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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.
Pellino-1 may be critically important for cell survival.
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.
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.
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.
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.
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.
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
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.
Our observations suggested that Peli-1 gene polymorphism rs329498 might contribute to SLE susceptibility in Chinese Han Population.
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.
Increased PELI1 expression and subsequent induction of BCL6 promotes lymphomagenesis.
Peptide PEL1 derived from the interleukin-1 receptor-associated kinase (IRAK)1-binding motif reveals a distinct phosphothreonine peptide binding preference.
GWAS study found two new SNPs associated with nickel dermatitis; SNPs are located in the NTN4 and PELI1 genes
Pellino1 interacts with the transcription factor Deformed Epidermal Autoregulatory Factor 1 (DEAF1).
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
role in interleukin-1-mediated signalling through interaction with interleukin-1 receptor-associated kinase 4-IRAK-tumor necrosis factor receptor-associated factor 6 complex
Smad6 bound to Pellino-1 promoted TGF-beta-mediated anti-inflammatory effects.
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
E3 ubiquitin ligase catalyzing the covalent attachment of ubiquitin moieties onto substrate proteins. Involved in the TLR and IL-1 signaling pathways via interaction with the complex containing IRAK kinases and TRAF6. Mediates 'Lys-63'-linked polyubiquitination of IRAK1 allowing subsequent NF-kappa-B activation (By similarity).
E3 ubiquitin-protein ligase pellino homolog 1
, pellino homolog 1
, pellino-related intracellular-signaling molecule
, protein pellino homolog 1
, pellino 1
, pellino protein
, pellino E3 ubiquitin protein ligase 1 L homeolog
, pellino E3 ubiquitin protein ligase 1 S homeolog
, pellino homolog 1b