Summary of Study ST000276
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 PR000154. The data can be accessed directly via it's Project DOI: 10.21228/M8688J This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
Study ID | ST000276 |
Study Title | IDH1 and Glioma knockdown idh1 |
Study Summary | This study is a part of series performed for the same researcher through pilot/feasibility grant program, so the publication is relevant reference for other studies (ST000199) This specific experiment is a pilot study to compare the metabolism of cells transformed using empty vector against cells transformed with vector carrying short hairpin RNA (shRNA) targeted to silence isocitrate dehydrogenase-1 (IDH1) gene. |
Institute | University of Michigan |
Department | Neurology |
Laboratory | Stegh Lab (Northwestern University) |
Last Name | Calvert |
First Name | Andrea |
Address | Evanston, IL |
a-calvert@u.northwestern.edu | |
Phone | 312-503-3134 |
Submit Date | 2014-06-11 |
Num Groups | 2 |
Total Subjects | 10 |
Study Comments | Subject IDs are updated to correcly show before/after exercise samples taken from the same person |
Raw Data File Type(s) | d |
Analysis Type Detail | GC-MS/LC-MS |
Release Date | 2016-01-13 |
Release Version | 1 |
Select appropriate tab below to view additional metadata details:
Project:
Project ID: | PR000154 |
Project DOI: | doi: 10.21228/M8688J |
Project Title: | Isocitrate dehydrogenase-1 and Glioma Studies |
Project Summary: | Dr. Stegh will define the role of a novel glioma oncoprotein, termed isocitrate dehydrogenase-1 (IDH1), in driving progression and therapy resistance of glioblastoma (GBM). Understanding the molecular basis of the therapy refractoriness of GBM is one of the most important areas of glioma research.IDH1 is a critical enzyme of the citric acid cycle (CAC) and is a master regulator of metabolism. Building on his preliminary studies, Dr. Stegh will molecularly characterize the precise mechanism, by which IDH1 protects glioma cells from therapy-induced cell death using glioma cell and mouse models. To target IDH1 signaling in GBM, he will leverage these model systems and mechanistical knowledge to develop and preclinically characterize RNA interference RNAi-based nanomaterials. He will generate RNAi-functionalized spherical nucleic acids (SNAs) that neutralize IDH1 expression in established gliomas. Due to the negative charge of the RNA backbone, however, siRNA oligonucleotides have many downsides, such as they trigger auto-immune responses, and cannot cross the blood-brain-barrier (BBB). In contrast, SNAs are able to transverse cellular membranes, do not require the use of toxic auxiliary reagents, and accumulate in cells and intracranial tumors very effectively. They also exhibit extraordinary stability in physiological environments, cross the BBB, are highly resistant to nuclease degradation, and thus, can move through biological fluids and avoid being destroyed as “foreign materials.” Dr. Stegh proposes to preclinically evaluate these IDH1-targeting nanoconjugates to provide a fundamentally novel treatment option of patients diagnosed with GBM, and will aid in successfully implementing RNAi-based therapies into neuro-oncological practice. |
Institute: | Northwestern University |
Department: | Neurology |
Laboratory: | Stegh Lab |
Last Name: | Stegh |
First Name: | Alexander |
Address: | Evanston, IL |
Email: | a-stegh@northwestern.edu |
Phone: | 312-503-2879 |
Subject:
Subject ID: | SU000296 |
Subject Type: | Human |
Subject Species: | Homo sapiens |
Taxonomy ID: | 9606 |
Species Group: | Human |
Factors:
Subject type: Human; Subject species: Homo sapiens (Factor headings shown in green)
mb_sample_id | local_sample_id | IDH1 Knockdown |
---|---|---|
SA012219 | S00014999 | No |
SA012220 | S00015002 | No |
SA012221 | S00015003 | No |
SA012222 | S00015001 | No |
SA012223 | S00015000 | No |
SA012224 | S00015007 | yes |
SA012225 | S00015008 | yes |
SA012226 | S00015005 | yes |
SA012227 | S00015004 | yes |
SA012228 | S00015006 | yes |
Showing results 1 to 10 of 10 |
Collection:
Collection ID: | CO000290 |
Collection Summary: | - |
Sample Type: | Cells, Cultured |
Treatment:
Treatment ID: | TR000310 |
Sample Preparation:
Sampleprep ID: | SP000304 |
Sampleprep Summary: | - |
Sampleprep Protocol Filename: | Gly-TCA-nucleotides_analysis_protocol-2015-03-09.docx |
Combined analysis:
Analysis ID | AN000440 | AN000441 |
---|---|---|
Analysis type | MS | MS |
Chromatography type | HILIC | GC |
Chromatography system | Agilent 1260 | Agilent 7890A |
Column | Phenomenex Luna NH2 (150 x 1mm,3um) | Agilent DB5-MS (30m × 0.25mm, 0.25um) |
MS Type | ESI | EI |
MS instrument type | QTOF | Single quadrupole |
MS instrument name | Agilent 6530 QTOF | Agilent 5975C |
Ion Mode | POSITIVE | POSITIVE |
Units | pmol/µg protein | pmol/µg protein |
Chromatography:
Chromatography ID: | CH000311 |
Methods ID: | AQM020 |
Methods Filename: | QTOF-002-HILIC-35min-1mm.m |
Instrument Name: | Agilent 1260 |
Column Name: | Phenomenex Luna NH2 (150 x 1mm,3um) |
Chromatography Type: | HILIC |
Chromatography ID: | CH001307 |
Methods ID: | AQM011 |
Methods Filename: | ALPHA_KETO_ACIDS-FULL.M.zip |
Instrument Name: | Agilent 7890A |
Column Name: | Agilent DB5-MS (30m × 0.25mm, 0.25um) |
Chromatography Type: | GC |
MS:
MS ID: | MS000381 |
Analysis ID: | AN000440 |
Instrument Name: | Agilent 6530 QTOF |
Instrument Type: | QTOF |
MS Type: | ESI |
Ion Mode: | POSITIVE |
Acquisition Parameters File: | Column1_solv1_jetstream+_grad9.m |
Processing Parameters File: | EX00317-MassHunterQuant-GlyTCA-DataAnalysis-LCMS-Method.m |
MS ID: | MS000382 |
Analysis ID: | AN000441 |
Instrument Name: | Agilent 5975C |
Instrument Type: | Single quadrupole |
MS Type: | EI |
Ion Mode: | POSITIVE |
Acquisition Parameters File: | ALPHA_KETO_ACIDS-FULL.M |
Processing Parameters File: | EX00317-MassHunterQuant-GlyTCA-DataAnalysis-GCMS-Method.m |