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Fig. 3. The nuclear accumulation of STAT1 and <t>STAT2</t> in response to IFN- is inhibited in HDV-transfected cells. Normal cells (Huh-7) or cells transfected with HDV cDNA [Huh-7 pS- VL(D3)] were seeded on glass coverslips and treated with 1000 U/mL IFN- for 30 minutes. Cells were ﬁxed with 4% paraformaldehyde, permeabilized with 0.2% Triton X-100, and stained with antisera to STAT1 (A) or STAT2 (B) and HDAg. Nuclei were counterstained with 4,6-diamidino-2-phenylindole (blue). Arrows point to cells successfully transfected with HDV.

Stat2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 337 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Hepatitis delta virus inhibits alpha interferon signaling."

Article Title: Hepatitis delta virus inhibits alpha interferon signaling.

Journal: Hepatology (Baltimore, Md.)

doi: 10.1002/hep.22654

Fig. 3. The nuclear accumulation of STAT1 and STAT2 in response to IFN- is inhibited in HDV-transfected cells. Normal cells (Huh-7) or cells transfected with HDV cDNA [Huh-7 pS- VL(D3)] were seeded on glass coverslips and treated with 1000 U/mL IFN- for 30 minutes. Cells were ﬁxed with 4% paraformaldehyde, permeabilized with 0.2% Triton X-100, and stained with antisera to STAT1 (A) or STAT2 (B) and HDAg. Nuclei were counterstained with 4,6-diamidino-2-phenylindole (blue). Arrows point to cells successfully transfected with HDV.

Figure Legend Snippet: Fig. 3. The nuclear accumulation of STAT1 and STAT2 in response to IFN- is inhibited in HDV-transfected cells. Normal cells (Huh-7) or cells transfected with HDV cDNA [Huh-7 pS- VL(D3)] were seeded on glass coverslips and treated with 1000 U/mL IFN- for 30 minutes. Cells were ﬁxed with 4% paraformaldehyde, permeabilized with 0.2% Triton X-100, and stained with antisera to STAT1 (A) or STAT2 (B) and HDAg. Nuclei were counterstained with 4,6-diamidino-2-phenylindole (blue). Arrows point to cells successfully transfected with HDV.

Techniques Used: Transfection, Staining

Fig. 4. HDV inhibition of IFN-–induced tyrosine phosphorylation of STAT1 and STAT2. Normal cells (Huh-7) and cells transfected with HDV cDNA [Huh-7 pSVL(D3)] were cultured for 9 days and then treated with 1000 U/mL IFN- for 30 minutes or left untreated. Equal amounts of cell lysates were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, transferred onto nitrocellulose membranes, and exam- ined with antibodies to phosphotyrosine 701-STAT1 (pY-STAT1), STAT1, phosphotyrosine 690-STAT2 (pY-STAT2), STAT2, p48, and HDAg. -Actin levels served as a loading control.

Figure Legend Snippet: Fig. 4. HDV inhibition of IFN-–induced tyrosine phosphorylation of STAT1 and STAT2. Normal cells (Huh-7) and cells transfected with HDV cDNA [Huh-7 pSVL(D3)] were cultured for 9 days and then treated with 1000 U/mL IFN- for 30 minutes or left untreated. Equal amounts of cell lysates were separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, transferred onto nitrocellulose membranes, and exam- ined with antibodies to phosphotyrosine 701-STAT1 (pY-STAT1), STAT1, phosphotyrosine 690-STAT2 (pY-STAT2), STAT2, p48, and HDAg. -Actin levels served as a loading control.

Techniques Used: Inhibition, Phospho-proteomics, Transfection, Cell Culture, Polyacrylamide Gel Electrophoresis, Control

Incubation:

Article Title: Fostamatinib (R788), a spleen tyrosine kinase inhibitor, sensitizes pancreatic cancer cells to oncolytic vesicular stomatitis virus
Article Snippet: .. Membranes were then incubated in TBS-T with 5% BSA or milk with 0.02% sodium azide and a 1:5,000 dilution of rabbit polyclonal anti-VSV antibodies (raised against VSV virions), a 1:1,000 dilution of rabbit anti-phospho-STAT1 (catalog number 9167S, Cell Signaling), a 1:1,000 dilution of rabbit anti-STAT1 (catalog number 14994T, clone D1K9Y, Cell Signaling), a 1:1,000 dilution of rabbit anti-phospho-STAT2 (catalog number PA5-97361clone p-Y690, Invitrogen), a 1:1,000 dilution of rabbit anti-STAT2 (catalog number 4594, Cell Signaling), a 1:1,000 dilution of rabbit anti-phospho-STAT3 (catalog number 9134P, clone Y705, Cell Signaling), a 1:1,000 dilution of mouse anti-STAT3 (catalog number 9139P, clone 124H6, Cell Signaling), rabbit anti-phospho-MAPK (catalog number 4370S,clone p-T202/Y204, Cell Signaling), a 1:1,000 dilution of rabbit anti-MAPK (catalog number 9102L Cell Signaling), rabbit anti-phospho-SYK (catalog number 2710Sclone p-Y525, Cell Signaling), a 1:1,000 dilution of rabbit anti-SYK (catalog number 13198S, Cell Signaling), a 1:1,000 dilution of rabbit anti-OAS2 (catalog number PA5-65422 Cell Signaling), a 1:1,000 dilution of rabbit anti-GAPDH (catalog number 1E6D9 Proteintech), 1:1,000 dilution of rabbit anti-phsopho-TBK1/NAK (catalog number 5483P, clone S172, Cell Signaling), and a 1:1,000 dilution of rabbit anti-MX1 (catalog number 13750-1-AP, Proteintech). .. Starbright Blue 700 goat anti-rabbit (Bio-Rad, 12004161) immunoglobulin G (IgG) fluorescent secondary antibodies at 1:5,000 dilutions were used for fluorescent western blotting detection using the Chemidoc MP imaging system from Bio-Rad.

Article Title: Distinct ZIKV strain signatures and type I IFN modulation reveal a protective role of brain endothelial interferon signaling in vitro and in vivo
Article Snippet: The samples were subjected to a 10% polyacrylamide gel electrophoresis (SDS-PAGE), followed by transfer to a nitrocellulose membrane (Merck). .. The membranes were blocked with 10% TBS containing 5% bovine serum albumin (BSA; Merck) for 1 h, and incubated with the antibodies anti-p-STAT1, anti-STAT1, anti-p-STAT2, anti-STAT2, anti-RIG-I, anti-TLR-3, and anti-β-actin (Cell Signaling Technology, Danvers, MA), overnight at 4 0 C. The membranes were washed and incubated with the respective HRP-conjugated secondary antibodies (Jackson ImmunoResearch Laboratories Inc., West Grove, PA) for 1 h and developed using the ECLTM Prime Western Blotting System kit (GE Healthcare, Boston, MA). .. The ratio between phosphorylated and nonphosphorylated proteins, as well as the ratio of total protein expression (sum of phosphorylated and nonphosphorylated) and β-actin, were calculated using ImageJ software.

Article Title: SENP5 enhances antiviral innate immunity by promoting AURKA-dependent STAT2 phosphorylation.
Article Snippet: .. Subsequently, the cells were incubated with primary antibodies against AURKA (Proteintech, IL, USA) and STAT2 (CST, MA, USA) at 4°C overnight. .. After being washed three times with PBS, the cells were stained with Alexa Fluor 488 goat anti-rabbit (ZSGB-BIO, AR TIC LE IN PR ES S Beijing, China) and Alexa Fluor 594 goat anti-mouse (ZSGB-BIO, Beijing, China) secondary antibodies for 1 h at room temperature.

Western Blot:

Article Title: Crimean-Congo hemorrhagic fever virus NSm protein inhibits the type I interferon signaling by binding to STAT2.
Article Snippet: .. Western blotting was performed as previously described using the following antibodies [10,12,13]: anti-HA (clone 3F10; Roche), anti-His (clone 9F2; Fujifilm Wako), anti-FLAG (catalog no. PM020; MBL), anti-VSIV M (clone 23H12; Kerafast), anti-VSIV G (clone P5D4; Sigma-Aldrich), anti-STAT2 (catalog no.: D9J7L; Cell Signaling Technology), anti-STAT1 (catalog no.: D19KY; Cell Signaling Technology), anti-STAT2 (phosphor Y690) (catalog no.: D3P2P; Cell Signaling Technology), anti-STAT1 (phosphor Y701) (catalog no.: D4A7; Cell Signaling Technology), anti-CCHFV Gn (in-house production) or anti-β-actin (catalog no. AC-15; Sigma-Aldrich). .. The band intensities of VSIV-G, VSIV-M, STAT1, pSTAT1, STAT2, pSTAT2, NSm-FLAG, and β-actin were quantified using ImageJ software (National Institutes of Health).

Article Title: Crimean-Congo hemorrhagic fever virus NSm protein inhibits the type I interferon signaling by binding to STAT2
Article Snippet: .. Western blotting was performed as previously described using the following antibodies [ , , ]: anti-HA (clone 3F10; Roche), anti-His (clone 9F2; Fujifilm Wako), anti-FLAG (catalog no. PM020; MBL), anti-VSIV M (clone 23H12; Kerafast), anti-VSIV G (clone P5D4; Sigma-Aldrich), anti-STAT2 (catalog no.: D9J7L; Cell Signaling Technology), anti-STAT1 (catalog no.: D19KY; Cell Signaling Technology), anti-STAT2 (phosphor Y690) (catalog no.: D3P2P; Cell Signaling Technology), anti-STAT1 (phosphor Y701) (catalog no.: D4A7; Cell Signaling Technology), anti-CCHFV Gn (in-house production) or anti-β-actin (catalog no. AC-15; Sigma-Aldrich). .. The band intensities of VSIV-G, VSIV-M, STAT1, pSTAT1, STAT2, pSTAT2, NSm-FLAG, and β-actin were quantified using ImageJ software (National Institutes of Health).

other:

Article Title: Elongator is required for pattern recognition receptor and type I interferon signaling in macrophages
Article Snippet: STAT2 , Mouse , CST , sc-514193 , 1:1000.

Image Search Results

A) Foci images of the DENV2 with ZIKV-equivalent STAT2-targeting mutations. B) Design of bimolecular fluorescence complementation (BiFC) assay for NS5-STAT2 interaction analysis in cells. C) Flow cytometry BiFC readouts of selected NS5 mutants with human STAT2. D) Foci images of DENV2 with single and combined STAT2-targeting mutations.

Journal: bioRxiv

Article Title: Disrupting IFIT1-STAT2 viral evasion synergy yields live-attenuated flavivirus with enhanced immune priming

doi: 10.64898/2026.06.04.729841

Figure Lengend Snippet: A) Foci images of the DENV2 with ZIKV-equivalent STAT2-targeting mutations. B) Design of bimolecular fluorescence complementation (BiFC) assay for NS5-STAT2 interaction analysis in cells. C) Flow cytometry BiFC readouts of selected NS5 mutants with human STAT2. D) Foci images of DENV2 with single and combined STAT2-targeting mutations.

Article Snippet: Similarly, the human STAT2 gene was sub-cloned from pUNO1-hSTAT2 (InvivoGen), fused with a C-terminal FLAG tag sequence, and cloned into a lentiviral plasmid under the control of the inducible CMVtight promoter, utilizing an mCherry expression cassette as a marker.

Techniques: Bimolecular Fluorescence Complementation Assay, Flow Cytometry

A) Heatmap of contact analysis of NS5-STAT2 interacting residues from four available NS5-STAT2 complex structures (top and middle, each number represents the numbers of contacts at each residue) with the corresponding mutation fitness data derived from DMS of DENV2 in Vero cells (bottom) . B) Western-blot analysis of STAT2 degradation during infection by DENV2 with selected NS5 mutations at the STAT2-contacting residues. C) Multi-step replication kinetics of the DENV2-WT, -P336G, -N730D, -P336G+N730D, and - P336G+Q845A in Vero cells infected at MOI = 0.1. D) Relative binding of the NS5 mutants with human STAT2 by co-immunoprecipitation assay.

Journal: bioRxiv

Article Title: Disrupting IFIT1-STAT2 viral evasion synergy yields live-attenuated flavivirus with enhanced immune priming

doi: 10.64898/2026.06.04.729841

Figure Lengend Snippet: A) Heatmap of contact analysis of NS5-STAT2 interacting residues from four available NS5-STAT2 complex structures (top and middle, each number represents the numbers of contacts at each residue) with the corresponding mutation fitness data derived from DMS of DENV2 in Vero cells (bottom) . B) Western-blot analysis of STAT2 degradation during infection by DENV2 with selected NS5 mutations at the STAT2-contacting residues. C) Multi-step replication kinetics of the DENV2-WT, -P336G, -N730D, -P336G+N730D, and - P336G+Q845A in Vero cells infected at MOI = 0.1. D) Relative binding of the NS5 mutants with human STAT2 by co-immunoprecipitation assay.

Techniques: Residue, Mutagenesis, Derivative Assay, Western Blot, Infection, Binding Assay, Co-Immunoprecipitation Assay

A) Foci images of DENV1-4 and ZIKV with P336G or N730D (DENV2 mutations). B) STAT2 degradation in A549 cells infected by DENV1-4 and ZIKV with P336G or N730D mutations. C) Multi-sequence alignment (MSA) of STAT2-interating residues across DENV1-4 (KDH, 16681, v1043, and H241, respectively) and ZIKV (SV0010) used in A) and B). MSA was performed with full-length NS5 sequences. The STAT2 interacting residues (based on the analysis performed in ) were then extracted from the aligned sequences and displayed using MView .

Journal: bioRxiv

Article Title: Disrupting IFIT1-STAT2 viral evasion synergy yields live-attenuated flavivirus with enhanced immune priming

doi: 10.64898/2026.06.04.729841

Figure Lengend Snippet: A) Foci images of DENV1-4 and ZIKV with P336G or N730D (DENV2 mutations). B) STAT2 degradation in A549 cells infected by DENV1-4 and ZIKV with P336G or N730D mutations. C) Multi-sequence alignment (MSA) of STAT2-interating residues across DENV1-4 (KDH, 16681, v1043, and H241, respectively) and ZIKV (SV0010) used in A) and B). MSA was performed with full-length NS5 sequences. The STAT2 interacting residues (based on the analysis performed in ) were then extracted from the aligned sequences and displayed using MView .

Techniques: Infection, Sequencing

Journal: bioRxiv

Article Title: Disrupting IFIT1-STAT2 viral evasion synergy yields live-attenuated flavivirus with enhanced immune priming

doi: 10.64898/2026.06.04.729841

Figure Lengend Snippet: A) Type-I IFN sensitivity of DENV2 with MTase, STAT2-targeting, and combined mutations (MTase+STAT2) in A549-WT and A549-IFIT1-KO, STAT2-KO, and PAF1-KO. The A549 cells were treated with IFN-α2 at 500U/ml for 4 hours before virus infection at MOI = 0.1. The virus titers (FFU/ml) for calculating IFN sensitivity were measured at 2 dpi. B) Multi-step replication kinetics of the DENV2 panel in WT A549 (left plot) and IFIT1-KO A549 (right plot). The A549 cells were infected with DENV2 at MOI = 0.1. C) Western-blot analysis of STAT2 expression level from the multi-step replication kinetics experiment in B). D) Flow cytometry measurement of STAT2 levels (as mean fluorescence intensity, MFI) in the infected and the bystander WT- and -IFIT1-KO A549 at 1 and 2 dpi (left and middle plot) and in the WT- and KO cells treated with type-I IFN at 500U/ml (right plot). E) Proteomic analysis showing differential human protein levels between WT- and IFIT1KO A549 at 2 dpi infected with either DENV2-E217A or DENV2-S150T+P336G+N730D as in B) (left volcano plot). The right heatmap shows the expression profile of ISGs with similar profile to STAT2 in different A549 cells (x-axis). F) Measurement of secreted IFN-β and TNF-α (pg/ml) of A549-WT and -IFIT1-KO cells infected with one of the three viruses, DENV2-WT, - E217A, or S150T+P336G+N730D (MOI = 1) at 1 and 2 dpi. The data points in the top bar plot from each virus were aggregated by cell types. The bottom paired line plots were matched by virus, with the data points in the IFIT1-KO being an average of the measurements from three IFIT1-KO clones. Statistical significance is indicated by brackets above the data sets. Exact p value is provided for each comparison (* ; ns, not significant). Statistical analysis was performed using an unpaired Student’s t-test for the top bar plots and a paired t-test for the bottom line plots.

Techniques: Virus, Infection, Western Blot, Expressing, Flow Cytometry, Fluorescence, Clone Assay, Comparison

A) Multi-step replication kinetics of the mutant DENV2 in STAT2-KO and PAF1-KO A549 cells. A549 cells were infected with DENV2 at MOI = 0.1. B) Western-blot analysis of IFIT1 and dengue NS3 expression in wild-type A549 cells during multi-step replication kinetics analysis in A). C) Flow cytometry of DENV2 infection by anti-NS3 in WT and IFIT1-KO A549 cells. D) Volcano plots illustrating the distribution of quantified proteins. The x-axis represents the fold change (LFC), and the y-axis represents the statistical significance as (-value). Proteins with a fold change > 2 and a p-value < 0.01 were considered significantly differentially expressed. Selected ISGs upregulated during DENV infections in WT- and IFIT1-KO A549 are labeled by their gene symbols. Aggregate data of DENV2-E217A and DENV2-S150T+P336G+N730D were used to represent the data of infected cells. E-F) Comparison between the cytokine concentrations (pg/ml) secreted from WT-A549 and those from IFIT1-KO-A549 infected with one of the three viruses, DENV2-WT, -E217A, or S150T+P336G+N730D (MOI = 1) at 1 and 2 dpi. The data points in the top bar plots (E) from each virus were aggregated by cell types. The bottom paired line plots (F) were matched by virus, with the data points in the IFIT1-KO being an average of the measurement from three IFIT1-KO clones. Statistical significance is indicated by brackets above the data sets. Exact values are provided for each comparison (* ; ns, not significant). Statistical analysis was performed using an unpaired Student’s t-test for the top bar plots and a paired t-test for the bottom line plots. G) Dose-response analysis of IFN-α2 and STAT2 level in A549 cells. A549 cells were treated with IFN-α2 48 hours before measurement by flow cytometry.

Journal: bioRxiv

Article Title: Disrupting IFIT1-STAT2 viral evasion synergy yields live-attenuated flavivirus with enhanced immune priming

doi: 10.64898/2026.06.04.729841

Figure Lengend Snippet: A) Multi-step replication kinetics of the mutant DENV2 in STAT2-KO and PAF1-KO A549 cells. A549 cells were infected with DENV2 at MOI = 0.1. B) Western-blot analysis of IFIT1 and dengue NS3 expression in wild-type A549 cells during multi-step replication kinetics analysis in A). C) Flow cytometry of DENV2 infection by anti-NS3 in WT and IFIT1-KO A549 cells. D) Volcano plots illustrating the distribution of quantified proteins. The x-axis represents the fold change (LFC), and the y-axis represents the statistical significance as (-value). Proteins with a fold change > 2 and a p-value < 0.01 were considered significantly differentially expressed. Selected ISGs upregulated during DENV infections in WT- and IFIT1-KO A549 are labeled by their gene symbols. Aggregate data of DENV2-E217A and DENV2-S150T+P336G+N730D were used to represent the data of infected cells. E-F) Comparison between the cytokine concentrations (pg/ml) secreted from WT-A549 and those from IFIT1-KO-A549 infected with one of the three viruses, DENV2-WT, -E217A, or S150T+P336G+N730D (MOI = 1) at 1 and 2 dpi. The data points in the top bar plots (E) from each virus were aggregated by cell types. The bottom paired line plots (F) were matched by virus, with the data points in the IFIT1-KO being an average of the measurement from three IFIT1-KO clones. Statistical significance is indicated by brackets above the data sets. Exact values are provided for each comparison (* ; ns, not significant). Statistical analysis was performed using an unpaired Student’s t-test for the top bar plots and a paired t-test for the bottom line plots. G) Dose-response analysis of IFN-α2 and STAT2 level in A549 cells. A549 cells were treated with IFN-α2 48 hours before measurement by flow cytometry.

Techniques: Mutagenesis, Infection, Western Blot, Expressing, Flow Cytometry, Labeling, Comparison, Virus, Clone Assay

Overall workflow of the study. Targeted* genes are ITGAM, PECAM1, CCL5, STAT1, STAT2, and CD44.

Journal: Cancer Medicine

Article Title: Linking Targeted Pancreatic Cancer Genes With Metabolic Disorders: A Cross‐Species Translational Pathway

doi: 10.1002/cam4.71775

Figure Lengend Snippet: Overall workflow of the study. Targeted* genes are ITGAM, PECAM1, CCL5, STAT1, STAT2, and CD44.

Article Snippet: The quality and quantity of RNA were determined by Nanodrop One (Thermofisher); all isolated RNA samples had A260/A280 ratios of 1.8–2.0. mRNA levels of ITGAM, PECAM, CCL5, CXCL10, STAT1, STAT2, and GZMB were determined by RT‐qPCR, relative to the housekeeping gene GAPDH, using the iTaq Universal One‐Step RT‐qPCR Kit (Bio‐Rad) and gene‐specific primers (Thermofisher; assay IDs: ITGAM Hs00167304_m1, PECAM1 Hs01065279_m1, CCL5 Hs00982282_m1, CXCL10 Hs00171042_m1, STAT1 Hs01013996_m1, STAT2 Hs01013115_g1, GZMB Hs00188051_m1).

Techniques:

(A–F): Targeted gene (ITGAM, PECAM1, CCL5, STAT1, STAT2, and CD44) expression plots across different samples showing comparatively higher expression levels in metabolically disordered (obese) mice and humans compared to healthy individuals. Plots with p < 0.05 are only considered. Overlapping jittered points reflect individual sample variability and were retained to preserve consistent visualisation across datasets.

Journal: Cancer Medicine

Article Title: Linking Targeted Pancreatic Cancer Genes With Metabolic Disorders: A Cross‐Species Translational Pathway

doi: 10.1002/cam4.71775

Figure Lengend Snippet: (A–F): Targeted gene (ITGAM, PECAM1, CCL5, STAT1, STAT2, and CD44) expression plots across different samples showing comparatively higher expression levels in metabolically disordered (obese) mice and humans compared to healthy individuals. Plots with p < 0.05 are only considered. Overlapping jittered points reflect individual sample variability and were retained to preserve consistent visualisation across datasets.

Techniques: Expressing, Metabolic Labelling

Violin plots showing the expression levels of genes of interest (ITGAM, PECAM1, CCL5, STAT1, STAT2, and CD44) across different clusters in the human pancreatic tissue, (A) non‐cancerous (control) and (B) cancerous. STAT1, STAT2, and CD44 have shown quite consistent expressions across all clusters. However, genes ITGAM, PECAM1, and CCL5 are highly expressed in clusters 8, 9, and 0 in cancerous compared to noncancerous. Identity signifies Cluster identities on the horizontal axis. Dataset used: GSE212966 .

Journal: Cancer Medicine

Article Title: Linking Targeted Pancreatic Cancer Genes With Metabolic Disorders: A Cross‐Species Translational Pathway

doi: 10.1002/cam4.71775

Figure Lengend Snippet: Violin plots showing the expression levels of genes of interest (ITGAM, PECAM1, CCL5, STAT1, STAT2, and CD44) across different clusters in the human pancreatic tissue, (A) non‐cancerous (control) and (B) cancerous. STAT1, STAT2, and CD44 have shown quite consistent expressions across all clusters. However, genes ITGAM, PECAM1, and CCL5 are highly expressed in clusters 8, 9, and 0 in cancerous compared to noncancerous. Identity signifies Cluster identities on the horizontal axis. Dataset used: GSE212966 .

Techniques: Expressing, Control

$Synovial tissue gene expression profiles in healthy controls and osteoarthritis (OA) patients. Box and whisker plots display ΔCt values (y‐axis; normalised to GAPDH) for (A) ITGAM, (B) PECAM, (C) CCL5, (D) CXCL10, (E) STAT1, (F) STAT2, and (G) GZMB, quantified by qPCR. The x‐axis compares groups: Healthy Controls (synovium from neck‐of‐femur fracture patients), OA Normal‐Weight, and OA Obese. Lower ΔCt reflects higher gene expression. Whiskers span the full data range, boxes represent the IQR (25th–75th percentiles), and the central line marks the mean. Significance thresholds: “*” p < 0.05, “**” p < 0.01, “***” p < 0.001 (One‐way ANOVA with Tukey post hoc test for normally distributed data; Kruskal–Wallis with Dunn's post hoc test for not‐normally distributed data).$

Journal: Cancer Medicine

Article Title: Linking Targeted Pancreatic Cancer Genes With Metabolic Disorders: A Cross‐Species Translational Pathway

doi: 10.1002/cam4.71775

Figure Lengend Snippet: Synovial tissue gene expression profiles in healthy controls and osteoarthritis (OA) patients. Box and whisker plots display ΔCt values (y‐axis; normalised to GAPDH) for (A) ITGAM, (B) PECAM, (C) CCL5, (D) CXCL10, (E) STAT1, (F) STAT2, and (G) GZMB, quantified by qPCR. The x‐axis compares groups: Healthy Controls (synovium from neck‐of‐femur fracture patients), OA Normal‐Weight, and OA Obese. Lower ΔCt reflects higher gene expression. Whiskers span the full data range, boxes represent the IQR (25th–75th percentiles), and the central line marks the mean. Significance thresholds: “*” p < 0.05, “**” p < 0.01, “***” p < 0.001 (One‐way ANOVA with Tukey post hoc test for normally distributed data; Kruskal–Wallis with Dunn's post hoc test for not‐normally distributed data).

Techniques: Gene Expression, Whisker Assay

Adipose tissue gene expression profiles in osteoarthritis (OA) patients stratified by BMI. Box‐and‐whisker plots display ΔCt values (y‐axis; normalised to GAPDH) for qPCR‐measured genes: (A) ITGAM, (B) PECAM, (C) CCL5, (D) CXCL10, (E) STAT1, (F) STAT2, and (G) GZMB. The x‐axis compares the OA Normal‐Weight and OA Obese groups. Lower ΔCt values indicate higher gene expression. Whiskers show the full data range, boxes span the IQR (25th–75th percentiles), and the central line denotes the median. Significance thresholds: p < 0.05, p < 0.01, p < 0.001 ( t ‐tests or Mann–Whitney tests if not normally distributed).

Journal: Cancer Medicine

Article Title: Linking Targeted Pancreatic Cancer Genes With Metabolic Disorders: A Cross‐Species Translational Pathway

doi: 10.1002/cam4.71775

Figure Lengend Snippet: Adipose tissue gene expression profiles in osteoarthritis (OA) patients stratified by BMI. Box‐and‐whisker plots display ΔCt values (y‐axis; normalised to GAPDH) for qPCR‐measured genes: (A) ITGAM, (B) PECAM, (C) CCL5, (D) CXCL10, (E) STAT1, (F) STAT2, and (G) GZMB. The x‐axis compares the OA Normal‐Weight and OA Obese groups. Lower ΔCt values indicate higher gene expression. Whiskers show the full data range, boxes span the IQR (25th–75th percentiles), and the central line denotes the median. Significance thresholds: p < 0.05, p < 0.01, p < 0.001 ( t ‐tests or Mann–Whitney tests if not normally distributed).

Techniques: Gene Expression, Whisker Assay, MANN-WHITNEY

Review

stat2 (Cell Signaling Technology Inc)

Structured Review

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1) Product Images from "Hepatitis delta virus inhibits alpha interferon signaling."

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