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antibodies against cd44  (Bio-Rad)


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    Structured Review

    Bio-Rad antibodies against cd44
    Antibodies Against Cd44, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 93/100, based on 36 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against cd44/product/Bio-Rad
    Average 93 stars, based on 36 article reviews
    antibodies against cd44 - by Bioz Stars, 2026-03
    93/100 stars

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    mRNA-drug interaction network and molecular docking analysis of hub genes with acetaminophen. A-C . mRNA-drugs network of hub genes. D . A molecular docking diagram of <t>Cd44</t> and acetaminophen. E . A molecular docking diagram of tnf and acetaminophen
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    Bio-Rad antibodies against cd44
    mRNA-drug interaction network and molecular docking analysis of hub genes with acetaminophen. A-C . mRNA-drugs network of hub genes. D . A molecular docking diagram of <t>Cd44</t> and acetaminophen. E . A molecular docking diagram of tnf and acetaminophen
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    Proteintech antibodies against cd44
    Histological changes in rats with tendinitis. (A) Injection schedule of PBS, collagenase I and etanercept in Sprague-Dawley rats. (B) H&E and Masson's trichrome staining 2 weeks post-injection of PBS, collagenase I + PBS and collagenase I + etanercept into tendon tissues. Red denotes collagen fibers; blue denotes the collapse of the collagen matrix. (C) Immunostaining for TNF-α on PBS-treated tendon tissue sections revealed negligible staining. Collagenase I-treated tendon tissue sections exhibited substantial positive staining (brown). (D) The percentages of TNF-α positive cells in tendon tissue. (E) SA-β-gal staining reveals little positive staining in PBS and collagenase I + etanercept groups, but substantial staining in collagenase I + PBS tendon tissues. (F) SA-β-gal-positive area (%) of tendon tissues. (G) Co-localization of <t>CD44</t> (green) with p53 (red) in tendon tissues. The nucleus inside the tendon tissues is labeled with DAPI (blue). Scale bar=50, 100, 200 µ m. * P<0.05, *** P<0.001. H&E, hematoxylin and eosin, SA-β-gal, senescence-associated β-galactosidase.
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    Image Search Results


    mRNA-drug interaction network and molecular docking analysis of hub genes with acetaminophen. A-C . mRNA-drugs network of hub genes. D . A molecular docking diagram of Cd44 and acetaminophen. E . A molecular docking diagram of tnf and acetaminophen

    Journal: Journal of Translational Medicine

    Article Title: Integration of angiogenesis and programmed cell death mechanisms unveils potential diagnostic and therapeutic targets in spinal cord injury

    doi: 10.1186/s12967-025-07405-2

    Figure Lengend Snippet: mRNA-drug interaction network and molecular docking analysis of hub genes with acetaminophen. A-C . mRNA-drugs network of hub genes. D . A molecular docking diagram of Cd44 and acetaminophen. E . A molecular docking diagram of tnf and acetaminophen

    Article Snippet: Primary antibodies against Cd44 (Proteintech Group, 1:1000), Icam1 (Proteintech Group, 1:1000), Tnf (Proteintech Group, 1:1000), Cd31 (Proteintech Group, 1:1000), N-Gsdmd (Proteintech Group, 1:2000) were incubated overnight at 4 °C, followed by HRP-conjugated secondary antibodies.

    Techniques:

    Single-cell transcriptomic profiling and hub-gene localization in SCI. A-B . UMAP visualization of single-cell RNA sequencing data, showing 22 transcriptionally distinct clusters further classified into 13 major cell types based on canonical markers. C . Stacked bar plot illustrating the proportions of each cell type in control versus SCI samples. D . Bubble plot displaying cluster-specific marker genes. E . Bubble plot showing expression of hub genes Cd44, Tnf, and Icam1 between control and sci groups, with dot size representing the percentage of cells expressing the gene and color indicating average expression level. F-H . Density plots depicting the distribution of hub genes across the umap space

    Journal: Journal of Translational Medicine

    Article Title: Integration of angiogenesis and programmed cell death mechanisms unveils potential diagnostic and therapeutic targets in spinal cord injury

    doi: 10.1186/s12967-025-07405-2

    Figure Lengend Snippet: Single-cell transcriptomic profiling and hub-gene localization in SCI. A-B . UMAP visualization of single-cell RNA sequencing data, showing 22 transcriptionally distinct clusters further classified into 13 major cell types based on canonical markers. C . Stacked bar plot illustrating the proportions of each cell type in control versus SCI samples. D . Bubble plot displaying cluster-specific marker genes. E . Bubble plot showing expression of hub genes Cd44, Tnf, and Icam1 between control and sci groups, with dot size representing the percentage of cells expressing the gene and color indicating average expression level. F-H . Density plots depicting the distribution of hub genes across the umap space

    Article Snippet: Primary antibodies against Cd44 (Proteintech Group, 1:1000), Icam1 (Proteintech Group, 1:1000), Tnf (Proteintech Group, 1:1000), Cd31 (Proteintech Group, 1:1000), N-Gsdmd (Proteintech Group, 1:2000) were incubated overnight at 4 °C, followed by HRP-conjugated secondary antibodies.

    Techniques: RNA Sequencing, Control, Marker, Expressing

    Mendelian randomization (MR) analysis of hub genes and SCI risk. A . TheMendelianrandomization of CD44 and SCl. B . TheMendelianrandomization of ICAM1 and SCl. C . TheMendelianrandomization of TNF and SCl. Odds ratios (ORs) with 95% confidence intervals are presented, with significant results highlighted in blue. No evidence of horizontal pleiotropy or heterogeneity was detected, supporting causal relationships between hub-gene variants and SCI

    Journal: Journal of Translational Medicine

    Article Title: Integration of angiogenesis and programmed cell death mechanisms unveils potential diagnostic and therapeutic targets in spinal cord injury

    doi: 10.1186/s12967-025-07405-2

    Figure Lengend Snippet: Mendelian randomization (MR) analysis of hub genes and SCI risk. A . TheMendelianrandomization of CD44 and SCl. B . TheMendelianrandomization of ICAM1 and SCl. C . TheMendelianrandomization of TNF and SCl. Odds ratios (ORs) with 95% confidence intervals are presented, with significant results highlighted in blue. No evidence of horizontal pleiotropy or heterogeneity was detected, supporting causal relationships between hub-gene variants and SCI

    Article Snippet: Primary antibodies against Cd44 (Proteintech Group, 1:1000), Icam1 (Proteintech Group, 1:1000), Tnf (Proteintech Group, 1:1000), Cd31 (Proteintech Group, 1:1000), N-Gsdmd (Proteintech Group, 1:2000) were incubated overnight at 4 °C, followed by HRP-conjugated secondary antibodies.

    Techniques:

    Validation of three hub genes at different time points after SCI. ( A–C ) mRNA expression of Cd44 at 1, 3, and 7 days post-SCI and in control group; ( d ) Western blot analysis of Cd44 protein expression and quantification. ( E–G ) mRNA expression of Icam1 at 1, 3, and 7 days post-SCI and in control group; ( H ) Western blot analysis of Icam1 protein expression and quantification. ( I–K ) mRNA expression of Tnf at 1, 3, and 7 days post-SCI and in control group; ( L ) Western blot analysis of Tnf protein expression and quantification. mRNA expression was normalized to GAPDH, and protein levels were normalized to β-actin. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001

    Journal: Journal of Translational Medicine

    Article Title: Integration of angiogenesis and programmed cell death mechanisms unveils potential diagnostic and therapeutic targets in spinal cord injury

    doi: 10.1186/s12967-025-07405-2

    Figure Lengend Snippet: Validation of three hub genes at different time points after SCI. ( A–C ) mRNA expression of Cd44 at 1, 3, and 7 days post-SCI and in control group; ( d ) Western blot analysis of Cd44 protein expression and quantification. ( E–G ) mRNA expression of Icam1 at 1, 3, and 7 days post-SCI and in control group; ( H ) Western blot analysis of Icam1 protein expression and quantification. ( I–K ) mRNA expression of Tnf at 1, 3, and 7 days post-SCI and in control group; ( L ) Western blot analysis of Tnf protein expression and quantification. mRNA expression was normalized to GAPDH, and protein levels were normalized to β-actin. Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001

    Article Snippet: Primary antibodies against Cd44 (Proteintech Group, 1:1000), Icam1 (Proteintech Group, 1:1000), Tnf (Proteintech Group, 1:1000), Cd31 (Proteintech Group, 1:1000), N-Gsdmd (Proteintech Group, 1:2000) were incubated overnight at 4 °C, followed by HRP-conjugated secondary antibodies.

    Techniques: Biomarker Discovery, Expressing, Control, Western Blot

    In vivo validation of acetaminophen treatment in SCI mice. A . Mechanical withdrawal thresholds (MPT) measured at baseline (0 d) and 1, 3, and 7 days after SCI. Acetaminophen significantly increased thresholds at day 7 compared with sci controls. B . Thermal pain thresholds assessed using the tail-flick test. Acetaminophen significantly prolonged latency at day 3 (*** p < 0.001) and remained elevated at day 7 (** p < 0.01). C-E . Western blot analysis and quantification of Cd44 and Tnf expression, showing significant reduction after acetaminophen treatment (* p < 0.05). F-H . Western blot analysis and quantification of Cd31 and N-Gsdmd expression, showing significant difference between groups (* p < 0.05,** p < 0.01). β-actin served as loading control

    Journal: Journal of Translational Medicine

    Article Title: Integration of angiogenesis and programmed cell death mechanisms unveils potential diagnostic and therapeutic targets in spinal cord injury

    doi: 10.1186/s12967-025-07405-2

    Figure Lengend Snippet: In vivo validation of acetaminophen treatment in SCI mice. A . Mechanical withdrawal thresholds (MPT) measured at baseline (0 d) and 1, 3, and 7 days after SCI. Acetaminophen significantly increased thresholds at day 7 compared with sci controls. B . Thermal pain thresholds assessed using the tail-flick test. Acetaminophen significantly prolonged latency at day 3 (*** p < 0.001) and remained elevated at day 7 (** p < 0.01). C-E . Western blot analysis and quantification of Cd44 and Tnf expression, showing significant reduction after acetaminophen treatment (* p < 0.05). F-H . Western blot analysis and quantification of Cd31 and N-Gsdmd expression, showing significant difference between groups (* p < 0.05,** p < 0.01). β-actin served as loading control

    Article Snippet: Primary antibodies against Cd44 (Proteintech Group, 1:1000), Icam1 (Proteintech Group, 1:1000), Tnf (Proteintech Group, 1:1000), Cd31 (Proteintech Group, 1:1000), N-Gsdmd (Proteintech Group, 1:2000) were incubated overnight at 4 °C, followed by HRP-conjugated secondary antibodies.

    Techniques: In Vivo, Biomarker Discovery, Tail Flick Test, Western Blot, Expressing, Control

    Histological changes in rats with tendinitis. (A) Injection schedule of PBS, collagenase I and etanercept in Sprague-Dawley rats. (B) H&E and Masson's trichrome staining 2 weeks post-injection of PBS, collagenase I + PBS and collagenase I + etanercept into tendon tissues. Red denotes collagen fibers; blue denotes the collapse of the collagen matrix. (C) Immunostaining for TNF-α on PBS-treated tendon tissue sections revealed negligible staining. Collagenase I-treated tendon tissue sections exhibited substantial positive staining (brown). (D) The percentages of TNF-α positive cells in tendon tissue. (E) SA-β-gal staining reveals little positive staining in PBS and collagenase I + etanercept groups, but substantial staining in collagenase I + PBS tendon tissues. (F) SA-β-gal-positive area (%) of tendon tissues. (G) Co-localization of CD44 (green) with p53 (red) in tendon tissues. The nucleus inside the tendon tissues is labeled with DAPI (blue). Scale bar=50, 100, 200 µ m. * P<0.05, *** P<0.001. H&E, hematoxylin and eosin, SA-β-gal, senescence-associated β-galactosidase.

    Journal: International Journal of Molecular Medicine

    Article Title: TNF-α induces premature senescence in tendon stem cells via the NF-κB and p53/p21/cyclin E/CDK2 signaling pathways

    doi: 10.3892/ijmm.2025.5581

    Figure Lengend Snippet: Histological changes in rats with tendinitis. (A) Injection schedule of PBS, collagenase I and etanercept in Sprague-Dawley rats. (B) H&E and Masson's trichrome staining 2 weeks post-injection of PBS, collagenase I + PBS and collagenase I + etanercept into tendon tissues. Red denotes collagen fibers; blue denotes the collapse of the collagen matrix. (C) Immunostaining for TNF-α on PBS-treated tendon tissue sections revealed negligible staining. Collagenase I-treated tendon tissue sections exhibited substantial positive staining (brown). (D) The percentages of TNF-α positive cells in tendon tissue. (E) SA-β-gal staining reveals little positive staining in PBS and collagenase I + etanercept groups, but substantial staining in collagenase I + PBS tendon tissues. (F) SA-β-gal-positive area (%) of tendon tissues. (G) Co-localization of CD44 (green) with p53 (red) in tendon tissues. The nucleus inside the tendon tissues is labeled with DAPI (blue). Scale bar=50, 100, 200 µ m. * P<0.05, *** P<0.001. H&E, hematoxylin and eosin, SA-β-gal, senescence-associated β-galactosidase.

    Article Snippet: Sections were incubated overnight at 4°C with primary antibodies against CD44 (cat. no. 15675-1-AP, Proteintech, 1:100) and p53 (cat. no. 60283-2-Ig, Proteintech, 1:100).

    Techniques: Injection, Staining, Immunostaining, Labeling