Summary of Study ST001150
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 PR000769. The data can be accessed directly via it's Project DOI: 10.21228/M88T11 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 | ST001150 |
Study Title | Metabolomics of a Mouse Model for Retinitis Pigmentosa |
Study Summary | Retinitis pigmentosa (RP) is a degenerative disease of the retina that affects approximately 1 million people worldwide. There are multiple genetic causes of this disease, for which, at present, there are no effective therapeutic strategies. We utilized broad spectrum metabolomics to identify perturbations in the metabolism of the rd10 mouse, a genetic model for RP. C57BL/6J and rd10 mice were raised in cyclic light followed by either light or dark adaptation at postnatal day (P) 18, an early stage in the degeneration process. Mice raised entirely in the dark until P18 were also evaluated. After euthanasia, retinas were removed and extracted for analysis by ultra-performance liquid chromatography-time of flight-mass spectrometry (UPLC-QTOF-MS). |
Institute | University of North Carolina at Chapel Hill |
Department | Department of Cell Biology & Physiology |
Last Name | Weiss |
First Name | Ellen |
Address | CB# 7545, 5340B MBRB, 111 Mason Farm Rd. Chapel Hill, NC 27599-7090 |
erweiss@med.unc.edu | |
Phone | 919-966-7683 |
Submit Date | 2019-03-18 |
Analysis Type Detail | LC-MS |
Release Date | 2019-07-17 |
Release Version | 1 |
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Project:
Project ID: | PR000769 |
Project DOI: | doi: 10.21228/M88T11 |
Project Title: | Metabolomics of a Mouse Model for Retinitis Pigmentosa |
Project Summary: | Retinitis pigmentosa (RP) is a degenerative disease of the retina that affects approximately 1 million people worldwide. There are multiple genetic causes of this disease, for which, at present, there are no effective therapeutic strategies. We utilized broad spectrum metabolomics to identify perturbations in the metabolism of the rd10 mouse, a genetic model for RP. C57BL/6J and rd10 mice were raised in cyclic light followed by either light or dark adaptation at postnatal day (P) 18, an early stage in the degeneration process. Mice raised entirely in the dark until P18 were also evaluated. After euthanasia, retinas were removed and extracted for analysis by ultra-performance liquid chromatography-time of flight-mass spectrometry (UPLC-QTOF-MS). |
Institute: | University of North Carolina |
Laboratory: | ERCMRC |
Last Name: | Sumner |
First Name: | Susan |
Address: | NRI, 500 Laureate Way, Kannapolis, NC, 28081, USA |
Email: | susan_sumner@unc.edu |
Phone: | 704-250-5066 |
Funding Source: | NIDDK U24DK097193 (Sumner, PI); Supplement to NEI R01EY12224 (Weiss, PI) |