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LC-MS/MS identified the TRIM16-binding proteins

ABSTRACT: Vascular calcification (VC) is highly prevalent in patients with chronic kidney disease (CKD). To date, effective treatments for VC are still lacking since the underlying mechanisms remains elusive. RNA-sequencing analysis revealed that the E3 ubiquitin ligase Tripartite motif 16 (TRIM16) may be a key modulator of VC. However, it remains unclear whether TRIM16-mediated ubiquitination contributes to VC. In the present study, we used LC-MS/MS to identify the substrates of TRIM16.

ORGANISM(S): Homo Sapiens

SUBMITTER: Jianyun Yan

PROVIDER: PXD051036 | iProX | Wed Mar 27 00:00:00 GMT 2024

REPOSITORIES: iProX

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TRIM16 Mediates K63-Linked Ubiquitination of DAB2 to Facilitate Vascular Calcification.

Lan Zirong Z Liang Qingchun Q Li Li L Liu Fang F Chen An A Ye Yuanzhi Y Feng Liyun L Zhang Zixi Z Zhang Xiuli X Ou Jing-Song JS Lu Lihe L Yan Jianyun J

Circulation research 20250627 4

<h4>Background</h4>Vascular calcification is highly prevalent in patients with chronic kidney disease (CKD), and the underlying mechanisms remain elusive. Several studies have indicated an important role of protein ubiquitination in vascular calcification. However, the role of E3 ubiquitin ligases in vascular calcification remains poorly understood.<h4>Methods</h4>Calcification of vascular smooth muscle cells (VSMCs) was induced by high phosphate. CKD mouse model was induced by an adenine diet, ...[more]

PMID: 40575853

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