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Proteintech tnfrsf12a
Correlation between the five signature genes . ( A ) Chord diagram of correlation. ( B ) Heat map of correlation. ( D–M ) Scatter plot of correlation among AKR1C2, SLC2A14, FTL, <t>TNFRSF12A,</t> and SLC2A3. * represents p<0.05; **represents p<0.01; ***represents p<0.01.

Correlation between the five signature genes . ( A ) Chord diagram of correlation. ( B ) Heat map of correlation. ( D–M ) Scatter plot of correlation among AKR1C2, SLC2A14, FTL, <t>TNFRSF12A,</t> and SLC2A3. * represents p<0.05; **represents p<0.01; ***represents p<0.01.

Tnfrsf12a, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 115 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/tnfrsf12a/GLUT3+Antibody/pmc12977075-103-35-43
Average 94 stars, based on 115 article reviews

tnfrsf12a - by Bioz Stars, 2026-09

94/100 stars

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1) Product Images from "A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage"

Article Title: A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage

Journal: International Journal of General Medicine

doi: 10.2147/IJGM.S581629

Figure Legend Snippet: Correlation between the five signature genes . ( A ) Chord diagram of correlation. ( B ) Heat map of correlation. ( D–M ) Scatter plot of correlation among AKR1C2, SLC2A14, FTL, TNFRSF12A, and SLC2A3. * represents p<0.05; **represents p<0.01; ***represents p<0.01.

Techniques Used:

Experimental verification of protein expression in the clinical sample. ( A ) The expression levels of AKR1C2, SLC2A14, FTL, TNFRSF12A, and SLC2A3 were detected by Western blot. ( B–F ) Protein quantification of the five signature genes. * represents p<0.05; ns represents no significance.

Figure Legend Snippet: Experimental verification of protein expression in the clinical sample. ( A ) The expression levels of AKR1C2, SLC2A14, FTL, TNFRSF12A, and SLC2A3 were detected by Western blot. ( B–F ) Protein quantification of the five signature genes. * represents p<0.05; ns represents no significance.

Techniques Used: Expressing, Western Blot

Blocking Assay:

Article Title: A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage
Article Snippet: .. After blocking with 5% BSA, the membranes were incubated overnight at 4°C with the following primary antibodies (all at 1:1000 dilution): AKR1C2 (#13035S, Cell Signaling Technology), FTL (#ab69090, Abcam), SLC2A14 (#PK35494-S, Abmart), SLC2A3 (#20403-1-AP, Proteintech), TNFRSF12A (#AWA10766, Abiowell), and GAPDH (#ab181602, ProteinTech). .. Following incubation with HRP-conjugated secondary antibodies, protein bands were visualized using an ECL detection reagent (Millipore, Germany) and imaged with a SmartChemi 910 Plus system (Sage, Beijing, China).

Article Title: A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage
Article Snippet: .. After blocking with 5% BSA, the membranes were incubated overnight at 4°C with the following primary antibodies (all at 1:1000 dilution): AKR1C2 (#13035S, Cell Signaling Technology), FTL (#ab69090, Abcam), SLC2A14 (#PK35494-S, Abmart), SLC2A3 (#20403-1-AP, Proteintech), TNFRSF12A (# AWA10766 , Abiowell), and GAPDH (#ab181602, ProteinTech). .. Following incubation with HRP-conjugated secondary antibodies, protein bands were visualized using an ECL detection reagent (Millipore, Germany) and imaged with a SmartChemi 910 Plus system (Sage, Beijing, China).

Incubation:

Article Title: A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage
Article Snippet: .. After blocking with 5% BSA, the membranes were incubated overnight at 4°C with the following primary antibodies (all at 1:1000 dilution): AKR1C2 (#13035S, Cell Signaling Technology), FTL (#ab69090, Abcam), SLC2A14 (#PK35494-S, Abmart), SLC2A3 (#20403-1-AP, Proteintech), TNFRSF12A (# AWA10766 , Abiowell), and GAPDH (#ab181602, ProteinTech). .. Following incubation with HRP-conjugated secondary antibodies, protein bands were visualized using an ECL detection reagent (Millipore, Germany) and imaged with a SmartChemi 910 Plus system (Sage, Beijing, China).

Image Search Results

Transcriptome analysis of the effect of TWEAK treatment on PDLSCs. (A) Venn diagram illustrating differentially expressed genes in PDLSCs following TWEAK treatment. (B) Multipoint differential scatter plot showing differentially expressed genes in PDLSCs following TWEAK treatment. (C) GO enrichment analysis comparing PDLSCs and PDLSCs treated with 50 ng/ml TWEAK. (D) KEGG enrichment analysis comparing PDLSCs and PDLSCs treated with 50 ng/ml TWEAK. (E) GO enrichment analysis comparing PDLSCs and PDLSCs treated with 100 ng/ml TWEAK. (F) KEGG enrichment analysis comparing PDLSCs and PDLSCs treated with 100 ng/ml TWEAK. (G) Western blot analysis was conducted to detect the levels of Fn14, NF-κB, P-NF-κB and NLRP3 in PDLSCs stimulated with 50 and 100 ng/ml TWEAK. (H) Statistical analysis of protein band intensities from (G) (n=3). (I) Western blot analysis of the levels of Fn14, NF-κB, P-NF-κB and NLRP3 in PDLSCs after Fn14 was silenced using an shRNA. (J) Statistical analysis of protein band intensities from (I) (n=3). Statistical analysis was performed using (G and H) one-way ANOVA or (I and J) a two-tailed Student's t-test. * P<0.05; ** P<0.01; *** P<0.001. Data are presented as the mean ± SD. FC, fold change; Fn14, fibroblast growth factor-inducible 14; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; ns, not significant; P-, phosphorylated; PDLSC, periodontal ligament stem cell; shRNA/sh, short hairpin RNA; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Journal: International Journal of Molecular Medicine

Article Title: TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF-κB pathway

doi: 10.3892/ijmm.2025.5679

Figure Lengend Snippet: Transcriptome analysis of the effect of TWEAK treatment on PDLSCs. (A) Venn diagram illustrating differentially expressed genes in PDLSCs following TWEAK treatment. (B) Multipoint differential scatter plot showing differentially expressed genes in PDLSCs following TWEAK treatment. (C) GO enrichment analysis comparing PDLSCs and PDLSCs treated with 50 ng/ml TWEAK. (D) KEGG enrichment analysis comparing PDLSCs and PDLSCs treated with 50 ng/ml TWEAK. (E) GO enrichment analysis comparing PDLSCs and PDLSCs treated with 100 ng/ml TWEAK. (F) KEGG enrichment analysis comparing PDLSCs and PDLSCs treated with 100 ng/ml TWEAK. (G) Western blot analysis was conducted to detect the levels of Fn14, NF-κB, P-NF-κB and NLRP3 in PDLSCs stimulated with 50 and 100 ng/ml TWEAK. (H) Statistical analysis of protein band intensities from (G) (n=3). (I) Western blot analysis of the levels of Fn14, NF-κB, P-NF-κB and NLRP3 in PDLSCs after Fn14 was silenced using an shRNA. (J) Statistical analysis of protein band intensities from (I) (n=3). Statistical analysis was performed using (G and H) one-way ANOVA or (I and J) a two-tailed Student's t-test. * P<0.05; ** P<0.01; *** P<0.001. Data are presented as the mean ± SD. FC, fold change; Fn14, fibroblast growth factor-inducible 14; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; ns, not significant; P-, phosphorylated; PDLSC, periodontal ligament stem cell; shRNA/sh, short hairpin RNA; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Article Snippet: The following antibodies were used for western blotting: Rabbit anti-Fn14 antibody (cat. no. bs-2493R; BIOSS), rabbit anti-NF-κB p65 (D14E12) antibody (cat. no. 8242; Cell Signaling Technology, Inc.), rabbit anti-phospho-NFκB p65 (Ser536) antibody (cat. no. 3033; Cell Signaling Technology, Inc.), rabbit anti-NLRP3 antibody (cat. no. bs-41293R; BIOSS), mouse anti-RUNX2 antibody (cat. no. ab76956; Abcam), rabbit anti-Sp7/Osterix antibody [ EPR21034 ] (cat. no. ab209484; Abcam), rabbit anti-OPG antibody (cat. no. ab73400; Abcam), mouse anti-ALP antibody [2F4] (cat. no. ab126820; Abcam), rabbit anti-TWEAK antibody (cat. no. PK93318; Abmart Pharmaceutical Technology Co., Ltd.), mouse anti-β-actin antibody (cat. no. T200068-8F10; ZENBIO Biotechnology Co., Ltd.), goat anti-mouse IgG H&L (HRP) (cat. no. 511103; ZENBIO Biotechnology Co., Ltd.) and goat anti-rabbit IgG H&L (HRP) (cat. no. 511203; ZENBIO Biotechnology Co., Ltd.).

Techniques: Western Blot, shRNA, Two Tailed Test

Inhibition of Fn14 and NF-κB effectively blocks TWEAK-induced alterations in PDLSC characteristics. (A) Western blot analysis was conducted to assess the levels of Fn14, NF-κB, P-NF-κB and NLRP3 in PDLSCs. (B) Statistical analysis of the intensities of the protein bands shown in (A) (n=3). (C) A CCK-8 assay was performed to generate the proliferation curve of PDLSCs. (D) Statistical analysis of the OD450 values of cells from each group on day 5 of the CCK-8 assay, as presented in (C) (n=6). (G) Results of ALP staining and (E) the corresponding statistical analysis of PDLSCs after osteogenic induction (n=6). Scale bar, 400 μ m. (H) Results of Alizarin Red staining and (F) the corresponding statistical analysis of PDLSCs following osteogenic induction (n=6). Scale bar, 400 μ m. (I) Reverse transcription-quantitative PCR was used to assess the mRNA expression levels of RUNX2 , SP7 , ALP and OPG in PDLSCs, with β-actin serving as an internal reference (n=4). (J) Western blot analysis was performed to detect the protein expression levels of RUNX2, SP7, ALP and OPG in PDLSCs, and (K) the grayscale values of the gel images were semi-quantitatively analyzed, with β-actin used as an internal reference (n=3). Statistical analysis was performed using a one-way ANOVA. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. Data are presented as the mean ± SD. ALP, alkaline phosphatase; CCK-8, Cell Counting Kit-8; Fn14, fibroblast growth factor-inducible 14; IOD, integral optical density; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; ns, not significant; OD450, optical density at 450 nm; OPG, osteoprotegerin; P-, phosphorylated; PDLSC, periodontal ligament stem cell; RUNX2, runt-related transcription factor 2; sh, short hairpin RNA; SP7, Sp7 transcription factor; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Journal: International Journal of Molecular Medicine

Article Title: TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF-κB pathway

doi: 10.3892/ijmm.2025.5679

Figure Lengend Snippet: Inhibition of Fn14 and NF-κB effectively blocks TWEAK-induced alterations in PDLSC characteristics. (A) Western blot analysis was conducted to assess the levels of Fn14, NF-κB, P-NF-κB and NLRP3 in PDLSCs. (B) Statistical analysis of the intensities of the protein bands shown in (A) (n=3). (C) A CCK-8 assay was performed to generate the proliferation curve of PDLSCs. (D) Statistical analysis of the OD450 values of cells from each group on day 5 of the CCK-8 assay, as presented in (C) (n=6). (G) Results of ALP staining and (E) the corresponding statistical analysis of PDLSCs after osteogenic induction (n=6). Scale bar, 400 μ m. (H) Results of Alizarin Red staining and (F) the corresponding statistical analysis of PDLSCs following osteogenic induction (n=6). Scale bar, 400 μ m. (I) Reverse transcription-quantitative PCR was used to assess the mRNA expression levels of RUNX2 , SP7 , ALP and OPG in PDLSCs, with β-actin serving as an internal reference (n=4). (J) Western blot analysis was performed to detect the protein expression levels of RUNX2, SP7, ALP and OPG in PDLSCs, and (K) the grayscale values of the gel images were semi-quantitatively analyzed, with β-actin used as an internal reference (n=3). Statistical analysis was performed using a one-way ANOVA. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. Data are presented as the mean ± SD. ALP, alkaline phosphatase; CCK-8, Cell Counting Kit-8; Fn14, fibroblast growth factor-inducible 14; IOD, integral optical density; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; ns, not significant; OD450, optical density at 450 nm; OPG, osteoprotegerin; P-, phosphorylated; PDLSC, periodontal ligament stem cell; RUNX2, runt-related transcription factor 2; sh, short hairpin RNA; SP7, Sp7 transcription factor; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Techniques: Inhibition, Western Blot, CCK-8 Assay, Staining, Reverse Transcription, Real-time Polymerase Chain Reaction, Expressing, Cell Counting, shRNA

Inhibition of Fn14 and NF-κB effectively blocks TWEAK-induced alterations in the microenvironmental regulatory potential of PDLSCs. (A) Expression levels of OPG (green) and RANKL (red) in PDLSCs were detected by immunofluorescence staining, followed by quantitative analysis of the MOD values for (B) RANKL and (C) OPG, and (D) the MOD ratio of RANKL/OPG (n=5). Scale bar, 200 μ m. (E) Expression levels of CD68 and CD163 in RAW264.7 macrophages were detected by immunofluorescence staining, followed by quantitative analysis of the MOD values for (F) CD68 and (G) CD163 (n=5). Scale bar, 200 μ m. Statistical analysis was performed using a one-way ANOVA. ** P<0.01; *** P<0.001; **** P<0.0001. Data are presented as the mean ± SD. Fn14, fibroblast growth factor-inducible 14; MOD, mean optical density; ns, not significant; OPGa, osteoprotegerin; PDLSC, periodontal ligament stem cell; RANKL, receptor activator of nuclear factor-κB ligand; sh, short hairpin RNA; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Journal: International Journal of Molecular Medicine

Article Title: TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF-κB pathway

doi: 10.3892/ijmm.2025.5679

Figure Lengend Snippet: Inhibition of Fn14 and NF-κB effectively blocks TWEAK-induced alterations in the microenvironmental regulatory potential of PDLSCs. (A) Expression levels of OPG (green) and RANKL (red) in PDLSCs were detected by immunofluorescence staining, followed by quantitative analysis of the MOD values for (B) RANKL and (C) OPG, and (D) the MOD ratio of RANKL/OPG (n=5). Scale bar, 200 μ m. (E) Expression levels of CD68 and CD163 in RAW264.7 macrophages were detected by immunofluorescence staining, followed by quantitative analysis of the MOD values for (F) CD68 and (G) CD163 (n=5). Scale bar, 200 μ m. Statistical analysis was performed using a one-way ANOVA. ** P<0.01; *** P<0.001; **** P<0.0001. Data are presented as the mean ± SD. Fn14, fibroblast growth factor-inducible 14; MOD, mean optical density; ns, not significant; OPGa, osteoprotegerin; PDLSC, periodontal ligament stem cell; RANKL, receptor activator of nuclear factor-κB ligand; sh, short hairpin RNA; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Techniques: Inhibition, Expressing, Immunofluorescence, Staining, shRNA

Journal: International Journal of Molecular Medicine

Article Title: TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF-κB pathway

doi: 10.3892/ijmm.2025.5679

Figure Lengend Snippet: Inhibition of the TWEAK/Fn14/NF-κB/NLRP3 pathway enhances the functional properties of iPDLSCs. (A) Expression profile of surface markers in iPDLSCs quantified using flow cytometry. (B) Levels of TWEAK, Fn14, NF-κB, P-NF-κB and NLRP3 in PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3, and (C) statistical analysis of the band density values (n=3). (D) Apoptosis levels in PDLSCs, iPDLSCs, and iPDLSCs after downregulation of Fn14, NF-κB and NLRP3 were detected using the TUNEL assay, and (E) statistical analysis of the average fluorescence intensity of TUNEL was performed (n=5). Scale bar, 200 μ m. (F) A Cell Counting Kit-8 assay was used to assess the proliferative potential of PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3, and (G) statistical analysis of the OD450 values on day 5 of the experiment was performed (n=6). (H) Transwell migration assay evaluating the migratory potential of PDLSCs, iPDLSCs, and iPDLSCs after Fn14, NF-κB or NLRP3 downregulation, with (I) quantification of the number of migrated cells (n=6). Scale bar, 400 μ m. (J) Wound healing assay evaluating the migratory potential of PDLSCs, iPDLSCs, and iPDLSCs after Fn14, NF-κB or NLRP3 downregulation, with (K) quantification of the percentage of wound closure (%) (n=16). Scale bar, 1 mm. (L) ALP staining was used to evaluate the mineralization potential of PDLSCs, iPDLSCs, and iPDLSCs after downregulation of Fn14, NF-κB or NLRP3, with (M) quantification of the integral optical density of the ALP-stained images (n=6). Scale bar, 400 μ m. (N) Alizarin Red staining was used to evaluate the mineralization potential of PDLSCs, iPDLSCs, and iPDLSCs after downregulation of Fn14, NF-κB or NLRP3, with (O) quantification of the integral optical density of the Alizarin Red-stained images (n=6). Scale bar, 400 μ m. (P) Reverse transcription-quantitative PCR was used to evaluate the mRNA expression levels of RUNX2 , SP7 , ALP and OPG in PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3 (n=4). (Q) Western blotting was used to detect the expression levels of RUNX2, SP7, ALP and OPG in PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3, and (R) statistical analysis of the band density values was performed (n=3). Statistical analysis was performed using a one-way ANOVA. * P<0.05; ** P<0.01; *** P<0.001; **** P<0.0001. Data are presented as the mean ± SD. ALP, alkaline phosphatase; Fn14, fibroblast growth factor-inducible 14; IOD, integral optical density; iPDLSC, inflammatory PDLSC; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; ns, not significant; OD450, optical density at 450 nm; OPG, osteoprotegerin; P-, phosphorylated; PDLSC, periodontal ligament stem cell; RUNX2, runt-related transcription factor 2; sh, short hairpin RNA; SP7, Sp7 transcription factor; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Techniques: Inhibition, Functional Assay, Expressing, Flow Cytometry, TUNEL Assay, Fluorescence, Cell Counting, Transwell Migration Assay, Wound Healing Assay, Staining, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, shRNA

Effect of inhibition of the tumor necrosis factor-like weak inducer of apoptosis/Fn14/NF-κB/NLRP3 pathway on the microenvironmental regulatory ability of iPDLSCs. (A) Immunofluorescence staining was used to detect the expression levels of RANKL and OPG in PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3, followed by statistical analysis of the average optical density values of (B) RANKL and (C) OPG, and (D) the RANKL/OPG ratio (n=5). Scale bar, 200 μ m. (E) Immunofluorescence staining was used to detect the expression levels of CD68 and CD163 in macrophages cocultured with PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3, followed by statistical analysis of the average optical density values of (F) CD68 and (G) CD163 (n=5). Scale bar, 200 μ m. Statistical analysis was performed using a one-way ANOVA. * P<0.05; ** P<0.01; **** P<0.0001. Data are presented as the mean ± SD. Fn14, fibroblast growth factor-inducible 14; iPDLSC, inflammatory PDLSC; MOD, mean optical density; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; ns, not significant; OPG, osteoprotegerin; PDLSC, periodontal ligament stem cell; RANKL, receptor activator of nuclear factor-κB ligand; sh, short hairpin RNA.

Journal: International Journal of Molecular Medicine

Article Title: TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF-κB pathway

doi: 10.3892/ijmm.2025.5679

Figure Lengend Snippet: Effect of inhibition of the tumor necrosis factor-like weak inducer of apoptosis/Fn14/NF-κB/NLRP3 pathway on the microenvironmental regulatory ability of iPDLSCs. (A) Immunofluorescence staining was used to detect the expression levels of RANKL and OPG in PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3, followed by statistical analysis of the average optical density values of (B) RANKL and (C) OPG, and (D) the RANKL/OPG ratio (n=5). Scale bar, 200 μ m. (E) Immunofluorescence staining was used to detect the expression levels of CD68 and CD163 in macrophages cocultured with PDLSCs, iPDLSCs, and iPDLSCs after the downregulation of Fn14, NF-κB and NLRP3, followed by statistical analysis of the average optical density values of (F) CD68 and (G) CD163 (n=5). Scale bar, 200 μ m. Statistical analysis was performed using a one-way ANOVA. * P<0.05; ** P<0.01; **** P<0.0001. Data are presented as the mean ± SD. Fn14, fibroblast growth factor-inducible 14; iPDLSC, inflammatory PDLSC; MOD, mean optical density; NLRP3, NOD-like receptor thermal protein domain-associated protein 3; ns, not significant; OPG, osteoprotegerin; PDLSC, periodontal ligament stem cell; RANKL, receptor activator of nuclear factor-κB ligand; sh, short hairpin RNA.

Techniques: Inhibition, Immunofluorescence, Staining, Expressing, shRNA

Effects of TWEAK and TWEAK-Fn14-IN-1 on the progression of rat periodontitis. (A) Micro-CT images of the rat maxilla, with the distance between the two red short lines representing the CEJ-ABC distance on the buccal side, and with statistical analysis of the (B) distance of CEJ-ABC (n=6), and (C) BV/TV at the root bifurcation of the maxillary second molar (n=6). Scale bar, 1 mm. Images of (D) H&E and (E) Masson's trichrome staining of rat periodontal tissues. Scale bar, 1 mm (top) or 100 μ m (bottom). (F) Representative images of TRAP/alkaline phosphatase double staining in the periodontal tissue of the rat maxillary second molar, with (G) quantification and statistical analysis of osteoclast numbers (TRAP-positive, multinucleated cells located in the bone resorption lacunae) at the mesial root (n=6). Red triangles indicate osteoclasts. Scale bar, 50 μ m. (H) Immunofluorescence staining of CD163 (green) and CD68 (red) in periodontal tissues, with (J) quantification of the mean fluorescence intensity of CD163 and (K) quantification of the mean fluorescence intensity of CD68 (n=6). Scale bar, 100 μ m. (I) Immunofluorescence staining of RUNX2 (green) and Periostin (red) in periodontal tissues, with (L) quantification of the mean fluorescence intensity of RUNX2 and (M) quantification of the mean fluorescence intensity of Periostin (n=6). Scale bar, 100 μ m. Blank represents the unmodeled group, PBS refers to the control group where PBS was used instead of TWEAK or TWEAK-Fn14-IN-1 during modeling, and TWEAK and TWEAK-Fn14-IN-1 represent experimental groups where the recombinant TWEAK protein or TWEAK-Fn14-IN-1 inhibitor was applied, respectively. Statistical analysis was performed using a one-way ANOVA. * P<0.05; ** P<0.01; **** P<0.0001. Data are presented as the mean ± SD. ABC, alveolar bone crest; BV/TV, bone volume to total volume; CEJ, cementoenamel junction; Fn14, fibroblast growth factor-inducible 14; MOD, mean optical density; ns, not significant; RUNX2, runt-related transcription factor 2; TRAP, tartrate-resistant acid phosphatase; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Journal: International Journal of Molecular Medicine

Article Title: TWEAK modulates the characteristics of periodontal ligament stem cells via the Fn14/NF-κB pathway

doi: 10.3892/ijmm.2025.5679

Figure Lengend Snippet: Effects of TWEAK and TWEAK-Fn14-IN-1 on the progression of rat periodontitis. (A) Micro-CT images of the rat maxilla, with the distance between the two red short lines representing the CEJ-ABC distance on the buccal side, and with statistical analysis of the (B) distance of CEJ-ABC (n=6), and (C) BV/TV at the root bifurcation of the maxillary second molar (n=6). Scale bar, 1 mm. Images of (D) H&E and (E) Masson's trichrome staining of rat periodontal tissues. Scale bar, 1 mm (top) or 100 μ m (bottom). (F) Representative images of TRAP/alkaline phosphatase double staining in the periodontal tissue of the rat maxillary second molar, with (G) quantification and statistical analysis of osteoclast numbers (TRAP-positive, multinucleated cells located in the bone resorption lacunae) at the mesial root (n=6). Red triangles indicate osteoclasts. Scale bar, 50 μ m. (H) Immunofluorescence staining of CD163 (green) and CD68 (red) in periodontal tissues, with (J) quantification of the mean fluorescence intensity of CD163 and (K) quantification of the mean fluorescence intensity of CD68 (n=6). Scale bar, 100 μ m. (I) Immunofluorescence staining of RUNX2 (green) and Periostin (red) in periodontal tissues, with (L) quantification of the mean fluorescence intensity of RUNX2 and (M) quantification of the mean fluorescence intensity of Periostin (n=6). Scale bar, 100 μ m. Blank represents the unmodeled group, PBS refers to the control group where PBS was used instead of TWEAK or TWEAK-Fn14-IN-1 during modeling, and TWEAK and TWEAK-Fn14-IN-1 represent experimental groups where the recombinant TWEAK protein or TWEAK-Fn14-IN-1 inhibitor was applied, respectively. Statistical analysis was performed using a one-way ANOVA. * P<0.05; ** P<0.01; **** P<0.0001. Data are presented as the mean ± SD. ABC, alveolar bone crest; BV/TV, bone volume to total volume; CEJ, cementoenamel junction; Fn14, fibroblast growth factor-inducible 14; MOD, mean optical density; ns, not significant; RUNX2, runt-related transcription factor 2; TRAP, tartrate-resistant acid phosphatase; TWEAK, tumor necrosis factor-like weak inducer of apoptosis.

Techniques: Micro-CT, Staining, Double Staining, Immunofluorescence, Fluorescence, Control, Recombinant

Differential gene screening and prognostic model construction. (A) The Venn diagram shows the gene intersection obtained from four differential gene screening methods (edgeR, DESeq2, Wilcoxon, and limma), with 86 common differential genes selected. (B) Univariate Cox regression identifies significant gene‐survival correlations, with hazard ratios (HR) and p ‐values illustrated in the forest plot. (C) LASSO regression cross‐validation determines the optimal λ value, with red dots representing the mean error of cross‐validation and gray bars indicating the standard deviation. (D) The LASSO regression path plot shows the trend of regression coefficients as λ values change, with coefficients gradually shrinking to zero and ultimately retaining a few key genes. (E) Multivariate Cox regression analysis selected three key genes: VAV3, TNFRSF12A, and PLA2G2A , showing their hazard ratios (HR) and p ‐values.

Journal: The FASEB Journal

Article Title: Lactate Metabolism‐Immune Regulation‐Related Gene Signature in Lower‐Grade Gliomas: Prognostic Model Development and Immune Characterization

doi: 10.1096/fj.202503738RR

Figure Lengend Snippet: Differential gene screening and prognostic model construction. (A) The Venn diagram shows the gene intersection obtained from four differential gene screening methods (edgeR, DESeq2, Wilcoxon, and limma), with 86 common differential genes selected. (B) Univariate Cox regression identifies significant gene‐survival correlations, with hazard ratios (HR) and p ‐values illustrated in the forest plot. (C) LASSO regression cross‐validation determines the optimal λ value, with red dots representing the mean error of cross‐validation and gray bars indicating the standard deviation. (D) The LASSO regression path plot shows the trend of regression coefficients as λ values change, with coefficients gradually shrinking to zero and ultimately retaining a few key genes. (E) Multivariate Cox regression analysis selected three key genes: VAV3, TNFRSF12A, and PLA2G2A , showing their hazard ratios (HR) and p ‐values.

Article Snippet: To further confirm the expression patterns and possible biological roles of the candidate genes in tumor tissues, we first analyzed the immunohistochemistry results of VAV3, TNFRSF12A, and PLA2G2A using the HPA (Human Protein Atlas) database.

Techniques: Biomarker Discovery, Standard Deviation

Construction and validation of the LMRIGs prognostic signature in LGG. (A) Distribution of survival status between high‐ and low‐risk patients. (B) ROC curves of the LMRIGs signature at 1, 3, and 5 years to evaluate predictive accuracy. (C) LGG patients stratified into high‐ and low‐risk groups based on risk scores. (D) Expression patterns of risk genes in different subgroups. (E) Heatmap of the expression of three LMRIGs genes ( VAV3, TNFRSF12A , and PLA2G2A ). (F) Kaplan–Meier survival analysis in the CGGA cohort, showing better prognosis in the low‐risk group. (G) ROC curves at 1, 3, and 5 years in the CGGA cohort. (H) Risk group classification in the CGGA validation cohort. (I) Expression patterns of risk genes in different subgroups. (J) Expression of risk genes in different subgroups of the CGGA cohort.

Journal: The FASEB Journal

Article Title: Lactate Metabolism‐Immune Regulation‐Related Gene Signature in Lower‐Grade Gliomas: Prognostic Model Development and Immune Characterization

doi: 10.1096/fj.202503738RR

Figure Lengend Snippet: Construction and validation of the LMRIGs prognostic signature in LGG. (A) Distribution of survival status between high‐ and low‐risk patients. (B) ROC curves of the LMRIGs signature at 1, 3, and 5 years to evaluate predictive accuracy. (C) LGG patients stratified into high‐ and low‐risk groups based on risk scores. (D) Expression patterns of risk genes in different subgroups. (E) Heatmap of the expression of three LMRIGs genes ( VAV3, TNFRSF12A , and PLA2G2A ). (F) Kaplan–Meier survival analysis in the CGGA cohort, showing better prognosis in the low‐risk group. (G) ROC curves at 1, 3, and 5 years in the CGGA cohort. (H) Risk group classification in the CGGA validation cohort. (I) Expression patterns of risk genes in different subgroups. (J) Expression of risk genes in different subgroups of the CGGA cohort.

Techniques: Biomarker Discovery, Expressing

Expression validation of key model genes and in vitro functional experiments of PLA2G2A. (A) Immunohistochemical results from the Human Protein Atlas (HPA) database show that the expression levels of VAV3, TNFRSF12A, and PLA2G2A are significantly higher in tumor tissues than in normal tissues. (B–D) qRT‐PCR results from clinical samples show that the mRNA levels of VAV3, TNFRSF12A , and PLA2G2A are significantly elevated in tumor tissues (* p < 0.05, *** p < 0.001, **** p < 0.0001). (E) Receiver operating characteristic curves (ROC) of PLA2G2A mRNA, TNFRSF12A mRNA, and VAV3 mRNA in subjects. (F, G) Western blot analysis of PLA2G2A protein expression in different glioma cell lines (* p < 0.05, ** p < 0.01, **** p < 0.0001). (H, I) After PLA2G2A knockdown in U251 cells using shRNA, Western blot confirmed transfection efficiency (*** p < 0.001, **** p < 0.0001). (J, K) After PLA2G2A knockdown in LN229 cells using shRNA, Western blot confirmed transfection efficiency (* p < 0.05, *** p < 0.001). (L, M) CCK‐8 assay results show that PLA2G2A downregulation significantly inhibits the proliferative ability of U251 and LN229 glioma cells (* p < 0.05, ** p < 0.01, **** p < 0.0001) (N) Immunofluorescence detection shows successful construction of stable U251 and LN229 transfected cells. (O) Transwell assay results show that PLA2G2A knockdown significantly reduces the migration and invasion abilities of U251 and LN229 tumor cells. (P) Quantitative analysis further confirms that the number of migrating and invading cells in the sh‐PLA2G2A treatment group is significantly lower than in the control group (* p < 0.05, ** p < 0.01, **** p < 0.0001).

Journal: The FASEB Journal

Article Title: Lactate Metabolism‐Immune Regulation‐Related Gene Signature in Lower‐Grade Gliomas: Prognostic Model Development and Immune Characterization

doi: 10.1096/fj.202503738RR

Figure Lengend Snippet: Expression validation of key model genes and in vitro functional experiments of PLA2G2A. (A) Immunohistochemical results from the Human Protein Atlas (HPA) database show that the expression levels of VAV3, TNFRSF12A, and PLA2G2A are significantly higher in tumor tissues than in normal tissues. (B–D) qRT‐PCR results from clinical samples show that the mRNA levels of VAV3, TNFRSF12A , and PLA2G2A are significantly elevated in tumor tissues (* p < 0.05, *** p < 0.001, **** p < 0.0001). (E) Receiver operating characteristic curves (ROC) of PLA2G2A mRNA, TNFRSF12A mRNA, and VAV3 mRNA in subjects. (F, G) Western blot analysis of PLA2G2A protein expression in different glioma cell lines (* p < 0.05, ** p < 0.01, **** p < 0.0001). (H, I) After PLA2G2A knockdown in U251 cells using shRNA, Western blot confirmed transfection efficiency (*** p < 0.001, **** p < 0.0001). (J, K) After PLA2G2A knockdown in LN229 cells using shRNA, Western blot confirmed transfection efficiency (* p < 0.05, *** p < 0.001). (L, M) CCK‐8 assay results show that PLA2G2A downregulation significantly inhibits the proliferative ability of U251 and LN229 glioma cells (* p < 0.05, ** p < 0.01, **** p < 0.0001) (N) Immunofluorescence detection shows successful construction of stable U251 and LN229 transfected cells. (O) Transwell assay results show that PLA2G2A knockdown significantly reduces the migration and invasion abilities of U251 and LN229 tumor cells. (P) Quantitative analysis further confirms that the number of migrating and invading cells in the sh‐PLA2G2A treatment group is significantly lower than in the control group (* p < 0.05, ** p < 0.01, **** p < 0.0001).

Techniques: Expressing, Biomarker Discovery, In Vitro, Functional Assay, Immunohistochemical staining, Quantitative RT-PCR, Western Blot, Knockdown, shRNA, Transfection, CCK-8 Assay, Immunofluorescence, Transwell Assay, Migration, Control

Schematic of lactate metabolism‐immune regulation‐related genes altering the tumor microenvironment in glioma. In glioma, clustering analysis based on lactate metabolism gene sets identified PLA2G2A, TNFRSF12A, and VAV3 as differentially expressed genes included in the predictive model. PLA2G2A alters the tumor microenvironment by remodeling the ECM, promoting tumor‐associated inflammation, and activating epithelial‐to‐mesenchymal transition (EMT), thereby enhancing tumor cell proliferation and invasion, ultimately leading to poor prognosis.

Journal: The FASEB Journal

Article Title: Lactate Metabolism‐Immune Regulation‐Related Gene Signature in Lower‐Grade Gliomas: Prognostic Model Development and Immune Characterization

doi: 10.1096/fj.202503738RR

Figure Lengend Snippet: Schematic of lactate metabolism‐immune regulation‐related genes altering the tumor microenvironment in glioma. In glioma, clustering analysis based on lactate metabolism gene sets identified PLA2G2A, TNFRSF12A, and VAV3 as differentially expressed genes included in the predictive model. PLA2G2A alters the tumor microenvironment by remodeling the ECM, promoting tumor‐associated inflammation, and activating epithelial‐to‐mesenchymal transition (EMT), thereby enhancing tumor cell proliferation and invasion, ultimately leading to poor prognosis.

Techniques:

Journal: International Journal of General Medicine

Article Title: A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage

doi: 10.2147/IJGM.S581629

Figure Lengend Snippet: Correlation between the five signature genes . ( A ) Chord diagram of correlation. ( B ) Heat map of correlation. ( D–M ) Scatter plot of correlation among AKR1C2, SLC2A14, FTL, TNFRSF12A, and SLC2A3. * represents p<0.05; **represents p<0.01; ***represents p<0.01.

Article Snippet: After blocking with 5% BSA, the membranes were incubated overnight at 4°C with the following primary antibodies (all at 1:1000 dilution): AKR1C2 (#13035S, Cell Signaling Technology), FTL (#ab69090, Abcam), SLC2A14 (#PK35494-S, Abmart), SLC2A3 (#20403-1-AP, Proteintech), TNFRSF12A (# AWA10766 , Abiowell), and GAPDH (#ab181602, ProteinTech).

Techniques:

Journal: International Journal of General Medicine

Article Title: A Five-Gene PANoptosis Signature Correlates with Immune Infiltration and Secondary Brain Injury in Intracerebral Hemorrhage

doi: 10.2147/IJGM.S581629

Figure Lengend Snippet: Experimental verification of protein expression in the clinical sample. ( A ) The expression levels of AKR1C2, SLC2A14, FTL, TNFRSF12A, and SLC2A3 were detected by Western blot. ( B–F ) Protein quantification of the five signature genes. * represents p<0.05; ns represents no significance.

Techniques: Expressing, Western Blot

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