Last update 01 Nov 2024

EEF2K

Last update 01 Nov 2024

Basic Info

Synonyms

Calcium/calmodulin-dependent eukaryotic elongation factor 2 kinase, CaMKIII, eEF-2 kinase

+ [3]

Introduction

Threonine kinase that regulates protein synthesis by controlling the rate of peptide chain elongation. Upon activation by a variety of upstream kinases including AMPK or TRPM7, phosphorylates the elongation factor EEF2 at a single site, renders it unable to bind ribosomes and thus inactive. In turn, the rate of protein synthesis is reduced.

Drugs associated with EEF2K

A-484954

Target

EEF2K

Mechanism

EEF2K inhibitors

Active Org.

Abbott Laboratories

Originator Org.

Abbott Laboratories

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

EEF2K inhibitors(Central South University)

Target

EEF2K

Mechanism

EEF2K inhibitors

Active Org.

Central South University

Originator Org.

Central South University

Active Indication

Triple Negative Breast Cancer

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

eEF2K (Johns Hopkins University)

Target

EEF2K

Mechanism

EEF2K inhibitors

Active Org.-

Originator Org.

University of Medicine & Dentistry of New Jersey

Active Indication-

Inactive Indication

Alzheimer Disease [+3]

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with EEF2K

100 Translational Medicine associated with EEF2K

0 Patents (Medical) associated with EEF2K

417

Literatures (Medical) associated with EEF2K

01 Dec 2024·Archives of Toxicology

Research advances on CaMKs-mediated neurodevelopmental injury

Review

Author: Xu, Bin ; Yang, Tianyao ; Yang, Jing ; Yang, Huajie ; Kong, Lingxu ; Liu, Wei

Calcium/calmodulin-dependent protein kinases (CaMKs) are important proteins in the calcium signaling cascade response pathway, which can broadly regulate biological functions in vivo. Multifunctional CaMKs play key roles in neural development, including neuronal circuit building, synaptic plasticity establishment, and neurotrophic factor secretion. Currently, four familial proteins, calcium/calmodulin-dependent protein kinase I (CaMKI), calcium/calmodulin-dependent protein kinase II (CaMKII), eukaryotic elongation factor 2 kinase (eEF2K, popularly known as CaMKIII) and calcium/calmodulin-dependent protein kinase IV (CaMKIV), are thought to have been the most extensively studied during neurodevelopment. Although their spatial structures are extremely similar, as well as the initial starting point of activation, both require the activation of calcium and calmodulin (CaM) complexes to be involved in the process, and the phosphorylation sites and modes of each member are different. Furthermore, due to the high structural similarity of CaMKs, their members may play synergistic roles in the regulation of neural development, but different CaMKs also have their own means of regulating neural development. In this review, we first describe the visualized protein structural forms of CaMKI, CaMKII, eEF2K and CaMKIV, and then describe the functions of each kinase in neurodevelopment. After that, we focus on four main mechanisms of neurodevelopmental damage caused by CaMKs: CaMKI/ERK/CREB pathway inhibition leading to dendritic spine structural damage; Ca²⁺/CaM/CaMKII through induction of mitochondrial kinetic disorders leading to neurodevelopmental damage; CaMKIII/eEF2 hyperphosphorylation affects the establishment of synaptic plasticity; and CaMKIV/JNK/NF-κB through induction of an inflammatory response leading to neurodevelopmental damage. In conclusion, we briefly discuss the pathophysiological significance of aberrant CaMK family expression in neurodevelopmental disorders, as well as the protective effects of conventional CaMKII and CaMKIII antagonists against neurodevelopmental injury.

01 Nov 2024·Bioactive Materials

Promotion of osteochondral repair through immune microenvironment regulation and activation of endogenous chondrogenesis via the release of apoptotic vesicles from donor MSCs

Article

Author: Zheng, Jinxuan ; Wu, Jiang ; Liu, Shuyun ; Yuan, Xun ; Ning, Chao ; Guo, Quanyi ; Guo, Weimin ; Yu, Rongcheng ; Liao, Chenxi ; Tang, Yiqi ; Yin, Han ; Zhao, Zhe ; Yan, Zineng ; Ding, Zhengang ; Sui, Xiang ; Tian, Guangzhao

Utilizing transplanted human umbilical cord mesenchymal stem cells (HUMSCs) for cartilage defects yielded advanced tissue regeneration, but the underlying mechanism remain elucidated.Early after HUMSCs delivery to the defects, we observed substantial apoptosis.The released apoptotic vesicles (apoVs) of HUMSCs promoted cartilage regeneration by alleviating the chondro-immune microenvironment.ApoVs triggered M2 polarization in macrophages while simultaneously facilitating the chondrogenic differentiation of endogenous MSCs.Mechanistically, in macrophages, miR-100-5p delivered by apoVs activated the MAPK/ERK signaling pathway to promote M2 polarization.In MSCs, let-7i-5p delivered by apoVs promoted chondrogenic differentiation by targeting the eEF2K/p38 MAPK axis.Consequently, a cell-free cartilage regeneration strategy using apoVs combined with a decellularized cartilage extracellular matrix (DCM) scaffold effectively promoted the regeneration of osteochondral defects.Overall, new mechanisms of cartilage regeneration by transplanted MSCs were unconcealed in this study.Moreover, we provided a novel exptl. basis for cell-free tissue engineering-based cartilage regeneration utilizing apoVs.

01 Oct 2024·Drug Discovery Today

Targeting eukaryotic elongation factor 2 kinase (eEF2K) with small-molecule inhibitors for cancer therapy

Review

Author: Wang, Huiping ; Jin, Wenke ; Guo, Chuanxin ; Zhang, Lan ; Fu, Leilei ; Li, Zixiang

Eukaryotic elongation factor 2 kinase (eEF2K) is a member of the α-kinase family that is activated by calcium/calmodulin. Of note, eEF2K is crucial for regulating translation and is often highly overexpressed in malignant cells. Therefore in this review, we summarize the molecular structure of eEF2K and its oncogenic roles in cancer. Moreover, we further discuss the inhibition of eEF2K with small-molecule inhibitors and other new emerging therapeutic strategies in cancer therapy. Taken together, these inspiring findings provide new insights into a promising strategy for inhibiting eEF2K to greatly improve future cancer therapy.

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EEF2K

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