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Status |
Public on Aug 31, 2022 |
Title |
Loss of GPHR in the brain |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
The Golgi apparatus plays a central role in the protein glycosylation where it is required for secretory trafficking. Abnormal morphology of the Golgi apparatus has been widely observed in neurodegenerative disease. Golgi pH regulator (GPHR) is an anion channel essential for acidification of the Golgi lumen and its essential for normal morphology and function of the Golgi apparatus. To address the Golgi dysfunction in neuronal cells, we established brain-specific GPHR knockout mice (GPHRf/f;Nes).
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Overall design |
The total RNA was prepared from GPHRf/f;Nes and control littermate mouse brain at P10.
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Contributor(s) |
Sou Y |
Citation(s) |
36056653 |
Submission date |
Jul 20, 2022 |
Last update date |
Nov 30, 2022 |
Contact name |
Yu-shin Sou |
E-mail(s) |
ysodaka@juntendo.ac.jp
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Phone |
0358021025
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Organization name |
Juntendo University Graduate School of Medicine
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Department |
Department of Cell Biology and Neuroscience
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Street address |
2-1-1 Hongo
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City |
Bunkyo-ku |
State/province |
Tokyo |
ZIP/Postal code |
113-8421 |
Country |
Japan |
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Platforms (1) |
GPL21163 |
Agilent-074809 SurePrint G3 Mouse GE v2 8x60K Microarray [Probe Name version] |
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Samples (2) |
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Relations |
BioProject |
PRJNA860354 |