Dataset Information

Aurora A phosphorylates PKM2 at T45.

ABSTRACT: Flag-PKM2 was expressed in H1299 cells. Then the H1299 cells were treated with DMSO or 100nM MLN8237. Then, cell lysate was incubated with anti-Flag M2-agarose. Elutes were separated with 10% SDS-PAGE. The gel was stained with Coomassie Brilliant Blue. Visualized bands were excised and subjected to LC-MS/MS analysis. Then the phosphorylation sites of PKM2 were identified.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Aoxing Cheng

LAB HEAD: Zhenye yang

PROVIDER: PXD036575 | Pride | 2023-03-11

REPOSITORIES: Pride

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Publications

Aurora A-mediated pyruvate kinase M2 phosphorylation promotes biosynthesis with glycolytic metabolites and tumor cell cycle progression.

Jiang Ya Y Wang Ting T Sheng Dandan D Han Chaoqiang C Xu Tian T Zhang Peng P You Weiyi W Fan Weiwei W Zhang Zhiyong Z Jin Tengchuan T Duan Xiaotao X Yuan Xiao X Liu Xing X Zhang Kaiguang K Ruan Ke K Shi Jue J Guo Jing J Cheng Aoxing A Yang Zhenye Z

The Journal of biological chemistry 20221002 11

Cancer cells have distinctive demands for intermediates from glucose metabolism for biosynthesis and energy in different cell cycle phases. However, how cell cycle regulators and glycolytic enzymes coordinate to orchestrate the essential metabolic processes are still poorly characterized. Here, we report a novel interaction between the mitotic kinase, Aurora A, and the glycolytic enzyme, pyruvate kinase M2 (PKM2), in the interphase of the cell cycle. We found Aurora A-mediated phosphorylation of ...[more]

PMID: 36198360

Similar Datasets

Project description:Purpose: PKM2-mediated metabolic switch to aerobic glycolysis plays a critical role in promoting cell survival and proliferation. However, little is known about the function of intestinal epithelial PKM2 in intestinal homeostasis. Here we investigated whether and how intestinal epithelial PKM2 modulates the morphology and function of the adult intestine in experimental murine colitis. Methods: Colonoscopic biopsies from the Crohn’s disease (CD) and ulcerative colitis (UC) patients (10 each) were analyzed for PKM2 expression. We also generated intestinal epithelial-specific Pkm2 knockout mice and employed them to examine PKM2 function. Mouse intestinal inflammation was induced with dextran sulfate sodium (DSS) in drinking water. Disease phenotypes were investigated by mouse survival, body weight, colon length and analysis of immune cell infiltration in colon, intestinal epithelial cell gene profiling and signal pathway. Results: Intestinal epithelial PKM2 level in UC and CD patients was significantly decreased compared to that from non-inflamed intestinal epithelium. Similar reduction of intestinal epithelial PKM2 was observed in mice with experimental colitis. Supporting the notion that PKM2 serves as a safeguard against colitis, intestinal epithelial-specific Pkm2-deficient (Pkm2-/-) mice displayed a severer intestinal inflammation, companying with shortened colon, disruption of epithelial tight junction, higher permeability, elevation of inflammatory cytokines and immune cell infiltration, compared with wild-type mice. Gene profiling and western blot analysis indicated that cell survival signaling, particularly the Akt/β-catenin pathways, were downregulated in Pkm2-/- mice. Functional assay using mouse primary colonic epithelial cells confirmed that Pkm2 reduction decreased proliferation and migration of epithelial cells, while enhanced expression of Pkm2 was associated with increased transcriptional activity of β-catenin. Moreover, increasing mouse intestinal epithelial Pkm2 expression via delivery of Pkm2-expressing plasmid attenuated DSS-induced experimental colitis. Conclusions: Intestinal epithelial PKM2, through activating Wnt/β-catenin signaling, induces a strong proliferative and migratory response that increases cell survival and wound healing under colitic condition.

			Action	DRS
	PKM-AuroraA-KD.xlsx	Xlsx
	PKM-AuroraA-WT.xlsx	Xlsx
	PKM2-AuroraA-KD.raw	Raw
	PKM2-AuroraA-WT.raw	Raw
	PKM2-DMSO.raw	Raw