CKAP2

更新于：2025-01-23

基本信息

别名

CKAP2、CTCL tumor antigen se20-10、cytoskeleton associated protein 2

+ [6]

简介

Possesses microtubule stabilizing properties. Involved in regulating aneuploidy, cell cycling, and cell death in a p53/TP53-dependent manner (By similarity).

关联

100 项与 CKAP2 相关的临床结果

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100 项与 CKAP2 相关的转化医学

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0 项与 CKAP2 相关的专利（医药）

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193

项与 CKAP2 相关的文献（医药）

2025-01-01·International Immunopharmacology

Neutrophils promote laser-induced choroidal neovascularization by increasing pro-inflammatory cytokines secretion and cell cycle arrest in retinal pigment epithelium

Article

作者: Qu, Yi ; Xu, Qian ; Li, Mengyao ; Fan, Qian ; Yan, Chenfei ; Li, Haiming ; Song, Xian

Inflammation is hypothesized to have essential functions in the development of wet age-related macular degeneration (AMD). Polymorphonuclear neutrophils (PMNs), recognized as major players in inflammation, are typically the first leukocytes to be recruited to an inflammatory site. Previous studies have identified neutrophil aggregates in the lesion site of the choroidal neovascularization model, and systemic depletion of neutrophils in adult mice is associated with reduced choroidal neovascularization (CNV) area, suggesting a pivotal role of PMNs in CNV pathogenesis. Here, we investigate the role of neutrophils in promoting CNV, a key feature of wet AMD. The malfunction and demise of retinal pigment epithelium cells are essential elements in CNV pathogenesis. Our hypothesis posits that neutrophils exacerbate CNV by influencing pro-inflammatory cytokines secreted by retinal pigment epithelium (RPE) cells. Using in vivo laser-induced CNV models with mice and in vitro experiments with the human ARPE-19 cell line, we demonstrated that co-culturing neutrophils with ARPE-19 cells induces an increase in pro-inflammatory cytokines and leads to S-phase cell cycle arrest, potentially through the induction of double-strand breaks (DSBs). Further exploration of this interaction revealed a potential pathway involving reactive oxygen species (ROS) and microRNA-23a, wherein PMNs induce DSBs by initiating the downregulation of LB1 via microRNA-23a. Additionally, we found that dHL-60 cell line could serve as a substitute for primary PMNs, highlighting its potential as a valuable tool in experimental models involving interactions with retinal cells. Our findings underscore the significant role of neutrophils in CNV pathogenesis, providing insights into potential therapeutic targets for wet AMD.

2024-11-28·Journal of Microbiology and Biotechnology

CKAP2 Regulated by TFDP1 Promotes Metastasis and Proliferation of Colorectal Cancer through Affecting the Tumor Microenvironment

Article

作者: Liu, Yang ; Cheng, Shi ; Zhong, Zhiqiang

The current pathological and physiological evaluation system for colorectal cancer (CRC) is limited; thus, effective biological targets to diagnose and treat this disease are urgently needed. In this study, we used qRT-PCR for detecting mRNA levels of genes. The levels of protein were identified by western blot, immunohistochemistry, and immunofluorescence assays. In addition, functional experiments were used to evaluate the role of cytoskeleton associated protein (CKAP) 2 in CRC cells and human umbilical vein endothelial cells (HUVECs). Bioinformatics analysis was employed to predict the binding relationship of CKAP2 and TFDP1, which was confirmed through dual luciferase reporter assay and immunoprecipitation assay. Furthermore, we injected human colorectal carcinoma HCT116 cells into mice flanks, and we injected Luciferase-labeled HCT116 cells into mice tail vein. HE staining was used to detect tumor nodules. As a result, high CKAP2 expression was found in CRC cells and tissues. CKAP2 silencing reduced CRC cell migration, invasion, proliferation, and epithelial-mesenchymal transition. Moreover, CKAP2 expression was positively associated with M2 macrophage levels. CKAP2 promoted protein expression of CD86, CD206, IL-1β, and CCL17. Moreover, CKAP2 promoted the proliferation of HUVECs and angiogenesis via affecting the tumor microenvironment (TME). We also found that CKAP2 could interact with TFDP1. The inhibitory impacts of TFDP1 downregulation on CRC cell' proliferation, migration, and invasion were reversed via CKAP2 overexpression. In vivo silencing of CKAP2 repressed tumor growth and metastasis. Overall, CKAP2 was positively regulated by TFDP1, which promoted tumorigenesis and metastasis in CRC.

2024-10-01·Journal of Cardiovascular Translational Research

Differential Expression of mRNA in Peripheral Blood Mononuclear Cells May Predict Postoperative Atrial Fibrillation in Coronary Artery Bypass Surgery Patients

Article

作者: Guo, Zhigang ; Liu, Xiankun ; Bai, Yunpeng ; Wang, Lianqun ; Jiang, Nan ; Tan, Mingqi

AbstractPostoperative Atrial Fibrillation (POAF) frequently follows Coronary Artery Bypass Grafting (CABG) surgery. This prospective study investigates genes linked to POAF in CABG patients, aiming to create a predictive model. Employing differential gene and methylation analyses, the study identified four genes (WARS2, CKAP2, CHI3L1, HSD17B6) associated with POAF. Preoperative plasma samples and clinical data were collected from 139 CABG patients, categorized into POAF (+) (43) and POAF (-) (96). Real-time quantitative PCR assessed gene expression, and a predictive model using the LASSO method demonstrated robust performance, with AUC values of 0.8895 in the training set and 0.7840 in the test set. This pioneering study integrates genomics and clinical data, suggesting WARS2, CKAP2, and CHI3L1 as potential indicators for POAF prediction.Graphical Abstract

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