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human cd44s pan specific antibody  (Bio-Techne corporation)


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    Bio-Techne corporation human cd44s pan specific antibody
    Human Cd44s Pan Specific Antibody, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 97/100, based on 83 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human cd44s pan specific antibody/product/Bio-Techne corporation
    Average 97 stars, based on 83 article reviews
    human cd44s pan specific antibody - by Bioz Stars, 2026-05
    97/100 stars

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    (a) Volcano plot representing significant genes (Log2FC ± 2 and p-value<0.05) identified in anti-miR-1307-5p vs SC from a total of 16211 genes. Red dots indicate significantly upregulated genes, blue dots indicate significantly downregulated genes, and grey dots represent non-significant genes (based on thresholds). (b) Ingenuity Pathway Analysis (IPA) network of significantly altered genes, with key hub genes highlighted in green (bold) indicate their central role in regulatory signaling. (c) Expression levels (Log2FC) of genes regulating the proliferation, cell-cycle progression, apoptosis resistance, EMT and angiogenesis regulators including E-CAD, N-CAD, VIM, VEGF-A, <t>CD44,</t> AKT, YAP1 and PI3K following miR-1307-5p inhibition. Expression levels were normalised against β-actin values, and relative quantification was performed using the ΔΔCt method. (d) Bar plot illustrating the log2 fold change (Log2FC) of selected genes (CCN2, SNAI1, and TGFB1) in the SC and anti-miR-1307-5p-treated cohort, along with their concordance with the TCGA HNSCC dataset. (e) Schematic representation of the proposed molecular mechanism. miR-1307-5p knockdown modulates key signaling pathways including TGF-β, AKT, YAP1 and MEK/ERK, leading to regulation of EMT/CSC traits, proliferation, angiogenesis, and apoptosis. This ultimately contributes to reversal of chemoresistance. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001).
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    (a) Volcano plot representing significant genes (Log2FC ± 2 and p-value<0.05) identified in anti-miR-1307-5p vs SC from a total of 16211 genes. Red dots indicate significantly upregulated genes, blue dots indicate significantly downregulated genes, and grey dots represent non-significant genes (based on thresholds). (b) Ingenuity Pathway Analysis (IPA) network of significantly altered genes, with key hub genes highlighted in green (bold) indicate their central role in regulatory signaling. (c) Expression levels (Log2FC) of genes regulating the proliferation, cell-cycle progression, apoptosis resistance, EMT and angiogenesis regulators including E-CAD, N-CAD, VIM, VEGF-A, <t>CD44,</t> AKT, YAP1 and PI3K following miR-1307-5p inhibition. Expression levels were normalised against β-actin values, and relative quantification was performed using the ΔΔCt method. (d) Bar plot illustrating the log2 fold change (Log2FC) of selected genes (CCN2, SNAI1, and TGFB1) in the SC and anti-miR-1307-5p-treated cohort, along with their concordance with the TCGA HNSCC dataset. (e) Schematic representation of the proposed molecular mechanism. miR-1307-5p knockdown modulates key signaling pathways including TGF-β, AKT, YAP1 and MEK/ERK, leading to regulation of EMT/CSC traits, proliferation, angiogenesis, and apoptosis. This ultimately contributes to reversal of chemoresistance. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001).
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    (a) Volcano plot representing significant genes (Log2FC ± 2 and p-value<0.05) identified in anti-miR-1307-5p vs SC from a total of 16211 genes. Red dots indicate significantly upregulated genes, blue dots indicate significantly downregulated genes, and grey dots represent non-significant genes (based on thresholds). (b) Ingenuity Pathway Analysis (IPA) network of significantly altered genes, with key hub genes highlighted in green (bold) indicate their central role in regulatory signaling. (c) Expression levels (Log2FC) of genes regulating the proliferation, cell-cycle progression, apoptosis resistance, EMT and angiogenesis regulators including E-CAD, N-CAD, VIM, VEGF-A, <t>CD44,</t> AKT, YAP1 and PI3K following miR-1307-5p inhibition. Expression levels were normalised against β-actin values, and relative quantification was performed using the ΔΔCt method. (d) Bar plot illustrating the log2 fold change (Log2FC) of selected genes (CCN2, SNAI1, and TGFB1) in the SC and anti-miR-1307-5p-treated cohort, along with their concordance with the TCGA HNSCC dataset. (e) Schematic representation of the proposed molecular mechanism. miR-1307-5p knockdown modulates key signaling pathways including TGF-β, AKT, YAP1 and MEK/ERK, leading to regulation of EMT/CSC traits, proliferation, angiogenesis, and apoptosis. This ultimately contributes to reversal of chemoresistance. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001).
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    (a) Volcano plot representing significant genes (Log2FC ± 2 and p-value<0.05) identified in anti-miR-1307-5p vs SC from a total of 16211 genes. Red dots indicate significantly upregulated genes, blue dots indicate significantly downregulated genes, and grey dots represent non-significant genes (based on thresholds). (b) Ingenuity Pathway Analysis (IPA) network of significantly altered genes, with key hub genes highlighted in green (bold) indicate their central role in regulatory signaling. (c) Expression levels (Log2FC) of genes regulating the proliferation, cell-cycle progression, apoptosis resistance, EMT and angiogenesis regulators including E-CAD, N-CAD, VIM, VEGF-A, <t>CD44,</t> AKT, YAP1 and PI3K following miR-1307-5p inhibition. Expression levels were normalised against β-actin values, and relative quantification was performed using the ΔΔCt method. (d) Bar plot illustrating the log2 fold change (Log2FC) of selected genes (CCN2, SNAI1, and TGFB1) in the SC and anti-miR-1307-5p-treated cohort, along with their concordance with the TCGA HNSCC dataset. (e) Schematic representation of the proposed molecular mechanism. miR-1307-5p knockdown modulates key signaling pathways including TGF-β, AKT, YAP1 and MEK/ERK, leading to regulation of EMT/CSC traits, proliferation, angiogenesis, and apoptosis. This ultimately contributes to reversal of chemoresistance. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001).
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    (a) Volcano plot representing significant genes (Log2FC ± 2 and p-value<0.05) identified in anti-miR-1307-5p vs SC from a total of 16211 genes. Red dots indicate significantly upregulated genes, blue dots indicate significantly downregulated genes, and grey dots represent non-significant genes (based on thresholds). (b) Ingenuity Pathway Analysis (IPA) network of significantly altered genes, with key hub genes highlighted in green (bold) indicate their central role in regulatory signaling. (c) Expression levels (Log2FC) of genes regulating the proliferation, cell-cycle progression, apoptosis resistance, EMT and angiogenesis regulators including E-CAD, N-CAD, VIM, VEGF-A, <t>CD44,</t> AKT, YAP1 and PI3K following miR-1307-5p inhibition. Expression levels were normalised against β-actin values, and relative quantification was performed using the ΔΔCt method. (d) Bar plot illustrating the log2 fold change (Log2FC) of selected genes (CCN2, SNAI1, and TGFB1) in the SC and anti-miR-1307-5p-treated cohort, along with their concordance with the TCGA HNSCC dataset. (e) Schematic representation of the proposed molecular mechanism. miR-1307-5p knockdown modulates key signaling pathways including TGF-β, AKT, YAP1 and MEK/ERK, leading to regulation of EMT/CSC traits, proliferation, angiogenesis, and apoptosis. This ultimately contributes to reversal of chemoresistance. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001).
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    Image Search Results


    (a) Volcano plot representing significant genes (Log2FC ± 2 and p-value<0.05) identified in anti-miR-1307-5p vs SC from a total of 16211 genes. Red dots indicate significantly upregulated genes, blue dots indicate significantly downregulated genes, and grey dots represent non-significant genes (based on thresholds). (b) Ingenuity Pathway Analysis (IPA) network of significantly altered genes, with key hub genes highlighted in green (bold) indicate their central role in regulatory signaling. (c) Expression levels (Log2FC) of genes regulating the proliferation, cell-cycle progression, apoptosis resistance, EMT and angiogenesis regulators including E-CAD, N-CAD, VIM, VEGF-A, CD44, AKT, YAP1 and PI3K following miR-1307-5p inhibition. Expression levels were normalised against β-actin values, and relative quantification was performed using the ΔΔCt method. (d) Bar plot illustrating the log2 fold change (Log2FC) of selected genes (CCN2, SNAI1, and TGFB1) in the SC and anti-miR-1307-5p-treated cohort, along with their concordance with the TCGA HNSCC dataset. (e) Schematic representation of the proposed molecular mechanism. miR-1307-5p knockdown modulates key signaling pathways including TGF-β, AKT, YAP1 and MEK/ERK, leading to regulation of EMT/CSC traits, proliferation, angiogenesis, and apoptosis. This ultimately contributes to reversal of chemoresistance. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001).

    Journal: bioRxiv

    Article Title: Inhibition of miR-1307 Reverses Resistance to Cisplatin in Drug-Resistant Oral Squamous Cell Carcinoma

    doi: 10.64898/2026.04.06.709730

    Figure Lengend Snippet: (a) Volcano plot representing significant genes (Log2FC ± 2 and p-value<0.05) identified in anti-miR-1307-5p vs SC from a total of 16211 genes. Red dots indicate significantly upregulated genes, blue dots indicate significantly downregulated genes, and grey dots represent non-significant genes (based on thresholds). (b) Ingenuity Pathway Analysis (IPA) network of significantly altered genes, with key hub genes highlighted in green (bold) indicate their central role in regulatory signaling. (c) Expression levels (Log2FC) of genes regulating the proliferation, cell-cycle progression, apoptosis resistance, EMT and angiogenesis regulators including E-CAD, N-CAD, VIM, VEGF-A, CD44, AKT, YAP1 and PI3K following miR-1307-5p inhibition. Expression levels were normalised against β-actin values, and relative quantification was performed using the ΔΔCt method. (d) Bar plot illustrating the log2 fold change (Log2FC) of selected genes (CCN2, SNAI1, and TGFB1) in the SC and anti-miR-1307-5p-treated cohort, along with their concordance with the TCGA HNSCC dataset. (e) Schematic representation of the proposed molecular mechanism. miR-1307-5p knockdown modulates key signaling pathways including TGF-β, AKT, YAP1 and MEK/ERK, leading to regulation of EMT/CSC traits, proliferation, angiogenesis, and apoptosis. This ultimately contributes to reversal of chemoresistance. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001).

    Article Snippet: The cells were stained, were suspended in 1 ml 1X PBS and stained with 5 μl of PE anti-human CD44 antibody (Miltenyi Biotec, USA) for 20 minutes in dark, washed with 1X PBS and resuspended in 100 μl 1X PBS.

    Techniques: Expressing, Inhibition, Quantitative Proteomics, Knockdown, Protein-Protein interactions

    (a) Representative images of the tumour morphology following treatment with sh-control, sh-control+Cis, sh-miR-1307-5p, and sh-miR-1307-5p+Cis. Tumours in the sh-miR-1307-5p and sh-miR-1307-5p+Cis-treated mice exhibit a visible reduction in size compared to SC and SC+Cis, respectively. H&E-stained tumour sections reveal decreased cell density, nuclear alterations, and disrupted tumour architecture, indicating reduced malignancy in the tumors of sh-miR-1307-5p and sh-miR-1307-5p+Cis as compared to sh-control, sh-control+Cis. (b) Tumour volume measurements demonstrate a significant reduction in sh-miR-1307 and sh-miR-1307+Cis groups compared to sh-control and sh-control+Cis. (c) Quantification of IHC staining for CD44, α-SMA and VIM expression (percentage of positive stained marker area) shows a marked decrease of CD44, α-SMA and VIM expression in treated groups, indicating suppression of CD44+ cancer stem cell populations. (d) IHC staining for CD44, α-SMA and VIM (brown) demonstrates a significant reduction in the expression in sh-miR-1307-5p and sh-miR-1307-5p+Cis-treated tumours. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001). sh-control-Scramble-control, Cis-Cisplatin.

    Journal: bioRxiv

    Article Title: Inhibition of miR-1307 Reverses Resistance to Cisplatin in Drug-Resistant Oral Squamous Cell Carcinoma

    doi: 10.64898/2026.04.06.709730

    Figure Lengend Snippet: (a) Representative images of the tumour morphology following treatment with sh-control, sh-control+Cis, sh-miR-1307-5p, and sh-miR-1307-5p+Cis. Tumours in the sh-miR-1307-5p and sh-miR-1307-5p+Cis-treated mice exhibit a visible reduction in size compared to SC and SC+Cis, respectively. H&E-stained tumour sections reveal decreased cell density, nuclear alterations, and disrupted tumour architecture, indicating reduced malignancy in the tumors of sh-miR-1307-5p and sh-miR-1307-5p+Cis as compared to sh-control, sh-control+Cis. (b) Tumour volume measurements demonstrate a significant reduction in sh-miR-1307 and sh-miR-1307+Cis groups compared to sh-control and sh-control+Cis. (c) Quantification of IHC staining for CD44, α-SMA and VIM expression (percentage of positive stained marker area) shows a marked decrease of CD44, α-SMA and VIM expression in treated groups, indicating suppression of CD44+ cancer stem cell populations. (d) IHC staining for CD44, α-SMA and VIM (brown) demonstrates a significant reduction in the expression in sh-miR-1307-5p and sh-miR-1307-5p+Cis-treated tumours. Error bars represent mean ± SD of three independent experiments. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001). sh-control-Scramble-control, Cis-Cisplatin.

    Article Snippet: The cells were stained, were suspended in 1 ml 1X PBS and stained with 5 μl of PE anti-human CD44 antibody (Miltenyi Biotec, USA) for 20 minutes in dark, washed with 1X PBS and resuspended in 100 μl 1X PBS.

    Techniques: Control, Staining, Immunohistochemistry, Expressing, Marker

    (a) MTT assay showing reduced proliferation of CD44+ cells following treatment with anti-miR-1307-5p EVs. Y-axis: %proliferation of CD44+ cells, X-axis: concentration (nM). (b) Bar graph quantifying flow cytometry results, demonstrating a significant change in G0/G1 and G2/M phases in anti-miR-1307-5p EVs treated cells as compared to SC EVs (c) Flow cytometry scatter plot for Annexin-V/PI stained CD44+ cells after co-culture with anti-miR-1307-5p EVs as compared to SC EVs with anti-miR-1307-5p EVs showing a significant increase of early apoptotic population (Annexin V+/PI−) for treated cells (d) Microscopic images showing the decrease in migratory ability of CD44+ cells when treated with anti-miR-1307 EVs as compared to SC EVs (scale: 10µM) (e) Confocal images illustrating reduction in the invasive potential of CD44+ spheroids treated with anti-miR-1307-5p EVs compared to SC EVs. Spheroids were stained with phalloidin (green) and DAPI (blue); imaged at 10X magnification. (f) Representative images showing reduced angiogenic potential of HUVECs when co-cultured with anti-miR-1307-5p EVs as compared to SC EVs (g) CAM Images showing disrupted vascular development after anti-miR-1307 EVs treatment. (h) Bar-graph depicting reduction in tumour volume for sh-miR-1307 EVs+Cis treated mice as compared to SC EVs+Cis. (i) NOD-SCID xenograft mice model depicting a decrease in the tumour size when injected with sh-miR-1307 EVs+Cis in the buccal cavity region as compared to SC EVs+Cis. H&E staining of tumour sections shows reduced tumour cell density, altered nuclear morphology, and increased necrosis in sh-miR-1307 EVs+Cis treated mice. The data was normalised to controls, experiments were performed in triplicate and error bars represent mean ± SD. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001). HUVECs: Human Large Vessel Endothelial Cells, CAM: chick chorioallantoic membrane model, sh-control- Scramble-control, Cis- Cisplatin.

    Journal: bioRxiv

    Article Title: Inhibition of miR-1307 Reverses Resistance to Cisplatin in Drug-Resistant Oral Squamous Cell Carcinoma

    doi: 10.64898/2026.04.06.709730

    Figure Lengend Snippet: (a) MTT assay showing reduced proliferation of CD44+ cells following treatment with anti-miR-1307-5p EVs. Y-axis: %proliferation of CD44+ cells, X-axis: concentration (nM). (b) Bar graph quantifying flow cytometry results, demonstrating a significant change in G0/G1 and G2/M phases in anti-miR-1307-5p EVs treated cells as compared to SC EVs (c) Flow cytometry scatter plot for Annexin-V/PI stained CD44+ cells after co-culture with anti-miR-1307-5p EVs as compared to SC EVs with anti-miR-1307-5p EVs showing a significant increase of early apoptotic population (Annexin V+/PI−) for treated cells (d) Microscopic images showing the decrease in migratory ability of CD44+ cells when treated with anti-miR-1307 EVs as compared to SC EVs (scale: 10µM) (e) Confocal images illustrating reduction in the invasive potential of CD44+ spheroids treated with anti-miR-1307-5p EVs compared to SC EVs. Spheroids were stained with phalloidin (green) and DAPI (blue); imaged at 10X magnification. (f) Representative images showing reduced angiogenic potential of HUVECs when co-cultured with anti-miR-1307-5p EVs as compared to SC EVs (g) CAM Images showing disrupted vascular development after anti-miR-1307 EVs treatment. (h) Bar-graph depicting reduction in tumour volume for sh-miR-1307 EVs+Cis treated mice as compared to SC EVs+Cis. (i) NOD-SCID xenograft mice model depicting a decrease in the tumour size when injected with sh-miR-1307 EVs+Cis in the buccal cavity region as compared to SC EVs+Cis. H&E staining of tumour sections shows reduced tumour cell density, altered nuclear morphology, and increased necrosis in sh-miR-1307 EVs+Cis treated mice. The data was normalised to controls, experiments were performed in triplicate and error bars represent mean ± SD. The statistical significance is indicated as: (*p<0.05; **p<0.01; ***p<0.001). HUVECs: Human Large Vessel Endothelial Cells, CAM: chick chorioallantoic membrane model, sh-control- Scramble-control, Cis- Cisplatin.

    Article Snippet: The cells were stained, were suspended in 1 ml 1X PBS and stained with 5 μl of PE anti-human CD44 antibody (Miltenyi Biotec, USA) for 20 minutes in dark, washed with 1X PBS and resuspended in 100 μl 1X PBS.

    Techniques: MTT Assay, Concentration Assay, Flow Cytometry, Staining, Co-Culture Assay, Cell Culture, Injection, Membrane, Control