integrin αvβ3 sc-7312 antibody  (Santa Cruz Biotechnology)

Journal: Science Advances

Article Title: Dynamic adaptive coassembled sericin protein orchestrating stem cell development for nucleus pulposus regeneration

doi: 10.1126/sciadv.adx2768

Figure Lengend Snippet: ( A ) The composition and structure of the NP in IVD tissue exhibited spatial heterogeneity, which support NP cell development and physiological function through dynamic mechanical regulation and biochemical signaling. ( B ) Inspired by the partitioned structure of ECM, bioactive sericin was coassembled with BPAA-GFF fibrillar networks, driven by phase separation–induced molecular network rearrangement. The resulting dynamic adaptive network activated stem cell integrin ligands to modulate cell-matrix interactions and promoted chondrogenic differentiation via rapid stress relaxation and biochemical factor induction. ( C ) In rat and rabbit IVD degeneration models, KGN-incorporated coassembled hydrogel effectively promoted BMSCs for NP regeneration.

Article Snippet: To investigate the role of integrin β3 in mediating stem cell adhesion and cytoskeletal regulation, functional inhibition was performed using the αvβ3 integrin antagonist cilengitide (MedChemExpress, USA).

Techniques:

Journal: Science Advances

Article Title: Dynamic adaptive coassembled sericin protein orchestrating stem cell development for nucleus pulposus regeneration

doi: 10.1126/sciadv.adx2768

Figure Lengend Snippet: ( A ) 3D coculture of stem cells with the coassembled BS gel. ( B ) Time-dependent gene expression trend of stem cells regulated by coassembled BS protein gel. ( C ) Up-regulated genes and their associated biological events based on Gene Ontology (GO) analysis comparing BS versus B. ( D ) Flow relationships between activated molecular pathways and up-regulated genes based on Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis comparing BS versus B. JAK-STAT, Janus kinase–signal transducer and activator of transcription; MAPK, mitogen-activated protein kinase. ( E ) Gene interaction network analysis and Gantt chart analysis of temporal gene expression in three gene categories. ( F ) Gene expression heatmap analysis comparing BS versus B, n = 3 independent samples. ( G ) In vitro validation of gene expression by qPCR, n = 3 independent samples. ( H ) Local interaction residues in molecular docking. Color-coded representation shows BPAA-GFF (green), sericin protein (magenta), and the integrin αvβ3 complex (blue and orange). ( I ) Time-course analysis of stem cells cocultured with the hydrogel at 1, 2, and 4 weeks. ( J ) Integrin β3 expression analysis at 1 week, n = 3 independent samples. ( K ) Cytoskeletal staining and cell aspect ratio analysis at 1 week. ( L ) YAP staining and nuclear/cytoplasmic ratio analysis. ( M ) Coassembled BS gel activates integrin-mediated cell-matrix interactions, driving YAP nuclear translocation and downstream mechanotransduction signaling. Statistical analyses were performed with Student’s t tests (unpaired and two-tailed): * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: To investigate the role of integrin β3 in mediating stem cell adhesion and cytoskeletal regulation, functional inhibition was performed using the αvβ3 integrin antagonist cilengitide (MedChemExpress, USA).

Techniques: Gene Expression, In Vitro, Biomarker Discovery, Expressing, Staining, Translocation Assay, Two Tailed Test

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: Gut microbial metabolite butyrate boosts p53-expressing telomerase-specific oncolytic adenovirus efficacy by enhancing infectivity and activating MHC-I/cGAS-STING

doi: 10.1007/s00262-025-04252-4

Figure Lengend Snippet: Enhancement of viral infectivity by butyrate A CT26, MC38, SW48, and HCT116 cells were treated with Ad-GFP (1000 MOI for CT26 and MC38, 100 MOI for SW48 and HCT116) with or without butyrate (2 mM) for 24 h, and were observed by fluorescence microscopy (n = 3–4). The lower panels show magnified views of the areas outlined by the red squares in the middle panels. Relative GFP intensity in butyrate-treated cells compared with mock-treated cells was measured in a randomly selected field in each well. Scale bar, 500 μm (upper and middle panels); 50 μm (lower panels). *, p < 0.05. **, p < 0.01. B HCT116 subcutaneous tumors were treated with Ad-GFP (5 × 10 7 PFU) intratumoral injection for 2 days with or without butyrate (1 mM) oral administration, starting 2 days prior to Ad-GFP injection (n = 6). Frozen sections of harvested tumors with or without butyrate treatment were observed by fluorescence microscopy, and GFP intensity was measured in three randomly selected fields in each tumor. Scale bar, 200 μm. *, p < 0.05. C CT26, MC38, SW48, and HCT116 cells were treated with butyrate (2 mM) for 2 days, and analyzed with flow cytometry for CAR, αvβ3, and αvβ5 (n = 3). MFI, mean fluorescence intensity. D HCT116 subcutaneous tumors were treated with or without butyrate (1 mM) oral administration for 7 days, and whole-cell lysates of the harvested tumors were analyzed by western blot for CAR and β-actin. Relative intensity of CAR compared with β-actin is indicated below the CAR bands. E MC38 and HCT116 cells were treated with Ad-GFP (1000 MOI for MC38, 100 MOI for HCT116) with or without butyrate (2 mM) for 24 h. Anti-CAR antibody was administered 2 h prior to Ad-GFP infection. These cells were observed by fluorescence microscopy. Scale bar, 50 μm. F SW48 and HCT116 cells were treated with butyrate (2 mM) and/or OBP-702 (10 MOI) for 0, 12, 24, or 48 h, and the whole-cell lysates were analyzed by western blot for p53, E1A, and β-actin. Relative intensity of E1A compared with β-actin is indicated below the E1A bands. G HCT116 subcutaneous tumors were treated with OBP-702 (5 × 10 7 PFU) intratumoral injection for 2, 12, 24, or 48 h with or without butyrate (1 mM) oral administration, starting 2 days prior to OBP-702 injection. Whole-cell lysates of the harvested tumors were analyzed by western blot for p53, E1A, and β-actin. Relative intensity of E1A compared with β-actin is indicated below the E1A bands

Article Snippet: Flow cytometry was performed for CAR (D3W3G, Cell Signaling Technology), αvβ3 (bs-1310R, Bioss antibodies, Woburn, MA, USA), αvβ5 (bs-1356R, Bioss Antibodies), and MHC-I (BE0077, Bio X Cell, Lebanon, NH, USA) using FACS Array and BD FACS Aria (BD Biosciences, San Jose, CA, USA), and analysis was performed using FlowJo software (BD Biosciences).

Techniques: Infection, Fluorescence, Microscopy, Injection, Flow Cytometry, Western Blot