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fndc5  (Bioss)
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Bioss fndc5
A : Serum GDF-8 levels; B : Serum CRP levels; C : Serum IL-6 levels; D : Serum <t>FNDC5</t> levels; E : Protein band patterns for RUNX2 and OCN; F : Relative expression levels of RUNX2 protein; G : Relative expression levels of OCN protein; Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD ( n = 10 per group). Group abbreviations (LD, MD, HD) are as defined in Table . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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Thermo Fisher gene exp fndc5 hs00401006 m1
A : Serum GDF-8 levels; B : Serum CRP levels; C : Serum IL-6 levels; D : Serum <t>FNDC5</t> levels; E : Protein band patterns for RUNX2 and OCN; F : Relative expression levels of RUNX2 protein; G : Relative expression levels of OCN protein; Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD ( n = 10 per group). Group abbreviations (LD, MD, HD) are as defined in Table . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
Gene Exp Fndc5 Hs00401006 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 89/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Obio Technology Corp Ltd press fndc5
A : Serum GDF-8 levels; B : Serum CRP levels; C : Serum IL-6 levels; D : Serum <t>FNDC5</t> levels; E : Protein band patterns for RUNX2 and OCN; F : Relative expression levels of RUNX2 protein; G : Relative expression levels of OCN protein; Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD ( n = 10 per group). Group abbreviations (LD, MD, HD) are as defined in Table . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
Press Fndc5, supplied by Obio Technology Corp Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Obio Technology Corp Ltd recombinant aav encoding fndc5
Diabetes induces cognitive deficits and decreases hippocampal <t>FNDC5/Irisin</t> expression in rats. ( A , B ) Dynamic changes in body weight and non-fasting blood glucose levels in CON and DM rats over 12 weeks ( n = 12). ( C – E ) Escape latency during MWM training at 4, 8, and 12 weeks ( n = 10 (4w and 8w); n = 12(12w)). ( F ) Average swimming speed during the spatial probe test ( n = 10 (4w and 8w); n = 12(12W)). ( G–I ) probe trial performance: number of platform crossings, latency to first platform crossing, and time spent in the target quadrant ( n = 10 (4w and 8w); n = 12(12W)). ( J ) Representative swimming trajectories on Day 1 and Day 5 of MWM training at different time points. ( K ) Serum Irisin concentrations measured by ELISA at 4, 8, and 12 weeks ( n = 3). ( L , M ) Western blot analysis of hippocampal FNDC5/Irisin expression at 4, 8, and 12 weeks ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant
Recombinant Aav Encoding Fndc5, supplied by Obio Technology Corp Ltd, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Santa Cruz Biotechnology immunoprecipitation
Diabetes induces cognitive deficits and decreases hippocampal <t>FNDC5/Irisin</t> expression in rats. ( A , B ) Dynamic changes in body weight and non-fasting blood glucose levels in CON and DM rats over 12 weeks ( n = 12). ( C – E ) Escape latency during MWM training at 4, 8, and 12 weeks ( n = 10 (4w and 8w); n = 12(12w)). ( F ) Average swimming speed during the spatial probe test ( n = 10 (4w and 8w); n = 12(12W)). ( G–I ) probe trial performance: number of platform crossings, latency to first platform crossing, and time spent in the target quadrant ( n = 10 (4w and 8w); n = 12(12W)). ( J ) Representative swimming trajectories on Day 1 and Day 5 of MWM training at different time points. ( K ) Serum Irisin concentrations measured by ELISA at 4, 8, and 12 weeks ( n = 3). ( L , M ) Western blot analysis of hippocampal FNDC5/Irisin expression at 4, 8, and 12 weeks ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant
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Santa Cruz Biotechnology rabbit anti fndc5 antibody
Diabetes induces cognitive deficits and decreases hippocampal <t>FNDC5/Irisin</t> expression in rats. ( A , B ) Dynamic changes in body weight and non-fasting blood glucose levels in CON and DM rats over 12 weeks ( n = 12). ( C – E ) Escape latency during MWM training at 4, 8, and 12 weeks ( n = 10 (4w and 8w); n = 12(12w)). ( F ) Average swimming speed during the spatial probe test ( n = 10 (4w and 8w); n = 12(12W)). ( G–I ) probe trial performance: number of platform crossings, latency to first platform crossing, and time spent in the target quadrant ( n = 10 (4w and 8w); n = 12(12W)). ( J ) Representative swimming trajectories on Day 1 and Day 5 of MWM training at different time points. ( K ) Serum Irisin concentrations measured by ELISA at 4, 8, and 12 weeks ( n = 3). ( L , M ) Western blot analysis of hippocampal FNDC5/Irisin expression at 4, 8, and 12 weeks ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant
Rabbit Anti Fndc5 Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Mimetics fndc5 knockout
Diabetes induces cognitive deficits and decreases hippocampal <t>FNDC5/Irisin</t> expression in rats. ( A , B ) Dynamic changes in body weight and non-fasting blood glucose levels in CON and DM rats over 12 weeks ( n = 12). ( C – E ) Escape latency during MWM training at 4, 8, and 12 weeks ( n = 10 (4w and 8w); n = 12(12w)). ( F ) Average swimming speed during the spatial probe test ( n = 10 (4w and 8w); n = 12(12W)). ( G–I ) probe trial performance: number of platform crossings, latency to first platform crossing, and time spent in the target quadrant ( n = 10 (4w and 8w); n = 12(12W)). ( J ) Representative swimming trajectories on Day 1 and Day 5 of MWM training at different time points. ( K ) Serum Irisin concentrations measured by ELISA at 4, 8, and 12 weeks ( n = 3). ( L , M ) Western blot analysis of hippocampal FNDC5/Irisin expression at 4, 8, and 12 weeks ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant
Fndc5 Knockout, supplied by Mimetics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech pde2a
Prognostic TMET genes defining TMET subtype phenotypes. (A) Univariate Cox regression analysis of TMET crosstalk genes in CRC. (B) Heatmap of the top 28 prognostically relevant TMET genes with significant differential expression (|logFC| > 0.15). (C,D) KEGG pathway enrichment of C1- and C2-upregulated TMET genes. (E,F) Kaplan–Meier survival curves stratified by CKMT2 and <t>PDE2A</t> expression. (G) PCA plot showing subtype separation driven by CKMT2 and PDE2A expression. (H) ROC curves evaluating the discriminatory performance of CKMT2 and PDE2A.
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Proteintech rabbit anti fndc5
Prognostic TMET genes defining TMET subtype phenotypes. (A) Univariate Cox regression analysis of TMET crosstalk genes in CRC. (B) Heatmap of the top 28 prognostically relevant TMET genes with significant differential expression (|logFC| > 0.15). (C,D) KEGG pathway enrichment of C1- and C2-upregulated TMET genes. (E,F) Kaplan–Meier survival curves stratified by CKMT2 and <t>PDE2A</t> expression. (G) PCA plot showing subtype separation driven by CKMT2 and PDE2A expression. (H) ROC curves evaluating the discriminatory performance of CKMT2 and PDE2A.
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Image Search Results


A : Serum GDF-8 levels; B : Serum CRP levels; C : Serum IL-6 levels; D : Serum FNDC5 levels; E : Protein band patterns for RUNX2 and OCN; F : Relative expression levels of RUNX2 protein; G : Relative expression levels of OCN protein; Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD ( n = 10 per group). Group abbreviations (LD, MD, HD) are as defined in Table . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Journal of Translational Medicine

Article Title: Targeting the PINK1/Parkin-FNDC5 pathway: a novel mechanism of icariin in regulating muscle-bone metabolic coupling in osteosarcopenia

doi: 10.1186/s12967-026-08017-0

Figure Lengend Snippet: A : Serum GDF-8 levels; B : Serum CRP levels; C : Serum IL-6 levels; D : Serum FNDC5 levels; E : Protein band patterns for RUNX2 and OCN; F : Relative expression levels of RUNX2 protein; G : Relative expression levels of OCN protein; Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD ( n = 10 per group). Group abbreviations (LD, MD, HD) are as defined in Table . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: After closing, incubate the membrane with anti-PINK1 (1:1000, Bioss, BS-22173R), Parkin (1:1000, Bioss, BS-23687R), LC3 (1:500, Solarbio, K008014P), p62 (1:1000, Bioss, BS-55207R), FNDC5 (1:1000, Bioss, BS-8486R), Runx2 (1:1000, BS-1134R), OCN (1:500, BS-4917R), Actin (1:20,000, Bioss, BS-10966R) as the internal control.

Techniques: Expressing

A : Western blot detection of mitochondrial autophagy-related protein bands in rat gastrocnemius and soleus muscles; B - D : Gray-scale analysis of PINK1, Parkin, and FNDC5 expression levels. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD ( n = 10 per group). Group abbreviations (LD, MD, HD) are as defined in Table . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Journal of Translational Medicine

Article Title: Targeting the PINK1/Parkin-FNDC5 pathway: a novel mechanism of icariin in regulating muscle-bone metabolic coupling in osteosarcopenia

doi: 10.1186/s12967-026-08017-0

Figure Lengend Snippet: A : Western blot detection of mitochondrial autophagy-related protein bands in rat gastrocnemius and soleus muscles; B - D : Gray-scale analysis of PINK1, Parkin, and FNDC5 expression levels. Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD ( n = 10 per group). Group abbreviations (LD, MD, HD) are as defined in Table . * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: After closing, incubate the membrane with anti-PINK1 (1:1000, Bioss, BS-22173R), Parkin (1:1000, Bioss, BS-23687R), LC3 (1:500, Solarbio, K008014P), p62 (1:1000, Bioss, BS-55207R), FNDC5 (1:1000, Bioss, BS-8486R), Runx2 (1:1000, BS-1134R), OCN (1:500, BS-4917R), Actin (1:20,000, Bioss, BS-10966R) as the internal control.

Techniques: Western Blot, Muscles, Expressing

A : FNDC5 protein band pattern; B : FNDC5 protein expression histogram; C : FNDC5 mRNA expression; D - F : Densitometric quantification of the protein bands shown in (G)༛ G : Western blot images show the protein expression levels of PINK1, Parkin, and FNDC5 in C2C12 myotubes under different treatment conditions༛ Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD. ns (not significant), ** p < 0.01, *** p < 0.001, **** p < 0.0001

Journal: Journal of Translational Medicine

Article Title: Targeting the PINK1/Parkin-FNDC5 pathway: a novel mechanism of icariin in regulating muscle-bone metabolic coupling in osteosarcopenia

doi: 10.1186/s12967-026-08017-0

Figure Lengend Snippet: A : FNDC5 protein band pattern; B : FNDC5 protein expression histogram; C : FNDC5 mRNA expression; D - F : Densitometric quantification of the protein bands shown in (G)༛ G : Western blot images show the protein expression levels of PINK1, Parkin, and FNDC5 in C2C12 myotubes under different treatment conditions༛ Statistical analysis was performed using one-way ANOVA followed by Tukey’s post hoc test. Data are expressed as mean ± SD. ns (not significant), ** p < 0.01, *** p < 0.001, **** p < 0.0001

Article Snippet: After closing, incubate the membrane with anti-PINK1 (1:1000, Bioss, BS-22173R), Parkin (1:1000, Bioss, BS-23687R), LC3 (1:500, Solarbio, K008014P), p62 (1:1000, Bioss, BS-55207R), FNDC5 (1:1000, Bioss, BS-8486R), Runx2 (1:1000, BS-1134R), OCN (1:500, BS-4917R), Actin (1:20,000, Bioss, BS-10966R) as the internal control.

Techniques: Expressing, Western Blot

Forest plots showing FNDC5 and results from different methods. A : Usual walking speed, B : Handgrip strength (left), C : Femoral neck bone mineral density, D : Forearm bone mineral density, E : Lumbar spine bone mineral density, F : Calcaneal bone mineral density

Journal: Journal of Translational Medicine

Article Title: Targeting the PINK1/Parkin-FNDC5 pathway: a novel mechanism of icariin in regulating muscle-bone metabolic coupling in osteosarcopenia

doi: 10.1186/s12967-026-08017-0

Figure Lengend Snippet: Forest plots showing FNDC5 and results from different methods. A : Usual walking speed, B : Handgrip strength (left), C : Femoral neck bone mineral density, D : Forearm bone mineral density, E : Lumbar spine bone mineral density, F : Calcaneal bone mineral density

Article Snippet: After closing, incubate the membrane with anti-PINK1 (1:1000, Bioss, BS-22173R), Parkin (1:1000, Bioss, BS-23687R), LC3 (1:500, Solarbio, K008014P), p62 (1:1000, Bioss, BS-55207R), FNDC5 (1:1000, Bioss, BS-8486R), Runx2 (1:1000, BS-1134R), OCN (1:500, BS-4917R), Actin (1:20,000, Bioss, BS-10966R) as the internal control.

Techniques:

Co-localization analysis of eQTL data at the FNDC5 locus with GWAS data for OS. A : Daily walking speed, B : Handgrip strength (left), C : Femoral neck bone mineral density, D : Forearm bone mineral density, E : Lumbar spine bone mineral density, F : Calcaneal bone mineral density

Journal: Journal of Translational Medicine

Article Title: Targeting the PINK1/Parkin-FNDC5 pathway: a novel mechanism of icariin in regulating muscle-bone metabolic coupling in osteosarcopenia

doi: 10.1186/s12967-026-08017-0

Figure Lengend Snippet: Co-localization analysis of eQTL data at the FNDC5 locus with GWAS data for OS. A : Daily walking speed, B : Handgrip strength (left), C : Femoral neck bone mineral density, D : Forearm bone mineral density, E : Lumbar spine bone mineral density, F : Calcaneal bone mineral density

Article Snippet: After closing, incubate the membrane with anti-PINK1 (1:1000, Bioss, BS-22173R), Parkin (1:1000, Bioss, BS-23687R), LC3 (1:500, Solarbio, K008014P), p62 (1:1000, Bioss, BS-55207R), FNDC5 (1:1000, Bioss, BS-8486R), Runx2 (1:1000, BS-1134R), OCN (1:500, BS-4917R), Actin (1:20,000, Bioss, BS-10966R) as the internal control.

Techniques:

Diabetes induces cognitive deficits and decreases hippocampal FNDC5/Irisin expression in rats. ( A , B ) Dynamic changes in body weight and non-fasting blood glucose levels in CON and DM rats over 12 weeks ( n = 12). ( C – E ) Escape latency during MWM training at 4, 8, and 12 weeks ( n = 10 (4w and 8w); n = 12(12w)). ( F ) Average swimming speed during the spatial probe test ( n = 10 (4w and 8w); n = 12(12W)). ( G–I ) probe trial performance: number of platform crossings, latency to first platform crossing, and time spent in the target quadrant ( n = 10 (4w and 8w); n = 12(12W)). ( J ) Representative swimming trajectories on Day 1 and Day 5 of MWM training at different time points. ( K ) Serum Irisin concentrations measured by ELISA at 4, 8, and 12 weeks ( n = 3). ( L , M ) Western blot analysis of hippocampal FNDC5/Irisin expression at 4, 8, and 12 weeks ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant

Journal: Journal of Translational Medicine

Article Title: FNDC5/irisin ameliorates diabetes-associated cognitive dysfunction via αVβ5-cAMP signaling to regulate oxidative stress, neuroinflammation and synaptic plasticity

doi: 10.1186/s12967-026-08066-5

Figure Lengend Snippet: Diabetes induces cognitive deficits and decreases hippocampal FNDC5/Irisin expression in rats. ( A , B ) Dynamic changes in body weight and non-fasting blood glucose levels in CON and DM rats over 12 weeks ( n = 12). ( C – E ) Escape latency during MWM training at 4, 8, and 12 weeks ( n = 10 (4w and 8w); n = 12(12w)). ( F ) Average swimming speed during the spatial probe test ( n = 10 (4w and 8w); n = 12(12W)). ( G–I ) probe trial performance: number of platform crossings, latency to first platform crossing, and time spent in the target quadrant ( n = 10 (4w and 8w); n = 12(12W)). ( J ) Representative swimming trajectories on Day 1 and Day 5 of MWM training at different time points. ( K ) Serum Irisin concentrations measured by ELISA at 4, 8, and 12 weeks ( n = 3). ( L , M ) Western blot analysis of hippocampal FNDC5/Irisin expression at 4, 8, and 12 weeks ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001; ns, not significant

Article Snippet: Recombinant AAV encoding FNDC5 (rAAV2/PHP.eB-Fndc5, pcAAV-CMV-Fndc5-3xFLAG-P2A-EGFP-WPRE, 1.35E + 13 v.g./ml) or control virus (rAAV2/PHP.eB-con, pcAAV-CMV-EGFP-WPRE, 2.40E + 13 v.g./ml) was purchased from OBIO Technology (Shanghai, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Western Blot

Overexpression of FNDC5/irisin ameliorates cognitive decline and hippocampal pathology. ( A ) Representative immunofluorescence image showing hippocampal AAV-FNDC5 injection. ( B – D ) quantification of FNDC5/Irisin protein expression (Western blot), mRNA expression ( n = 3). ( E ) Serum Irisin levels measured by ELISA ( n = 3). ( F ) Representative swimming trajectories in the MWM probe test on Day 1 and Day 5. ( G ) Escape latency during MWM training trials across groups ( n = 12). ( H – K ) Probe trial performance: number of platform crossings, latency to first platform crossing, time spent in the target quadrant and swimming speed ( n = 12). ( L , M ) Representative HE and Nissl staining images of the cortex and hippocampal subregions (CA1, CA3, DG) in different groups. Scale bar: 100 μm. ( N ) Quantification of Nissl-positive neuronal cells in cortex and hippocampal subregions ( n = 3). ( O – Q ) Western blot analysis of APP, phosphorylated Tau (P-Tau), and total Tau expression in hippocampal tissues ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant

Journal: Journal of Translational Medicine

Article Title: FNDC5/irisin ameliorates diabetes-associated cognitive dysfunction via αVβ5-cAMP signaling to regulate oxidative stress, neuroinflammation and synaptic plasticity

doi: 10.1186/s12967-026-08066-5

Figure Lengend Snippet: Overexpression of FNDC5/irisin ameliorates cognitive decline and hippocampal pathology. ( A ) Representative immunofluorescence image showing hippocampal AAV-FNDC5 injection. ( B – D ) quantification of FNDC5/Irisin protein expression (Western blot), mRNA expression ( n = 3). ( E ) Serum Irisin levels measured by ELISA ( n = 3). ( F ) Representative swimming trajectories in the MWM probe test on Day 1 and Day 5. ( G ) Escape latency during MWM training trials across groups ( n = 12). ( H – K ) Probe trial performance: number of platform crossings, latency to first platform crossing, time spent in the target quadrant and swimming speed ( n = 12). ( L , M ) Representative HE and Nissl staining images of the cortex and hippocampal subregions (CA1, CA3, DG) in different groups. Scale bar: 100 μm. ( N ) Quantification of Nissl-positive neuronal cells in cortex and hippocampal subregions ( n = 3). ( O – Q ) Western blot analysis of APP, phosphorylated Tau (P-Tau), and total Tau expression in hippocampal tissues ( n = 3). Data are expressed as mean ± SD. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant

Article Snippet: Recombinant AAV encoding FNDC5 (rAAV2/PHP.eB-Fndc5, pcAAV-CMV-Fndc5-3xFLAG-P2A-EGFP-WPRE, 1.35E + 13 v.g./ml) or control virus (rAAV2/PHP.eB-con, pcAAV-CMV-EGFP-WPRE, 2.40E + 13 v.g./ml) was purchased from OBIO Technology (Shanghai, China).

Techniques: Over Expression, Immunofluorescence, Injection, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Staining

RNA-seq analysis reveals transcriptional regulation by FNDC5/Irisin in hippocampal tissue. ( A ) Volcano plot of differentially expressed genes (DEGs) in the hippocampus of AAV-NC vs. AAV-FNDC5 rats ( n = 6). ( B ) Top 20 enriched KEGG pathways in DEGs ( n = 6). ( C ) The bubble plot of top 30 GO signaling pathways enriched by DEGs ( n = 6)

Journal: Journal of Translational Medicine

Article Title: FNDC5/irisin ameliorates diabetes-associated cognitive dysfunction via αVβ5-cAMP signaling to regulate oxidative stress, neuroinflammation and synaptic plasticity

doi: 10.1186/s12967-026-08066-5

Figure Lengend Snippet: RNA-seq analysis reveals transcriptional regulation by FNDC5/Irisin in hippocampal tissue. ( A ) Volcano plot of differentially expressed genes (DEGs) in the hippocampus of AAV-NC vs. AAV-FNDC5 rats ( n = 6). ( B ) Top 20 enriched KEGG pathways in DEGs ( n = 6). ( C ) The bubble plot of top 30 GO signaling pathways enriched by DEGs ( n = 6)

Article Snippet: Recombinant AAV encoding FNDC5 (rAAV2/PHP.eB-Fndc5, pcAAV-CMV-Fndc5-3xFLAG-P2A-EGFP-WPRE, 1.35E + 13 v.g./ml) or control virus (rAAV2/PHP.eB-con, pcAAV-CMV-EGFP-WPRE, 2.40E + 13 v.g./ml) was purchased from OBIO Technology (Shanghai, China).

Techniques: RNA Sequencing, Protein-Protein interactions

Metabolomic profiling reveals the effects of FNDC5/irisin overexpression on hippocampal metabolites in diabetic rats. ( A ) Representative total ion current (TIC) chromatograms of hippocampal metabolites from different groups, showing the overall metabolic fingerprinting ( n = 6). ( B ) QC sample correlation plots, demonstrating the stability and reliability of the metabolomic analysis ( n = 5). ( C ) Principal component analysis (PCA) score plot, illustrating the separation of metabolic profiles among CON, DM, AAV-NC, and AAV-FNDC5 groups ( n = 6). ( D ) Volcano plot of differential metabolites between groups, with red dots representing significantly altered metabolites (|log 2 FC| >1, p < 0.05) ( n = 6). ( E ) Hierarchical clustering heatmap of differential metabolites, showing distinct metabolic patterns across groups. Each row represents a metabolite, and each column represents a sample; colors indicate relative metabolite intensities ( n = 6). ( F ) KEGG pathway enrichment analysis of differential metabolites. Pathways related to cAMP signaling, riboflavin metabolism, citrate cycle (TCA cycle), arginine and proline metabolism, and GABAergic synapse (red boxes) are significantly enriched ( n = 6). ( G – L ) violin plots showing the relative abundances of representative metabolites involved in key pathways, including ( G ) riboflavin, ( H ) phosphatidic acid, ( I ) glutamine, ( J ) citric acid, ( K ) arginine, and ( L ) GABA ( n = 6). ( M ) Differential gene-metabolite co-expression network analysis. Data are presented as mean ± SD; ns: not significant, ** p < 0.001

Journal: Journal of Translational Medicine

Article Title: FNDC5/irisin ameliorates diabetes-associated cognitive dysfunction via αVβ5-cAMP signaling to regulate oxidative stress, neuroinflammation and synaptic plasticity

doi: 10.1186/s12967-026-08066-5

Figure Lengend Snippet: Metabolomic profiling reveals the effects of FNDC5/irisin overexpression on hippocampal metabolites in diabetic rats. ( A ) Representative total ion current (TIC) chromatograms of hippocampal metabolites from different groups, showing the overall metabolic fingerprinting ( n = 6). ( B ) QC sample correlation plots, demonstrating the stability and reliability of the metabolomic analysis ( n = 5). ( C ) Principal component analysis (PCA) score plot, illustrating the separation of metabolic profiles among CON, DM, AAV-NC, and AAV-FNDC5 groups ( n = 6). ( D ) Volcano plot of differential metabolites between groups, with red dots representing significantly altered metabolites (|log 2 FC| >1, p < 0.05) ( n = 6). ( E ) Hierarchical clustering heatmap of differential metabolites, showing distinct metabolic patterns across groups. Each row represents a metabolite, and each column represents a sample; colors indicate relative metabolite intensities ( n = 6). ( F ) KEGG pathway enrichment analysis of differential metabolites. Pathways related to cAMP signaling, riboflavin metabolism, citrate cycle (TCA cycle), arginine and proline metabolism, and GABAergic synapse (red boxes) are significantly enriched ( n = 6). ( G – L ) violin plots showing the relative abundances of representative metabolites involved in key pathways, including ( G ) riboflavin, ( H ) phosphatidic acid, ( I ) glutamine, ( J ) citric acid, ( K ) arginine, and ( L ) GABA ( n = 6). ( M ) Differential gene-metabolite co-expression network analysis. Data are presented as mean ± SD; ns: not significant, ** p < 0.001

Article Snippet: Recombinant AAV encoding FNDC5 (rAAV2/PHP.eB-Fndc5, pcAAV-CMV-Fndc5-3xFLAG-P2A-EGFP-WPRE, 1.35E + 13 v.g./ml) or control virus (rAAV2/PHP.eB-con, pcAAV-CMV-EGFP-WPRE, 2.40E + 13 v.g./ml) was purchased from OBIO Technology (Shanghai, China).

Techniques: Metabolomic, Over Expression, Expressing

FNDC5/Irisin colocalizes with neurons, microglia, and astrocytes to regulate inflammatory homeostasi. ( A – D ) Representative immunofluorescence images showing the colocalization of Irisin (red) with neuronal marker NeuN (purple), astrocyte marker GFAP (green), and microglial marker Iba1 (yellow) in the ( A ) cortex, ( B ) hippocampal CA3 region, ( C ) hippocampal CA1 region, and ( D ) hippocampal DG region. Nuclei were counterstained with DAPI (blue). ( n = 3, scale bar = 100 μm). ( E – H ) Quantitative analysis of relative fluorescence intensity for Irisin ( E , G ) and NeuN ( F , H ) in cortical ( E , F ) and hippocampal ( G , H ) subregions (CA1, CA3, DG, cortex) ( n = 3). ( I ) FNDC5/Irisin colocalizes with neurons, microglia, and astrocytes ( n = 3). ( J ) Heatmap showing the expression patterns of pro-inflammatory (red) and anti-inflammatory (blue) factors in different groups, as determined by multiplex assay ( n = 3). ( K – R ) Quantitative analysis of pro-inflammatory factors including ( K ) IL-1β, ( L ) IL-6, ( M ) TNF-α, ( N ) KC/GRO, and anti-inflammatory factors including ( O ) IL-4, ( P ) IL-10, ( Q ) IL-13, ( R ) IL-1β/IL-10 ratio in hippocampal tissues ( n = 3). Data are presented as mean ± SD; ns: not significant, p < 0.05, p < 0.01, ** p < 0.001

Journal: Journal of Translational Medicine

Article Title: FNDC5/irisin ameliorates diabetes-associated cognitive dysfunction via αVβ5-cAMP signaling to regulate oxidative stress, neuroinflammation and synaptic plasticity

doi: 10.1186/s12967-026-08066-5

Figure Lengend Snippet: FNDC5/Irisin colocalizes with neurons, microglia, and astrocytes to regulate inflammatory homeostasi. ( A – D ) Representative immunofluorescence images showing the colocalization of Irisin (red) with neuronal marker NeuN (purple), astrocyte marker GFAP (green), and microglial marker Iba1 (yellow) in the ( A ) cortex, ( B ) hippocampal CA3 region, ( C ) hippocampal CA1 region, and ( D ) hippocampal DG region. Nuclei were counterstained with DAPI (blue). ( n = 3, scale bar = 100 μm). ( E – H ) Quantitative analysis of relative fluorescence intensity for Irisin ( E , G ) and NeuN ( F , H ) in cortical ( E , F ) and hippocampal ( G , H ) subregions (CA1, CA3, DG, cortex) ( n = 3). ( I ) FNDC5/Irisin colocalizes with neurons, microglia, and astrocytes ( n = 3). ( J ) Heatmap showing the expression patterns of pro-inflammatory (red) and anti-inflammatory (blue) factors in different groups, as determined by multiplex assay ( n = 3). ( K – R ) Quantitative analysis of pro-inflammatory factors including ( K ) IL-1β, ( L ) IL-6, ( M ) TNF-α, ( N ) KC/GRO, and anti-inflammatory factors including ( O ) IL-4, ( P ) IL-10, ( Q ) IL-13, ( R ) IL-1β/IL-10 ratio in hippocampal tissues ( n = 3). Data are presented as mean ± SD; ns: not significant, p < 0.05, p < 0.01, ** p < 0.001

Article Snippet: Recombinant AAV encoding FNDC5 (rAAV2/PHP.eB-Fndc5, pcAAV-CMV-Fndc5-3xFLAG-P2A-EGFP-WPRE, 1.35E + 13 v.g./ml) or control virus (rAAV2/PHP.eB-con, pcAAV-CMV-EGFP-WPRE, 2.40E + 13 v.g./ml) was purchased from OBIO Technology (Shanghai, China).

Techniques: Immunofluorescence, Marker, Fluorescence, Expressing, Multiplex Assay

FNDC5/Irisin overexpression improves dendritic complexity and synaptic plasticity in diabetic rats. ( A ) Representative Golgi staining images showing dendritic morphology in hippocampal CA1, CA3 subregions, and COR across CON, DM, AAV-NC, and AAV-FNDC5 groups. ( B – D ) Sholl analysis quantifying dendritic intersections at different radial distances from the soma for ( B ) total dendrites, ( C ) basal dendrites, and ( D ) apical dendrites. Insets show schematic representations of dendritic arborization patterns ( n = 3). ( E – G ) Quantitative analysis of total dendritic length in ( E ) CA1, ( F ) CA3, and ( G ) CDR regions. ( H ) Representative images of synaptic structures in CA1, CA3, and COR regions visualized by Golgi staining. ( n = 3, scale bar: 10 μm). ( I – K ) Quantitative analysis of synaptic density in ( I ) CA1, ( J ) CA3, and ( K ) COR regions ( n = 3). ( L – N ) Quantitative analysis of dendritic spine subtypes including mushroom spines, stubby spines, and thin spines in hippocampal subregions ( n = 3). ( O ) TEM images showing ultrastructural changes of synapses; Red boxes indicate magnified areas of synaptic regions. Scale bar: 2 μm and 500 nm. ( P – T ) Western blot analysis of BDNF, NGF, PSD-95, and SYN in hippocampal tissues ( n = 3). Data are presented as mean ± SD; ns: not significant, p < 0.05, p < 0.01, ** p < 0.001

Journal: Journal of Translational Medicine

Article Title: FNDC5/irisin ameliorates diabetes-associated cognitive dysfunction via αVβ5-cAMP signaling to regulate oxidative stress, neuroinflammation and synaptic plasticity

doi: 10.1186/s12967-026-08066-5

Figure Lengend Snippet: FNDC5/Irisin overexpression improves dendritic complexity and synaptic plasticity in diabetic rats. ( A ) Representative Golgi staining images showing dendritic morphology in hippocampal CA1, CA3 subregions, and COR across CON, DM, AAV-NC, and AAV-FNDC5 groups. ( B – D ) Sholl analysis quantifying dendritic intersections at different radial distances from the soma for ( B ) total dendrites, ( C ) basal dendrites, and ( D ) apical dendrites. Insets show schematic representations of dendritic arborization patterns ( n = 3). ( E – G ) Quantitative analysis of total dendritic length in ( E ) CA1, ( F ) CA3, and ( G ) CDR regions. ( H ) Representative images of synaptic structures in CA1, CA3, and COR regions visualized by Golgi staining. ( n = 3, scale bar: 10 μm). ( I – K ) Quantitative analysis of synaptic density in ( I ) CA1, ( J ) CA3, and ( K ) COR regions ( n = 3). ( L – N ) Quantitative analysis of dendritic spine subtypes including mushroom spines, stubby spines, and thin spines in hippocampal subregions ( n = 3). ( O ) TEM images showing ultrastructural changes of synapses; Red boxes indicate magnified areas of synaptic regions. Scale bar: 2 μm and 500 nm. ( P – T ) Western blot analysis of BDNF, NGF, PSD-95, and SYN in hippocampal tissues ( n = 3). Data are presented as mean ± SD; ns: not significant, p < 0.05, p < 0.01, ** p < 0.001

Article Snippet: Recombinant AAV encoding FNDC5 (rAAV2/PHP.eB-Fndc5, pcAAV-CMV-Fndc5-3xFLAG-P2A-EGFP-WPRE, 1.35E + 13 v.g./ml) or control virus (rAAV2/PHP.eB-con, pcAAV-CMV-EGFP-WPRE, 2.40E + 13 v.g./ml) was purchased from OBIO Technology (Shanghai, China).

Techniques: Over Expression, Staining, Western Blot

FNDC5/Irisin activates the PKA-CREB signaling pathway via the integrin αVβ5 receptor to regulate synaptic plasticity. ( A – C ) Western blot analysis of phosphorylated PKA (P-PKA), total PKA, phosphorylated CREB (P-CREB), and total CREB in hippocampal tissues from CON, DM, AAV-NC, and AAV-FNDC5 groups ( n = 3). ( D – H ) Western blot analysis of P-PKA, total PKA, P-CREB, total CREB, PSD-95, and SYN in SY5Y cells under different treatments ( n = 3). ( I – K ) Western blot analysis of P-PKA, total PKA, P-CREB, and total CREB in SY5Y cells treated with cilengitide trifluoroacetate (avβ5 inhibitor) ( n = 3). Data are presented as mean ± SD; ns: not significant, p < 0.05, p < 0.01, ** p < 0.001, * p < 0.0001

Journal: Journal of Translational Medicine

Article Title: FNDC5/irisin ameliorates diabetes-associated cognitive dysfunction via αVβ5-cAMP signaling to regulate oxidative stress, neuroinflammation and synaptic plasticity

doi: 10.1186/s12967-026-08066-5

Figure Lengend Snippet: FNDC5/Irisin activates the PKA-CREB signaling pathway via the integrin αVβ5 receptor to regulate synaptic plasticity. ( A – C ) Western blot analysis of phosphorylated PKA (P-PKA), total PKA, phosphorylated CREB (P-CREB), and total CREB in hippocampal tissues from CON, DM, AAV-NC, and AAV-FNDC5 groups ( n = 3). ( D – H ) Western blot analysis of P-PKA, total PKA, P-CREB, total CREB, PSD-95, and SYN in SY5Y cells under different treatments ( n = 3). ( I – K ) Western blot analysis of P-PKA, total PKA, P-CREB, and total CREB in SY5Y cells treated with cilengitide trifluoroacetate (avβ5 inhibitor) ( n = 3). Data are presented as mean ± SD; ns: not significant, p < 0.05, p < 0.01, ** p < 0.001, * p < 0.0001

Article Snippet: Recombinant AAV encoding FNDC5 (rAAV2/PHP.eB-Fndc5, pcAAV-CMV-Fndc5-3xFLAG-P2A-EGFP-WPRE, 1.35E + 13 v.g./ml) or control virus (rAAV2/PHP.eB-con, pcAAV-CMV-EGFP-WPRE, 2.40E + 13 v.g./ml) was purchased from OBIO Technology (Shanghai, China).

Techniques: Western Blot

Prognostic TMET genes defining TMET subtype phenotypes. (A) Univariate Cox regression analysis of TMET crosstalk genes in CRC. (B) Heatmap of the top 28 prognostically relevant TMET genes with significant differential expression (|logFC| > 0.15). (C,D) KEGG pathway enrichment of C1- and C2-upregulated TMET genes. (E,F) Kaplan–Meier survival curves stratified by CKMT2 and PDE2A expression. (G) PCA plot showing subtype separation driven by CKMT2 and PDE2A expression. (H) ROC curves evaluating the discriminatory performance of CKMT2 and PDE2A.

Journal: Frontiers in Pharmacology

Article Title: Metabolic profiling of the TME uncovers the contrasting impacts of CKMT2 and PDE2A in CRC progression and therapeutic response

doi: 10.3389/fphar.2026.1732137

Figure Lengend Snippet: Prognostic TMET genes defining TMET subtype phenotypes. (A) Univariate Cox regression analysis of TMET crosstalk genes in CRC. (B) Heatmap of the top 28 prognostically relevant TMET genes with significant differential expression (|logFC| > 0.15). (C,D) KEGG pathway enrichment of C1- and C2-upregulated TMET genes. (E,F) Kaplan–Meier survival curves stratified by CKMT2 and PDE2A expression. (G) PCA plot showing subtype separation driven by CKMT2 and PDE2A expression. (H) ROC curves evaluating the discriminatory performance of CKMT2 and PDE2A.

Article Snippet: Membranes were blocked with 5% bovine serum albumin (BSA) in TBST buffer and incubated overnight at 4 °C with a primary antibody against CKMT2 (Proteintech, #23995-1-AP, Rabbit, 1:1,000) and PDE2A (Proteintech, #55306-1-AP,Rabbit, 1:1,000).

Techniques: Quantitative Proteomics, Expressing

Single-cell resolution of TMET gene expression. (A,B) t-SNE plots showing major cell populations in CRC single-cell datasets EMTAB8107 and GSE166555 . (C,D) Distribution of malignant, immune, and stromal lineages across datasets. (E–H) Expression patterns of C1- and C2-associated TMET genes in EMTAB8107. (I–L) Corresponding expression patterns in GSE166555 . (M–P) Dot plots showing TMET gene expression across cell types. (Q–T) t-SNE plots illustrating PDE2A and CKMT2 expression in both datasets. C1: high-risk; C2: low-risk.

Journal: Frontiers in Pharmacology

Article Title: Metabolic profiling of the TME uncovers the contrasting impacts of CKMT2 and PDE2A in CRC progression and therapeutic response

doi: 10.3389/fphar.2026.1732137

Figure Lengend Snippet: Single-cell resolution of TMET gene expression. (A,B) t-SNE plots showing major cell populations in CRC single-cell datasets EMTAB8107 and GSE166555 . (C,D) Distribution of malignant, immune, and stromal lineages across datasets. (E–H) Expression patterns of C1- and C2-associated TMET genes in EMTAB8107. (I–L) Corresponding expression patterns in GSE166555 . (M–P) Dot plots showing TMET gene expression across cell types. (Q–T) t-SNE plots illustrating PDE2A and CKMT2 expression in both datasets. C1: high-risk; C2: low-risk.

Article Snippet: Membranes were blocked with 5% bovine serum albumin (BSA) in TBST buffer and incubated overnight at 4 °C with a primary antibody against CKMT2 (Proteintech, #23995-1-AP, Rabbit, 1:1,000) and PDE2A (Proteintech, #55306-1-AP,Rabbit, 1:1,000).

Techniques: Single Cell, Gene Expression, Expressing

Risk stratification based on PDE2A and CKMT2. (A,B) Risk stratification of CRC patients using LASSO regression based on PDE2A and CKMT2 expression. (C) Bar plot illustrating the distribution of CRC patients according to risk scores derived from PDE2A and CKMT2. (D) Kaplan-Meier survival curve comparing overall survival (OS) between risk subgroups. (E) Sankey diagram mapping the distribution of CRC patients across molecular clusters, risk subgroups, PDE2A and CKMT2 expression levels, and vital status. (F) PCA plot visualizing the dimensional separation of risk subgroups. (G) PCA plot depicting the segregation of gene-based subgroups. (H) Heatmap displaying PDE2A and CKMT2 expression across risk subgroups and their associations with clinical and molecular features. (I–L) Bar plots showing the distribution of gene-based subtypes across cancer stages and molecular classifications, including MSI, CMS, and CIMP status.

Journal: Frontiers in Pharmacology

Article Title: Metabolic profiling of the TME uncovers the contrasting impacts of CKMT2 and PDE2A in CRC progression and therapeutic response

doi: 10.3389/fphar.2026.1732137

Figure Lengend Snippet: Risk stratification based on PDE2A and CKMT2. (A,B) Risk stratification of CRC patients using LASSO regression based on PDE2A and CKMT2 expression. (C) Bar plot illustrating the distribution of CRC patients according to risk scores derived from PDE2A and CKMT2. (D) Kaplan-Meier survival curve comparing overall survival (OS) between risk subgroups. (E) Sankey diagram mapping the distribution of CRC patients across molecular clusters, risk subgroups, PDE2A and CKMT2 expression levels, and vital status. (F) PCA plot visualizing the dimensional separation of risk subgroups. (G) PCA plot depicting the segregation of gene-based subgroups. (H) Heatmap displaying PDE2A and CKMT2 expression across risk subgroups and their associations with clinical and molecular features. (I–L) Bar plots showing the distribution of gene-based subtypes across cancer stages and molecular classifications, including MSI, CMS, and CIMP status.

Article Snippet: Membranes were blocked with 5% bovine serum albumin (BSA) in TBST buffer and incubated overnight at 4 °C with a primary antibody against CKMT2 (Proteintech, #23995-1-AP, Rabbit, 1:1,000) and PDE2A (Proteintech, #55306-1-AP,Rabbit, 1:1,000).

Techniques: Expressing, Derivative Assay

Validation of PDE2A and CKMT2 in colorectal cancer. (A,C) GEPIA-based comparison of CKMT2 and PDE2A mRNA expression in normal and CRC tissues. (B,D) qPCR validation in FHC, SW480, and HCT116 cell lines. (E–H) Western blot analysis and quantification of CKMT2 and PDE2A protein expression. (I,J) Representative IHC images and quantitative comparison in CRC and adjacent normal tissues (n = 63). (K) Heatmap of protein expression in relation to clinicopathological features. (L,M) Representative IHC images and Pearson correlation analysis showing inverse expression of CKMT2 and PDE2A.

Journal: Frontiers in Pharmacology

Article Title: Metabolic profiling of the TME uncovers the contrasting impacts of CKMT2 and PDE2A in CRC progression and therapeutic response

doi: 10.3389/fphar.2026.1732137

Figure Lengend Snippet: Validation of PDE2A and CKMT2 in colorectal cancer. (A,C) GEPIA-based comparison of CKMT2 and PDE2A mRNA expression in normal and CRC tissues. (B,D) qPCR validation in FHC, SW480, and HCT116 cell lines. (E–H) Western blot analysis and quantification of CKMT2 and PDE2A protein expression. (I,J) Representative IHC images and quantitative comparison in CRC and adjacent normal tissues (n = 63). (K) Heatmap of protein expression in relation to clinicopathological features. (L,M) Representative IHC images and Pearson correlation analysis showing inverse expression of CKMT2 and PDE2A.

Article Snippet: Membranes were blocked with 5% bovine serum albumin (BSA) in TBST buffer and incubated overnight at 4 °C with a primary antibody against CKMT2 (Proteintech, #23995-1-AP, Rabbit, 1:1,000) and PDE2A (Proteintech, #55306-1-AP,Rabbit, 1:1,000).

Techniques: Biomarker Discovery, Comparison, Expressing, Western Blot

External validation of the prognostic impact of PDE2A and CKMT2. (A,B) Kaplan-Meier survival curves illustrating differences in recurrence-free survival (RFS, n = 1,336) and overall survival (OS, n = 1,061) between CRC patients with high and low PDE2A expression. (C,D) Kaplan-Meier survival curves depicting differences in recurrence-free survival (RFS, n = 1,336) and overall survival (OS, n = 1,061) between CRC patients with high and low CKMT2 expression.

Journal: Frontiers in Pharmacology

Article Title: Metabolic profiling of the TME uncovers the contrasting impacts of CKMT2 and PDE2A in CRC progression and therapeutic response

doi: 10.3389/fphar.2026.1732137

Figure Lengend Snippet: External validation of the prognostic impact of PDE2A and CKMT2. (A,B) Kaplan-Meier survival curves illustrating differences in recurrence-free survival (RFS, n = 1,336) and overall survival (OS, n = 1,061) between CRC patients with high and low PDE2A expression. (C,D) Kaplan-Meier survival curves depicting differences in recurrence-free survival (RFS, n = 1,336) and overall survival (OS, n = 1,061) between CRC patients with high and low CKMT2 expression.

Article Snippet: Membranes were blocked with 5% bovine serum albumin (BSA) in TBST buffer and incubated overnight at 4 °C with a primary antibody against CKMT2 (Proteintech, #23995-1-AP, Rabbit, 1:1,000) and PDE2A (Proteintech, #55306-1-AP,Rabbit, 1:1,000).

Techniques: Biomarker Discovery, Expressing

Impact of PDE2A and CKMT2 on immunotherapy response. (A,B) Kaplan-Meier survival curves showing overall survival (OS, n = 1,061) differences between patients with high and low PDE2A and CKMT2 expression. (C,D) Box plot and ROC curves comparing PDE2A expression between immunotherapy responders (n = 355) and non-responders (n = 570). (E,F) Box plot and ROC curves comparing CKMT2 expression between immunotherapy responders (n = 355) and non-responders (n = 570).

Journal: Frontiers in Pharmacology

Article Title: Metabolic profiling of the TME uncovers the contrasting impacts of CKMT2 and PDE2A in CRC progression and therapeutic response

doi: 10.3389/fphar.2026.1732137

Figure Lengend Snippet: Impact of PDE2A and CKMT2 on immunotherapy response. (A,B) Kaplan-Meier survival curves showing overall survival (OS, n = 1,061) differences between patients with high and low PDE2A and CKMT2 expression. (C,D) Box plot and ROC curves comparing PDE2A expression between immunotherapy responders (n = 355) and non-responders (n = 570). (E,F) Box plot and ROC curves comparing CKMT2 expression between immunotherapy responders (n = 355) and non-responders (n = 570).

Article Snippet: Membranes were blocked with 5% bovine serum albumin (BSA) in TBST buffer and incubated overnight at 4 °C with a primary antibody against CKMT2 (Proteintech, #23995-1-AP, Rabbit, 1:1,000) and PDE2A (Proteintech, #55306-1-AP,Rabbit, 1:1,000).

Techniques: Expressing