DOCK4

Last update 08 May 2025

Basic Info

Synonyms

dedicator of cytokinesis 4, Dedicator of cytokinesis protein 4, DOCK4

+ [2]

Introduction

Functions as a guanine nucleotide exchange factor (GEF) that promotes the exchange of GDP to GTP, converting inactive GDP-bound small GTPases into their active GTP-bound form (PubMed:12628187, PubMed:16464467). Involved in regulation of adherens junction between cells (PubMed:12628187). Plays a role in cell migration (PubMed:20679435). Has a higher guanine nucleotide exchange factor activity compared to other isoforms.

100 Clinical Results associated with DOCK4

100 Translational Medicine associated with DOCK4

0 Patents (Medical) associated with DOCK4

110

Literatures (Medical) associated with DOCK4

31 Dec 2025·Annals of Medicine

Construction of a novel radioresistance-related signature for prediction of prognosis, immune microenvironment and anti-tumour drug sensitivity in non-small cell lung cancer

Article

Author: Chen, Min ; Zhang, Lisha ; Wang, Meifang ; Huang, Litao ; Zhang, Xiaoqiao ; Wang, Dandan ; Chen, Yong ; Chen, Yanhui ; Sun, Junjun ; Chen, Yanliang ; Zhou, Chan

BACKGROUNDNon-small cell lung cancer (NSCLC) is a fatal disease, and radioresistance is an important factor leading to treatment failure and disease progression. The objective of this research was to detect radioresistance-related genes (RRRGs) with prognostic value in NSCLC.METHODSThe weighted gene coexpression network analysis (WGCNA) and differentially expressed genes (DEGs) analysis were performed to identify RRRGs using expression profiles from TCGA and GEO databases. The least absolute shrinkage and selection operator (LASSO) regression and random survival forest (RSF) were used to screen for prognostically relevant RRRGs. Multivariate Cox regression was used to construct a risk score model. Then, Immune landscape and drug sensitivity were evaluated. The biological functions exerted by the key gene LBH were verified by in vitro experiments.RESULTSNinety-nine RRRGs were screened by intersecting the results of DEGs and WGCNA, then 11 hub RRRGs associated with survival were identified using machine learning algorithms (LASSO and RSF). Subsequently, an eight-gene (APOBEC3B, DOCK4, IER5L, LBH, LY6K, RERG, RMDN2 and TSPAN2) risk score model was established and demonstrated to be an independent prognostic factor in NSCLC on the basis of Cox regression analysis. The immune landscape and sensitivity to anti-tumour drugs showed significant disparities between patients categorized into different risk score subgroups. In vitro experiments indicated that overexpression of LBH enhanced the radiosensitivity of A549 cells, and knockdown LBH reversed the cytotoxicity induced by X-rays.CONCLUSIONOur study developed an eight-gene risk score model with potential clinical value that can be adopted for choice of drug treatment and prognostic prediction. Its clinical routine use may assist clinicians in selecting more rational practices for individuals, which is important for improving the prognosis of NSCLC patients. These findings also provide references for the development of potential therapeutic targets.

01 Jun 2025·Breast Cancer Research and Treatment

A potential therapeutic molecule target: lncRNA AK023507 inhibits the metastasis of breast cancer by regulating the WNT/DOCK4/β-catenin axis

Article

Author: Cai, Yangjun ; Song, Dandan ; Hu, Xiaoqu ; Hu, Yingying ; Kan, Yang ; Diao, Biyu ; Xie, Bojian

PURPOSEBreast cancer (BC) has become the most common malignant tumor in women worldwide. This study was carried out to find and validate a novel molecular therapeutic target for BC.METHODSLong non-coding RNA (lncRNA) AK023507 was selected as the study objects through microarray analysis. The function of lncRNA AK023507 was verified by various cell function experiments in vitro, subcutaneous tumorigenesis experiments, and lung metastasis model experiments in vivo. The RNA pull-down experiment and Western blot experiment were used to confirm the mechanism regulation pathway and the recovery experiment was used to verify it. TCGA datasets were used for clinical and immune function prediction analysis.RESULTSIn vitro cell function tests and in vivo experiments suggested that overexpression of lncRNA AK023507 inhibited the proliferation and metastasis of BC cells. The RNA pull-down experiment and Western blot analysis validated that lncRNA AK023507 interacted with the dedicator of cytokinesis 4 (DOCK4) protein. Analysis of public databases predicted that DOCK4 is a potential prognostic risk factor associated with epithelial-mesenchymal transition (EMT) and central memory T cell (TCM) cellular immune infiltration.CONCLUSIONSLncRNA AK023507 inhibits the proliferation and metastasis of BC by regulating the DOCK4/β-catenin axis. This discovery will provide new potential therapeutic targets for BC.

01 Apr 2025·Arteriosclerosis, Thrombosis, and Vascular Biology

Transcytosis of LDL Across Arterial Endothelium: Mechanisms and Therapeutic Targets

Review

Author: Weinberg, Peter D. ; de Liedekerke Beaufort, Gaetan C. ; Bolanle, Israel O.

Transport of LDL (low-density lipoprotein) from plasma to arterial intima is thought to be rate limiting in the development of atherosclerosis. Its variation likely determines where lesions develop within arteries and might account for some of the currently unexplained difference in disease susceptibility between individuals. It may also be critical in the development of lipid-rich, unstable plaques. Mechanisms have been controversial but recent evidence suggests that caveolar transcytosis across endothelial cells is the dominant pathway. Receptors involved are LDLR (LDL receptor), SR-B1 (scavenger receptor class B type 1), and ALK1 (activin receptor-like kinase 1). The role of LDLR is influenced by IL-1β (interleukin-1β); the role of SR-B1 by HDL (high-density lipoprotein), DOCK4 (dedicator of cytokinesis 4), GPER (G-protein–coupled estrogen receptor), and HMGB1 (high mobility group box 1); and the role of ALK1 by BMP (bone morphogenetic protein) 9. Additionally, BMP4 stimulates transcytosis and FSTL1 (follistatin-like 1 protein) inhibits it. Fundamental transcytotic mechanisms include caveola formation, undocking, trafficking, and docking; they are influenced by cholesterol-lowering agents, MYDGF (myeloid-derived growth factor), MFSD2a (major facilitator superfamily domain containing 2a) in the blood-brain barrier, and inhibitors of dynamin-2 and tubulin polymerization. The relative merits of different therapeutic approaches are discussed, with statins, colchicine, benzimidazoles, and metformin being existing drugs that might be repurposed and salidroside and glycyrrhizic acid being nutraceuticals worth investigating. Finally, we discuss evidence against the ferry-boat model of transcytosis, the contributions of receptor-mediated, fluid-phase, and active transcytosis, and where inhibition of transcytosis might be most beneficial.

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