Summary of Study ST001303
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 PR000884. The data can be accessed directly via it's Project DOI: 10.21228/M8DX2P 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 | ST001303 |
Study Title | TGF-Beta 3 heterozygous mice |
Study Type | Mice nephropathy in lipotoxic model |
Study Summary | Transforming growth factor β (TGFβ) family comprises the main player in the development of fibrosis including three isoforms: TGFβ1, TGFβ2 and TGFβ3. TGFβ3 may play an antifibrotic role at the renal level, counteracting the role of TGFβ1, using a mouse model heterozygous for the TGFβ3 gene (TGFβ3+/-). Partial deletion of TGFβ3 causes in the mice albuminuria, loss of glomerular filtration rate, accelerated fibrosis, epithelial-to-mesenchymal transition and increment of glomerular basement membrane thickening. |
Institute | University Rey Juan Carlos |
Department | Basics Science of Health |
Last Name | Lanzon |
First Name | Borja |
Address | Avenida de Atenas S/N |
borja.lanzon@urjc.es | |
Phone | 663692554 |
Submit Date | 2019-12-19 |
Num Groups | 2 |
Total Subjects | 14 |
Num Males | 14 |
Raw Data Available | Yes |
Raw Data File Type(s) | d |
Analysis Type Detail | GC-MS/LC-MS |
Release Date | 2020-03-03 |
Release Version | 1 |
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Project:
Project ID: | PR000884 |
Project DOI: | doi: 10.21228/M8DX2P |
Project Title: | TGFβ3 heterozygous mice |
Project Type: | Mice nephropathy in lipotoxic model |
Project Summary: | Transforming growth factor β (TGFβ) family comprises the main player in the development of fibrosis including three isoforms: TGFβ1, TGFβ2 and TGFβ3. TGFβ3 may play an antifibrotic role at the renal level, counteracting the role of TGFβ1, using a mouse model heterozygous for the TGFβ3 gene (TGFβ3+/-). Partial deletion of TGFβ3 causes in the mice albuminuria, loss of glomerular filtration rate, accelerated fibrosis, epithelial-to-mesenchymal transition and increment of glomerular basement membrane thickening. |
Institute: | University Rey Juan Carlos |
Department: | Basics Science of Health |
Last Name: | Lanzon |
First Name: | Borja |
Address: | Avenida de Atenas S/N, Alcorcón, Madrid, 28922, Spain |
Email: | borja.lanzon@urjc.es |
Phone: | 663692554 |