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Study shows that IRAK1 was over-expressed in human hepatocellular carcinoma (HCC (show FAM126A ELISA Kits)) tumor tissues and provides evidence that IRAK1 promotes cell proliferation and protects against apoptosis in HCC (show FAM126A ELISA Kits).
These results suggest that the IRAK1-binding protein OPTN (show OPTN ELISA Kits) negatively regulates IL-1beta (show IL1B ELISA Kits)/LPS (show IRF6 ELISA Kits)-induced NF-kappaB (show NFKB1 ELISA Kits) activation by preventing polyubiquitination of TRAF6 (show TRAF6 ELISA Kits).
IRAK1 regulates lipid accumulation by modulating CD36 (show CD36 ELISA Kits)-mediated uptake and ABCA1 (show ABCA1 ELISA Kits)-, ABCG1 (show ABCG1 ELISA Kits)-dependent cholesterol efflux.
High IRAK1 expression is associated with multiple myeloma.
TLR4 (show TLR4 ELISA Kits)- and TLR2 (show TLR2 ELISA Kits)-induced IRAK-ERK (show EPHB2 ELISA Kits) pathway cross-talks with p67phox (show NCF2 ELISA Kits)-Nox-2 (show CYBB ELISA Kits) for reactive oxygen species generation, thus regulating IL-1beta (show IL1B ELISA Kits) transcription and processing in monocytic cells.
Data suggest that, in monocytes and macrophages, the interleukin-1B- (IL1B (show IL1B ELISA Kits))-stimulated trans-autophosphorylation of IRAK4 (interleukin-1 receptor-associated kinase 4 (show IRAK4 ELISA Kits)) is initiated by MYD88- (myeloid differentiation primary response gene 88 (show MYD88 ELISA Kits))-induced dimerization of IRAK4 (show IRAK4 ELISA Kits). In contrast, IRAK1 is inactive in unstimulated monocytes/macrophages and is converted to an active protein kinase (show CDK7 ELISA Kits) in response to IL1B (show IL1B ELISA Kits).
Data indicate the complexity of interactions between Pin1 (show PIN1 ELISA Kits) and activated IRAK1, suggesting that phosphorylation of neighboring Ser (show SIGLEC1 ELISA Kits)/Thr (show TRH ELISA Kits)-Pro motifs in proteins might provide competitive advantage at cellular concentrations for engaging with Pin1 (show PIN1 ELISA Kits).
IRAK1 is a direct target of miR (show MLXIP ELISA Kits)-146b and has functional roles to inhibit various aggressive papillary thyroid carcinoma cell activities.
our data strongly suggest that AQCA-mediated suppression of inflammatory responses could be managed by a direct interference of signaling cascades including IRAK and Syk (show SYK ELISA Kits), linked to the activation of NF-kappaB (show NFKB1 ELISA Kits) and AP-1 (show FOSB ELISA Kits).
The IRAK1 rs3027898 was not associated with RA, whereas C allele of miR (show MLXIP ELISA Kits)-146a rs2910164 was found to be protective.
these findings identify a transcription-independent, rapid, and nongenomic glucocorticoid suppression of TLR9 (show TLR9 ELISA Kits) ligand-mediated IRAK1 ubiquitination as a novel mechanism for restraining acute inflammatory reactions
These results suggest that the IRAK1-binding protein OPTN (show OPTN ELISA Kits) negatively regulates IL-1beta (show IL1B ELISA Kits)/LPS (show TLR4 ELISA Kits)-induced NF-kappaB (show NFKB1 ELISA Kits) activation by preventing polyubiquitination of TRAF6 (show TRAF6 ELISA Kits).
Data, including data from studies in knockout mice, suggest that Irak1 is involved in regulating glucose metabolism and insulin (show INS ELISA Kits) sensitivity in skeletal muscle (but not in liver and not in obesity due to high-fat diet); insulin (show INS ELISA Kits) sensitivity is 30% higher in Irak1 knockout mice on chow diet, but Irak1 deletion does not affect development of glucose intolerance due to high-fat diet.
Suppression of IRAK1 or IRAK4 (show IRAK4 ELISA Kits) Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding-Defective Mutant of ABIN1 (show TNIP1 ELISA Kits)
Torreya nucifera butanol fraction exhibits anti-inflammatory activities by direct inhibition of macrophage Src (show SRC ELISA Kits)/Syk (show SYK ELISA Kits)/NF-kappaB (show NFKB1 ELISA Kits) and IRAK1/AP-1 (show JUN ELISA Kits) signaling.
IRAK1 is involved in TLR4 (show TLR4 ELISA Kits)-mediated downregulation of ABCA1 (show ABCA1 ELISA Kits) expression and lipid accumulation in VSMCs.
plays an important role in intestinal inflammation by mediating T cell activation, differentiation, and accumulation in the gut (show GUSB ELISA Kits)
Mangiferin ameliorates colitis by inhibiting IRAK1 phosphorylation in NF-kappaB (show NFKB1 ELISA Kits) and MAPK (show MAPK1 ELISA Kits) pathways
miR (show MLXIP ELISA Kits)-146a ameliorates liver ischemia/reperfusion injury in vivo and hypoxia/reoxygenation injury in vitro by directly suppressing IRAK1 and TRAF6 (show TRAF6 ELISA Kits).
miR (show MLXIP ELISA Kits)-146a attenuates sepsis-induced cardiac dysfunction by preventing NF-kappaB (show NFKB1 ELISA Kits) activation, inflammatory cell infiltration, and inflammatory cytokine production via targeting of IRAK and TRAF6 (show TRAF6 ELISA Kits) in both cardiomyocytes and inflammatory monocytic cells.
Results describe a new full-length gene model for the bovine IRAK1 gene.
ALOX5AP (show ALOX5AP ELISA Kits), CPNE3 (show CPNE3 ELISA Kits), IL1R2 (show IL1R2 ELISA Kits), IL6 (show IL6 ELISA Kits), TLR2 (show TLR2 ELISA Kits), TLR4 (show TLR4 ELISA Kits), and THY1 (show THY1 ELISA Kits) were upregulated in blood polymorphonuclear cells in negative energy balance versus positive energy balance cows.
This gene encodes the interleukin-1 receptor-associated kinase 1, one of two putative serine/threonine kinases that become associated with the interleukin-1 receptor (IL1R) upon stimulation. This gene is partially responsible for IL1-induced upregulation of the transcription factor NF-kappa B. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
interleukin-1 receptor-associated kinase 1
, Pelle homolog
, interleukin-1 receptor-associated kinase-1
, pelle-like protein kinase
, interleukin receptor associated kinase 1