Fig 1: Gene distribution of CAPG between different expression levels. In total 515 samples of LGG and 152 samples of HGG were selected, and the expression of CAPG is shown. LGG, low grade gliomas; HGG, high grade gliomas; CAPG, capping protein gene.
Fig 2: Gene expression of CAPG between normal and human glioma. The gene expression profiling data of 529 glioblastoma tissues and 10 normal samples in TCGA database were chosen to re-analyze the mRNA levels of CAPG. P<0.05. TCGA, The Cancer Genome Atlas; CAPG, capping protein gene.
Fig 3: Rho cell motility pathway was positively correlated with CapG. NES, normalized enrichment score
Fig 4: Ectopic CapG overexpression strengthened MLC2 phosphorylation and inhibited Rac1 activity. A Total MLC2 and phosphorylated MLC2 in CapG overexpressing 6-10B cells and the NC group. B Total rac1 and pulled-down GTP-rac1 in CapG overexpressing 6-10B and HNE1 cells and corresponding NC groups. a-Tubulin is used as a loading control. NC, negative control. Grouped blots were cropped from different parts of the same gel and from different exposures
Fig 5: Overview of the CapG-involved motility pathway. It is derived from the present study outcomes that CapG is involved in Rho motility pathway independent of ROCK and inactivates Rac1. It is reasonably deduced that CapG-mediated Ca2+ signaling and Ca2+-dependent MLCK contribute to MLC phosphorylation. Arrows indicate activation. Truncated arrows mean inhibition. ROCK, rho-associated protein kinase; p-MLC, phosphorylated-myosin light chain; MLCK, myosin light chain kinase
Supplier Page from Abcam for Anti-Actin Regulatory Protein CAPG/MCP antibody