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a novel miR (show MLXIP Proteins)-155-Peli1-c-Rel (show NFkBP65 Proteins) pathway that specifically regulates Tfh cell generation and function.
These findings reveal a novel mechanism that endotoxin tolerance reprograms mitogen-activated protein kinase (show MAPK1 Proteins) signaling by suppressing Pellino 1-mediated K63-linked ubiquitination of cIAP2 (show BIRC3 Proteins), K48-linked ubiquitination, and degradation of TRAF3 (show TRAF3 Proteins).
The nonredundant role of Pellino1 in immune receptor signaling is in part due (show IRAK1 Proteins)to its different substrate specificity.
Pellino1 interacts with the transcription factor Deformed Epidermal Autoregulatory Factor 1 (DEAF1 (show DEAF1 Proteins)).
Peli1 is a microglia-specific mediator of autoimmune neuroinflammation that works by regulating Traf3 (show TRAF3 Proteins) degradation
These results demonstrate that the ligands that signal via MyD88 (show MYD88 Proteins) do not always employ the same protein kinase (show CDK7 Proteins) to activate Pellino 1 and show that the activiation of NF-kappaB (show NFKB1 Proteins) and mitogen-activated protein kinases.
Peli1 as a critical factor in the maintenance of peripheral T cell tolerance and demonstrate a previously unknown mechanism of c-Rel (show NFkBP65 Proteins) regulation.
Pellino-1 protein may have a cellular function distinct from previously identified functions.
IKKepsilon (show IKBKE Proteins)/TBK1 (show TBK1 Proteins) mediate the activation of Pellino 1's E3 ligase activity, as well as inducing the transcription of its gene and protein expression in response to TLR3 (show TLR3 Proteins) and TLR4 (show TLR4 Proteins) agonists.
miR (show MLXIP Proteins)-21 expression was upregulated during early stages of liver regeneration. Targeting of Peli1 by miR (show MLXIP Proteins)-21 could potentially provide the basis for a negative feedback cycle regulating NF-kappaB (show NFKB1 Proteins) signaling.
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 (show BCL6 Proteins) promotes lymphomagenesis.
Peptide PEL1 derived from the interleukin-1 receptor-associated kinase (IRAK)1 (show IRAK1 Proteins)-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
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 (show CA8 Proteins)
role in interleukin-1-mediated signalling through interaction with interleukin-1 receptor-associated kinase 4 (show IRAK4 Proteins)-IRAK (show IRAK1 Proteins)-tumor necrosis factor (show TNF Proteins) receptor-associated factor 6 complex
Smad6 (show SMAD6 Proteins) bound to Pellino-1 promoted TGF-beta (show TGFB1 Proteins)-mediated anti-inflammatory effects.
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
, protein pellino homolog 1
, pellino homolog 1
, pellino-related intracellular-signaling molecule
, pellino 1
, pellino protein