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.
| Study ID | ST001320 |
| Study Title | Examination of labeled glucose utilization in central carbon metabolism in HeLa cells post WNT stimulation |
| Study Type | In vitro |
| Study Summary | HeLa 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 |
| Department | Biological Chemisty |
| Laboratory | Christofk Lab |
| Last Name | Christofk |
| First Name | Heather |
| Address | 615 Charles E Young Drive South Los Angeles, CA 90095 |
| hchristofk@mednet.ucla.edu | |
| Phone | (310) 794-4248 |
| Submit Date | 2020-02-19 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | raw(Thermo) |
| Analysis Type Detail | LC-MS |
| Release Date | 2020-07-18 |
| Release Version | 1 |
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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 |
