Summary of Study ST003531
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 PR002173. The data can be accessed directly via it's Project DOI: 10.21228/M8R23J 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 | ST003531 |
Study Title | Micropeptide hSPAR, a glutamine regulator, suppresses tumor growth via TRIM21-P27KIP1-mTOR pathway - human MDA-MB-231 breast cancer cell |
Study Summary | hSPAR, a microprotein, is capable of specifically inhibiting the mTOR signaling activity and cell proliferation in MDA-MB-231 cells. Glutamine, an essential amino acid, plays a crucial role in regulating the mTOR signal. Our data indicate that in MDA-MB-231 cells, overexpressing hSPAR inhibits glutamine uptake, consequently suppressing the activation of the mTOR signaling. |
Institute | University of Science and Technology of China |
Last Name | Wang |
First Name | Wei |
Address | Division of Life Sciences and Medicine, 443 Huangshan Road, Hefei city, Anhui Province |
WW571@mail.ustc.edu.cn | |
Phone | 18604523231 |
Submit Date | 2024-10-09 |
Raw Data Available | Yes |
Raw Data File Type(s) | mzML |
Analysis Type Detail | LC-MS |
Release Date | 2025-01-06 |
Release Version | 1 |
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Treatment:
Treatment ID: | TR003669 |
Treatment Summary: | MDA-MB-231 breast cancer cells were transfected with empty vector, ΔATG1+2, hSPAR or hSPAR-C for 48 hours. |