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PERK/CHOP Contributes to the CGK733-induced Vesicular Calcium Sequestration Which Is Accompanied by Non-Apoptotic Cell Death

PERK/CHOP Contributes to the CGK733-induced Vesicular Calcium Sequestration Which Is Accompanied by Non-Apoptotic Cell Death

Yufeng Wang, Yasuhiro Kuramitsu, Byron Baron, Takao Kitagawa, Junko Akada, Kazuhiro Tokuda, Dan Cui, Kazuyuki Nakamura

Oncotarget. 2015 Sep 22;6(28):25252-65.

PMID: 26259235

Abstract:

Calcium ions (Ca(2+)) are indispensable for the physiology of organisms and the molecular regulation of cells. We observed that CGK733, a synthetic chemical substance, induced non-apoptotic cell death and stimulated reversible calcium sequestration by vesicles in pancreatic cancer cells. The endoplasmic reticulum (ER) stress eukaryotic translation initiation factor 2-alpha kinase 3/C/EBP homologous protein (PERK/CHOP) signaling pathway was shown to be activated by treatment with CGK733. Ionomycin, an ER stress drug and calcium ionophore, can activate PERK/CHOP signaling and accelerate CGK733-induced calcium sequestration. Knockdown of CHOP diminished CGK733-induced vesicular calcium sequestration, but had no effects on the cell death. Proteomic analysis demonstrated that the ER-located calcium-binding proteins, calumenin and protein S100-A11, were altered in CGK733-treated cells compared to non-treated controls. Our study reveals that CGK733-induced intracellular calcium sequestration is correlated with the PERK/CHOP signaling pathway and may also be involved in the dysregulations of calcium-binding proteins.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
IAR4242694	CGK733			Price

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