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Proteomic analysis of mousekidney cortices with and without VPS34 knockout

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

INSTRUMENT(S): Q Exactive

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Kidney

SUBMITTER: Markus Rinschen

LAB HEAD: Markus Rinschen

PROVIDER: PXD007092 | Pride | 2024-01-26

REPOSITORIES: Pride

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			Action	DRS
	20170424_Q1_AWH_ColID_336_ProjID_553_Benzing_sample01.raw	Raw
	20170424_Q1_AWH_ColID_336_ProjID_553_Benzing_sample02.raw	Raw
	20170424_Q1_AWH_ColID_336_ProjID_553_Benzing_sample03.raw	Raw
	20170424_Q1_AWH_ColID_336_ProjID_553_Benzing_sample04.raw	Raw
	20170424_Q1_AWH_ColID_336_ProjID_553_Benzing_sample05.raw	Raw

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1 - 5 of 9

Publications

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

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

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

2024-01-26 | PXD007093 | Pride

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

PPARs and c-Myc regulate metabolism of renal tubules

Project description:Different segments of renal tubules have distinct metabolic features and functions, and defective metabolism in renal tubules is involved in the pathobiology of kidney diseases. However, the mechanisms underlying the metabolic regulation in renal tubules remain to be defined. We demonstrated that the renal proximal tubule (PT) has high expression of fatty acid and lipid metabolism enzymes, which is transcriptionally upregulated by abundantly expressed peroxisome proliferator-activated receptor (PPAR)/γ to support active lipid metabolism. In contrast, the renal distal tubule (DT) has elevated glycolytic enzyme expression corresponding with high rates of glycolysis, and this increased expression is mediated by abundantly expressed c-Myc. In addition, Nrf2 upregulated glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and NADP-dependent malic enzyme 1 expression for NADPH production and antioxidation in the DT. Highly expressed PPARγ transcriptionally enhanced expression of the protease iRhom2 in the PT, which suppressed epidermal growth factor (EGF) expression and secretion, inhibiting EGF receptor activation-dependent glycolytic gene expression and maintaining the low level of glycolysis. PPARγ inhibition reduced iRhom2 expression and increased EGF and GLUT1 expression in the PT in mice, resulting in hypertrophy of renal tubules and inhibited kidney functions, which can be rescued by inhibition of glycolysis via treatment with 2-deoxy-D-glucose. These findings delineate instrumental molecular mechanisms underlying the active lipid metabolism and suppressed glycolysis in the PT and active glycolysis in the DT and reveal critical roles for PPARs and c-Myc in maintaining metabolic homeostasis in the kidney

2018-11-15 | PXD007828 | 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

Pro-oxidant therapy by a vitamin K precursor targets PI 3-Kinase VPS34 function

Project description:Men taking anti-oxidant vitamin E supplements have increased prostate cancer (PC) risk. Whether pro- oxidants protect from PC remained unclear. We show that a pro-oxidant vitamin K precursor (MSB) suppresses PC progression in mice killing cells through an oxidative cell death: MSB antagonizes the essential class III PI 3-Kinase VPS34 the regulator of endosome identity and sorting through oxidation of key cysteines pointing to a redox checkpoint in sorting. Testing MSB in a myotubular myopathy model that is driven by loss of MTM1 the phosphatase antagonist of VPS34 we show that dietary MSB improved muscle histology function and extended life span. These findings enhance our understanding of pro-oxidant selectivity and show how definition of the pathways they impinge on can give rise to unexpected therapeutic opportunities.

2024-04-02 | GSE148011 | GEO

Analysis of isotope incorporation in differentiated and undifferentiated podocytes

Project description:We subjected podocytes (either differentiated or undifferentiated) to a pulse with stable isotope labeled amino acids for 24, 48, 72 and 96h.

2018-05-01 | PXD006887 | 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

Proteomic analysis of cultured primary urinary cells from M. Fabry Patients

Project description:We analyzed the proteome of primary urinary cells from patients with M. Fabry as compared to primary urinary cells from healthy control samples

2018-10-17 | PXD007081 | Pride

Deep mapping of the mouse podocyte proteome

Project description:We analyzed the proteome of mouse FACS-sorted podocytes. We compared podocytes ("green cells") with non-podocyte ("red cells") cells of the glomerulus.

2018-06-21 | PXD003306 | Pride

Analysis of the cultured podocyte phosphoproteome

Project description:The renal filtration barrier is critically maintained by the renal podocyte, a postmitotic, neuron-like epithelial cell type. Cultured podocyte cell lines – both in the differentiated and undifferentiated state - are a widely utilized tool to estimate cytoskeletal rearrangement processes in vitro. Here, we mapped the podocyte proteome at a depth of more than 7000 proteins. The data dissects the dynamic range of the podocyte proteome during differentiation. The data also demonstrates an absolute quantitative analysis of proteins mutated in forms of hereditary disease and demonstrates expression of several proteins not expressed in other, standard cell lines. We validated differentially regulated proteins using immunoblot and functional assays estimating lysosomal and proteasomal function. Comparison with deep mapping RNAseq data from the native podocyte, preliminary fingerprint data from the native proteome and staining intensities from the human protein atlas was performed to estimate similiarities between the cultured and native podocyte proteome, unravelling that at least 26 high-abundant native, podocyte-specific proteins, were not identified in the dataset. Notably, this data detected general perturbations in proteostatic mechanisms as a key alteration during podocyte differentiation, with increased proteasome activity in the undifferentiated state and markedly increased expression of lysosomal proteins in the differentiated state. We also performed a comparative phosphoproteomic analysis with published data from the native glomerul. These data also suggests a preference of phosphorylation of actin associated proteins in the differentiated state. The dataset obtained here, a valuable resource, warrants and provides the means for deep mapping of the native podocyte proteome and phosphoproteome in a similar manner.

2016-07-04 | PXD004013 | Pride

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