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The proteomics of Desert Hedgehog (DHH) in endothelial cells (HUVECs)

ABSTRACT: To unravel the direct mechanism of DHH to prevent EndoMT and to identify potential DHH interacting proteins, we analyzed HUVECs treated with either adenovirus-Flag-DHH (Ad-DHH) or control adenovirus (Ad-NC) together with 3 cytokines (TGF-β1, IL-1β, and TNF-α at 10 ng/ml) for 3 days. We precipitated DHH from overexpressed ECs followed by mass spectrometry.

ORGANISM(S): Homo Sapiens

SUBMITTER: Jianping Weng

PROVIDER: PXD052429 | iProX | Tue May 21 00:00:00 BST 2024

REPOSITORIES: iProX

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the proteomics of IGFBP6 in endothelial cells (HUVECs)

Project description:To unravel the direct mechanism of the anti-inflammatory effects of IGFBP6 in ECs, we analysed HUVECs treated with either adenovirus-Flag-IGFBP6 (Ad-IGFBP6) or control adenovirus (Ad-NC). We precipitated IGFBP6 from overexpressed ECs followed by mass spectrometry.

2024-05-13 | PXD052204 |

Enhanced Pathogenicity of Th17 cells Generated in the Absence of Transforming Growth Factor-β Signaling

Project description:CD4+ T cells that selectively produce interleukin (IL)-17, are critical for host defense and autoimmunity1-4. Crucial for T helper17 (Th17) cells in vivo5,6, IL-23 has been thought to be incapable of driving initial differentiation. Rather, IL-6 and transforming growth factor (TGF)-β1 have been argued to be the factors responsible for initiating specification7-10. Herein, we show that Th17 differentiation occurs in the absence of TGF-β signaling. Neither IL-6 nor IL-23 alone efficiently generated Th17 cells; however, these cytokines in combination with IL-1β effectively induced IL-17 production in naïve precursors, independently of TGF-β. Epigenetic modification of the Il17a/Il17f and Rorc promoters proceeded without TGF-β1, allowing the generation of cells that co-expressed Rorγt and T-bet. T-bet+Rorγt+ Th17 cells are generated in vivo during experimental allergic encephalomyelitis (EAE), and adoptively transferred Th17 cells generated with IL-23 in the absence of TGF-β1 were more pathogenic in this experimental disease. These data suggest a new model for Th17 differentiation. Consistent with genetic data linking the IL23R with autoimmunity, our findings re-emphasize the role of IL-23 and therefore have important implications for the development of new therapies. Mouse T helper 17 cell differentiation with or without TGFB

2010-08-31 | E-GEOD-23505 | biostudies-arrayexpress

Enhanced Pathogenicity of Th17 cells Generated in the Absence of Transforming Growth Factor-β Signaling: ChIPSeq

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2010-08-31 | E-GEOD-23681 | biostudies-arrayexpress

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2020-04-22 | PXD015780 | Pride

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Project description:To analyse whether the activation of TGF-ß signalling (recombinant hTGF-ß, 5 ng/mL; PeproTech) is able to invoke a full phenotype- switch, we performed RNA sequencing of melanoma cultures from two independent melanoma cell lines at two different time point after TGF-β1 (5 ng/ml, preprotech).

2020-04-17 | GSE148767 | GEO

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2021-08-11 | GSE105053 | GEO

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2023-11-01 | GSE218814 | GEO

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