Proteomics

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Regulation of hyperoxia-induced neonatal lung injury via posttranslational cysteine redox modifications

ABSTRACT: Lung tissue from normoxia- or hyperoxia-treated control or SCNN1B overexpression mice were processed with a redox proteomics workflow and analyzed by LC-MS/MS with TMT based quantification. Data was searched with MS-GF+ using PNNL's DMS Processing pipeline.

INSTRUMENT(S): Q Exactive Plus

ORGANISM(S): Mus Musculus (ncbitaxon:10090)

SUBMITTER: Wei-Jun Qian  

PROVIDER: MSV000090157 | MassIVE | Thu Aug 18 12:24:00 BST 2022

SECONDARY ACCESSION(S): PXD036154

REPOSITORIES: MassIVE

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Regulation of hyperoxia-induced neonatal lung injury via post-translational cysteine redox modifications.

Zhang Tong T   Day Nicholas J NJ   Gaffrey Matthew M   Weitz Karl K KK   Attah Kwame K   Mimche Patrice N PN   Paine Robert R   Qian Wei-Jun WJ   Helms My N MN  

Redox biology 20220719

Preterm infants and patients with lung disease often have excess fluid in the lungs and are frequently treated with oxygen, however long-term exposure to hyperoxia results in irreversible lung injury. Although the adverse effects of hyperoxia are mediated by reactive oxygen species, the full extent of the impact of hyperoxia on redox-dependent regulation in the lung is unclear. In this study, neonatal mice overexpressing the beta-subunit of the epithelial sodium channel (β-ENaC) encoded by Scnn1  ...[more]

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