Kui Cui

Dec 26, 2024 | mdpi.com | Kui Cui

1. IntroductionBreast cancer is one of the most prevalent cancers and a leading cause of death among women. The search for new therapeutic targets and treatment strategies is urgently needed. Central to this interest is CD200, a cell surface glycoprotein involved in the negative regulation of immune responses [1,2]. CD200 binds to its cognitive receptor, CD200R, and the CD200/CD200R interactions regulate the immune tolerance and weaken antitumor immunity within the tumor microenvironment [3].

Aug 27, 2024 | biorxiv.org | Bo Zhu |Krishan Lal Gupta |Kui Cui |Beibei Wang

AbstractRationale: Low density cholesterol receptor (LDLR) in the liver is critical for the clearance of low-density lipoprotein cholesterol (LDL-C) in the blood. In atherogenic conditions, proprotein convertase subtilisin/kexin 9 (PCSK9) secreted by the liver, in a nonenzymatic fashion, binds to LDLR on the surface of hepatocytes, preventing its recycling and enhancing its degradation in lysosomes, resulting in reduced LDL-C clearance.

Jul 30, 2024 | biorxiv.org | Beibei Wang |Kui Cui |Bo Zhu |Yunzhou Dong

AbstractSmooth muscle cells in major arteries play a crucial role in regulating coronary artery disease. Conversion of smooth muscle cells into other adverse cell types in the artery propels the pathogenesis of the disease. Curtailing artery plaque buildup by modulating smooth muscle cell reprograming presents us a new opportunity to thwart coronary artery disease.

Feb 9, 2024 | biorxiv.org | Sudarshan Bhattacharjee |Hao Wu |Beibei Wang |Kui Cui

AbstractThis study investigates the molecular underpinnings of endothelial dysfunction in diabetes, focusing on the roles of Disabled-2 (Dab2) and Forkhead Box M1 (FoxM1) in VEGFR2 signaling and endothelial cell function. Our research reveals critical insights into the downregulation of Dab2 and FoxM1 in endothelial cells (ECs) under hyperglycemic conditions that leads to impaired angiogenesis and delayed wound healing.

Jan 8, 2024 | biorxiv.org | Beibei Wang |Kui Cui |Bo Zhu |Yunzhou Dong

AbstractHypothesis: VSMC play crucial roles in atherosclerosis via phenotypic switching. The trans-differentiation of VSMC into other cell types might contribute to atherosclerotic lesion development, progression, and the subsequent diseases such as myocardial infarction or stroke. Epsins, a family of endocytic adaptors, are crucial for atherosclerosis development and progression; yet, the role of epsins in VSMC phenotypic modulation is unknown.