Ontology highlight
ABSTRACT:
PROVIDER: PRJNA613474 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR11351604.fastq.gz | Fastqsanger.gz | |||
| SRR11351605.fastq.gz | Fastqsanger.gz | |||
| SRR11351606.fastq.gz | Fastqsanger.gz | |||
| SRR11351607.fastq.gz | Fastqsanger.gz | |||
| SRR11351608.fastq.gz | Fastqsanger.gz |
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Project description:Mass Spectrometry Data for the manuscript "Numb positively regulates Hedgehog signaling at the ciliary pocket"
2022-08-03 | MSV000090077 | MassIVE
Project description:The primary cilium is a signaling compartment that interprets Hedgehog signals through changes of its protein, lipid and second messenger compositions. Here, we combine proximity labeling of cilia with quantitative mass spectrometry to unbiasedly profile the time-dependent alterations of the ciliary proteome in response to Hedgehog. This approach correctly identifies the three factors known to undergo Hedgehog-regulated ciliary redistribution and reveals two such additional proteins. First, we find that a regulatory subunit of the cAMP-dependent protein kinase (PKA) rapidly exits cilia together with the G protein-coupled receptor GPR161 in response to Hedgehog; and we propose that the GPR161/PKA module senses and amplifies cAMP signals to modulate ciliary PKA activity. Second, we identify the phosphatase Paladin as a cell type-specific regulator of Hedgehog signaling that enters primary cilia upon pathway activation. The broad applicability of quantitative ciliary proteome profiling promises a rapid characterization of ciliopathies and their underlying signaling malfunctions.
2021-04-07 | PXD024367 | Pride
Project description:The primary cilium is a signaling compartment that interprets Hedgehog signals through changes of its protein, lipid and second messenger compositions. Here, we combine proximity labeling of cilia with quantitative mass spectrometry to unbiasedly profile the time-dependent alterations of the ciliary proteome in response to Hedgehog. This approach correctly identifies the three factors known to undergo Hedgehog-regulated ciliary redistribution and reveals two such additional proteins. First, we find that a regulatory subunit of the cAMP-dependent protein kinase (PKA) rapidly exits cilia together with the G protein-coupled receptor GPR161 in response to Hedgehog; and we propose that the GPR161/PKA module senses and amplifies cAMP signals to modulate ciliary PKA activity. Second, we identify the phosphatase Paladin as a cell type-specific regulator of Hedgehog signaling that enters primary cilia upon pathway activation. The broad applicability of quantitative ciliary proteome profiling promises a rapid characterization of ciliopathies and their underlying signaling malfunctions.
2021-04-07 | PXD024361 | Pride
Project description:The primary cilium is a signaling compartment that interprets Hedgehog signals through changes of its protein, lipid and second messenger compositions. Here, we combine proximity labeling of cilia with quantitative mass spectrometry to unbiasedly profile the time-dependent alterations of the ciliary proteome in response to Hedgehog. This approach correctly identifies the three factors known to undergo Hedgehog-regulated ciliary redistribution and reveals two such additional proteins. First, we find that a regulatory subunit of the cAMP-dependent protein kinase (PKA) rapidly exits cilia together with the G protein-coupled receptor GPR161 in response to Hedgehog; and we propose that the GPR161/PKA module senses and amplifies cAMP signals to modulate ciliary PKA activity. Second, we identify the phosphatase Paladin as a cell type-specific regulator of Hedgehog signaling that enters primary cilia upon pathway activation. The broad applicability of quantitative ciliary proteome profiling promises a rapid characterization of ciliopathies and their underlying signaling malfunctions.
2021-04-07 | PXD024366 | Pride
Project description:Ciliary Hedgehog signaling restricts injury-induced adipogenesis
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Project description:Purpose: The response to Hedgehog signaling in the limb is driven by GLI bound enhancers and the majority of Hh targets in the developing limb bud are regulated solely by the activity of GLI-repressor. Currently, we do not have a comprehensive understanding of how GLI bound enhancers respond to Hedgehog signaling. The goal of this study is to identify how GLI bound enhancers are regulated by Hedgehog signaling and specifically by GLI-repressor. Methods: ATAC-seq was done in embryonic day 10.5 posterior limb buds from control and Shh-null embryos to identify GLI enhancers that change chromatin accessibility in response to Hedgehog signaling. Results: We found that Hedgehog signaling regulates the chromatin accessibility of a subset of GLI binding regions. This subset of GLI bound enhancers has reduced accessibility in the absence of Hedgehog signaling and largely overlaps with GLI enhancers that also have reduced H3K27ac in the absence of Hedgehog signaling.
2020-01-21 | GSE107877 | GEO
Project description:The Hedgehog (Hh) signaling pathway is essential for embryonic development and tissue homeostasis, and its dysregulation contributes to severe developmental disorders and various cancers. Despite its biological importance, a detailed understanding of the dynamic interactions and phosphorylation events that regulate this pathway remains incomplete. To address this gap, we employed a comprehensive systems-level approach combining proximity-dependent biotinylation (BioID), phosphoproteomics, and advanced computational analyses to generate an extensive and dynamic map of the mammalian Hh signaling pathway. Using stable NIH-3T3 and HEK293 cell lines expressing key Hh components, we systematically characterized protein-protein interactions (PPIs) and phosphorylation dynamics in response to pathway activation and during primary cilia progression. Our workflow identified numerous ciliary proteins, highlighting the essential role of primary cilia and phosphorylation in Hh signaling regulation. To further explore the contribution of primary cilia, we analyzed interaction networks during cilia absence, formation, and resorption. These analyses revealed that the mammalian Hh signaling network is modular, consisting of four distinct functional groups: core membrane/ciliary regulators, intracellular signaling regulators, trafficking/scaffolding regulators, and downstream transcriptional regulators. Each module displayed specialized roles within the signaling cascade, closely linked to cell cycle regulation.
2025-03-17 | MSV000097352 | MassIVE
Project description:Primary cilia are tiny membrane protrusions emanating from the surface of almost all mammalian cell types. Recently, a picture has emerged of the primary cilium functioning as a cellular antenna that senses extracellular stimuli via receptors, locally processes the signal using cilia-specific signalling pathways, and transduces this information into a cellular response. Components of the cyclic AMP (cAMP) signalling cascade have been proposed to be part of the ciliary signalling pathways. We aimed to shed light on whether ciliary cAMP signaling controls gene expression, and if yes, which gene expression program is particularly targeted by ciliary cAMP signaling. To this end, we targeted an optogenetic tool to increase cAMP levels (bPAC) to the primary cilium in murine, kidney-derived inner medullary collecting duct (mIMCD-3) cells (mIMCD-3 cilia-bPAC cells). As controls, we used cells were bPAC is targeted to the cytosol (mIMCD-3 cyto-bPAC cells) and wild-type cells (mIMCD-3 WT cells). We increased cAMP levels by light stimulation and next analysed gene expression using bulk RNA-sequencing. As an additional control, we also included WT cells treated with the compound Forskolin, which targets endogeneous adenylyl cyclases and thus, in principle, is believed to increase cAMP levels in both compartments, cilium and cell soma.
2022-05-11 | GSE182339 | GEO
Project description:Tetraspanin-enriched Membrane Domains Regulate Vascular Leakage by Membrane Cholesterol Accessibility to Balance Antagonistic GTPases
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Project description:Regulation of endothelial nutrient transport is poorly understood. Vascular endothelial growth factor (VEGF)-B signaling in endothelial cells promotes uptake and transcytosis of fatty acids (FA) from the bloodstream to the underlying tissue, advancing pathological lipid accumulation and lipotoxicity in diabetic complications. Here we demonstrate a VEGF-B dependent obstruction of endothelial glucose transport attributed to plasma membrane lipid alterations affecting glucose transporter 1 function, which was independent of FA uptake. Specifically, VEGF-B signaling impaired recycling of low-density lipoprotein receptor to the plasma membrane, leading to reduced cholesterol uptake and membrane cholesterol loading, decreasing endothelial glucose uptake capacity. Inhibiting VEGF-B in vivo was accordingly linked to reconstitution of membrane cholesterol and induction of glucose uptake, of particular relevance for conditions inferring insulin resistance and diabetic complications. In summary, our study reveals a novel mechanism of action for VEGF-B in endothelial nutrient uptake and highlights the impact of membrane cholesterol for the regulation of endothelial glucose transport.
2020-04-06 | GSE146108 | GEO