gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Myeloid differentiation primary response gene 88

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. [provided by RefSeq, Feb 2010] (from NCBI)
Top mentioned proteins: TLR4, V1a, TLR2, Interleukin-6, CAN
Papers using MyD88 antibodies
Constitutive activation of epithelial TLR4 augments inflammatory responses to mucosal injury and drives colitis-associated tumorigenesis.
Chandra Dhyan, In PLoS ONE, 2010
... BSA; Calbiochem, La Jolla, CA), cell-permeable peptide set comprising peptides that inhibit human TIRAP and MyD88 functions (IMGENEX, San Diego, CA), active ...
The metagenomics RAST server - a public resource for the automatic phylogenetic and functional analysis of metagenomes.
Vidal-Puig Antonio J., In PLoS Biology, 2007
... Receptor (rabbit polyclonal, sc-25103), Insulin Receptor β (goat polyclonal, sc-31369), UCP1 (goat polyclonal sc-6529), and MyD88 (goat polyclonal, sc-8197) were from Santa Cruz Biotechnology, Inc ...
MyD88- and Bruton's tyrosine kinase-mediated signals are essential for T cell-independent pathogen-specific IgM responses.
Zimmer Jacques, In PLoS ONE, 2006
... Primary anti-MyD88 antibody was obtained from AnaSpec, Inc ...
Staphylococcal enterotoxin B potentiates LPS-induced hepatic dysfunction in chronically catherized rats.
Giambartolomei Guillermo H., In PLoS ONE, 2000
... Primary anti-MyD88 antibody was obtained from AnaSpec, Inc., (San Jose, CA) ...
Inhibition of Interleukin 1 Receptor/Toll-like Receptor Signaling through the Alternatively Spliced, Short Form of MyD88 Is Due to Its Failure to Recruit IRAK-4
Tschopp Jürg et al., In The Journal of Experimental Medicine, 1999
... (Eastman Kodak Co.), anti–vesicular stomatitis virus (VSV; Sigma-Aldrich), anti–IRAK-1 (Qbiogene or Santa Cruz Biotechnology, Inc.), anti-MyD88 (ProSci Inc.), and anti-E (Amersham ...
more suppliers
Papers on MyD88
Primary role for TLR-driven TNF rather than cytosolic immune detection in restricting Coxiella burnetii phase II replication within mouse macrophages.
Shin et al., Ribeirão Preto, Brazil. In Infect Immun, Feb 2016
Furthermore, the TLR signaling adaptors MyD88 and Trif are required for cytokine responses and restricting bacterial replication.
Roles of TLR2, TLR4, and MyD88 during pulmonary Coxiella burnetii infection.
Jutila et al., Bozeman, United States. In Infect Immun, Feb 2016
Here, we assessed the roles for TLR2, TLR4, and MyD88 in pulmonary C. burnetii infection and compared responses to those that occurred in TLR2 and TLR4 deficient animals following peripheral infection.
Subtype-specific addiction of the activated B-cell subset of diffuse large B-cell lymphoma to FOXP1.
Tucker et al., Austin, United States. In Proc Natl Acad Sci U S A, Feb 2016
Genome-wide analyses revealed direct and indirect FOXP1 transcriptional enforcement of ABC-DLBCL hallmarks, including the classical NF-κB and MYD88 (myeloid differentiation primary response gene 88) pathways.
Innate control of actin nucleation determines two distinct migration behaviours in dendritic cells.
Lennon-Duménil et al., France. In Nat Cell Biol, Jan 2016
Following TLR4-MyD88-induced maturation, Arp2/3-dependent actin enrichment at the cell front is markedly reduced.
Saturated fatty acids trigger TLR4-mediated inflammatory response.
Hermsdorff et al., Viçosa, Brazil. In Atherosclerosis, Jan 2016
Those molecules can induce TLR4 inflammatory response by MyD88-dependent and/or MyD88-independent pathways that, in turn, promotes the expression of proinflammatory transcript factors such as factor nuclear kappa B (NF-κB), which plays a crucial role in the induction of inflammatory mediators (cytokines, chemokines, or costimulatory molecules) implicated in the development and progression of many chronic diseases.
Sequential Activation of Two Pathogen-Sensing Pathways Required for Type I Interferon Expression and Resistance to an Acute DNA Virus Infection.
Sigal et al., Philadelphia, United States. In Immunity, Jan 2016
Toll-like receptor 9 (TLR9), its adaptor MyD88, the downstream transcription factor interferon regulatory factor 7 (IRF7), and type I interferons (IFN-I) are all required for resistance to infection with ectromelia virus (ECTV).
The immunobiology of Campylobacter jejuni: Innate immunity and autoimmune diseases.
Phongsisay, Fukuoka, Japan. In Immunobiology, Jan 2016
Furthermore, C. jejuni targets MyD88, NLRP3 inflammasome, TIR-domain-containing adapter-inducing interferon-β (TRIF), sialic acid-binding immunoglobulin-like lectins (Siglecs), macrophage galactose-type lectin (MGL), and immunoglobulin-like receptors (TREM2, LMIR5/CD300b).
Toll-like receptors: potential targets for lupus treatment.
Zuo et al., Shanghai, China. In Acta Pharmacol Sin, Dec 2015
A number of downstream proteins in the TLR signaling cascade (such as MyD88, IRAKs and IFN-α) are identified as potential therapeutic targets for SLE treatment.
Blood-Brain Barrier Deterioration and Hippocampal Gene Expression in Polymicrobial Sepsis: An Evaluation of Endothelial MyD88 and the Vagus Nerve.
Diamond et al., New York City, United States. In Plos One, Dec 2015
In particular, MyD88-dependent activation of brain microvascular endothelial cells and a resulting loss of blood-brain barrier integrity have been proposed to play an important role in the effects of systemic inflammation on the CNS.
Expression of the Receptor for Advanced Glycation End Products in Epicardial Fat: Link with Tissue Thickness and Local Insulin Resistance in Coronary Artery Disease.
Corsi Romanelli et al., Milano, Italy. In J Diabetes Res, Dec 2015
EAT expression of RAGE, GLUT4, adiponenctin, GLO1, HMGB1, TLR-4, and MyD88 was analyzed by microarray.
Molecular Pathogenesis of Ehrlichia chaffeensis Infection.
Rikihisa, Columbus, United States. In Annu Rev Microbiol, Nov 2015
The central role of MyD88, but not Toll-like receptors, suggests that Ehrlichia species have unique inflammatory molecules.
The many faces of small B cell lymphomas with plasmacytic differentiation and the contribution of MYD88 testing.
Campo et al., Pittsburgh, United States. In Virchows Arch, Nov 2015
The discovery of MYD88 L265P mutations in the vast majority of LPLs has had a major impact on the study of these lymphomas.
CD47 blockade triggers T cell-mediated destruction of immunogenic tumors.
Xu et al., Beijing, China. In Nat Med, Oct 2015
In addition, the antitumor effects of CD47 blockade required expression of the cytosolic DNA sensor STING, but neither MyD88 nor TRIF, in CD11c+ cells, suggesting that cytosolic sensing of DNA from tumor cells is enhanced by anti-CD47 treatment, further bridging the innate and adaptive responses.
MyD88 Adaptor-Dependent Microbial Sensing by Regulatory T Cells Promotes Mucosal Tolerance and Enforces Commensalism.
Chatila et al., Boston, United States. In Immunity, Sep 2015
We report that Treg-cell-specific deletion of the TLR adaptor MyD88 resulted in deficiency of intestinal Treg cells, a reciprocal increase in T helper 17 (Th17) cells and heightened interleukin-17 (IL-17)-dependent inflammation in experimental colitis.
Targeting B cell receptor signaling with ibrutinib in diffuse large B cell lymphoma.
Staudt et al., Bethesda, United States. In Nat Med, Aug 2015
ABC tumors with BCR mutations responded to ibrutinib frequently (5/9; 55.5%), especially those with concomitant myeloid differentiation primary response 88 (MYD88) mutations (4/5; 80%), a result that is consistent with in vitro cooperation between the BCR and MYD88 pathways.
Antiinflammation effect of human placental multipotent mesenchymal stromal cells is mediated by prostaglandin E2 via a myeloid differentiation primary response gene 88-dependent pathway.
Huang et al., Taipei, Taiwan. In Anesthesiology, 2012
antiinflammation effect of human placental multipotent mesenchymal stromal cells is mediated, at least in part, by prostaglandin E2 via a myeloid differentiation primary response gene 88-dependent pathway
MYD88 L265P somatic mutation in Waldenström's macroglobulinemia.
Hunter et al., Boston, United States. In N Engl J Med, 2012
MYD88 L265P is a commonly recurring mutation in patients with Waldenstrom's macroglobulinemia that can be useful in differentiating Waldenstrom's macroglobulinemia and non-IgM LPL from B-cell disorders that have some of the same features.
MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells.
Miller et al., New York City, United States. In J Exp Med, 2012
MyD88 inhibition amplifies dendritic cell capacity to promote pancreatic carcinogenesis via Th2 cells
IL-1R-MyD88 signaling in keratinocyte transformation and carcinogenesis.
Trinchieri et al., Bethesda, United States. In J Exp Med, 2012
MyD88 exerts a cell-intrinsic function in RAS-mediated transformation of keratinocytes.
Extracellularly delivered single-stranded viral RNA causes neurodegeneration dependent on TLR7.
Lehnardt et al., Berlin, Germany. In J Immunol, 2012
Activation of Toll-like receptor (TLR)7, a receptor sensing single-stranded viral RNA, causes neuronal cell death through the adapter molecule MyD88 and caspase-3 in a cell-autonomous fashion.
More papers using MyD88 antibodies
MyD88-5 links mitochondria, microtubules, and JNK3 in neurons and regulates neuronal survival
Ding Aihao et al., In The Journal of Experimental Medicine, 1981
... We thank Krista LaPerle for pathological evaluation of the MyD88-5 knockout mice; Lee Gould for taking confocal images of the transgenic mouse brain; Nat Heinz ...
share on facebooktweetadd +1mail to friends