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β1 integrin antibody  (Developmental Studies Hybridoma Bank)


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    Structured Review

    Developmental Studies Hybridoma Bank β1 integrin antibody
    <t>β1</t> <t>integrin</t> signaling facilitates Arp2/3‐dependent migration on type I collagen. (A) Volcano plot of RNAseq results comparing Arpc4 KO versus control in 8025 and R254 cells. Functional annotation of downregulated genes (8025 cells, n = 379; R254 cells, n = 328) after Arpc4 knock‐out in murine PDAC cells. Top 10 annotations are shown. Reference genome: GRCm39. (B) Western blot shows expression levels of Arpc4, β1 integrin and p‐MLC2 in control and Arpc4 KO cells, Hsp90 as a loading control. (C) Panels depict single‐cell trajectories on plates coated with type I collagen with treatment of 100 μg/mL IgG or β1‐Integrin antibody. Quantitative analysis for migrated distance and velocity of cells in each group. (D) Representative phase‐contrast pictures show the morphology of control 8025 cells in type I collagen (left, scale bars: 200 μm) with treatment of 100 μg/mL IgG or β1‐Integrin antibody at various time points. Quantitative analysis of size for the structures formed by PDAC cells (right). p ‐values for β1‐Integrin antibody vs. IgG are 0.0002 (Day 3), <0.0001 (Day 5), and 0.011 (Day 7).
    β1 Integrin Antibody, supplied by Developmental Studies Hybridoma Bank, used in various techniques. Bioz Stars score: 95/100, based on 385 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/β1 integrin antibody/product/Developmental Studies Hybridoma Bank
    Average 95 stars, based on 385 article reviews
    β1 integrin antibody - by Bioz Stars, 2026-05
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    Images

    1) Product Images from "Arp2/3 complex and β1 integrin drive an invasive front through extracellular matrix adaptation in pancreatic cancer"

    Article Title: Arp2/3 complex and β1 integrin drive an invasive front through extracellular matrix adaptation in pancreatic cancer

    Journal: International Journal of Cancer

    doi: 10.1002/ijc.70376

    β1 integrin signaling facilitates Arp2/3‐dependent migration on type I collagen. (A) Volcano plot of RNAseq results comparing Arpc4 KO versus control in 8025 and R254 cells. Functional annotation of downregulated genes (8025 cells, n = 379; R254 cells, n = 328) after Arpc4 knock‐out in murine PDAC cells. Top 10 annotations are shown. Reference genome: GRCm39. (B) Western blot shows expression levels of Arpc4, β1 integrin and p‐MLC2 in control and Arpc4 KO cells, Hsp90 as a loading control. (C) Panels depict single‐cell trajectories on plates coated with type I collagen with treatment of 100 μg/mL IgG or β1‐Integrin antibody. Quantitative analysis for migrated distance and velocity of cells in each group. (D) Representative phase‐contrast pictures show the morphology of control 8025 cells in type I collagen (left, scale bars: 200 μm) with treatment of 100 μg/mL IgG or β1‐Integrin antibody at various time points. Quantitative analysis of size for the structures formed by PDAC cells (right). p ‐values for β1‐Integrin antibody vs. IgG are 0.0002 (Day 3), <0.0001 (Day 5), and 0.011 (Day 7).
    Figure Legend Snippet: β1 integrin signaling facilitates Arp2/3‐dependent migration on type I collagen. (A) Volcano plot of RNAseq results comparing Arpc4 KO versus control in 8025 and R254 cells. Functional annotation of downregulated genes (8025 cells, n = 379; R254 cells, n = 328) after Arpc4 knock‐out in murine PDAC cells. Top 10 annotations are shown. Reference genome: GRCm39. (B) Western blot shows expression levels of Arpc4, β1 integrin and p‐MLC2 in control and Arpc4 KO cells, Hsp90 as a loading control. (C) Panels depict single‐cell trajectories on plates coated with type I collagen with treatment of 100 μg/mL IgG or β1‐Integrin antibody. Quantitative analysis for migrated distance and velocity of cells in each group. (D) Representative phase‐contrast pictures show the morphology of control 8025 cells in type I collagen (left, scale bars: 200 μm) with treatment of 100 μg/mL IgG or β1‐Integrin antibody at various time points. Quantitative analysis of size for the structures formed by PDAC cells (right). p ‐values for β1‐Integrin antibody vs. IgG are 0.0002 (Day 3), <0.0001 (Day 5), and 0.011 (Day 7).

    Techniques Used: Migration, RNA sequencing, Control, Functional Assay, Knock-Out, Western Blot, Expressing, Single Cell



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    Image Search Results


    β1 integrin signaling facilitates Arp2/3‐dependent migration on type I collagen. (A) Volcano plot of RNAseq results comparing Arpc4 KO versus control in 8025 and R254 cells. Functional annotation of downregulated genes (8025 cells, n = 379; R254 cells, n = 328) after Arpc4 knock‐out in murine PDAC cells. Top 10 annotations are shown. Reference genome: GRCm39. (B) Western blot shows expression levels of Arpc4, β1 integrin and p‐MLC2 in control and Arpc4 KO cells, Hsp90 as a loading control. (C) Panels depict single‐cell trajectories on plates coated with type I collagen with treatment of 100 μg/mL IgG or β1‐Integrin antibody. Quantitative analysis for migrated distance and velocity of cells in each group. (D) Representative phase‐contrast pictures show the morphology of control 8025 cells in type I collagen (left, scale bars: 200 μm) with treatment of 100 μg/mL IgG or β1‐Integrin antibody at various time points. Quantitative analysis of size for the structures formed by PDAC cells (right). p ‐values for β1‐Integrin antibody vs. IgG are 0.0002 (Day 3), <0.0001 (Day 5), and 0.011 (Day 7).

    Journal: International Journal of Cancer

    Article Title: Arp2/3 complex and β1 integrin drive an invasive front through extracellular matrix adaptation in pancreatic cancer

    doi: 10.1002/ijc.70376

    Figure Lengend Snippet: β1 integrin signaling facilitates Arp2/3‐dependent migration on type I collagen. (A) Volcano plot of RNAseq results comparing Arpc4 KO versus control in 8025 and R254 cells. Functional annotation of downregulated genes (8025 cells, n = 379; R254 cells, n = 328) after Arpc4 knock‐out in murine PDAC cells. Top 10 annotations are shown. Reference genome: GRCm39. (B) Western blot shows expression levels of Arpc4, β1 integrin and p‐MLC2 in control and Arpc4 KO cells, Hsp90 as a loading control. (C) Panels depict single‐cell trajectories on plates coated with type I collagen with treatment of 100 μg/mL IgG or β1‐Integrin antibody. Quantitative analysis for migrated distance and velocity of cells in each group. (D) Representative phase‐contrast pictures show the morphology of control 8025 cells in type I collagen (left, scale bars: 200 μm) with treatment of 100 μg/mL IgG or β1‐Integrin antibody at various time points. Quantitative analysis of size for the structures formed by PDAC cells (right). p ‐values for β1‐Integrin antibody vs. IgG are 0.0002 (Day 3), <0.0001 (Day 5), and 0.011 (Day 7).

    Article Snippet: The cultures were then incubated at 37°C in a 5% CO2 atmosphere for 12 h. For those groups receiving blocking antibody treatments, the media also included 100 μg/mL of IgG (I‐1195, Leinco Technologies, St. Louis, MO) or β1‐integrin antibody (AIIB2, Developmental Studies Hybridoma Bank, Iowa City, IA).

    Techniques: Migration, RNA sequencing, Control, Functional Assay, Knock-Out, Western Blot, Expressing, Single Cell

    Schematic illustration of the NIR-responsive dynamic wrinkle platform for the non-invasive harvesting of pre-primed cell sheets and their application in volumetric muscle loss (VML) repair. (A) The process of obtaining and applying pre-conditioned cell sheets for VML repair. (B) NIR-triggered dynamic reconfiguration of the wrinkle topography remotely switches the interfacial adhesion state. (C) This reconfiguration alters cellular mechanotransduction and focal adhesion density, leading to cell sheet detachment when the interfacial mechanical force (Fm) surpasses the cell-substrate adhesion force (Fc). (D) Immunofluorescence staining of focal adhesion-related markers (integrin β1, talin, pFAK(Y397), paxillin, and YAP/TAZ) and cytoskeleton in cells under control and mechanical stimulation conditions.

    Journal: Bioactive Materials

    Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

    doi: 10.1016/j.bioactmat.2026.01.046

    Figure Lengend Snippet: Schematic illustration of the NIR-responsive dynamic wrinkle platform for the non-invasive harvesting of pre-primed cell sheets and their application in volumetric muscle loss (VML) repair. (A) The process of obtaining and applying pre-conditioned cell sheets for VML repair. (B) NIR-triggered dynamic reconfiguration of the wrinkle topography remotely switches the interfacial adhesion state. (C) This reconfiguration alters cellular mechanotransduction and focal adhesion density, leading to cell sheet detachment when the interfacial mechanical force (Fm) surpasses the cell-substrate adhesion force (Fc). (D) Immunofluorescence staining of focal adhesion-related markers (integrin β1, talin, pFAK(Y397), paxillin, and YAP/TAZ) and cytoskeleton in cells under control and mechanical stimulation conditions.

    Article Snippet: FAK Antibody (sc-271126), pFAK(Y3978556s), talin (sc: 4021s), paxillin (sc: 365379), integrin β1 (sc: 374429), and YAP (cst: 14074s), TAZ (cst: 83669s) were ordered from Santa Cruz Biotechnology.

    Techniques: Immunofluorescence, Staining, Control

    Immunofluorescence staining of focal adhesion-related markers and cytoskeleton in cells under control and mechanical stimulation conditions. Left (Control group): Immunofluorescence staining shows focal adhesion-associated proteins (green channels). These correspond to integrin β1(A), talin (B), pFAK/FAK (C), paxillin (D), YAP (E), and TAZ (F) in each row. F-actin and FAK are shown in the red channel. The rightmost column of each row displays merged images. These integrate focal adhesion marker signals (green), F-actin (red), and DAPI-stained nuclei (blue). Yellow indicates co-localization of focal adhesion markers and F-actin. Right (After mechanical stimulation group): Immunofluorescence staining displays the same set of focal adhesion-related proteins and F-actin in cells after mechanical stimulation. Merged images are presented in the same format as the control group.

    Journal: Bioactive Materials

    Article Title: Pre-priming cell sheet therapy enabled by dynamic wrinkled electroactive substrate for muscle reconstruction

    doi: 10.1016/j.bioactmat.2026.01.046

    Figure Lengend Snippet: Immunofluorescence staining of focal adhesion-related markers and cytoskeleton in cells under control and mechanical stimulation conditions. Left (Control group): Immunofluorescence staining shows focal adhesion-associated proteins (green channels). These correspond to integrin β1(A), talin (B), pFAK/FAK (C), paxillin (D), YAP (E), and TAZ (F) in each row. F-actin and FAK are shown in the red channel. The rightmost column of each row displays merged images. These integrate focal adhesion marker signals (green), F-actin (red), and DAPI-stained nuclei (blue). Yellow indicates co-localization of focal adhesion markers and F-actin. Right (After mechanical stimulation group): Immunofluorescence staining displays the same set of focal adhesion-related proteins and F-actin in cells after mechanical stimulation. Merged images are presented in the same format as the control group.

    Article Snippet: FAK Antibody (sc-271126), pFAK(Y3978556s), talin (sc: 4021s), paxillin (sc: 365379), integrin β1 (sc: 374429), and YAP (cst: 14074s), TAZ (cst: 83669s) were ordered from Santa Cruz Biotechnology.

    Techniques: Immunofluorescence, Staining, Control, Marker

    Fluorescence images and quantification of nanoparticle uptake in TNFα-activated ECs under the following conditions: (A) VCAM1 blockade, (B) β1-integrin blockade on nanoparticles, and (C) CPZ treatment. Red: IA@MoNP, MoNP, or bare NP; blue: DAPI-stained nuclei. Scale bar = 50 μm. (A–B) *p < 0.05 vs. IgG antibody; # p < 0.05 vs. MoNP. (C) *p < 0.05 vs. control ECs; # p < 0.05 vs. bare NP. Data are presented as mean ± SD from n = 3 independent experiments.

    Journal: bioRxiv

    Article Title: Integrin Activation Enhances Lesion-Specific Targeting of Monocyte-Mimetic Nanoparticles in Atherosclerosis

    doi: 10.64898/2026.03.04.707824

    Figure Lengend Snippet: Fluorescence images and quantification of nanoparticle uptake in TNFα-activated ECs under the following conditions: (A) VCAM1 blockade, (B) β1-integrin blockade on nanoparticles, and (C) CPZ treatment. Red: IA@MoNP, MoNP, or bare NP; blue: DAPI-stained nuclei. Scale bar = 50 μm. (A–B) *p < 0.05 vs. IgG antibody; # p < 0.05 vs. MoNP. (C) *p < 0.05 vs. control ECs; # p < 0.05 vs. bare NP. Data are presented as mean ± SD from n = 3 independent experiments.

    Article Snippet: Membrane proteins were assessed by Western blot using antibodies against CD11b (Cell Signaling #17800, 1:1000), Na + /K + ATPase (Cell Signaling #3010, 1:1000), α4-integrin (Invitrogen #PA5-20599, 1:1000), and β1-integrin (Cell Signaling #4706S, 1:1000).

    Techniques: Fluorescence, Staining, Control

    (A) Schematic illustration of the experimental design. (B) IVIS imaging and quantification of nanoparticle accumulation in partially ligated LCA of ApoE -/- mice. (C) Representative cross-sectional fluorescence images of the LCA. Red: IA@MoNP or MoNP; green: elastin fibers; blue: DAPI-stained nuclei. Scale bar = 100 μm. (D–E) IVIS analysis showing (D) biodistribution in major organs across nanoparticle formulations and (E) reduction of IA@MoNP signal in the LCA following β1-integrin blockade on nanoparticles. (B) *p < 0.05 vs. RCA; # p < 0.05 vs. MoNP; (E) *p < 0.05 vs. IgG antibody. Data are presented as mean ± SD from n = 4 mice each group.

    Journal: bioRxiv

    Article Title: Integrin Activation Enhances Lesion-Specific Targeting of Monocyte-Mimetic Nanoparticles in Atherosclerosis

    doi: 10.64898/2026.03.04.707824

    Figure Lengend Snippet: (A) Schematic illustration of the experimental design. (B) IVIS imaging and quantification of nanoparticle accumulation in partially ligated LCA of ApoE -/- mice. (C) Representative cross-sectional fluorescence images of the LCA. Red: IA@MoNP or MoNP; green: elastin fibers; blue: DAPI-stained nuclei. Scale bar = 100 μm. (D–E) IVIS analysis showing (D) biodistribution in major organs across nanoparticle formulations and (E) reduction of IA@MoNP signal in the LCA following β1-integrin blockade on nanoparticles. (B) *p < 0.05 vs. RCA; # p < 0.05 vs. MoNP; (E) *p < 0.05 vs. IgG antibody. Data are presented as mean ± SD from n = 4 mice each group.

    Article Snippet: Membrane proteins were assessed by Western blot using antibodies against CD11b (Cell Signaling #17800, 1:1000), Na + /K + ATPase (Cell Signaling #3010, 1:1000), α4-integrin (Invitrogen #PA5-20599, 1:1000), and β1-integrin (Cell Signaling #4706S, 1:1000).

    Techniques: Imaging, Fluorescence, Staining