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AGAP2-AS1 was upregulated and transcriptionally induced by SP1 in breast cancer..ChIP assays showed that AGAP2-AS1-bound CBP increased the enrichment of H3K27ac at the promoter region of MyD88, thus resulting in the upregulation of MyD88. Gain- and loss-of-function assays confirmed that the NF-kappaB pathway was activated by MyD88 and AGAP2-AS1
Activates the NFkappaB (zeige NFKB1 Proteine) pathway through the Tolllike receptor 4 (TLR4 (zeige TLR4 Proteine))/myeloid differentiation factor 88 (MyD88)/IkappaBalpha (zeige NFKBIA Proteine) axis.
explored the detection method and clinical relevance of MYD88 mutations in Chinese patients with Chronic Lymphocytic Leukemia
The combination of Ligusticum chuanxiong and Radix Paeoniae protects against focal cerebral ischaemia via TLR4 (zeige TLR4 Proteine)/MyD88/MAPK (zeige MAPK1 Proteine)/NF-kappaB (zeige NFKB1 Proteine) signalling pathway in rat model of middle cerebral artery stroke.
MYD88 Gene Polymorphism is not associated with Chronic Lymphocytic Leukemia.
17.6% of cases with primary CNS diffuse large B-cell lymphoma had homozygous/hemizygous MYD88 mutations, which has not been previously reported
MyD88 mutation status did not correlate with overall survival (OS), post-ASCT OS, or progression-free survival (PFS) for Diffuse Large B Cell Lymphoma Patients undergoing Autologous Stem Cell Transplantation.
Inducible activation of MyD88 and CD40 (zeige CD40 Proteine) in CAR T cells with a small-molecule drug not only enhances their effector function, resulting in potent antitumor activity in preclinical solid tumors, but also enables their remote control post infusion.
loss of MyD88 is essential for retinoic acid-facilitated differentiation of human embryonal carcinoma cells.
Study supports that MYD88 status is a necessary biomarker in patients with primary cutaneous large B-cell lymphomas for diagnosis, prognosis, and management.
Study shows the identification two novel variants of MyD88 gene in mouse. The novel transcript and protein isoform MYD88N1 was expressed in several tissues while the MyD88N2 variant was found only in the brain. The existence of different transcription factors binding sites observed after promoter analysis indicates their role in the critical control of gene expression at different developmental stages.
by promoting the initial antigen-specific B cell proliferation and differentiation, B cell-intrinsic MyD88 signaling enhanced both T-independent and T-dependent antibody responses elicited by Bacterial phage Qbeta-derived virus-like particle. This finding will provide additional insight into the role of Toll (zeige TLR4 Proteine)-Like Receptor signaling in antiviral immunity, autoimmune diseases, and vaccine design.
This study demonstrates that the synergistic effect between TLR4 (zeige TLR4 Proteine) and TLR3 (zeige TLR3 Proteine) in macrophages is an important determinant in acute lung injury and, more importantly, that TLR3 (zeige TLR3 Proteine) up-regulation is dependent on TLR4 (zeige TLR4 Proteine)-MyD88-NF-kappaB (zeige NFKB1 Proteine) signaling.
Results provide evidence that Bbsal autophagy prevents autoactivation or enhancement of inflammatory signals by targeting monomeric MyD88. Also, MyD88 was shown to interact with TRAF6 (zeige TRAF6 Proteine).
we confirmed the essential role of MyD88-dependent signalling in recruiting neutrophils and controlling P. aeruginosa-induced pulmonary infection
MyD88 protein levels are increased during in vitro myogenesis and in conditions that promote skeletal muscle growth in vivo.
The results suggested that dioscin prevents LPSinduced ALI through inhibiting the TLR4 (zeige TLR4 Proteine)/MyD88 signaling pathway via upregulation of HSP70 (zeige HSP70 Proteine).
The results indicate that IgM (zeige CD40LG Proteine)-restricted PCMZL may harbour distinct molecular genetic characteristics, as evidenced by activating MYD88 mutations, which may explain some of the peculiar clinical and histological features found in this population.
In the initial periods of AP progression, an increased expression of MMP9 (zeige MMP9 Proteine) in the TLR2 KO and MyD88 KO mice was observed. In the final periods of AP progression, a reduction of MMP2 (zeige MMP2 Proteine) expression and an increase of MMP9 (zeige MMP9 Proteine) expression in the TLR2 KO mice were observed. MMP2 (zeige MMP2 Proteine) and MMP9 (zeige MMP9 Proteine) production was modulated for TLR2 and MyD88 during apical periodontitis progression
MyD88 deficiency considerably protected mice from the development of streptozotocin (STZ)-induced diabetes and delayed the onset of diabetes in Non-Obese Diabetic mice. MyD88 signaling in myeloid cells is a critical pathogenic factor in autoimmune diabetes, which is antagonized by TRIF (zeige RNF138 Proteine)-dependent responses. This depends at least in part on their opposite effects in regulating IDO (zeige IDO1 Proteine) in phagocytes exposed to apoptotic cells.
a novel function of MyD88 in the regulation of metabolism that appears to be independent of its known roles in immunity and development.
propose that dMyD88 is the functional homolog of TIRAP (zeige TIRAP Proteine) and that both proteins function as sorting adaptors to recruit downstream signaling adaptors to activated receptors
DmMyD88 encodes an essential component of the Toll (zeige TLR4 Proteine) pathway in dorsoventral pattern formation.
We show that there is a direct interaction between Kra and Tube presumably mediated by the death domains present in both proteins.
both the heterodimeric and heterotrimeric complexes form kidney-shaped structures and that Tube is bivalent and has separate high affinity binding sites for dMyD88 and Pelle (zeige IRAK1 Proteine).
These results suggest that porcine circovirus 2 induces IL-8 (zeige IL8 Proteine) secretion via the TLR2/MyD88/NF-kappaB (zeige NFKB1 Proteine) signalling pathway.
At 30 days after autotransplantation of a pig kidney, mRNA expression increases for MyD88.
These results suggest that an MyD88-dependent signaling pathway is present in newborn as well as in adult swine and that it is involved in the innate immune system of these animals.
microbiota-induced, Myd88-dependent signaling inhibits host Notch (zeige NOTCH1 Proteine) signaling in the intestinal epithelium, thereby promoting secretory cell fate determination
Fish IRF6 (zeige IRF6 Proteine) is distinguished from the homolog of mammals by being a positive regulator of IFN transcription and phosphorylated by MyD88 and TBK1 (zeige TBK1 Proteine), suggesting that differences in the IRF6 (zeige IRF6 Proteine) regulation pattern exist between lower and higher vertebrates.
DrIRF1 works in concert with MyD88 to activate zebrafish IFNvarphi3 but not IFNvarphi1. These results provide insights into the evolving function of IRF1 (zeige IRF1 Proteine) as a positive IFN regulator.
MyD88 signaling has an important protective role during early pathogenesis.
MyD88-dependent signaling is involved in the innate immune response of the developing zebrafish embryo, a model for the study of vertebrate innate immunity.
L. rhamnosus GR-1 ameliorates the E. coli-induced disruption of cellular ultrastructure, subsequently reducing the percentage of bovine endometrial epithelial cells apoptosis and limiting inflammatory responses, partly via attenuation of MyD88-dependent and MyD88-independent pathway activation
Modulated cytokine expression in Bovine viral diarrhea virus type 2 infected macrophages was associated with decreased MyD88 expression.
The study demonstrates that in cattle, animals heterozygous at the MyD88 A625C polymorphic marker have a 5-fold reduced risk for active pulmonary tuberculosis.
MyD88 plays a functional role in transducing LPS (zeige IRF6 Proteine) signaling from TLR-4 (zeige TLR4 Proteine) to downstream effector molecules involved in NF-kappaB (zeige NFKB1 Proteine) activation
MyD88 interacts with interferon (zeige IFNA Proteine) regulatory factor (IRF) 3 (zeige IRF3 Proteine) and IRF7 (zeige IRF7 Proteine) in Atlantic salmon (Salmo salar)
the salmon MyD88 was cloned and its expression was analysed.
This gene encodes a cytosolic adapter protein that plays a central role in the innate and adaptive immune response. This protein functions as an essential signal transducer in the interleukin-1 and Toll-like receptor signaling pathways. These pathways regulate that activation of numerous proinflammatory genes. The encoded protein consists of an N-terminal death domain and a C-terminal Toll-interleukin1 receptor domain. Patients with defects in this gene have an increased susceptibility to pyogenic bacterial infections. Alternate splicing results in multiple transcript variants.
myeloid differentiation primary response gene (88)
, myeloid differentiation primary response protein MyD88
, myeloid differentiation primary response protein MyD88-B
, Toll/IL-1 receptor binding protein MyD88-B
, myeloid differentiation primary response gene 88
, myeloid differentiation primary response factor 88
, myeloid differentiation factor 88
, myeloid differentiation primary response protein 88
, myeloid differentiation response protein 88