Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Orbitrap Fusion Lumos
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Cell Culture
SUBMITTER: 
Michael Podolsky
LAB HEAD: Michael J. Podolsky
PROVIDER: PXD048563 | Pride | 2024-05-22
REPOSITORIES: pride
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| MP1593_2ndbatch_DDA_Mut.raw | Raw | |||
| MP1593_2ndbatch_DDA_WT.raw | Raw | |||
| peptides.txt | Txt | |||
| proteinGroups.txt | Txt | |||
| supp_data_3.xlsx | Xlsx |
Items per page: 5 1 - 5 of 5 |
Publications
Genome-wide screens identify SEL1L as an intracellular rheostat controlling collagen turnover.
Podolsky Michael J MJ Kheyfets Benjamin B Pandey Monika M Beigh Afaq H AH Yang Christopher D CD Lizama Carlos O CO Datta Ritwik R Lin Liangguang L LL Wang Zhihong Z Wolters Paul J PJ McManus Michael T MT Qi Ling L Atabai Kamran K
Nature communications 20240220 1
Accumulating evidence has implicated impaired extracellular matrix (ECM) clearance as a key factor in fibrotic disease. Despite decades of research elucidating the effectors of ECM clearance, relatively little is understood regarding the upstream regulation of this process. Collagen is the most abundant constituent of normal and fibrotic ECM in mammalian tissues. Its catabolism occurs through extracellular proteolysis and cell-mediated uptake of collagen fragments for intracellular degradation. ...[more]
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