Browse our anti-MYD88 (MYD88) Antibodies

Human Myeloid Differentiation Primary Response Gene (88) (MYD88) interaction partners

1. explored the detection method and clinical relevance of MYD88 mutations in Chinese patients with Chronic Lymphocytic Leukemia

2. The combination of Ligusticum chuanxiong and Radix Paeoniae protects against focal cerebral ischaemia via TLR4 (show TLR4 Antibodies)/MyD88/MAPK (show MAPK1 Antibodies)/NF-kappaB (show NFKB1 Antibodies) signalling pathway in rat model of middle cerebral artery stroke.

3. MYD88 Gene Polymorphism is not associated with Chronic Lymphocytic Leukemia.

4. 17.6% of cases with primary CNS diffuse large B-cell lymphoma had homozygous/hemizygous MYD88 mutations, which has not been previously reported

5. 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.

6. Inducible activation of MyD88 and CD40 (show CD40 Antibodies) 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.

7. loss of MyD88 is essential for retinoic acid-facilitated differentiation of human embryonal carcinoma cells.

8. Study supports that MYD88 status is a necessary biomarker in patients with primary cutaneous large B-cell lymphomas for diagnosis, prognosis, and management.

9. Among age >65 patients, the MyD88 L265P mutation portended a worse overall survival compared with the MyD88 wild type

10. Results show that MyD88 protein is necessary to activate autophagy in HSV-1-infected THP-1 (show GLI2 Antibodies) cells.

Mouse (Murine) Myeloid Differentiation Primary Response Gene (88) (MYD88) interaction partners

1. The results indicate that IgM (show CD40LG Antibodies)-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.

2. In the initial periods of AP progression, an increased expression of MMP9 (show MMP9 Antibodies) in the TLR2 KO and MyD88 KO mice was observed. In the final periods of AP progression, a reduction of MMP2 (show MMP2 Antibodies) expression and an increase of MMP9 (show MMP9 Antibodies) expression in the TLR2 KO mice were observed. MMP2 (show MMP2 Antibodies) and MMP9 (show MMP9 Antibodies) production was modulated for TLR2 and MyD88 during apical periodontitis progression

3. 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 (show RNF138 Antibodies)-dependent responses. This depends at least in part on their opposite effects in regulating IDO (show IDO1 Antibodies) in phagocytes exposed to apoptotic cells.

4. the present study indicated that MyD88 and TRIF (show RNF138 Antibodies) blockades serve notable and equivalent roles in protecting cardiac deterioration from severe sepsis by attenuating cytokine release, reducing neutrophil infiltration and alleviating apoptosis.

5. Results show that interleukin-33 (show IL33 Antibodies) acts to express Schaffer collateral/CA1 (show CA1 Antibodies) long term potentiation (LTP (show SCP2 Antibodies)) relevant to spatial learning and memory in a myeloid differentiation factor 88 (MyD88)-dependent manner.

6. We also define the likely cellular candidates for this MyD88-dependent step. These findings suggest that symptom management is possible without ameliorating protective antiviral immune responses

7. These findings establish the T-cell intrinsic IL-18R/MyD88 pathway as a crucial element for induction of cognate Th1 (show HAND1 Antibodies) responses against an important human pathogen.

8. The findings suggest that MyD88 in primary sensory neurons plays an active role in regulating IL-1beta (show IL1B Antibodies) signaling and neuroinflammation in the peripheral and the central nervous systems, and contributes to the maintenance of persistent pain.

9. These findings elucidate a novel mechanism of inflammation-associated osteoclastogenesis, which involves TLR4 (show TLR4 Antibodies) recognition of gamma-glutamyltranspeptidase and subsequent activation of MyD88-dependent signaling.

10. The intracellular adaptor protein MyD88-independent TLR2 activation induced by Porphyromonas gingivalis stimulates PI3K signaling that drives inflammation but at the same time depresses phagocytosis and enables phagocytosed bacteria to escape lysosomal degradation.

Fruit Fly (Drosophila melanogaster) Myeloid Differentiation Primary Response Gene (88) (MYD88) interaction partners

1. a novel function of MyD88 in the regulation of metabolism that appears to be independent of its known roles in immunity and development.

2. propose that dMyD88 is the functional homolog of TIRAP (show TIRAP Antibodies) and that both proteins function as sorting adaptors to recruit downstream signaling adaptors to activated receptors

3. DmMyD88 encodes an essential component of the Toll (show TLR4 Antibodies) pathway in dorsoventral pattern formation.

4. We show that there is a direct interaction between Kra and Tube presumably mediated by the death domains present in both proteins.

5. 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 (show IRAK1 Antibodies).

Pig (Porcine) Myeloid Differentiation Primary Response Gene (88) (MYD88) interaction partners

1. These results suggest that porcine circovirus 2 induces IL-8 (show IL8 Antibodies) secretion via the TLR2/MyD88/NF-kappaB (show NFKB1 Antibodies) signalling pathway.

2. At 30 days after autotransplantation of a pig kidney, mRNA expression increases for MyD88.

3. 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.

Zebrafish Myeloid Differentiation Primary Response Gene (88) (MYD88) interaction partners

1. microbiota-induced, Myd88-dependent signaling inhibits host Notch (show NOTCH1 Antibodies) signaling in the intestinal epithelium, thereby promoting secretory cell fate determination

2. Fish IRF6 (show IRF6 Antibodies) is distinguished from the homolog of mammals by being a positive regulator of IFN transcription and phosphorylated by MyD88 and TBK1 (show TBK1 Antibodies), suggesting that differences in the IRF6 (show IRF6 Antibodies) regulation pattern exist between lower and higher vertebrates.

3. DrIRF1 works in concert with MyD88 to activate zebrafish IFNvarphi3 but not IFNvarphi1. These results provide insights into the evolving function of IRF1 (show IRF1 Antibodies) as a positive IFN regulator.

4. MyD88 signaling has an important protective role during early pathogenesis.

5. MyD88-dependent signaling is involved in the innate immune response of the developing zebrafish embryo, a model for the study of vertebrate innate immunity.

Cow (Bovine) Myeloid Differentiation Primary Response Gene (88) (MYD88) interaction partners

1. 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

2. Modulated cytokine expression in Bovine viral diarrhea virus type 2 infected macrophages was associated with decreased MyD88 expression.

3. The study demonstrates that in cattle, animals heterozygous at the MyD88 A625C polymorphic marker have a 5-fold reduced risk for active pulmonary tuberculosis.

4. MyD88 plays a functional role in transducing LPS (show IRF6 Antibodies) signaling from TLR-4 (show TLR4 Antibodies) to downstream effector molecules involved in NF-kappaB (show NFKB1 Antibodies) activation

Atlantic Salmon (Salmo salar) Myeloid Differentiation Primary Response Gene (88) (MYD88) interaction partners

1. MyD88 interacts with interferon (show IFNA Antibodies) regulatory factor (IRF) 3 (show IRF3 Antibodies) and IRF7 (show IRF7 Antibodies) in Atlantic salmon (Salmo salar)

2. the salmon MyD88 was cloned and its expression was analysed.