DOCK3

Last update 08 May 2025

Basic Info

Synonyms

dedicator of cytokinesis 3, Dedicator of cytokinesis protein 3, DOCK3

+ [5]

Introduction

Potential guanine nucleotide exchange factor (GEF). GEF proteins activate some small GTPases by exchanging bound GDP for free GTP. Its interaction with presenilin proteins as well as its ability to stimulate Tau/MAPT phosphorylation suggest that it may be involved in Alzheimer disease. Ectopic expression in nerve cells decreases the secretion of amyloid-beta APBA1 protein and lowers the rate of cell-substratum adhesion, suggesting that it may affect the function of some small GTPase involved in the regulation of actin cytoskeleton or cell adhesion receptors (By similarity).

100 Clinical Results associated with DOCK3

100 Translational Medicine associated with DOCK3

0 Patents (Medical) associated with DOCK3

131

Literatures (Medical) associated with DOCK3

01 Feb 2025·Brain and Behavior

Exploring the Relationship Between Serum Neuronal Pentraxin 2 and Poststroke Cognitive Impairment in Patients With First‐Episode Acute Ischemic Stroke

Article

Author: Gu, Shiyuan ; Ma, Wenyang ; Li, Jie

ABSTRACTBackground and Objective: Neuronal pentraxin 2 (NPTX2) is associated with cognitive impairment in some neurodegenerative diseases. However, few studies focused on the association between NPTX2 and poststroke cognitive impairment (PSCI). Hence, this study aimed to investigate the association between serum NPTX2 levels and PSCI.Methods: A total of 134 participants with acute ischemic stroke (AIS) and 42 normal controls were enrolled in this study. Admission baseline information was collected, and serum NPTX2 levels were determined within 24 h using enzyme‐linked immunosorbent assay (ELISA) at hospital admission. All subjects were evaluated for cognitive function using the MoCA (Montreal Cognitive Assessment) scale at 3 months after stroke onset, and patients with AIS were divided into PSCI and PSNCI (poststroke no cognitive impairment) groups, with a total MoCA score < 26 defined as PSCI. This study analyzed the relationship between serum NPTX2 and MoCA score and the risk factors of PSCI. The receiver operating characteristic (ROC) curve was to evaluate the diagnostic value of serum NPTX2 levels on PSCI.Results: Among the 134 AIS participants, 53 (38.8%) patients suffered from PSCI at 3 months after stroke onset. The serum levels of NPTX2 in the PSCI group, PSNCI group, and normal controls group were significantly different (p < 0.05). The serum NPTX2 levels in the PSCI and PSNCI groups were higher than normal control group, and the serum NPTX2 levels in the PSCI group were lower than PSNCI group (p < 0.05). Serum NPTX2 levels were positively correlated with the total score of MoCA (r = 0.329, p < 0.01), and also positively correlated with some subcognitive domains of MoCA (visuospatial and executive functions, naming, delayed memory, and attention). ROC curve indicated that serum NPTX2 predicted cognitive impairment in AIS patients. Multivariate Logistic regression analysis indicated serum NPTX2 was an independent protective factor for PSCI (odds ratio [OR] = 0.075, 95% CI 0.010–0.812, p < 0.01).Conclusions: Lower serum NPTX2 levels were associated with PSCI within 3 months in patients with first‐episode AIS. Lower levels of serum NPTX2 may be associated with impairment in visuospatial and executive functions, naming, delayed memory, and attention, while a further larger‐scale study is needed to verify our findings.

01 Feb 2025·Alzheimer's & Dementia

The genetic landscape of early‐onset Alzheimer's disease in China

Article

Author: Jia, Jian‐Ping ; Wei, Yi‐Ping ; Liu, Wen‐Ying ; Wang, Qi‐Geng ; Wang, Qi ; Li, Fang‐Yu ; Cao, Shu‐Man ; Li, Yan ; Li, Ying ; Qin, Wei

AbstractINTRODUCTIONResearch on somatic and germline mutations in Chinese individuals with early‐onset Alzheimer's disease (EOAD) has been limited.METHODSWe conducted whole‐genome sequencing of blood DNA from 108 patients with EOAD and 116 controls. The analysis included somatic and germline mutations across coding and non‐coding regions, mutational signature determination, pathway enrichment identification, and predictive model.RESULTSThe mutational burden was significantly higher in the EOAD group compared to the control group. The prevalence of single‐base substitution signature 5, which is strongly associated with aging, was much higher in patients with EOAD than in controls. EOAD‐specific somatic mutations were identified in genes such as MIR31HG, TUBB4B, and APP. Germline mutations in DOCK3, PCSK5, and PDE4D were significantly associated with age of dementia onset. Furthermore, a predictive model comprising 15 mutations demonstrated an area under the curve of 0.78.DISCUSSIONThe accumulation of senescence‐related somatic mutations may increase the risk of developing EOAD.Highlights

Whole genome sequencing was used to find somatic and germline mutations in Chinese individuals with early‐onset Alzheimer's disease (EOAD).

Total number and burden of blood somatic mutations were significantly higher.

The prevalence of single‐base substitution signature 5 was notably elevated in EOAD.

EOAD‐specific somatic mutations were identified in MIR31HG, TUBB4B, and APP.

DOCK3, PCSK5, and PDE4D germline mutations were associated with the age of EOAD onset.

01 Nov 2024·Journal of Lipid Research

The two major splice variants of scavenger receptor BI differ by their interactions with lipoproteins and cellular localization in endothelial cells

Article

Author: Schlumpf, Eveline ; von Eckardstein, Arnold ; Frey, Kathrin ; Potapenko, Anton ; Robert, Jérôme ; Rohrer, Lucia ; Wollscheid, Bernd

The scavenger receptor BI (SR-BI) facilitates the transport of both HDL and LDL through endothelial cells. Its two splice variants, SR-BI_var1 and SR-BI_var2, differ in their carboxy terminal domains. Only SR-BI_var1 contains the putative binding sites for the adapter proteins PDZ domain containing protein 1 (PDZK1) and dedicator of cytokinesis 4 (DOCK4), which limit the cell surface abundance and internalization of the receptor. To investigate the cellular localization of the SR-BI variants and their interaction with lipoproteins in endothelial cells, EA.hy926 cells were stably transfected with vectors encoding untagged, GFP- or mCherry-tagged constructs of the two SR-BI variants. Additionally, the cells were transfected with shRNAs against PDZK1 or DOCK4. Microscopy investigation showed that SR-BI_var1 was predominantly localized on the cell surface together with clathrin whereas SR-BI_var2 was absent from the cell surface but retrieved in endosomes and lysosomes. Accordingly, only SR-BI_var1 increased lipoprotein binding to endothelial while HDL and LDL uptake were enhanced by both variants. Silencing of PDZK1 or DOCK4 only reduced HDL association in SR-BI_var2 overexpressing cells while LDL association was reduced both in WT and SR-BI_var2 overexpressing cells. In conclusion, either SR-BI variant facilitates the uptake of HDL and LDL into endothelial cells, however by different mechanisms and trafficking routes. This dual role may explain why the loss of DOCK4 or PDZK1 differently affects the uptake of HDL and LDL in different endothelial cells.

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DOCK3

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