PAI-1-dependent inactivation of SMAD4-modulated junction and adhesion complex in obese endometrial cancer. Lin et al.
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Figure 1C. Representative sections of tissue microarrays immunofluorescently stained with the white adipose tissue 7 (WAT7) homing peptide, a known marker specific for ASCs (pink-red; see white arrows), CD31 for endothelial cells (green), and DAPI for nuclei (blue). Figure 4B-C. PLA indicating protein-protein interactions of PAI-1 and low-density lipoprotein receptor-related protein 1 (LRP1) on the cell surface (B) or intracellular (C). Figure 4F.PLA demonstrating protein-protein interactions of SMAD4 and ubiquitin due to ASC-CM exposure in the presence or absence of the following inhibitors: tiplaxtinin (Tip) for PAI-1, RAP for LRP1, and protease inhibitor MG132. Micrograph images showing positive PLA signal (green) for SMAD4-ubiquitin interactions. DAPI was used to stain nuclei (blue).
图1C。经白色脂肪组织7(WAT7)归巢肽(一种特异性识别脂肪源干细胞(ASCs)的已知标志物,荧光信号呈粉红红色,详见白色箭头)、内皮细胞标志物CD31(荧光信号呈绿色)以及细胞核染色剂DAPI(荧光信号呈蓝色)免疫荧光染色的组织微阵列代表性切片。 图4B-C。原位邻近连接实验(PLA)用于展示纤溶酶原激活物抑制剂-1(PAI-1)与低密度脂蛋白受体相关蛋白1(LRP1)在细胞表面(B)或胞内(C)的蛋白质相互作用。 图4F。原位邻近连接实验(PLA)展示了在分别加入或不加入以下抑制剂的情况下,经脂肪源干细胞条件培养基(ASC-CM)处理后,SMAD4与泛素之间的蛋白质相互作用:PAI-1抑制剂替普瑞宁(Tip)、LRP1抑制剂RAP以及蛋白酶抑制剂MG132。显微图像显示SMAD4与泛素相互作用的阳性PLA信号呈绿色,同时以DAPI对细胞核进行染色(呈蓝色)。



