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Human TRAF6 Protein expressed in HEK-293 Cells - ABIN2734115
Tikhanovich, Kuravi, Artigues, Villar, Dorko, Nawabi, Roberts, Weinman: Dynamic Arginine Methylation of Tumor Necrosis Factor (TNF) Receptor-associated Factor 6 Regulates Toll-like Receptor Signaling. in The Journal of biological chemistry 2015
Human TRAF6 Protein expressed in Wheat germ - ABIN1323514
Nakada, Tai, Panier, Al-Hakim, Iemura, Juang, ODonnell, Kumakubo, Munro, Sicheri, Gingras, Natsume, Suda, Durocher: Non-canonical inhibition of DNA damage-dependent ubiquitination by OTUB1. in Nature 2010
TRAF6 plays a role in Epithelial-mesenchymal transition phenotypes, the generation and maintenance of cancer stem cells in squamous cell carcinoma of head and neck.
TIFAB gene may act as a Coronary Artery Aneurysm susceptibility locus in patients with Kawasaki Disease.
TRAF6 is a novel PIK3CA regulator whose deregulated overexpression represents a mechanism for PI3K overactivation in tumors.
TRAF6 was identified as an independent prognostic factor of glioblastoma multiforme, with ability to promote tumor invasiveness via elevating expression of MMP9.
Results show that TRAF6 is upregulated in SACC samples, especially in SACC with metastasis, which is closely correlated with an aggressive phenotype and shorter life survival span in SACC patients.
Genetic polymorphisms of TRAF6 are associated with decreased peritoneal immune activation and an increased risk of spontaneous bacterial peritonitis.
The overexpression of miR-146a significantly increased the ErbB4 expression, decreased the expression of TRAF6, IRAK1, caspase 3, and the phosphorylation level of NF-kappaB, and also increased the Bcl-2/Bax ratio, suggesting the inhibition of inflammation and apoptosis.
TRAF6 can promote the proliferation of stromal cells of benign prostatic hyperplasia via Akt/mTOR signaling.
Study identified IRAK1 and TRAF6 are direct targets of miR-146a in cervical cancer cells. Their expression is downregulated by miR-146a to promote cell viability.
Immune profiling of human prostate epithelial cells in health and pathology determined by expression of p38/TRAF-6/ERK MAP kinases pathways has been reported.
Downregulation of miR-124 in human osteosarcoma tissues and cell lines may increase the expression of TRAF6 protein. miR-124 may inhibit cell cycle progression and invasion of osteosarcoma cells, and promote apoptosis by regulating TRAF6.
Low TRAF6 expression is associated with posterior longitudinal ligament ossification.
these results suggest that miR-146a-5p affects proliferation and apoptosis in a cellular context-dependent manner and selectively disarms the TRAF6-mediated branch of the TGF-beta signaling in oral squamous cell carcinoma cell lines by sparing Smad4 involvement
MALT1 and TRAF6 cooperatively interact with CARMA1-BCL10 filaments and form CARMA1-BCL10-MALT1-TRAF6 signalosome.
our data demonstrated that miR146b5p, as a tumor suppressor, mediated temozolomide resistance in GBM cells through negatively regulating TRAF6 expression, indicating that miR146b5p and its targeted genes would be potential therapeutic targets for glioma therapy.
genetic association studies in Han population in southern China: Data suggest that, in subjects with type 2 diabetes, an SNP in NLRX1 (rs4245191) is associated with macro-vascular complications and cerebral infarction in the population studied; no such association was found for two other SNPs in NLRX1 (rs10790286, rs561830) or for two SNPs in TRAF6 (rs5030445, rs16928973). (NLRX1 = NLR family member-X1)
protein-protein interaction studies on TRAF6 and BSG to get molecular level insights of the reactions.
miR-146a suppresses the inflammatory response in human white adipocytes via targeting the expression of IRAK1 and TRAF6.
miRNA146a expression was significantly higher in hepatitis C patients with a best cut off value 1.63 to discriminate between hepatitis C patients and healthy controls. Meanwhile, it was negatively correlated to IRAK1 and TRAF6 levels and positively correlated to viral load in hepatitis C patients.
Suggest role for EBV-EBER1 in the induction of increased TRAF6 expression in the peripheral B cells of Sjogren's patients.
Conditional deletion of TRAF6 in the intestinal epithelium causes a complete loss of M cells in Peyer patches (PPs), resulting in impaired antigen uptake into PPs.
the expression of TRAF6 in T cells might be implicated in tissue-specific sialadenitis by regulating the chemokine-chemokine receptor system
The data suggest that TFAF6 inhibition reduces choroidal neovascularization formation via down-regulating expression of HIF-1a and VEGF and activation of macrophages and microglia.
Traf6 plays a crucial role in regulating M1 osteoclast and M2 foreign body giant cell polarization.
Authors report that the deletion of TRAF6 in hematopoietic lineage cells resulted in the upregulation of HSPCs in the fetal liver at the prenatal period. However, in the early postnatal period, deletion of TRAF6 drastically diminished HSPCs in the bone marrow (BM), with severe defects in BM development and extramedullary hematopoiesis in the spleen being identified.
Study demonstrated that TRAF6 plays an important role in the process of aseptic inflammatory loosening caused by periprosthetic debris, and Low intensity pulsed ultrasound was found to inhibit such inflammation through increasing the level of FBXL2, and further increasing ubiquitination of TRAF6.
atorvastatin treatment may protect BV2 microglia and hippocampal neurons from oxygenglucose deprivationinduced neuronal inflammatory injury by suppressing the TLR4/TRAF6/NFkappaB pathway. This may provide a potential strategy for the treatment of neuronal injury.
these findings identify IPMK as a key determinant of TRAF6 stability and elucidate the physiological function of IPMK in TLR-induced innate immunity.
Results demonstrate that TRAF6 interacts with MyD88 and suggest that TRAF6 participates in protection from basal autophagy.
Klf4 Alleviates Lipopolysaccharide-Induced Inflammation by Inducing Expression of MCP-1 Induced Protein 1 to Deubiquitinate TRAF6.
TRAF6 RING dimer employs a concerted allosteric mechanism using both subunits of the TRAF6 dimer to promote ubiquitin (Ub) transfer.
miR-146a-mediated control of Traf6 expression Is required for the attenuation of proinflammatory cytokine responses, control of T cell tolerance, and prevention of autoimmunity.
Data indicate TNF receptor associated factor 6 (TRAF6) as an essential molecular switch leading to cardiac hypertrophy in a transforming growth factor beta-activated kinase 1 (TAK1), -dependent manner.
Berberine hydrochloride targets TRAF6 and NFATc1.
The authors found that keratin 8 suppressed toll-like receptor-induced nuclear factor (NF)-kappaB activation and interacted with the adaptor tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6) to prevent its polyubiquitination.
MiR-146a/ MiR-146b could down-regulate the TRAF6 and IRAK1 expression and promote proliferation, migration and angiogenesis ability of endothelial progenitor cells, which could be important for recovery of patients with hyperacute ischemic stroke.
TRAF6 coiled-coil oligomerization domain primes its interaction with Ubc13/Ub~Ubc13 to confer processivity. Long polyUb chain assembly requires coiled-coil domain of TRAF6
TRAF6 is a key promoter of ischemic signaling cascades and neuronal death after cerebral ischemia/reperfusion injury. TRAF6 upregulation binds and ubiquitinates Rac1 directly, which promotes neuron death through neuroinflammation and neuro-oxidative signals.
we found that reactive oxygen species-induced autophagy acts as a negative feedback regulator of JNK activity by dissociating Atg9/mAtg9 from dTRAF2/TRAF6 in Drosophila.
null mutant of DTRAF2 showed immune deficiencies in which NF-kappaB nuclear translocation and antimicrobial gene transcription against microbial infection were severely impaired
TRAF6 is a novel NS3-interacting protein that inhibits classical swine fever virus replication via activation of NF-kappaB-signaling pathways.
we have now analyzed the in vivo function of Traf6 in the innate immune response without interference of adaptive immunity
Full-length traf6 was functionally characterized.
The protein encoded by this gene is a member of the TNF receptor associated factor (TRAF) protein family. TRAF proteins are associated with, and mediate signal transduction from, members of the TNF receptor superfamily. This protein mediates signaling from members of the TNF receptor superfamily as well as the Toll/IL-1 family. Signals from receptors such as CD40, TNFSF11/RANCE and IL-1 have been shown to be mediated by this protein. This protein also interacts with various protein kinases including IRAK1/IRAK, SRC and PKCzeta, which provides a link between distinct signaling pathways. This protein functions as a signal transducer in the NF-kappaB pathway that activates IkappaB kinase (IKK) in response to proinflammatory cytokines. The interaction of this protein with UBE2N/UBC13, and UBE2V1/UEV1A, which are ubiquitin conjugating enzymes catalyzing the formation of polyubiquitin chains, has been found to be required for IKK activation by this protein. This protein also interacts with the transforming growth factor (TGF) beta receptor complex and is required for Smad-independent activation of the JNK and p38 kinases. This protein has an amino terminal RING domain which is followed by four zinc-finger motifs, a central coiled-coil region and a highly conserved carboxyl terminal domain, known as the TRAF-C domain. Two alternatively spliced transcript variants, encoding an identical protein, have been reported.
E3 ubiquitin-protein ligase TRAF6
, RING finger protein 85
, TNF receptor-associated factor 6
, interleukin-1 signal transducer
, TNF receptor-associated factor 6-B
, TNF-receptor-associated factor 2
, TNF-receptor associated factor 6
, TNF receptor-associated factor 6-like
, TNF receptor-associated factor 6-A
, TNF receptor-associated factor 6, E3 ubiquitin protein ligase