Literature summary for 2.7.11.20 extracted from

Cheng, Y.; Ren, X.; Yuan, Y.; Shan, Y.; Li, L.; Chen, X.; Zhang, L.; Takahashi, Y.; Yang, J.W.; Han, B.; Liao, J.; Li, Y.; Harvey, H.; Ryazanov, A.; Robertson, G.P.; Wan, G.; Liu, D.; Chen, A.F.; Tao, Y.; Yang, J.M.
eEF-2 kinase is a critical regulator of Warburg effect through controlling PP2A-A synthesis (2016), Oncogene, 2016, 1-16.

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Activating Compound

Activating Compound	Comment	Organism	Structure
Calmodulin	required	Homo sapiens

Metals/Ions

Metals/Ions	Comment	Organism	Structure
Ca2+	required	Homo sapiens
Mg2+	required	Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates	Organism	Comment (Nat. Sub.)	Natural Products	Comment (Nat. Pro.)	Rev.	Reac.
ATP + [elongation factor 2]	Homo sapiens	-	ADP + [elongation factor 2] phosphate	-	?

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	O00418	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
breast cancer cell	-	Homo sapiens	-
MCF-7 cell	-	Homo sapiens	-
MDA-MB-231 cell	-	Homo sapiens	-
MDA-MB-468 cell	-	Homo sapiens	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
ATP + [elongation factor 2]	-	Homo sapiens	ADP + [elongation factor 2] phosphate	-	?

Synonyms

Synonyms	Comment	Organism
calcium/calmodulin-dependent protein kinase III	-	Homo sapiens
eEF-2 kinase	-	Homo sapiens
EEF-2K	-	Homo sapiens
eukaryotic elongation factor 2 kinase	-	Homo sapiens
eukaryotic elongation factor-2 kinase	-	Homo sapiens

Cofactor

Cofactor	Comment	Organism	Structure
ATP	-	Homo sapiens

General Information

General Information	Comment	Organism
malfunction	knockdown of eEF-2K expression leads to a significant increase in phosphatase 2A-A (PP2A-A) protein synthesis and remarkable downregulation of c-Myc and pyruvate kinase M2 isoform, the key glycolytic enzyme transcriptionally activated by c-Myc. In addition, depletion of eEF-2K reduces the ability of the transformed cells to proliferate and enhance the sensitivity of tumor cells to chemotherapy both in vitro and in vivo. The glucose level is significantly higher in the conditioned medium of the cells with eEF-2K knockdown than that of the control cells. Activation of adenosine monophosphate-activated protein kinase, which increases phosphorylation of AMPK at Thr172, is observed in the cells subjected to silencing of eEF-2K expression. Downregulation of PKM2 mRNA and protein in the cells deficient in eEF-2K, but Overexpression of c-Myc reverses the eEF-2K-mediated downregulation of PKM2 mRNA expression. Silencing of eEF-2K expression blunts the hypoxia-stimulated glycolysis and reduces survival of hypoxic tumor cells. Phenotype, overview	Homo sapiens
physiological function	phosphorylation of eEF-2 by eEF-2K is an essential system in regulation of global protein synthesis. Cancer cells predominantly metabolize glucose by glycolysis to produce energy in order to meet their metabolic requirement, a phenomenon known as Warburg effect. Enzyme eEF-2 kinase is a critical regulator of Warburg effect through controlling synthesis of protein phosphatase 2A-A (PP2A-A), a key factor that facilitates the ubiquitin-proteasomal degradation of c-Myc protein. Eukaryotic elongation factor-2 kinase (eEF-2K) has a negative regulator of protein synthesis, has a critical role in promoting glycolysis in cancer cells. eEF-2K is required for the hypoxia-stimulated glycolysis and promotes survival of hypoxic tumor cells. Enzyme eEF-2K activates PKM2 through stabilizing c-Myc protein, MG132, a proteasome inhibitor, can rescue the downregulation of c-Myc in the cells with knockdown of eEF-2K expression. eEF-2K is supportive to growth and proliferation of tumor cells	Homo sapiens

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Release 2023.1 (January 2023)