Human FGF‑BP Antibody

Detection of Human FGF-BP by Western Blot

miR-217 targets KLF5 by binding to its 3’UTR.A. miR-217 decreased the KLF5, FGF-BP and Cyclin D1 protein levels in HCC1806 and HCC1937 TNBC cells. KLF5, FGF-BP and Cyclin D1 protein levels were detected by using WB. beta -actin was used as the loading control. B. The putative wild type binding sites of miR-217 on KLF5 3’UTR and its mutants. C. miR-217 mimics significantly inhibits the KLF5 3’UTR luciferase reporter activity through the second putative binding site. HEK293T cells were transfected with miR-217 mimics and pMIR-KLF5 3’-UTR or miR-217 binding sites mutated pMIR-KLF5 3’-UTR reporters (mut1, mut2 or mut1,2) together with the pCMV-Renilla control. Image collected and cropped by CiteAb from the following publication (https://dx.plos.org/10.1371/journal.pone.0176395), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse FGF-BP by Immunohistochemistry

mTORC1-STAT3-FGFBP1 pathway regulates angiogenesis in an OVA-induced chronic asthma model.A The timeline to establish OVA-induced chronic asthma models and therapeutic interventions (see the “Materials and methods” section for details). The mice were divided into three groups: the control group (Control), OVA-induced chronic asthma group (OVA), and rapamycin-treated group (Rapa). B The total number of leukocytes and eosinophil count in the BALF were counted using Wright–Giemsa staining. C Representative photographs of H&E staining (upper panels) and Masson’s staining (lower panels) of lung tissues (scale bar: 100 μm). D Inflammation score (left panels) and Wat/Pbm (right panels) of lung tissues. E Immunoblotting of the indicated proteins in lung tissues. F IHC analysis of the indicated proteins in lung tissues (scale bar: 100 μm). n = 8 mice per group. Results are shown as mean ± SD. **P < 0.01; ***P < 0.001; ****P < 0.0001. G Schematic illustration of activated mTORC1-STAT3-FGFBP1 signaling pathway promotes angiogenesis in airway epithelial cells. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/34341336), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Mouse FGF-BP by Immunohistochemistry

PLA promotes angiogenesis through FGFBP1.A NCI-H292 cells, stably expressed shRNA targeting FGFBP1 (shFGFBP1) or a control shRNA (shSc), were treated with 20 μg/mL PLA for 24 h. Western blot (upper panel) and ELISA (lower panel) were performed to detect the protein levels of FGFBP1 in cell lysates and supernatants, respectively. B–E NCI-H292/shFGFBP1 and NCI-H292/shSc cells were treated with PLA (20 μg/mL) for 24 h and the cell-conditioned media were collected for tube formation assay (B, C) and CAM assay (D, E). B, D Representative micrographs of tube formation assay (B) and CAM assay (D). C, E Quantitations of total branching points of tube formation assay (C) and new vessels of CAM assay (E). F NCI-H292 cells infected with lentivirus harboring a vector encoding FGFBP1 (LvFGFBP1) or the empty vector (LvNC). Western blot (upper panel) and ELISA (lower panel) were performed to detect the protein levels of FGFBP1 in cell lysates and supernatants, respectively. (G–J) The cell-conditioned media of NCI-H292/LvFGFBP1 and NCI-H292/LvNC cells were collected for tube formation assay (G, H) and CAM assay (I, J). G, I Representative micrographs of tube formation assay (G) and CAM assay (I). H, J Quantitation of total branching points of tube formation assay (H) and new vessels of CAM assay (J). n = 6 chick embryos per group. Results are shown as mean ± SD. ***P < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/34341336), licensed under a CC-BY license. Not internally tested by R&D Systems.