNA expression levels of <t>NUBPL,</t> NCKAP1, <t>MYL6,</t> <t>MYH9</t> and MYH10 in male mice myocardial tissue (n = 6). Data are presented as mean ± SEM. (*p < 0.05, **p < 0.01.)
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    Fig. 2. Identification of DE-DRMs in individuals with EP. (A) The heatmap of expression levels for nine DE-DRMs. (B) The expression levels of 11 DRMs were exhibited between Ctrl and EP groups in boxplots. (C) Correlation analysis of nine DE-DRMs. Red and green colors represent positive and negative correlations, respectively. (D) The PPI analysis of DE-DMRs showed that SLC3A2 interacted with SLC7A11, while NDUFS1 interacted with NDUFA11, <t>NUBPL,</t> and LRPPRC. Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; EP, epilepsy; Ctrl, control; PPI, protein-protein interaction; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, <t>mitochondrial;</t> LRPPRC, leucine rich pentatricopeptide repeat containing. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Fig. 2. Identification of DE-DRMs in individuals with EP. (A) The heatmap of expression levels for nine DE-DRMs. (B) The expression levels of 11 DRMs were exhibited between Ctrl and EP groups in boxplots. (C) Correlation analysis of nine DE-DRMs. Red and green colors represent positive and negative correlations, respectively. (D) The PPI analysis of DE-DMRs showed that SLC3A2 interacted with SLC7A11, while NDUFS1 interacted <t>with</t> <t>NDUFA11,</t> <t>NUBPL,</t> and LRPPRC. Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; EP, epilepsy; Ctrl, control; PPI, protein-protein interaction; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Image Search Results


    Identification of potential biomarkers in ATC/PDTC. A , volcano plot of DEPs in ATC/PDTC versus PTC with |log 2 FC| ≥ 1 and p < 0.05. B , correlation analysis of FCGR2A with NET formation markers PADI4 across groups. C , single-cell RNA-seq data ( GSE232237 ) showing FCGR2A expression predominantly in macrophages, with the highest expression in ATC. D , correlation analysis of FCGR2A expression with M0 macrophages, NK cells, and B cells examined by Spearman analysis. E , representative figures of IHC analysis validation of FCGR2A, UBE2C, and NUBPL expression in ATC (n = 11), PDTC (n = 7), and PTC (n = 10) tissues. The numbers at the upper left corner of each IHC image (0–3) indicate the immunoreactivity score for the representative case. The IHC scores were fully plotted in the bar plots assessed by pairwise student’s t tests. ns, not significant; ∗ p < 0.05; ∗∗∗ p < 0.001; and ∗∗∗∗ p < 0.0001. ATC, anaplastic thyroid carcinoma; FCGR2A, Fc fragment of IgG receptor IIa; IHC, immunohistochemistry; log 2 FC, log 2 fold change; NK, natural killer; PDTC, poorly differentiated thyroid carcinoma; PTC, papillary thyroid carcinoma; PADI4, peptidyl arginine deiminase 4; NUBPL, nucleotide-binding protein-like; UBE2C, ubiquitin-conjugating enzyme E2 C.

    Journal: Molecular & Cellular Proteomics : MCP

    Article Title: Multiomics Profiling Reveals Distinct Immunosuppression and Metabolic Dysregulation in Aggressive Subtypes of Thyroid Cancer

    doi: 10.1016/j.mcpro.2026.101513

    Figure Lengend Snippet: Identification of potential biomarkers in ATC/PDTC. A , volcano plot of DEPs in ATC/PDTC versus PTC with |log 2 FC| ≥ 1 and p < 0.05. B , correlation analysis of FCGR2A with NET formation markers PADI4 across groups. C , single-cell RNA-seq data ( GSE232237 ) showing FCGR2A expression predominantly in macrophages, with the highest expression in ATC. D , correlation analysis of FCGR2A expression with M0 macrophages, NK cells, and B cells examined by Spearman analysis. E , representative figures of IHC analysis validation of FCGR2A, UBE2C, and NUBPL expression in ATC (n = 11), PDTC (n = 7), and PTC (n = 10) tissues. The numbers at the upper left corner of each IHC image (0–3) indicate the immunoreactivity score for the representative case. The IHC scores were fully plotted in the bar plots assessed by pairwise student’s t tests. ns, not significant; ∗ p < 0.05; ∗∗∗ p < 0.001; and ∗∗∗∗ p < 0.0001. ATC, anaplastic thyroid carcinoma; FCGR2A, Fc fragment of IgG receptor IIa; IHC, immunohistochemistry; log 2 FC, log 2 fold change; NK, natural killer; PDTC, poorly differentiated thyroid carcinoma; PTC, papillary thyroid carcinoma; PADI4, peptidyl arginine deiminase 4; NUBPL, nucleotide-binding protein-like; UBE2C, ubiquitin-conjugating enzyme E2 C.

    Article Snippet: Primary antibodies—including FCGR2A (RRID: AB_2246912 , Cat.15625-1-AP, Proteintech, 1:600 dilution), ubiquitin-conjugating enzyme E2 C (UBE2C) (RRID: AB_11232220 , Cat.66087-1-Ig, Proteintech, 1:500), and nucleotide-binding protein-like (NUBPL) (RRID: AB_2878402 , Cat.17393-1-AP, Proteintech, 1:200)—were diluted in antibody dilution buffer and applied to tissue sections.

    Techniques: Single Cell, RNA Sequencing, Expressing, Biomarker Discovery, Immunohistochemistry, Binding Assay, Ubiquitin Proteomics

    FIGURE 8 | Male mouse data for myocardial injury in the IC model. (A) Changes in body weight between the Control and IC groups of mice (n = 8). (B) Changes in serum LDH levels between the control and IC groups (n = 8). (C) Representative haematoxylin and eosin (HE) staining of myo- cardial tissue showing histological changes in the control and IC groups. Scale bar = 100 μm. (D) Masson's trichrome staining depicting the myocar- dial infarction area. Scale bar = 500 μm. (E) Echocardiography results showing heart rate, left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) (n = 8). (E) Relative mRNA expression levels of NUBPL, NCKAP1, MYL6, MYH9 and MYH10 in male mice myocardial tissue (n = 6). Data are presented as mean ± SEM. (*p < 0.05, **p < 0.01.)

    Journal: Journal of cellular and molecular medicine

    Article Title: A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy.

    doi: 10.1111/jcmm.70475

    Figure Lengend Snippet: FIGURE 8 | Male mouse data for myocardial injury in the IC model. (A) Changes in body weight between the Control and IC groups of mice (n = 8). (B) Changes in serum LDH levels between the control and IC groups (n = 8). (C) Representative haematoxylin and eosin (HE) staining of myo- cardial tissue showing histological changes in the control and IC groups. Scale bar = 100 μm. (D) Masson's trichrome staining depicting the myocar- dial infarction area. Scale bar = 500 μm. (E) Echocardiography results showing heart rate, left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), left ventricular end-diastolic diameter (LVEDD) and left ventricular end-systolic diameter (LVESD) (n = 8). (E) Relative mRNA expression levels of NUBPL, NCKAP1, MYL6, MYH9 and MYH10 in male mice myocardial tissue (n = 6). Data are presented as mean ± SEM. (*p < 0.05, **p < 0.01.)

    Article Snippet: Sodium pentobarbital (Sigma, 57–33- 0, USA), and antibodies: MYH9 (Rabbit, 11,128- 1- AP, Proteintech, China), NUBPL (Rabbit, 17,393- 1- AP, Proteintech, China), MYL6 (Mouse, 68,142- 1- Ig, Proteintech, China), NCKAP1 (Rabbit, 12,140- 1- AP, Proteintech, China), MYH10 (Rabbit, 19,673- 1- AP, Proteintech, China), β- actin (Mouse, 60,008- 1- Ig, Proteintech, China), goat anti- rat IgG (HRP Conjugate) (98,164, CST, USA) and goat antimouse IgG (HRP Conjugate) (91,196, CST, USA).

    Techniques: Control, Staining, Expressing

    FIGURE 9 | (A) IHC expression of MYH9, NUBPL, MYL6, MYH10 and NCKAP1 in myocardial cells of male mice in the control and IC groups (20× and 40×). (B) Western blot bands showing protein expression of MYH9, NUBPL, MYL6, MYH10 and NCKAP1 in male mouse myocardial tis- sue. (mean ± SD, n = 4). (*p ≤ 0.05, **p ≤ 0.01.)

    Journal: Journal of cellular and molecular medicine

    Article Title: A Novel Disulfidptosis-Related Diagnostic Gene Signature and Differential Expression Validation in Ischaemic Cardiomyopathy.

    doi: 10.1111/jcmm.70475

    Figure Lengend Snippet: FIGURE 9 | (A) IHC expression of MYH9, NUBPL, MYL6, MYH10 and NCKAP1 in myocardial cells of male mice in the control and IC groups (20× and 40×). (B) Western blot bands showing protein expression of MYH9, NUBPL, MYL6, MYH10 and NCKAP1 in male mouse myocardial tis- sue. (mean ± SD, n = 4). (*p ≤ 0.05, **p ≤ 0.01.)

    Article Snippet: Sodium pentobarbital (Sigma, 57–33- 0, USA), and antibodies: MYH9 (Rabbit, 11,128- 1- AP, Proteintech, China), NUBPL (Rabbit, 17,393- 1- AP, Proteintech, China), MYL6 (Mouse, 68,142- 1- Ig, Proteintech, China), NCKAP1 (Rabbit, 12,140- 1- AP, Proteintech, China), MYH10 (Rabbit, 19,673- 1- AP, Proteintech, China), β- actin (Mouse, 60,008- 1- Ig, Proteintech, China), goat anti- rat IgG (HRP Conjugate) (98,164, CST, USA) and goat antimouse IgG (HRP Conjugate) (91,196, CST, USA).

    Techniques: Expressing, Control, Western Blot

    Fig. 2. Identification of DE-DRMs in individuals with EP. (A) The heatmap of expression levels for nine DE-DRMs. (B) The expression levels of 11 DRMs were exhibited between Ctrl and EP groups in boxplots. (C) Correlation analysis of nine DE-DRMs. Red and green colors represent positive and negative correlations, respectively. (D) The PPI analysis of DE-DMRs showed that SLC3A2 interacted with SLC7A11, while NDUFS1 interacted with NDUFA11, NUBPL, and LRPPRC. Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; EP, epilepsy; Ctrl, control; PPI, protein-protein interaction; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: Neurobiology of disease

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.

    doi: 10.1016/j.nbd.2025.106789

    Figure Lengend Snippet: Fig. 2. Identification of DE-DRMs in individuals with EP. (A) The heatmap of expression levels for nine DE-DRMs. (B) The expression levels of 11 DRMs were exhibited between Ctrl and EP groups in boxplots. (C) Correlation analysis of nine DE-DRMs. Red and green colors represent positive and negative correlations, respectively. (D) The PPI analysis of DE-DMRs showed that SLC3A2 interacted with SLC7A11, while NDUFS1 interacted with NDUFA11, NUBPL, and LRPPRC. Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; EP, epilepsy; Ctrl, control; PPI, protein-protein interaction; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: The cultured neurons were immobilized with 4 % paraformaldehyde for 30 min, permeated with 0.1 % Triton X-100 for 10 min, and blocked with 5 % bovine serum albumin (BSA) for 1 h. These neurons were incubated with primary antibodies (overnight, 4 ◦C): anti-glycogen synthase 1 (GYS1) antibody (Sangon Biotech, D122431, dilution: 1:100), anti-NADH:ubiquinone oxidoreductase core subunit S1 (NDUFS1) antibody (Abcam, ab185733, dilution: 1:100), anti-3oxoacyl-ACP synthase, mitochondrial (OXSM) antibody (Boster, A12866–1, dilution: 1:100), anti-leucine rich pentatricopeptide repeat containing (LRPPRC) antibody (Abcam, ab259927, dilution: 1:200), anti-NADH:ubiquinone oxidoreductase subunit A11 (NDUFA11) antibody (Abclonal, A16239, dilution: 1:100) (Yang et al., 2022), anti-NUBP iron‐sulfur cluster assembly factor, mitochondrial (NUBPL) antibody (Boster, A10634–1, dilution: 1:100), anti-NCK associated protein 1 (NCKAP1) antibody (Bioworld Technology, BS71703, dilution: 1:50), anti-SLC3A2 antibody (Santa, sc-390,154, dilution: 1:50), and antiSLC7A11 antibody (Abcam, ab307601, dilution: 1:500).

    Techniques: Expressing, Control

    Fig. 8. The expression of DE-DRMs in seizures models (in vitro and in vivo). (A) Constructing the in vitro seizures model. The amplitude and frequency of neuronal APs in the Mg2+-free group were significantly increased (n = 6 in each group; Independent sample t-test; #, P < 0.01). (B) Protein expression of nine DE-DRMs in the in vitro seizures model. The expression of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in the Mg2+-free group, while the expression of SLC7A11 was significantly increased in Mg2+-free group (n = 6 in each group; Independent sample t-test; #, P < 0.01). (C) Con structing the in vivo seizures model. No epileptoid discharges were observed in six rats of the Ctrl group, while significant epileptoid discharges were observed in six rats of the PTZ group (scale: Y-axis,50uV; X-axis, 0.5 s). (D) Protein expression of nine DE-DRMs in vivo models. The expressions of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in PTZ group, while the expression of SLC7A11 was significantly increased in PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; APs, action potentials; GYS1, glycogen synthase 1; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; OXSM, 3-oxoacyl-ACP synthase, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NCKAP1, NCK associated protein 1; PTZ, pentylenetetrazol.

    Journal: Neurobiology of disease

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.

    doi: 10.1016/j.nbd.2025.106789

    Figure Lengend Snippet: Fig. 8. The expression of DE-DRMs in seizures models (in vitro and in vivo). (A) Constructing the in vitro seizures model. The amplitude and frequency of neuronal APs in the Mg2+-free group were significantly increased (n = 6 in each group; Independent sample t-test; #, P < 0.01). (B) Protein expression of nine DE-DRMs in the in vitro seizures model. The expression of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in the Mg2+-free group, while the expression of SLC7A11 was significantly increased in Mg2+-free group (n = 6 in each group; Independent sample t-test; #, P < 0.01). (C) Con structing the in vivo seizures model. No epileptoid discharges were observed in six rats of the Ctrl group, while significant epileptoid discharges were observed in six rats of the PTZ group (scale: Y-axis,50uV; X-axis, 0.5 s). (D) Protein expression of nine DE-DRMs in vivo models. The expressions of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in PTZ group, while the expression of SLC7A11 was significantly increased in PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; APs, action potentials; GYS1, glycogen synthase 1; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; OXSM, 3-oxoacyl-ACP synthase, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NCKAP1, NCK associated protein 1; PTZ, pentylenetetrazol.

    Article Snippet: The cultured neurons were immobilized with 4 % paraformaldehyde for 30 min, permeated with 0.1 % Triton X-100 for 10 min, and blocked with 5 % bovine serum albumin (BSA) for 1 h. These neurons were incubated with primary antibodies (overnight, 4 ◦C): anti-glycogen synthase 1 (GYS1) antibody (Sangon Biotech, D122431, dilution: 1:100), anti-NADH:ubiquinone oxidoreductase core subunit S1 (NDUFS1) antibody (Abcam, ab185733, dilution: 1:100), anti-3oxoacyl-ACP synthase, mitochondrial (OXSM) antibody (Boster, A12866–1, dilution: 1:100), anti-leucine rich pentatricopeptide repeat containing (LRPPRC) antibody (Abcam, ab259927, dilution: 1:200), anti-NADH:ubiquinone oxidoreductase subunit A11 (NDUFA11) antibody (Abclonal, A16239, dilution: 1:100) (Yang et al., 2022), anti-NUBP iron‐sulfur cluster assembly factor, mitochondrial (NUBPL) antibody (Boster, A10634–1, dilution: 1:100), anti-NCK associated protein 1 (NCKAP1) antibody (Bioworld Technology, BS71703, dilution: 1:50), anti-SLC3A2 antibody (Santa, sc-390,154, dilution: 1:50), and antiSLC7A11 antibody (Abcam, ab307601, dilution: 1:500).

    Techniques: Expressing, In Vitro, In Vivo

    Fig. 9. Verifying the PPI in seizures models (in vivo and in vitro). (A-B) colocation analysis indicated that SLC7A11 colocalized with SLC3A2, NDUFS1 colocalized with LRPPRC, NDUFS1 colocalized with NUBPL, and NDUFS1 colocalized with NDUFA11 in both primary neurons and hippocampal tissue. (C–D) Pooled quan tification of protein immunoprecipitation showed a significant increment in the pull-down of SLC7A11 and a significant reduction in the pull-down of NDUFA11 in both the Mg2+-free group and PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: PPI, protein-protein interaction; SLC3A2,solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; LRPPRC, leucine rich pentatricopeptide repeat containing; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; PTZ, pentylenetetrazol.

    Journal: Neurobiology of disease

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.

    doi: 10.1016/j.nbd.2025.106789

    Figure Lengend Snippet: Fig. 9. Verifying the PPI in seizures models (in vivo and in vitro). (A-B) colocation analysis indicated that SLC7A11 colocalized with SLC3A2, NDUFS1 colocalized with LRPPRC, NDUFS1 colocalized with NUBPL, and NDUFS1 colocalized with NDUFA11 in both primary neurons and hippocampal tissue. (C–D) Pooled quan tification of protein immunoprecipitation showed a significant increment in the pull-down of SLC7A11 and a significant reduction in the pull-down of NDUFA11 in both the Mg2+-free group and PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: PPI, protein-protein interaction; SLC3A2,solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; LRPPRC, leucine rich pentatricopeptide repeat containing; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; PTZ, pentylenetetrazol.

    Article Snippet: The cultured neurons were immobilized with 4 % paraformaldehyde for 30 min, permeated with 0.1 % Triton X-100 for 10 min, and blocked with 5 % bovine serum albumin (BSA) for 1 h. These neurons were incubated with primary antibodies (overnight, 4 ◦C): anti-glycogen synthase 1 (GYS1) antibody (Sangon Biotech, D122431, dilution: 1:100), anti-NADH:ubiquinone oxidoreductase core subunit S1 (NDUFS1) antibody (Abcam, ab185733, dilution: 1:100), anti-3oxoacyl-ACP synthase, mitochondrial (OXSM) antibody (Boster, A12866–1, dilution: 1:100), anti-leucine rich pentatricopeptide repeat containing (LRPPRC) antibody (Abcam, ab259927, dilution: 1:200), anti-NADH:ubiquinone oxidoreductase subunit A11 (NDUFA11) antibody (Abclonal, A16239, dilution: 1:100) (Yang et al., 2022), anti-NUBP iron‐sulfur cluster assembly factor, mitochondrial (NUBPL) antibody (Boster, A10634–1, dilution: 1:100), anti-NCK associated protein 1 (NCKAP1) antibody (Bioworld Technology, BS71703, dilution: 1:50), anti-SLC3A2 antibody (Santa, sc-390,154, dilution: 1:50), and antiSLC7A11 antibody (Abcam, ab307601, dilution: 1:500).

    Techniques: In Vivo, In Vitro, Immunoprecipitation

    Fig. 2. Identification of DE-DRMs in individuals with EP. (A) The heatmap of expression levels for nine DE-DRMs. (B) The expression levels of 11 DRMs were exhibited between Ctrl and EP groups in boxplots. (C) Correlation analysis of nine DE-DRMs. Red and green colors represent positive and negative correlations, respectively. (D) The PPI analysis of DE-DMRs showed that SLC3A2 interacted with SLC7A11, while NDUFS1 interacted with NDUFA11, NUBPL, and LRPPRC. Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; EP, epilepsy; Ctrl, control; PPI, protein-protein interaction; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: Neurobiology of disease

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.

    doi: 10.1016/j.nbd.2025.106789

    Figure Lengend Snippet: Fig. 2. Identification of DE-DRMs in individuals with EP. (A) The heatmap of expression levels for nine DE-DRMs. (B) The expression levels of 11 DRMs were exhibited between Ctrl and EP groups in boxplots. (C) Correlation analysis of nine DE-DRMs. Red and green colors represent positive and negative correlations, respectively. (D) The PPI analysis of DE-DMRs showed that SLC3A2 interacted with SLC7A11, while NDUFS1 interacted with NDUFA11, NUBPL, and LRPPRC. Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; EP, epilepsy; Ctrl, control; PPI, protein-protein interaction; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: The paraffin sections were incubated with the first primary antibodies (overnight, 4 ◦C) which were as follows: anti-SLC7A11 antibody (Abcam, ab307601, dilution: 1:500), antiLRPPRC antibody (Abcam, ab259927, dilution: 1:200), anti-NDUFA11 antibody (Abclonal, A16239, dilution: 1:100), anti-NUBPL antibody (Boster, A10634–1, dilution: 1:100).

    Techniques: Expressing, Control

    Fig. 8. The expression of DE-DRMs in seizures models (in vitro and in vivo). (A) Constructing the in vitro seizures model. The amplitude and frequency of neuronal APs in the Mg2+-free group were significantly increased (n = 6 in each group; Independent sample t-test; #, P < 0.01). (B) Protein expression of nine DE-DRMs in the in vitro seizures model. The expression of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in the Mg2+-free group, while the expression of SLC7A11 was significantly increased in Mg2+-free group (n = 6 in each group; Independent sample t-test; #, P < 0.01). (C) Con structing the in vivo seizures model. No epileptoid discharges were observed in six rats of the Ctrl group, while significant epileptoid discharges were observed in six rats of the PTZ group (scale: Y-axis,50uV; X-axis, 0.5 s). (D) Protein expression of nine DE-DRMs in vivo models. The expressions of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in PTZ group, while the expression of SLC7A11 was significantly increased in PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; APs, action potentials; GYS1, glycogen synthase 1; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; OXSM, 3-oxoacyl-ACP synthase, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NCKAP1, NCK associated protein 1; PTZ, pentylenetetrazol.

    Journal: Neurobiology of disease

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.

    doi: 10.1016/j.nbd.2025.106789

    Figure Lengend Snippet: Fig. 8. The expression of DE-DRMs in seizures models (in vitro and in vivo). (A) Constructing the in vitro seizures model. The amplitude and frequency of neuronal APs in the Mg2+-free group were significantly increased (n = 6 in each group; Independent sample t-test; #, P < 0.01). (B) Protein expression of nine DE-DRMs in the in vitro seizures model. The expression of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in the Mg2+-free group, while the expression of SLC7A11 was significantly increased in Mg2+-free group (n = 6 in each group; Independent sample t-test; #, P < 0.01). (C) Con structing the in vivo seizures model. No epileptoid discharges were observed in six rats of the Ctrl group, while significant epileptoid discharges were observed in six rats of the PTZ group (scale: Y-axis,50uV; X-axis, 0.5 s). (D) Protein expression of nine DE-DRMs in vivo models. The expressions of GYS1, NDUFS1, OXSM, LRPPRC, NDUFA11, NUBPL, NCKAP1, and SLC3A2 were not significantly changed in PTZ group, while the expression of SLC7A11 was significantly increased in PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: DE-DRMs, differentially expressed disulfidptosis-related molecules; APs, action potentials; GYS1, glycogen synthase 1; SLC3A2, solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; OXSM, 3-oxoacyl-ACP synthase, mitochondrial; LRPPRC, leucine rich pentatricopeptide repeat containing; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NCKAP1, NCK associated protein 1; PTZ, pentylenetetrazol.

    Article Snippet: The paraffin sections were incubated with the first primary antibodies (overnight, 4 ◦C) which were as follows: anti-SLC7A11 antibody (Abcam, ab307601, dilution: 1:500), antiLRPPRC antibody (Abcam, ab259927, dilution: 1:200), anti-NDUFA11 antibody (Abclonal, A16239, dilution: 1:100), anti-NUBPL antibody (Boster, A10634–1, dilution: 1:100).

    Techniques: Expressing, In Vitro, In Vivo

    Fig. 9. Verifying the PPI in seizures models (in vivo and in vitro). (A-B) colocation analysis indicated that SLC7A11 colocalized with SLC3A2, NDUFS1 colocalized with LRPPRC, NDUFS1 colocalized with NUBPL, and NDUFS1 colocalized with NDUFA11 in both primary neurons and hippocampal tissue. (C–D) Pooled quan tification of protein immunoprecipitation showed a significant increment in the pull-down of SLC7A11 and a significant reduction in the pull-down of NDUFA11 in both the Mg2+-free group and PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: PPI, protein-protein interaction; SLC3A2,solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; LRPPRC, leucine rich pentatricopeptide repeat containing; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; PTZ, pentylenetetrazol.

    Journal: Neurobiology of disease

    Article Title: Identifying disulfidptosis-related biomarkers in epilepsy based on integrated bioinformatics and experimental analyses.

    doi: 10.1016/j.nbd.2025.106789

    Figure Lengend Snippet: Fig. 9. Verifying the PPI in seizures models (in vivo and in vitro). (A-B) colocation analysis indicated that SLC7A11 colocalized with SLC3A2, NDUFS1 colocalized with LRPPRC, NDUFS1 colocalized with NUBPL, and NDUFS1 colocalized with NDUFA11 in both primary neurons and hippocampal tissue. (C–D) Pooled quan tification of protein immunoprecipitation showed a significant increment in the pull-down of SLC7A11 and a significant reduction in the pull-down of NDUFA11 in both the Mg2+-free group and PTZ group (n = 6 in each group; Independent sample t-test; #, P < 0.01). Abbreviations: PPI, protein-protein interaction; SLC3A2,solute carrier family 3 member 2; SLC7A11, solute carrier family 7 member 11; NDUFS1, NADH:ubiquinone oxidoreductase core subunit S1; LRPPRC, leucine rich pentatricopeptide repeat containing; NUBPL, NUBP iron‑sulfur cluster assembly factor, mitochondrial; NDUFA11, NADH:ubiquinone oxidoreductase subunit A11; PTZ, pentylenetetrazol.

    Article Snippet: The paraffin sections were incubated with the first primary antibodies (overnight, 4 ◦C) which were as follows: anti-SLC7A11 antibody (Abcam, ab307601, dilution: 1:500), antiLRPPRC antibody (Abcam, ab259927, dilution: 1:200), anti-NDUFA11 antibody (Abclonal, A16239, dilution: 1:100), anti-NUBPL antibody (Boster, A10634–1, dilution: 1:100).

    Techniques: In Vivo, In Vitro, Immunoprecipitation