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anti-Human IRAK4 Antikörper:
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Human Monoclonal IRAK4 Primary Antibody für ICS - ABIN1176904
Hatao, Muroi, Hiki, Ogawa, Mimura, Kaminishi, Tanamoto: Prolonged Toll-like receptor stimulation leads to down-regulation of IRAK-4 protein. in Journal of leukocyte biology 2004
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Human Monoclonal IRAK4 Primary Antibody für ICS - ABIN1176905
Li, Strelow, Fontana, Wesche: IRAK-4: a novel member of the IRAK family with the properties of an IRAK-kinase. in Proceedings of the National Academy of Sciences of the United States of America 2002
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Human Polyclonal IRAK4 Primary Antibody für ICC, ELISA - ABIN1002520
Wesche, Gao, Li, Kirschning, Stark, Cao: IRAK-M is a novel member of the Pelle/interleukin-1 receptor-associated kinase (IRAK) family. in The Journal of biological chemistry 1999
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Monoclonal IRAK4 Primary Antibody für DB, IHC (fro) - ABIN534253
Lehmann, Krüger, Park, Derkow, Rosenberger, Baumgart, Trimbuch, Eom, Hinz, Kaul, Habbel, Kälin, Franzoni, Rybak, Nguyen, Veh, Ninnemann, Peters, Nitsch, Heppner, Golenbock, Schott, Ploegh, Wulczyn et al.: An unconventional role for miRNA: let-7 activates Toll-like receptor 7 and causes neurodegeneration. ... in Nature neuroscience 2012
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Human Monoclonal IRAK4 Primary Antibody für FACS, IHC - ABIN969218
Pathak, De Souza, Salte, Wiker, Asjö: HIV induces both a down-regulation of IRAK-4 that impairs TLR signalling and an up-regulation of the antibiotic peptide dermcidin in monocytic cells. in Scandinavian journal of immunology 2009
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Human Polyclonal IRAK4 Primary Antibody für IHC (fro), WB - ABIN2475135
Linder, Sziegoleit, Brattström, Tydén, Groth: Pancreatic elastase 1 after pancreatic transplantation. in Pancreas 1991
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Human Polyclonal IRAK4 Primary Antibody für ELISA, WB - ABIN547388
Lye, Mirtsos, Suzuki, Suzuki, Yeh: The role of interleukin 1 receptor-associated kinase-4 (IRAK-4) kinase activity in IRAK-4-mediated signaling. in The Journal of biological chemistry 2004
Dimethyl fumarate blocks IRAK4-MyD88 interactions and IRAK4-mediated cytokine production in a cysteine 13-dependent manner.
structures reveal conformational flexibility of unphosphorylated IRAK4 and provide unexpected insights into the potential use of small molecules to modulate IRAK4 activity in cancer, autoimmunity, and inflammation
miR-544 may participate in controlling inflammation and apoptosis after ischemia-reperfusion by targeting IRAK4.
Defective MyD88, IRAK4 but not NF-kB inhibit IL-1beta, MCP-1 and IP-10 production.
Interleukin-1 receptor-associated kinase 4 (IRAK-4) involved in the pathway produces cytokines that initiate and maintain inflammation through Toll-like receptors and interleukin-1 receptors on the membranes of innate immune cells are stimulated with antigens
Inhibition of IRAK4-L abrogates leukaemic growth, particularly in acute myeloid leukaemia (AML) cells with higher expression of the IRAK4-L isoform. Collectively, mutations in U2AF1 induce expression of therapeutically targetable 'active' IRAK4 isoforms and provide a genetic link to activation of chronic innate immune signalling in myelodysplastic syndromes and AML.
Data show that interleukin 1 receptor associated kinase 4 (IRAK4) and EPH receptor A2 (EphA2) were the functional targets of miR-302b.
Therefore, the IRAK4-MyD88 scaffolding function is essential for IL-1 signaling, but IRAK4 kinase activity can control IL-1 signal strength by modulating the association of IRAK4, MyD88, and IRAK1.
our results indicate that IRAK4 has a critical scaffold function in myddosome formation and that its kinase activity is dispensable for myddosome assembly and activation of the NF-kappaB and MAPK pathways but is essential for MyD88-dependent production of inflammatory cytokines. Our findings suggest that the scaffold function of IRAK4 may be an attractive target for treating inflammatory and autoimmune diseases.
rs4251545 of IRAK4 (p.Ala428Thr) modified the susceptibility to HBV-related HCC via increased proliferation rate and reduced production of inflammatory cytokines and chemokines
synthetic routes with moderate to high yields have been developed to produce the reference standard 9, demethylated precursor 8 and target tracer [11C]9. The radiosynthesis employed [11C]CH3OTf for N-[11C]methylation at the piperazin position of the desmethyl precursor, followed by product purification and isolation using a semi-preparative RP HPLC combined with SPE. [11C]9 was obtained in high radiochemical yield, radioc
The high mRNA levels of IRAK1 and IRAK4 were correlated with the development of Behcet's disease, which suggested that IRAK1 and IRAK4 might participate in the pathogenesis of Behcet's disease
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.
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, TAK1, and IKKB in monocytes; IRAK4 activation of TAK1-IKKB-IRF5 axis leads to induction of cytokines and interferons following TLR7/TLR8 stimulation. (IRAK4 = interleukin-1 receptor-associated kinase 4; IRF5 = interferon regulatory factor-5; TAK1 = MAPK kinase kinase 7; IKKB = I-kappa B kinase; TLR = toll-like receptor)
AMPK activation inhibited IL-1beta-stimulated CXCL10 secretion, associated with reduced interleukin-1 receptor associated kinase-4 (IRAK4) phosphorylation.
By CRISPR/Cas9-induced inactivation of TLR9, MyD88, IRAK4 and IRAK1 we confirm that BZLF1 repression is dependent on functional TLR9 and MyD88 signaling, and identify IRAK4 as an essential element for TLR9-induced repression of BZLF1 expression upon BCR cross-linking
the polymorphisms in TLR-MyD88-NF-kappaB signaling pathway confer genetic susceptibility to Type 2 diabetes mellitus and diabetic nephropathy.
data show that in pericytes, MyD88 and IRAK4 are key regulators of 2 major injury responses: inflammatory and fibrogenic.
Data suggest that, in monocytes and macrophages, the interleukin-1B- (IL1B)-stimulated trans-autophosphorylation of IRAK4 is initiated by MYD88- (myeloid differentiation primary response gene 88)-induced dimerization of IRAK4. In contrast, IRAK1 (interleukin-1 receptor-associated kinase 1) is inactive in unstimulated monocytes/macrophages and is converted to an active protein kinase in response to IL1B.
Pharmacological inhibition or siRNA mediated knockdown of IRAK1/4 attenuated Nod1-mediated activation of NF-kappaB, JNK, and the expression of proinflammatory cytokines. These results reveal that Nod1-mediated lipolysis promoted accumulation of DAG, which engaged PKCdelta and IRAK1/4 to augment inflammation in 3T3-L1 adipocytes.
IRAK4 kinase activity is prerequisite for regulating innate immunity during infections with intracellular bacteria. The loss of IRAK4 kinase activity underlies deficient cytokine and microbicidal responses during infection with intracellular bacteria L. monocytogenes or M. smegmatis via impaired activation of IRAK1, MAPKs, and NF-kappaB but increases bacterial burdens, correlating with decreased induction of NO.
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 or IRAK4 Catalytic Activity, but Not Type 1 IFN Signaling, Prevents Lupus Nephritis in Mice Expressing a Ubiquitin Binding-Defective Mutant of ABIN1
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-302b or IRAK4 siRNA silencing inhibits downstream NF-kappaB 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-93 inhibits IRAK4 expression by binding directly to the 3'-UTR of IRAK4.
Intact IRAK4 function inhibited heart-specific migration of bone-marrow-derived CCR5(+) cells.
In macrophages from IRAK4(KDKI) mice, IRAK4 kinase deficiency decreased LPS signaling but did not prevent endotoxin tolerance. A TLR2-TLR1 agonist attenuated TLR2-elicited homo- & heterotolerance at the level of MAPK activation.
During bacterial infection, PGN-mediated TLR2 signaling induces miR-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- and IRAK-4-deficient mice and humans.
Signaling via IRAK4 is essential for the activation of innate immune cells, development of parasite-specific acquired immunity, and host resistance to infection with T. gondii.
Induction of endotoxin tolerance in vivo inhibits expression of proinflammatory mediators via impaired activation of IRAK4, p38, and NF-kappaB and increases expression of negative regulators of TLR4 pathways.
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