Human Lamin B1 Antibody

Detection of Human Lamin B1 by Western Blot. Western blot shows lysates of Jurkat human acute T cell leukemia cell line and MOLT-4 human acute lymphoblastic leukemia cell line. PVDF membrane was probed with 2 µg/mL of Mouse Anti-Human Lamin B1 Monoclonal Antibody (Catalog # MAB8525) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF018). A specific band was detected for Lamin B1 at approximately 68 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.

Lamin B1 in Human Liver. Lamin B1 was detected in immersion fixed paraffin-embedded sections of human liver using Mouse Anti-Human Lamin B1 Monoclonal Antibody (Catalog # MAB8525) at 3 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Mouse IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC001). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to nuclear membrane. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.

Lamin B1 in HeLa Human Cell Line. Lamin B1 was detected in immersion fixed HeLa human cervical epithelial carcinoma cell line using Mouse Anti-Human Lamin B1 Monoclonal Antibody (Catalog # MAB8525) at 8 µg/mL for 3 hours at room temperature. Cells were stained using the NorthernLights™ 557-conjugated Anti-Mouse IgG Secondary Antibody (red; Catalog # NL007) and counterstained with DAPI (blue). Specific staining was localized to nuclear membrane. View our protocol for Fluorescent ICC Staining of Cells on Coverslips.

Detection of Lamin B1 by Western Blot LCZ696 suppresses LPS-induced activation of the TLR4/Myd88 pathway in HUVECs.Cells were stimulated with LPS (1 μg/mL) in the presence or absence of LCZ696 (20 μM) for 24 hours. (A). The levels of TLR4 and Myd88 were measured using Western blot; (B). Nuclear levels of NF-kappa B p65 (***P < 0.005 vs. control group; ##, ###P < 0.01, 0.005 vs. LPS group). Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/33839697), licensed under a CC-BY license. Not internally tested by R&D Systems.

Detection of Lamin B1 by Western Blot Pristimerin suppresses endothelial cellular motilities required for angiogenesis through inactivating Shh/Gli1 signaling pathway. A Pristimerin suppressed nucleus translocation of Gli1 in endothelial cells. After incubating with Shh (100 ng/mL) and pristimerin (125, 250, and 500 nM) for 24 h, the HUVECs and HMEC-1 cells were stained with Gli1 antibody and Alexa Fluor 488 Donkey anti-Rabbit IgG. DAPI was used to label the nucleus. The cells were observed and photographed with a laser scanning confocal microscope. Scale bar: 20 μm. b, c Pristimerin inhibits Gli1 distribution in endothelial cells. The HUVECs and HMEC-1 cells were incubated with Shh and pristimerin for 24 h, and then lysed with a NE-PERTM Nucleus and Cytoplasmic Extraction Kit. After that, proteins were subjected to western blotting assay. beta -actin and Lamin B were set as loading control. The quantitative data were presented as ratios of Gli1/ beta -actin and Gli1/Lamin B. The representative blot and quantitative data were shown in B&C, respectively. d, e Pristimerin inactivated Shh/Gli1 and its downstream signaling pathway. The cells were treated with Shh and pristimerin for 24 h and lysed using RIPA buffer. Total proteins were subjected to western blotting assay. The representative blot and quantitative data were shown in d, e, respectively. The data are presented as mean ± SEM, n = 3. ***P < 0.001 compared with the control group; #P < 0.05 and ###P < 0.001 compared with the SHH-treated group. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/32286274), licensed under a CC-BY license. Not internally tested by R&D Systems.