aiib2 β1 integrin  (Developmental Studies Hybridoma Bank)

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

Journal: bioRxiv

Article Title: Nascent extracellular matrix converts biomaterial cues into cell fate decisions

doi: 10.64898/2026.01.10.698826

Figure Lengend Snippet: a. Timeline and schematic showing the blocking of cell adhesion to nECM using an integrin β1 (ITGB1) function perturbing antibody for 1 hour pre-embedding and for 7 consecutive days . b. Representative fluorescent images of the incorporation of EdU in chondrocytes cultured without (Ctrl) and with ITGB1 inhibition (ITGB1i) in high and low modification hydrogels at day 7 (scale bar = 100 μm). c. Quantification of the incorporation of EdU in chondrocytes cultured without (Ctrl) and with ITGB1 inhibition (ITGB1i) in high and low modification hydrogels at day 7 (low-Ctrl: n = 23 ROIs, N = 3; low-ITGB1i: n = 30 ROIs, N = 3; high-Ctrl: n = 23 ROIs, N = 3; low-ITGB1i: n = 27 ROIs, N = 3). d. Representative fluorescent images of Sox9 immunofluorescence (dashed line outlines nuclei) of chondrocytes cultured without (Ctrl) and with ITGB1 inhibition (ITGB1i) in low and high modification hydrogels at day 7 (scale bar = 10 μm). e. Quantification of Sox9 nucleus-to-cytoplasm (NC) ratio of chondrocytes cultured without (Ctrl) and with ITGB1 inhibition (ITGB1i) in low and high modification hydrogels at day 7 (low-Ctrl: n = 138 cells, N = 4; low-ITGB1i: n = 133 cells, N = 4; high-Ctrl: n = 124 cells, N = 4; high-ITGBi: n = 138 cells, N = 4). a-e. N = number of independent experiments ****p < 0.0001, *p < 0.05, error bar = standard deviation, ns: no significant difference by two-way ANOVA with Tukey’s multiple comparisons test.

Article Snippet: For perturbation studies, media was supplemented with either an anti-CD44 antibody (DSHB, H4C4, 2.5 μg/mL, day 0-3) or anti-integrin β1 antibody (anti-ITGB1, DSHB, AIIB2, 2.5 μg/mL, day 0-7).

Techniques: Blocking Assay, Cell Culture, Inhibition, Modification, Immunofluorescence, Standard Deviation