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Title: Emerging roles of downstream of kinase 3 in cell signaling
Authors: Loh, Jia Tong
Teo, Joey Kay Hui
Lim, Hong-Hwa
Lam, Kong-Peng
Keywords: Science::Biological sciences
Issue Date: 2020
Source: Loh, J. T., Teo, J. K. H., Lim, H.-H., & Lam, K.-P. (2020). Emerging roles of downstream of kinase 3 in cell signaling. Frontiers in Immunology, 11, 566192-. doi:10.3389/fimmu.2020.566192
Project: NMRC/OFYIRG/083/2018 
Journal: Frontiers in Immunology 
Abstract: Downstream of kinase (Dok) 3 is a member of the Dok family of adaptor proteins known to regulate signaling pathways downstream of various immunoreceptors. As Dok-3 lacks intrinsic catalytic activity, it functions primarily as a molecular scaffold to facilitate the nucleation of protein complexes in a regulated manner and hence, achieve specificity in directing signaling cascades. Since its discovery, considerable progress has been made toward defining the role of Dok-3 in limiting B cell-receptor signaling. Nonetheless, Dok-3 has since been implicated in the signaling of Toll-like and C-type lectin receptors. Emerging data further demonstrate that Dok-3 can act both as an activator and inhibitor, in lymphoid and non-lymphoid cell types, suggesting Dok-3 involvement in a plethora of signal transduction pathways. In this review, we will focus on the structure and expression profile of Dok-3 and highlight its role during signal transduction in B cells, innate cells as well as in bone and lung tissues.
ISSN: 1664-3224
DOI: 10.3389/fimmu.2020.566192
Rights: © 2020 Loh, Teo, Lim and Lam. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Fulltext Permission: open
Fulltext Availability: With Fulltext
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