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Overexpression of Peli1 inhibits noncanonical NF-kappaB activation and alleviates lupus-like disease. PELI1 levels negatively correlate with disease severity in SLE patients.
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Pellino-1 may be critically important for cell survival.
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This study demonstrates Pellino 1 (PELI1) as an important modulator that exerts opposite regulatory functions on apoptosis and necroptosis, two distinct forms of regulated cell death mechanisms.
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The study demonstrates that cytosolic Pellino-1-mediated K63-linked ubiquitination of IRF5 in M1 macrophages regulates glucose intolerance in obesity, suggesting a cytosolic mediator function of Pellino-1 in TLR4/IFN-gamma receptor-IRF5 axis during M1 polarization.
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Pellino 1 expression acts as an inhibitory signal of the homeostatic regulation of mitotic cell cycle and checkpoint, and thus contributes to the initiation and progression of neoplastic chromosome aneuploidy.
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Pellino-1 overexpression activated PI3K/Akt and ERK signaling pathways and elicited an epithelial-mesenchymal transition (EMT) phenotype of lung adenocarcinoma cells. Pellino-1-mediated EMT was demonstrated through morphology, the upregulation of Vimentin, Slug and Snail expression and the downregulation of E-cadherin and beta-catenin expression.
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Results indicate that Pellino-1 contributes to lung oncogenesis through the overexpression of inhibitor of apoptosis protein 2 (cIAP2) and promotion of cell survival and chemoresistance.
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Our results suggest that PELI1 might participate in B-cell maturation or oncogenic activation of aggressive B-cell lymphomas, both during and after germinal center stages
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The combination of low Pellino3 levels together with high and inducible Pellino1 expression may be an important determinant of the degree of inflammation triggered upon Toll-like receptor 2 engagement by Helicobacter pylori and/or its components, contributing to Helicobacter pylori-associated pathogenesis by directing the incoming signal toward an NF-kB-mediated proinflammatory response.
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Our observations suggested that Peli-1 gene polymorphism rs329498 might contribute to SLE susceptibility in Chinese Han Population.
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The study results in the Chinese Han population showed that PELI1 is a member of a constellation of genetic factors that may contribute to the pathogenesis of systemic lupus erythematosus.
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Increased PELI1 expression and subsequent induction of BCL6 promotes lymphomagenesis.
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Peptide PEL1 derived from the interleukin-1 receptor-associated kinase (IRAK)1-binding motif reveals a distinct phosphothreonine peptide binding preference.
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GWAS study found two new SNPs associated with nickel dermatitis; SNPs are located in the NTN4 and PELI1 genes
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Pellino1 interacts with the transcription factor Deformed Epidermal Autoregulatory Factor 1 (DEAF1).
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incomplete KD, IVIG nonresponsiveness, long febrile days, and the rs7604693 genetic variant in the PELI1 gene are major risk factors for the development of CALs
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role in interleukin-1-mediated signalling through interaction with interleukin-1 receptor-associated kinase 4-IRAK-tumor necrosis factor receptor-associated factor 6 complex
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Smad6 bound to Pellino-1 promoted TGF-beta-mediated anti-inflammatory effects.
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kinase-inactive IRAK proteins can associate with Pellino proteins, thus excluding the possibility that their inability to regulate Pellino degradation is due to lack of association with the Pellino proteins