Image13_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Table_1_CircHADHA-augmented autophagy suppresses tumor growth of colon cancer by regulating autophagy-related gene via miR-361.docx by Ying Shi (115282)

“…<p>Colon cancer undergoes a traditional pathway from colon polyps to colon cancer. …”

Image4_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Image7_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Image3_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Table_2_CircHADHA-augmented autophagy suppresses tumor growth of colon cancer by regulating autophagy-related gene via miR-361.docx by Ying Shi (115282)

“…<p>Colon cancer undergoes a traditional pathway from colon polyps to colon cancer. …”

Table1_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.DOCX by Susana Lechuga (9554969)

Image12_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Image11_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Image2_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Image1_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Image6_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

Image5_Coactosin-like protein 1 regulates integrity and repair of model intestinal epithelial barriers via actin binding dependent and independent mechanisms.TIF by Susana Lechuga (9554969)

The Synthetic β-Nitrostyrene Derivative CYT-Rx20 Inhibits Esophageal Tumor Growth and Metastasis via PI3K/AKT and STAT3 Pathways by Wen-Chin Chiu (3139899)

Image_4_RGS10 mitigates high glucose-induced microglial inflammation via the reactive oxidative stress pathway and enhances synuclein clearance in microglia.tif by Jaegwon Chung (488604)

Image_1_RGS10 mitigates high glucose-induced microglial inflammation via the reactive oxidative stress pathway and enhances synuclein clearance in microglia.TIF by Jaegwon Chung (488604)

Image_3_RGS10 mitigates high glucose-induced microglial inflammation via the reactive oxidative stress pathway and enhances synuclein clearance in microglia.TIF by Jaegwon Chung (488604)

Image_2_RGS10 mitigates high glucose-induced microglial inflammation via the reactive oxidative stress pathway and enhances synuclein clearance in microglia.TIF by Jaegwon Chung (488604)

Table 1_Chronic BPAF exposure differentially enhances fat deposition in mice fed normal or high-fat diets via lipid metabolism dysregulation.xlsx by Ziquan Lv (690020)

“…This study aims to investigate the impact of BPAF exposure on obesity and lipid metabolism in male mice subjected to either a normal chow diet (ND) or a high-fat diet (HFD).…”

DataSheet1_Proteasome Inhibition Suppresses KIT-Independent Gastrointestinal Stromal Tumors Via Targeting Hippo/YAP/Cyclin D1 Signaling.PDF by Ting Chen (15205)

“…<p>Purpose: Gastrointestinal stromal tumors (GISTs) are the most common malignant tumor of mesenchymal origin of the digestive tract. A yet more challenging resistance mechanism involves transition from oncogenic KIT to a new imatinib-insensitive oncogenic driver, heralded by loss of KIT expression. …”