Fig 2: Conditional Deletion of RhoA in the Small Intestine Causes Defects in Epithelial Architecture(A) Western blotting of RHOA, Cdc42, Rac1, and effectors of RHOA (MLC2 and p-MLC2) in isolated small intestinal crypts from 1- to 2-month-old control WT or RhoA KO mice.(B) Representative H&E staining of control WT or RhoA KO duodenum sections.(C and D) Representative immunofluorescence by anti-RHOA and anti-E-cadherin in control WT (C) or RhoA KO (D) duodenum sections.

Fig 3: Inversin affects the activity of the Rho GTPases.Activity of Rac-1, RhoA and Cdc42 was determined by pull-down in migrating inv+/+ and inv−/− MEFs 30 min (A) or 4 h (B) after scratch. Histograms represent the mean ± S.E.M. of three independent experiments.

Fig 4: ACTN1 regulates Hippo signaling activity and Rho GTPases activities. a The Cancer Genome Atlas (TCGA) RNA sequencing data of HCC cohort were downloaded and divided into two ACTN1-high and ACTN1-low groups. Gene set enrichment analysis (GSEA) was then preformed. False discovery rate (FDR) was set at 0.25. b Western blotting analysis of phospho-LATS1, LATS1, phospho-YAP and YAP in sh-ACTN1–1 and sh-Ctrl MHCC-97H cells. The activities of RhoA, Cdc42 and Rac1 were measured by pull-down assays in sh-ACTN1–1 and sh-Ctrl MHCC-97H cells. Statistical analyses of densitometry were shown at right. The experiments were repeated three times. c Real-time qPCR analysis of the mRNA levels of CTGF, ANKRD1 and CYR61 in sh-ACTN1–1 and sh-Ctrl MHCC-97H cells. The experiments were repeated three times. d Correlation analysis of ACTN1 expression with YAP target genes in the TCGA cohort. *P < 0.05; **P < 0.01

Fig 5: Model showing how PRRSV utilizes viral apoptotic mimicry and TIM-induced macropinocytosis as an alternative pathway to infect host cells. In addition to CME, TIM-1/4 recognizes PRRSV as apoptotic mimicry and induces macropinocytosis via the Rac1/Cdc42-Pak1 signaling pathway. PRRSV enters SNX5-macropinosomes via macropinocytosis as an alternative pathway, where CD163 functions as an indispensable receptor.