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Regulation of glucose transporters by protein kinases in cancer cells

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abstract #3699 esmo 2017_AH.pdf210.36 KBAdobe PDF Ver/Abrir
Regulation of glucose_mdx361.036.pdf61.67 KBAdobe PDF Ver/Abrir

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Resumo(s)

Background: Cancer cells require increased glucose supply to sustain proliferation. One mechanism involves increased expression of glucose transporter (GLUT) genes. But insulin has revealed that protein phosphorylation is another key mechanism in glucose uptake regulation: insulin binding to responsive cells triggers a signalling cascade with phosphorylation of TBC1D4, a negative regulator of endosomal GLUT trafficking, so that more transporters are inserted into the plasma membrane. Previous work from the host lab has identified the family of WNK protein kinases and shown that WNK1 can also phosphorylate TBC1D4 and promote GLUT translocation to the cell surface. Our objective is to understand the contribution of WNK1 to glucose uptake in colorectal cancer cells. Our objective is to understand the contribution of WNK1 to glucose uptake in colorectal cancer cells.

Descrição

ESMO 2017 - 42nd European Society of Medical Oncology Congress 2017, 8-12 September 2017, Madrid, Spain

Palavras-chave

WNK Protein Kinases Colorectal Cancer Transporte de Glucose Vias de Transdução de Sinal e Patologias Associadas Cancro Coloretal

Contexto Educativo

Citação

Ann Oncol. 2017 Sept;28(Suppl 5):50-52. doi:10.1093/annonc/mdx361.036.

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Editora

Oxford University Press/European Society for Medical Oncology

Licença CC

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