Proteomics

Dataset Information

0

Plasma proteomics of BACE1, 2, and double KO mice


ABSTRACT: The beta-secretase BACE1 is a central drug target for Alzheimer’s disease. Clinically tested, BACE1-directed inhibitors also block the homologous protease BACE2. Yet, little is known about physiological BACE2 substrates and functions in vivo. Here, we performed glycoprotein enrichment and subsequent discovery proteomics to identify substrates of the protease BACE2 in plasma of mice. Therefore, we analysed plasma from BACE2 KO, BACE1/2 double KO and WT controls, as well as BACE1 KO with a separate WT control. Inactivation of BACE2, but not BACE1, inhibited shedding of VEGFR3/FLT4. Thus, sVEGFR3 represents a pharmacodynamic plasma marker for BACE2 activity in vivo.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Blood Plasma

SUBMITTER: Stephan Mueller  

LAB HEAD: Stefan F. Lichtenthaler

PROVIDER: PXD041577 | Pride | 2024-06-27

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
Plasma_002.raw Raw
Plasma_003.raw Raw
Plasma_004.raw Raw
Plasma_006.raw Raw
Plasma_007.raw Raw
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Publications


The β-secretase β-site APP cleaving enzyme (BACE1) is a central drug target for Alzheimer's disease. Clinically tested, BACE1-directed inhibitors also block the homologous protease BACE2. Yet little is known about physiological BACE2 substrates and functions in vivo. Here, we identify BACE2 as the protease shedding the lymphangiogenic vascular endothelial growth factor receptor 3 (VEGFR3). Inactivation of BACE2, but not BACE1, inhibited shedding of VEGFR3 from primary human lymphatic endothelial  ...[more]

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