Proteomics

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Endothelin-1, over-expressed in SOD1G93A mice, aggravates injury of NSC34-hSOD1G93A cells through complicated molecular mechanism revealed by quantitative proteomics analysis


ABSTRACT: Using proteomic analysis, we revealed that 110 proteins were differentially expressed in NSC34-hSOD1G93A cells after ET-1 treatment in our experiments, of which 54 were up-regulated and 56 were down-regulated. Bioinformatics analysis showed that the differentially expressed proteins (DEPs) were primarily enriched in hippo signaling pathway-multiple species, ABC transporters, ErbB signaling pathway and so on. These results provide further insights on the potential roles of ET-1 in ALS. Our study presents a new promising therapeutic target to protect MNs of ALS.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Differentiation In Spinal Cord

DISEASE(S): Amyotrophic Lateral Sclerosis

SUBMITTER: Yingzhen Zhang  

LAB HEAD: Guo Yansu

PROVIDER: PXD037555 | Pride | 2023-03-11

REPOSITORIES: Pride

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Endothelin-1, over-expressed in SOD1<sup>G93A</sup> mice, aggravates injury of NSC34-hSOD1G93A cells through complicated molecular mechanism revealed by quantitative proteomics analysis.

Zhang Yingzhen Y   Chen Lin L   Li Zhongzhong Z   Li Dongxiao D   Wu Yue Y   Guo Yansu Y  

Frontiers in cellular neuroscience 20221201


Endothelin-1 (ET-1), a secreted signaling peptide, is suggested to be involved in multiple actions in various tissues including the brain, but its role in amyotrophic lateral sclerosis (ALS) remains unknown. In this study, we detected the expression changes as well as the cellular localization of ET-1, endothelin A (ET-A) and endothelin B (ET-B) receptors in spinal cord of transgenic SOD1-G93A (TgSOD1-G93A) mice, which showed that the two ET receptors (ET-Rs) expressed mainly on neurons and decr  ...[more]

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