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| 2.07 MB | Adobe PDF |
Advisor(s)
Abstract(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.
Description
Abstract Review publicado em: EMJ Oncol. 5[1]: pp 50-52.
Keywords
Cancer Cell WNK Protein Kinases Glucose Transport Cancro Coloretal Vias de Transdução de Sinal e Patologias Associadas
