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Analysis of the mouse kidney cortex phosphoproteome of VPS34 knockout and control animals

ABSTRACT: We generated phosphoproteomics data of renal cortices of mice with and without tubule-specific vps34 knockout.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Kidney

SUBMITTER: Markus Rinschen

LAB HEAD: Markus Rinschen

PROVIDER: PXD007093 | Pride | 2024-01-26

REPOSITORIES: Pride

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VPS34-dependent control of apical membrane function of proximal tubule cells and nutrient recovery by the kidney.

Rinschen Markus M MM Harder Jennifer L JL Carter-Timofte Madalina E ME Zanon Rodriguez Luis L Mirabelli Carmen C Demir Fatih F Kurmasheva Naziia N Ramakrishnan Suresh K SK Kunke Madlen M Tan Yifan Y Billing Anja A Dahlke Eileen E Larionov Alexey A AA Bechtel-Walz Wibke W Aukschun Ute U Grabbe Marlen M Nielsen Rikke R Christensen Erik I EI Kretzler Matthias M Huber Tobias B TB Wobus Christiane E CE Olagnier David D Siuzdak Gary G Grahammer Florian F Theilig Franziska F

Science signaling 20221129 762

The lipid kinase VPS34 orchestrates autophagy, endocytosis, and metabolism and is implicated in cancer and metabolic disease. The proximal tubule in the kidney is a key metabolic organ that controls reabsorption of nutrients such as fatty acids, amino acids, sugars, and proteins. Here, by combining metabolomics, proteomics, and phosphoproteomics analyses with functional and superresolution imaging assays of mice with an inducible deficiency in proximal tubular cells, we revealed that VPS34 contr ...[more]

PMID: 36445937

Similar Datasets

Proteomic analysis of mousekidney cortices with and without VPS34 knockout

Project description:We analyzed the proteome of mouse with a tubule-specific VPS34 knockout and compared it to control mice.

2024-01-26 | PXD007092 | Pride

VPS34 regulates RAB7 activation and Retromer localization to autophagosomes and mitophagy in oocytes

Project description:To investigate the role of Vps34 during oocyte development, we crossed female Vps34f/f mice with Gdf9-Cre and Zp3-Cre male transgenic mice for Cre recombinase specifically in oocytes at either primordial or early growing stages. Our results revealed that Vps34 plays a key role in oocyte cytoplasmic maturation. In order to reveal the changes in oocyte transcriptome level caused by Vps34 deletion, we conducted transcriptome sequencing on oocytes at GV stage, MII stage and 2cell embryo of ZcKO, and analyzed the changes in transcripts at these three stages. Transcriptome sequencing results showed that the oocytes and 2cell embryos of ZcKO were enriched with a large number of transcription and transport-related differential genes, and the 2cell stage had the most differential genes, which was the key period for the occurrence of major ZGA. Further analysis of transcription-related genes revealed that the enriched major ZGA genes were all down-regulated in 2cell of ZcKO mice. In addition, differential genes involved in autophagy were enriched in ZcKO 2cell, with HPG abnormally increased. Autophagy is the main degradation pathways of maternal proteins in early embryonic development, and degradation of maternal proteins is necessary for the normal process of ZGA, which occurs prior to major ZGA and even during oocyte maturation, when defects appear to be irremediable later. These results suggest that Vps34 deletion leads to degradation inhibition of maternal factors and impaired major ZGA, leading to embryonic development arrest.

2023-09-01 | GSE216465 | GEO

Analysis of the urinary proteome of mice with and without VPS34 knockout

Project description:We analyzed the effect of tubular VPS34 knockout on the urinary proteome.

2024-01-26 | PXD007106 | Pride

Proteome for Usp11 knockout E17.5 cortex

Project description:Since Usp11 encodes a DUB, we reasoned that Usp11 deficiency may lead to increased ubiquitination and destabilization of a protein that functions in neuronal differentiation and migration.To define the molecular mechanism of Usp11 deficiency on cortical development, we performed a label-free quantitative liquid chromatography-tandem Mass Spectrometry (LC-MS/MS) analysis to detect the protein expression profiles in E17.5 WT and Usp11 KO cortices in four biological repeats.

2021-01-29 | PXD021587 | Pride

Ubiquitinated sites on VPS34 by UBE3C LC-MSMS

Project description:Ubiquitinated sites on VPS34 identified by LC-MS/MS analysis of VPS34 derived from in vivo ubiquitination assays of UBE3C-transfected or -untransfected 293T cells.

2021-02-19 | PXD023959 | Pride

Antileukemic activity of the VPS34-IN1 inhibitor in acute myeloid leukemia

Project description:Acute myeloid leukemia (AML) is an aggressive disease with a poor prognosis. Vacuolar protein sorting 34 (VPS34) is a member of the phosphatidylinositol-3-kinase lipid kinase family that controls the canonical autophagy pathway and vesicular trafficking. Using a recently developed specific inhibitor (VPS34-IN1), we found that a VPS34 block induces apoptosis in AML cells but not in normal CD34+ hematopoietic cells. Complete and acute inhibition of VPS34 was required for the anti-leukemic activity of VPS34-IN1. This inhibitor also has pleiotropic effects against various cellular functions related to class III PI3K in AML cells that may explain their survival impairment. VPS34-IN1 inhibits basal and L-asparaginase-induced autophagy in AML cells. A synergistic cell death activity of this drug was also demonstrated. VPS34-IN1 was additionally found to impair vesicular trafficking and mTORC1 signaling. From an unbiased approach based on phosphoproteomic analysis, we identified that VPS34-IN1 specifically inhibits STAT5 phosphorylation downstream of FLT3-ITD signaling in AML. The identification of the mechanisms controlling FLT3-ITD signaling by VPS34 represents an important insight into the oncogenesis of AML and could lead to new therapeutic strategies.

2020-11-11 | PXD016839 | Pride

Gene expression change in Gata2 conditional knockout mice adult renal collecting duct

Project description:We would like to know the gene expression pattern in absence of transcription factor GATA2 in adult renal collecting duct We used Gata2 flox::Pax8-rtTA::Tet-Cre to make a doxycycline induced Gata2 renal tubule cell specific knockout mice We performed microarray analyses using DBA-lectin and magnetic beads purifed collecting duct cells from WT (n=3) or Gata2 CKO mice (n=3) at 4-weeks after doxycycline induction

2013-11-19 | E-GEOD-52448 | biostudies-arrayexpress

Transcription profiling of human renal proximal tube endothelial cells at 24h and 1%oxygen

Project description:Aim of the study was to characterize the transcriptional response of human primary renal proximal tubule endothelial cells (RPTEC) to low oxygen stress. Experiment Overall Design: Passage 4 renal proximal tubule epithelial cells were exposed to a humidified atmosphere consisting of either 5% CO2 and 95% air (20% O2, normoxia) or 5% CO2, 1% oxygen and 95% nitrogen (hypoxia) for 24 hours. Total RNA was extracted immediately after exposure. Three independent biological replicates were performed, resulting in 6 samples (3 control and 3 low oxygen).

2008-10-25 | E-GEOD-12792 | biostudies-arrayexpress

Ubiquitin chain types on ubiquitinated VPS34 in the presence or absence of UBE3C in vitro LC-MSMS

Project description:We identified VPS34 as the direct substrate of UBE3C E3 ligase in vivo and in vitro. Next, to analyze the ubiquitin chain on VPS34 that was assembled by UBE3C in vitro.

2021-02-17 | PXD023986 | Pride

Lack of phosphatidylinositol 3-kinase VPS34 in regulatory T cells leads to a fatal lymphoproliferative disorder without affecting their development

Project description:Regulatory T (Treg) cells are essential for the maintenance of immunological tolerance, yet the molecular components required for their maintenance and effector functions remain incompletely defined. Inactivation of VPS34 in Treg cells led to an early, lethal phenotype, with massive effector T cell activation and inflammation, like mice lacking Treg cells completely. However, VPS34-deficient Treg cells developed normally, populated the peripheral lymphoid organs and effectively supressed conventional T cells in vitro. Our data suggest that VPS34 is required for the maturation of Treg cells or that mature Treg cells depend on VPS34 for survival. Functionally, we observed that lack of VPS34 activity impairs cargo processing upon transendocytosis, that defective autophagy contributes to, but is not sufficient to explain this lethal phenotype, and that loss of VPS34 activity induces a state of heightened metabolic activity that may interfere with metabolic networks required for maintenance or suppressive functions of Treg cells.

2024-01-29 | PXD048981 | Pride

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