No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human TRAF6 Antibodies:
anti-Mouse (Murine) TRAF6 Antibodies:
anti-Rat (Rattus) TRAF6 Antibodies:
Go to our pre-filtered search.
Human Polyclonal TRAF6 Primary Antibody for IHC, WB - ABIN6713396
Liu, He, Zhang, Li, Zhu, Dong, Zhang, Xing, Wang, Qiao, Chen: Neuroprotective effect of early and short-time applying sophoridine in pMCAO rat brain: down-regulated TRAF6 and up-regulated p-ERK1/2 expression, ameliorated brain infaction and edema. in Brain research bulletin 2012
Show all 5 Pubmed References
Human Polyclonal TRAF6 Primary Antibody for IF, WB - ABIN6714483
Zeng, Zhao, Ma, Jiang, Tu: Protosappanin A inhibits oxidative and nitrative stress via interfering the interaction of transmembrane protein CD14 with Toll-like receptor-4 in lipopolysaccharide-induced BV-2 microglia. in International immunopharmacology 2012
Show all 3 Pubmed References
Human Polyclonal TRAF6 Primary Antibody for IF, WB - ABIN541206
Takeda, Kaisho, Akira: Toll-like receptors. in Annual review of immunology 2003
Show all 3 Pubmed References
Cow (Bovine) Polyclonal TRAF6 Primary Antibody for IHC (fro), IHC (p) - ABIN537432
Ichii, Otsuka, Sasaki, Namiki, Hashimoto, Kon: Altered expression of microRNA miR-146a correlates with the development of chronic renal inflammation. in Kidney international 2012
Show all 3 Pubmed References
Human Polyclonal TRAF6 Primary Antibody for ICC, ELISA - ABIN1003297
Wu: Assembly of post-receptor signaling complexes for the tumor necrosis factor receptor superfamily. in Advances in protein chemistry 2004
Show all 4 Pubmed References
Cow (Bovine) Polyclonal TRAF6 Primary Antibody for IHC, IHC (p) - ABIN4361692
Zapata, Krajewska, Krajewski, Kitada, Welsh, Monks, McCloskey, Gordon, Kipps, Gascoyne, Shabaik, Reed: TNFR-associated factor family protein expression in normal tissues and lymphoid malignancies. in Journal of immunology (Baltimore, Md. : 1950) 2000
Show all 3 Pubmed References
Human Polyclonal TRAF6 Primary Antibody for FACS, WB - ABIN4361690
Yoshida, Jono, Kai, Li: The tumor suppressor cylindromatosis (CYLD) acts as a negative regulator for toll-like receptor 2 signaling via negative cross-talk with TRAF6 AND TRAF7. in The Journal of biological chemistry 2005
Show all 2 Pubmed References
Human Polyclonal TRAF6 Primary Antibody for ELISA, ICC - ABIN6265707
Zhang, Fei, Tao, Li, Shen, Wang, Liu, Xu: Neuroprotective Effect of Modified Xijiao Dihuang Decoction against Oxygen-Glucose Deprivation and Reoxygenation-Induced Injury in PC12 Cells: Involvement of TLR4-MyD88/NF-κB Signaling Pathway. in Evidence-based complementary and alternative medicine : eCAM 2018
Human Polyclonal TRAF6 Primary Antibody for IHC, WB - ABIN6672306
Teng, Luo, Yu, Chen, Huang, Chen, Xie, Zeng, Luo, Xiong, Liu, Hou, Feng: CRISPR/Cas9-mediated deletion of miR-146a enhances antiviral response in HIV-1 infected cells. in Genes and immunity 2018
These results reveal that TRAF6 regulates YAP signaling by promoting the ubiquitination and degradation of MST1 in pancreatic cancer.
This study for the first time ever demonstrated an association between a genetic variant of TRAF6 and low bone mineral density among patients with rheumatoid arthritis.
Downregulation of miR146a in human cervical cancer cells induced TRAF6 and NFkappaB protein expression. The inhibition of TRAF6 attenuated the effects of antimiR146a on the function of Th17 cell differentiation to modulate cervical cancer cell growth and apoptosis. Collectively, miR146a regulated the function of Th17 cell differentiation through NFkappaB signaling by targeting TRAF6.
Tumor necrosis factor receptor-associated factor 6 (TRAF6)-mediated proto-oncogene protein Akt (AKT) ubiquitination and subsequent phosphorylation played an essential role in the control of tumor cell malignant behavior.
the interaction of TRAF6 with c-Cbl causes lysine 48-linked polyubiquitination for both negative feedback regulation and signaling cross-talk between RANKL and IFN-gamma.
we show that knockdown of TRAF6 sensitizes MM cells to treatment with bortezomib when co-cultured with stromal cells. Inhibiting TRAF6 represents a promising strategy to target MM cells in the BM microenvironment.
miR323 suppresses nerve cell apoptosis in cerebral infarction via the TGFbeta1/SMAD3 signaling pathway.
MALT1 activation by TRAF6 in lymphocytes needs neither BCL10 nor CARD11.
TARBP2 participates in the interaction between IRF7 and TRAF6, thereby suppressing TRAF6-mediated K63-linked ubiquitination of IRF7.
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.
miR-590-3p has the ability to suppress LPS-induced Acute Kidney Injury and podocyte apoptosis by targeting TRAF6
our data suggest that NUMBL and TAK1 are reciprocally regulated and that NUMBL acts as an endogenous regulator of NF-kappaB signaling and osteoclastogenesis by targeting the TAK1-TRAF6-NEMO axis.
TRAF6 is required for hematopoietic stem cell homeostasis by maintaining a minimal threshold level of IKKbeta/NF-kappaB signaling.
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.
Low TRAF6 expression is associated with posterior longitudinal ligament ossification.
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.
protein-protein interaction studies on TRAF6 and BSG to get molecular level insights of the reactions.
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.
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