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Analysis of the TNFR1-SC from HOIP-proficient and -deficient A549 cells

ABSTRACT: This study aimed at determining which components of the TNFR1-SC are recruited in dependency of HOIP.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Permanent Cell Line Cell, Cell Culture

DISEASE(S): Lung Adenocarcinoma

SUBMITTER: Silvia Surinova

LAB HEAD: Silvia Surinova

PROVIDER: PXD008497 | Pride | 2018-09-25

REPOSITORIES: Pride

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			Action	DRS
	parameters.txt	Txt
	proteinGroups.txt	Txt
	regmssu_Q141121_225.raw	Raw
	regmssu_Q141121_228.raw	Raw
	regmssu_Q141121_237.raw	Raw

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Analysis of the TBK1 interactors from TBK1-deficient A549 cells reconstituted with moTAP TBK1 or empty vector

Project description:This study aimed at determining the proteins that interact with TBK1.

2018-09-25 | PXD010777 | Pride

Site-specific ubiquitination of the E3 ligase HOIP regulates apoptosis and immune signaling

Project description:HOIP, the catalytic component of the Linear Ubiquitin chain Assembly Complex (LUBAC), is a critical regulator of inflammation. However, how HOIP itself is regulated to control inflammatory responses is unclear. Here, we discover that site-specific ubiquitination of K784 within HOIP promotes Tumour Necrosis Factor (TNF)-induced inflammatory signalling. A HOIP K784R mutant is catalytically active but shows reduced induction of an NF-B reporter relative to wild type HOIP. HOIP K784 is evolutionarily conserved, equivalent to HOIP K778 in mice. We generated HoipK778R/K778R knockin mice, which show no overt developmental phenotypes; however, in response to TNF, HoipK778R/K778R mouse embryonic fibroblasts display suppressed NF-B activation and increased apoptotic markers. On the other hand, HOIP K778R enhances the TNF-induced formation of TNFR complex II, and an interaction between TNFR complex II and LUBAC. Loss of the LUBAC component SHARPIN leads to embryonic lethality in HoipK778R/K778R mice, which is rescued by knockout of TNFR1. We propose that site-specific ubiquitination of HOIP regulates a LUBAC-dependent switch between survival and apoptosis in TNF-signalling.

2020-08-31 | PXD021217 | Pride

Gene expression of IKK1/2 deficient thymocytes

Project description:CD8SP TCRhi thymocytes were sorted from TNFR1-/- and TNFR1-/- CD4Cre+ IKK1fx/fx IKK2fx/fx R26REYFPfx/fx mice. RNA was produced from the sorted cells and sequencing performed. Samples 1,2 and 3 were from TNFR1-/- mice Samples 4, 5, 6 and 7 were from TNFR1-/- CD4Cre+ IKK1fx/fx IKK2fx/fx R26REYFPfx/fx mice

2017-07-05 | E-MTAB-4778 | biostudies-arrayexpress

protein-protein interaction dataset TNFR1-mediated NFkB signaling

Project description:Most MS-based approaches to study protein-protein interactions require homogenization of the cells, which leads to loss of the cellular structures, dilution of proteins and formation of incorrect protein complexes. Furthermore, several purification and washing steps are needed, which can lead to the loss of (weaker) interactions. We recently developed a new method for studying protein complexes without interfering with the cellular integrity; Virotrap. By trapping and purifying protein complexes in virus-like particles, we avoid cell lysis and preserve intact complexes during the purification process. Here, we present a protein-protein interaction network of the TNFR1-induced NF-κB and apoptosis pathway, using TRADD, FADD, TRAF2, cIAP1, NEMO, TANK, HOIL1, HOIP, SHARPIN, A20, ABIN1 and ABIN2 as baits in Virotrap. Virotrap was applied both under resting conditions as well as upon TNF stimulation, which reveals dynamic interactions in TNFR1-induced NF-κB signaling. The found interactions compromise both known interactors as well as novel ones that might serve as valuable resource for further unraveling the molecular mechanisms controlling inflammation, cellular proliferation and cell death.

2018-11-06 | PXD009366 | Pride

Comprehensive proteome profiling of nuclear and cytoplasmic fractions of rat Sertoli cells.

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2017-01-18 | PXD003050 | Pride

Expression data from isolated SHARPIN-deficient thymic Treg cells

Project description:One of the ubiquitin ligases, LUBAC, is a trimetric complex composed of SHARPIN, HOIL-1, and HOIP. LUBAC works at the proximal TCR signaling pathway allowing normal Treg development. We used microarrays to detail the global programme of gene expression underlying LUBAC-mediated signaling pathway in Treg cells.

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Comparative proteomic analysis of exosomes derived from endothelial cells and Schwann cells

Project description:Exosomes derived from endothelial cells and Schwann cells have been employed as novel treatments of neurological diseases, including peripheral neuropathy. Exosomal cargo plays a critical role in mediating recipient cell function. In this study, we thus performed a comprehensive proteomic analysis of exosomes derived from healthy mouse dermal microvascular endothelial cells (EC-Exo) and healthy mouse Schwann cells (SC-Exo). We detected 1,817and 1,579 proteins in EC-Exo and SC-Exo, respectively. Among them, 1506 proteins were present in both EC-Exo and SC-Exo, while 311 and 73 proteins were detected only in EC-Exo and SC-Exo, respectively. Bioinformatic analysis revealed that EC-Exo enriched proteins were involved in the neurovascular function, while SC-Exo enriched proteins were related to lipid metabolism. Western blot analysis of 14 enriched proteins revealed that EC-Exo contained proteins involved in mediating endothelial function such as delta-like 4 (DLL4) and endothelial NOS (NOS3), whereas SC-Exo had proteins involved in mediating glial function such as apolipoprotein A-I (APOA1) and phospholipid transfer protein (PLTP). Collectively, the present study indicates cargo protein profiles are distinct between EC-Exo and SC-Exo, suggesting potential roles of EC-Exo and SC-Exo mainly in mediating neurovascular and myelin functions, respectively.

2023-08-20 | PXD041547 | Pride

Paracrine IFN response limits ZIKV infection in human Sertoli cells

Project description:Zika virus (ZIKV) is unique among mosquito-borne flaviviruses in its ability to be sexually transmitted. The testes have been implicated as sites of long-term ZIKV replication, and our previous studies have identified Sertoli cells (SC), the nurse cells of the seminiferous epithelium that govern spermatogenesis, as major targets of ZIKV infection. To improve our understanding of the host-ZIKV interaction within human testicular cells, we analyzed ZIKV-induced proteome changes in SC and mixed seminiferous tubule cells (STC) using high-throughput liquid chromatography-tandem mass spectrometry (LC-MS/MS). We found that ZIKV infection in SC and STC induced distinct IFN-stimulated proteins and impacted pathways and functional networks associated with innate antiviral defense. IFN signaling was the most significantly enriched pathway and MX1 was the most abundant IFN-stimulated protein in both SC and STC. Increased levels of MX1 at later time points of infection coincided with diminished propagation of ZIKV in SC, whereas silencing of MX1 and IFIT1 enhanced peak ZIKV titers in SC. Furthermore, although downstream IFN-I signaling was found to be functional and restricted ZIKV replication in SC, in comparison to A549 cells, SC exhibited dampened expression of IFN-I/III-stimulated genes despite higher levels of virus progeny and IFN-I/III transcripts. Together, this study highlights the IFN-I/III response as a driver of the antiviral state that limits ZIKV infection in SC and suggests that delayed and reduced robustness of innate antiviral defense in SC may contribute to ZIKV persistence in the testes.

2021-09-10 | PXD025133 | Pride

Schwann cell plasticity regulates neuroblastic tumor cell differentiation

Project description:The remarkable plasticity of Schwann cells (SCs) is essential for nerve regeneration but also contributes to neuropathies and cancer progression. It has not yet been investigated whether the adaptive potential of SCs is manifested in stromal, tumor associated SCs characteristically found within a benign subtype of neuroblastic tumors (NBTs). We here performed transcriptome profiling of human NBTs, rich and poor in SC stroma, as well as human injured nerves, rich in repair SCs, revealing that stromal SCs exhibit a repair SC characteristic gene expression signature. In turn, primary repair SCs had a pro-differentiating and anti-proliferative effect on NBT cell lines after direct and trans-well co-culture. Within the pool of secreted stromal/repair SC factors, we identified EGFL8, a matricellular protein with so far undescribed function, to induce neuronal differentiation of aggressive NBT cells. EGFL8 expression further correlated with favorable tumor stage and increased patient survival. Our findings suggest that stromal SCs exert nerve repair associated functions in the tumor-environment and underline the therapeutic value of SC-derived factors for aggressive, SC stroma-poor NBTs.

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Project description:LUBAC (linear ubiquitin assembly complex) consists of HOIP, HOIL1 and SHARPIN. HOIP deficiency has been characterized by immunodeficiency, autoinflammation and amylopectinosis. To explore the molecular mechanism of the autoinflammation, we performed a transcriptome-wide analysis using whole blood and unstimulated PBMCs of a HOIP deficiency patient.

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