Summary of study ST001320

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000897. The data can be accessed directly via it's Project DOI: 10.21228/M8R704 This work is supported by NIH grant, U2C- DK119886.

See: https://www.metabolomicsworkbench.org/about/howtocite.php

This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.

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Study IDST001320
Study TitleExamination of labeled glucose utilization in central carbon metabolism in HeLa cells post WNT stimulation
Study TypeIn vitro
Study SummaryHeLa cells were treated with media containing either vehicle or WNT in combination with UC13-glucose for 20 min or 60 min.
Institute
University of California, Los Angeles
DepartmentBiological Chemisty
LaboratoryChristofk Lab
Last NameChristofk
First NameHeather
Address615 Charles E Young Drive South Los Angeles, CA 90095
Emailhchristofk@mednet.ucla.edu
Phone(310) 794-4248
Submit Date2020-02-19
Raw Data AvailableYes
Raw Data File Type(s).raw
Analysis Type DetailLC-MS
Release Date2020-07-18
Release Version1
Heather Christofk Heather Christofk
https://dx.doi.org/10.21228/M8R704
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000897
Project DOI:doi: 10.21228/M8R704
Project Title:GSK3 inhibits macropinocytosis and lysosomal activity through the Wnt destruction complex machinery
Project Summary:Canonical Wnt signaling is emerging as a major regulator of endocytosis. Here we report that mutation of Axin1, a tumor-suppressor part of the β-catenin destruction complex, results in the activation of macropinocytosis in Alexander hepatocellular carcinoma (HCC) cells. Axin1 binds Glycogen Synthase Kinase 3 (GSK3), and we found that inhibition of GSK3 by Lithium chloride (LiCl), CHIR99021 or dominant-negative GSK3 triggered macropinocytosis. GSK3 inhibition caused a rapid increase in endolysosomes that was independent of new protein synthesis. GSK3 inhibition or Axin1 mutation increased lysosomal activity, which could be followed with tracers for active cathepsin D, β-glucosidase, and ovalbumin degradation. Microinjection of LiCl into the blastula cavity of Xenopus embryos caused a striking increase in dextran macropinocytosis. The effects of GSK3 inhibition on macropinocytosis and protein degradation in endolysosomes were blocked by the macropinocytosis inhibitors EIPA or IPA-2, suggesting that the increased membrane trafficking drives lysosomal activity and nutrient acquisition.
Institute:University of California, Los Angeles
Department:Biological Chemisty
Laboratory:De Robertis Lab
Last Name:De Robertis
First Name:Edward
Address:5-612A MRL
Email:ederobertis@mednet.ucla.edu
Phone:(310) 206-1401
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