Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
IRAK-4 Arg12 is also essential for Myddosome assembly and signalling and we propose that phosphorylated Ser8 induces the N-terminal loop to fold into an alpha-helix. This conformer is stabilised by an electrostatic interaction between phospho-Ser8 and Arg12 and would destabilise a critical interface between IRAK-4 and MyD88 (show MYD88 Proteins).
Our data established IRAK4 as a novel therapeutic target for PDAC treatment. Development of potent IRAK4 inhibitors is needed for clinical testing.
Data suggest that IRAK4 activity regulates activation of IRF5 (show IRF5 Proteins), TAK1 (show MAP3K7 Proteins), and IKKB (show IKBKB Proteins) in monocytes; IRAK4 activation of TAK1 (show MAP3K7 Proteins)-IKKB (show IKBKB Proteins)-IRF5 (show IRF5 Proteins) axis leads to induction of cytokines and interferons following TLR7 (show TLR7 Proteins)/TLR8 (show TLR8 Proteins) stimulation. (IRAK4 = interleukin-1 receptor-associated kinase 4; IRF5 (show IRF5 Proteins) = interferon regulatory factor-5 (show IRF5 Proteins); TAK1 (show MAP3K7 Proteins) = MAPK (show MAPK1 Proteins) kinase kinase 7; IKKB (show IKBKB Proteins) = I-kappa B kinase; TLR = toll (show TLR4 Proteins)-like receptor)
AMPK (show PRKAA1 Proteins) activation inhibited IL-1beta (show IL1B Proteins)-stimulated CXCL10 (show CXCL10 Proteins) secretion, associated with reduced interleukin-1 receptor associated kinase-4 (IRAK4) phosphorylation.
By CRISPR/Cas9-induced inactivation of TLR9 (show TLR9 Proteins), MyD88 (show MYD88 Proteins), IRAK4 and IRAK1 (show IRAK1 Proteins) we confirm that BZLF1 repression is dependent on functional TLR9 (show TLR9 Proteins) and MyD88 (show MYD88 Proteins) signaling, and identify IRAK4 as an essential element for TLR9 (show TLR9 Proteins)-induced repression of BZLF1 expression upon BCR (show BCR Proteins) cross-linking
the polymorphisms in TLR-MyD88 (show MYD88 Proteins)-NF-kappaB (show NFKB1 Proteins) signaling pathway confer genetic susceptibility to Type 2 diabetes mellitus and diabetic nephropathy.
data show that in pericytes, MyD88 (show MYD88 Proteins) and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic.
Data suggest that, in monocytes and macrophages, the interleukin-1B- (IL1B (show IL1B Proteins))-stimulated trans-autophosphorylation of IRAK4 is initiated by MYD88- (myeloid differentiation primary response gene 88 (show MYD88 Proteins))-induced dimerization of IRAK4. In contrast, IRAK1 (interleukin-1 receptor-associated kinase 1 (show IRAK1 Proteins)) is inactive in unstimulated monocytes/macrophages and is converted to an active protein kinase (show CDK7 Proteins) in response to IL1B (show IL1B Proteins).
IRAK4 - Gene involved in innate immunity that have been associated with Chronic Rhinosinusitis.
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.
IRAK4 kinase activity contributes to murine lupus and could represent a new therapeutic target.
Data demonstrate that IRAK-4 is essential for innate and adaptive immunity and necessary for efficient control of mycobacterial infections.
Suppression of IRAK1 (show IRAK1 Proteins) or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding-Defective Mutant of ABIN1 (show TNIP1 Proteins)
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 Proteins)-302b or IRAK4 siRNA silencing inhibits downstream NF-kappaB (show NFKB1 Proteins) 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 Proteins)-93 inhibits IRAK4 expression by binding directly to the 3'-UTR of IRAK4.
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