<HashMap><database>bioimages</database><scores/><additional><omics_type>Unknown</omics_type><submitter/><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-BIAD1435</full_dataset_link><repository>bioimages</repository><figure_sub>Specimen</figure_sub><figure_sub>Study Component</figure_sub><figure_sub>organisation</figure_sub><figure_sub>Biosample</figure_sub><figure_sub>Associations</figure_sub><figure_sub>Image acquisition</figure_sub><pubmed_authors>Darren Reece Williams</pubmed_authors><pubmed_authors>Sang Hoon LEE</pubmed_authors></additional><is_claimable>false</is_claimable><name>Targeting phosphatase DUSP22 ameliorates skeletal muscle wasting via Akt independent JNK-FOXO3a repression</name><description>Skeletal muscle wasting results from numerous conditions, such as sarcopenia, glucocorticoid therapy or intensive care. It prevents independent living in the elderly, predisposes to secondary diseases, and ultimately reduces lifespan. There is no approved drug therapy and the major causative mechanisms are not fully understood. Dual specificity phosphatase 22 (DUSP22) is a pleiotropic signaling molecule that plays important roles in immunity and cancer. However, the role of DUSP22 in skeletal muscle wasting is unknown. In this study, DUSP22 was found to be upregulated in sarcopenia patients and models of skeletal muscle wasting. DUSP22 knockdown or pharmacological inhibition with BML-260 prevented multiple forms of muscle wasting. Mechanistically, targeting DUSP22 suppressed FOXO3a, a mast</description><dates><release>2024-10-26T00:00:00Z</release><modification>2024-10-26T12:51:21.143Z</modification><creation>2024-10-26T12:51:21.143Z</creation></dates><accession>S-BIAD1435</accession><cross_references/></HashMap>