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Last update 08 May 2025

CKAP2

Last update 08 May 2025

Basic Info

Synonyms

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

+ [6]

Introduction

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

Drugs associated with CKAP2

FR900359

Target

CKAP2 x GNA11 x GNAQ x NOSs

Mechanism

CKAP2 modulators [+3]

Active Org.

Hefei Institutes of Physical Science [+3]

Originator Org.

Hoshi University

Active Indication

Stomach Cancer [+2]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CKAP2

100 Translational Medicine associated with CKAP2

0 Patents (Medical) associated with CKAP2

188

Literatures (Medical) associated with CKAP2

01 May 2025·International Journal of Biological Macromolecules

Bulk transcriptome and single-nucleus RNA sequencing analyses highlight the role of recombination activating 1 in non-alcoholic fatty liver disease

Article

Author: Chen, Guangshun ; Zhao, Miao ; Guo, Junjie ; Zhang, Yu ; Li, Jiequn ; Li, Qiang ; Wen, Yifan ; Luo, Xiaohua ; Deng, Hongbo

Non-alcoholic fatty liver disease (NAFLD) is a prevalent chronic condition with an incompletely understood pathogenesis. In this study, five candidate genes-RAG1, CKAP2, CENPK, TYMS, and BUB1-were identified as being associated with NAFLD progression through integrative bioinformatics analyses. A predictive model incorporating these genes demonstrated strong robustness and diagnostic accuracy. Single-nucleus RNA sequencing analysis further revealed that RAG1 plays a potential role in hepatocytes of NAFLD patients. Functional experiments using RNA interference to suppress RAG1 expression in HepG2 cells treated with oleic and palmitic acids showed reduced total glyceride and cholesterol levels, mitigated lipid accumulation, and alterations in pathways related to lipid metabolism, inflammation, and fibrosis. Furthermore, adeno-associated virus-specific knockdown of RAG1 in hepatocytes attenuated hepatic steatosis in high-fat diet-fed mice. These findings suggest that investigating the molecular mechanisms of hub genes like RAG1 may advance our understanding of NAFLD pathogenesis and inform therapeutic development.

01 Jan 2025·International Immunopharmacology

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

Article

Author: 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.

28 Nov 2024·Journal of Microbiology and Biotechnology

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

Article

Author: 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.

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CKAP2

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