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The estimated prevalence of IRAK4 gene polymorphism found in a Portuguese Caucasian population was 26.8 % (CI 95%) [20.1, 34.7 %]. A model to predict the inflammatory response in the maxillary sinus in the presence etiological factors of dental origin was constructed.
This is the first study to show an association between single nucleotide polymorphisms in IRAK1 (show IRAK1 ELISA Kits), IRAK4 and MyD88 (show MYD88 ELISA Kits), and the presence of severe invasive pneumococcal disease.
Src (show SRC ELISA Kits), Syk (show SYK ELISA Kits), IRAK1 (show IRAK1 ELISA Kits), and IRAK4 have roles in anti-inflammatory responses mediated by dietary flavonoid Kaempferol
findings suggest that rare, functional variants in MYD88, IRAK4 or IKBKG do not significantly contribute to IPD susceptibility in adults at the population level
High mRNA levels of IRAK1 (show IRAK1 ELISA Kits) and IRAK4 correlated with VKH disease activity.
Studies indicate that interleukin-1 receptor-associated kinase 4 protein (IRAK4), a serine/threonine kinase, plays a key role in both inflammation and oncology diseases.
by bolstering the IgM(+)IgD(+)CD27(+) B-cell subset, IRAK-4 and MyD88 promote optimal T-independent IgM antibody responses against bacteria in humans.
delineation of the latter responses identified a narrow repertoire of transcriptional programs affected by loss of MyD88 (show MYD88 ELISA Kits) function or IRAK4 function
Data show that dimerization is crucial for IRAK4 autophosphorylation in vitro and ligand dependent signaling in cells.
these studies suggest that not only the loss of protein expression but also the defect of Myddosome formation couldcause IRAK4 and MyD88 (show MYD88 ELISA Kits) deficiency syndromes.
PMA treatment during a vulnerable period can alter brain development. IL-18 and IRAK-4 appear to be important for the development of PMA induced injury.
enforced expression of miR (show MLXIP ELISA Kits)-302b or IRAK4 siRNA silencing inhibits downstream NF-kappaB (show NFKB1 ELISA Kits) signalling and airway leukocyte infiltration, thereby alleviating lung injury and increasing survival in P. aeruginosa-infected mice.
Our results demonstrate that osteoclasts and FBGCs are reciprocally regulated and identify IRAK4 as a potential therapeutic target to inhibit stimulated osteoclastogenesis and rescue inhibited FBGC formation
Suggest FC-99 is a potential therapeutic molecule that alleviated experimental sepsis by directly inhibiting IRAK4 activation.
MiR (show MLXIP ELISA Kits)-93 inhibits IRAK4 expression by binding directly to the 3'-UTR (show UTS2R ELISA Kits) of IRAK4.
Intact IRAK4 function inhibited heart-specific migration of bone-marrow-derived CCR5 (show CCR5 ELISA Kits)(+) cells.
In macrophages from IRAK4(KDKI) mice, IRAK4 kinase deficiency decreased LPS (show TLR4 ELISA Kits) signaling but did not prevent endotoxin tolerance. A TLR2 (show TLR2 ELISA Kits)-TLR1 (show TLR1 ELISA Kits) agonist attenuated TLR2 (show TLR2 ELISA Kits)-elicited homo- & heterotolerance at the level of MAPK (show MAPK1 ELISA Kits) activation.
During bacterial infection, PGN (show SPG7 ELISA Kits)-mediated TLR2 (show TLR2 ELISA Kits) signaling induces miR (show MLXIP ELISA Kits)-132/-212 to downregulate IRAK4.
IRAK4-deficient mice exhibit increased susceptibility and decreased cytokine production in vivo upon Streptococcus pneumoniae infection.
Experimental and natural infections in MyD88 (show MYD88 ELISA Kits)- and IRAK-4-deficient mice and humans.
This gene encodes a kinase that activates NF-kappaB in both the Toll-like receptor (TLR) and T-cell receptor (TCR) signaling pathways. The protein is essential for most innate immune responses. Mutations in this gene result in IRAK4 deficiency and recurrent invasive pneumococcal disease. Multiple transcript variants encoding different isoforms have been found for this gene.
interleukin-1 receptor-associated kinase 4
, interleukin-1 receptor-associated kinase 4-like
, Interleukin-1 receptor-associated kinase 4
, renal carcinoma antigen NY-REN-64
, NY-REN-64 antigen
, interleukin-1 receptor associated kinase 4