Proteomics

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Induction of muscle atrophy by tumor and dexamethasone regulates a distinct set of proteins from atrophy caused by aging

ABSTRACT: To assess changes in the muscle proteome that due to tumor burden and dexamethasone treatments and compare proteomic changes that occur in atrophy due to tumor burden and dexamethasone treatment with atrophy caused by aging. Regulators of muscle atrophy induced by diseases such as cancer or drugs such as dexamethasone are largely unknown. We would therefore like to determine the proteomic signature of atrophying muscle caused by tumor burden (LLC cell injected mice) and dexamethasone treatment in order to examine possible biomarkers and regulators of muscle atrophy. We would also like to compared the proteomic signature of different modes of muscle atrophy to determine similarities and differences in the possible biomarkers and regulators.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Skeletal Muscle Tissue, Tibialis Anterior

DISEASE(S): Muscular Atrophy,Cachexia

SUBMITTER: Zuo-Fei Yuan  

LAB HEAD: Fabio Demontis

PROVIDER: PXD027490 | Pride | 2022-02-22

REPOSITORIES: Pride

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Dataset's files

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Action DRS
Dexamethasone_F1.mzXML Mzxml
Dexamethasone_F1.pepXML Pepxml
Dexamethasone_F1.raw Raw
Dexamethasone_F10.mzXML Mzxml
Dexamethasone_F10.pepXML Pepxml
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Publications

Integrated genomic and proteomic analyses identify stimulus-dependent molecular changes associated with distinct modes of skeletal muscle atrophy.

Hunt Liam C LC   Graca Flavia A FA   Pagala Vishwajeeth V   Wang Yong-Dong YD   Li Yuxin Y   Yuan Zuo-Fei ZF   Fan Yiping Y   Labelle Myriam M   Peng Junmin J   Demontis Fabio F  

Cell reports 20211101 6

Skeletal muscle atrophy is a debilitating condition that occurs with aging and disease, but the underlying mechanisms are incompletely understood. Previous work determined that common transcriptional changes occur in muscle during atrophy induced by different stimuli. However, whether this holds true at the proteome level remains largely unexplored. Here, we find that, contrary to this earlier model, distinct atrophic stimuli (corticosteroids, cancer cachexia, and aging) induce largely different  ...[more]

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