Semaphorin 3B Antibody - BSA Free

Immunocytochemistry/ Immunofluorescence: Semaphorin 3B Antibody [NB100-2218]

Immunocytochemistry/Immunofluorescence: Semaphorin 3B Antibody [NB100-2218] - SEMA3B antibody was tested in Neuro-2a cells with Dylight 488 (green). Nuclei and alpha-tubulin were counterstained with DAPI (blue) and Dylight 550 (red).

Immunohistochemistry: Semaphorin 3B Antibody [NB100-2218]

Immunohistochemistry: Semaphorin 3B Antibody [NB100-2218] - IHC analysis of SEMA3B in mouse kidney using DAB with hematoxylin counterstain.

Simple Western: Semaphorin 3B Antibody [NB100-2218]

Simple Western: Semaphorin 3B Antibody [NB100-2218] - Simple Western lane view shows a specific band for SEMA3B in 1.0 mg/ml of HeLa lysate. This experiment was performed under reducing conditions using the 12-230 kDa separation system.

Western Blot: Semaphorin 3B Antibody - BSA Free [NB100-2218] -

SEMA3B‐AS1 requires SEMA3B/NRP1 to suppress angiogenesis. (A) Protein network analysis of possible SEMA3B interacted proteins. The red square highlights NRP1. (B) SEMA3B and NRP1 colocalize in the blood vessels of colorectal carcinoma (CRC) patients. The scale bars indicate 100 and 20 μm in pictures at 100× or 400× magnifications, respectively. (C) Both SEMA3B and vascular endothelial growth factor (VEGF) interact with NRP1, as analyzed by coIP. (D) NRP1 can bind with more SEMA3B and less VEGF after SEMA3B‐AS1 overexpression. (E–G) SEMA3B‐AS1 required SEMA3B/NRP1 to suppress the human umbilical vein endothelial cell (HUVEC) invasion (E), tubule formation in vitro (F), and angiogenesis in the chorioallantoic membrane (CAM) assay (G). Scale bars indicate 50 μm (E) and 100 μm (F), respectively. The yellow circles in (G) indicate locations where conditioned medium was used. (H) Schematic diagram showing the mechanism of action of SEMA3B‐AS1 in CRC. SEMA3B‐AS1 was downregulated in colorectal carcinoma and consequently decreased EP300 recruitment. In turn, the reduction in EP300 recruitment suppressed the accumulation of the active marker H3K9ac and repressed SEMA3B levels. Subsequently, the receptor NRP1 interacted with less SEMA3B, and then, the VEGF pathway was activated, which induced angiogenesis and colorectal carcinoma progression.*p < 0.05; **p < 0.01; ***p < 0.001. Source: Illustration created with BioRender (available online: https://biorender.com/ (accessed on 15 June 2022)). Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/37701532), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: Semaphorin 3B Antibody - BSA Free [NB100-2218] -

SEMA3B‐AS1 requires SEMA3B/NRP1 to suppress angiogenesis. (A) Protein network analysis of possible SEMA3B interacted proteins. The red square highlights NRP1. (B) SEMA3B and NRP1 colocalize in the blood vessels of colorectal carcinoma (CRC) patients. The scale bars indicate 100 and 20 μm in pictures at 100× or 400× magnifications, respectively. (C) Both SEMA3B and vascular endothelial growth factor (VEGF) interact with NRP1, as analyzed by coIP. (D) NRP1 can bind with more SEMA3B and less VEGF after SEMA3B‐AS1 overexpression. (E–G) SEMA3B‐AS1 required SEMA3B/NRP1 to suppress the human umbilical vein endothelial cell (HUVEC) invasion (E), tubule formation in vitro (F), and angiogenesis in the chorioallantoic membrane (CAM) assay (G). Scale bars indicate 50 μm (E) and 100 μm (F), respectively. The yellow circles in (G) indicate locations where conditioned medium was used. (H) Schematic diagram showing the mechanism of action of SEMA3B‐AS1 in CRC. SEMA3B‐AS1 was downregulated in colorectal carcinoma and consequently decreased EP300 recruitment. In turn, the reduction in EP300 recruitment suppressed the accumulation of the active marker H3K9ac and repressed SEMA3B levels. Subsequently, the receptor NRP1 interacted with less SEMA3B, and then, the VEGF pathway was activated, which induced angiogenesis and colorectal carcinoma progression.*p < 0.05; **p < 0.01; ***p < 0.001. Source: Illustration created with BioRender (available online: https://biorender.com/ (accessed on 15 June 2022)). Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/37701532), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: Semaphorin 3B Antibody - BSA Free [NB100-2218] -

SEMA3B, the sense‐cognate gene for SEMA3B‐AS1, is a key downstream target of SEMA3B‐AS1. (A) Genomic location of SEMA3B and SEMA3B‐AS1 from the ENCODE collection. Higher levels of epigenetic modification marks on histone 3 at lysine 9 (H3K9ac) and several transcription factor binding site uniform peaks of EP300 were observed within the SEMA3B promoter region. (B and C) The correlation between SEMA3B‐AS1 transcript levels and SEMA3B mRNA levels in colorectal carcinoma tissues was measured according to our data (n = 30; B) and The Cancer Genome Atlas (TCGA) cohort (n = 622; C). (D and E) SEMA3B‐AS1 regulated the expression of SEMA3B at the mRNA (D) and protein (E) levels. *p < 0.05; **p < 0.01; ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/37701532), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Immunohistochemistry: Semaphorin 3B Antibody - BSA Free [NB100-2218] -

SEMA3B overexpression inhibits angiogenesis and the vascular endothelial growth factor (VEGF) pathway. (A) Gene set enrichment analysis (GSEA) showed the enrichment of the VEGF pathway in CRC cells with SEMA3B downregulation. (B) Overexpression of SEMA3B‐AS1 or SEMA3B increased the content of SEMA3B protein in the supernatant of colorectal cancer cells. (C) Colorectal carcinoma (CRC) cell supernatant overexpressing SEMA3B‐AS1 or SEMA3B inhibited the invasion ability of endothelial cells. Representative images (left) and the statistical analysis (right) are shown. Scale bars indicate 50 μm. (D) CRC cell supernatant overexpressing SEMA3B‐AS1 or SEMA3B inhibited the tube formation of endothelial cells in vitro. Scale bars indicate 100 μm. (E) The chorioallantoic membrane (CAM) assay was used to examine blood vessel formation after stimulation with the supernatants from the indicated cells. The yellow circles indicate locations where conditioned medium was used. *p < 0.05; **p < 0.01; ***p < 0.001. Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/37701532), licensed under a CC-BY license. Not internally tested by Novus Biologicals.