Results 11 to 20 of about 58,596 (215)

HSP110 and MYD88: blame the chaperone [PDF]

open access: yesBlood, 2018
In this issue of Blood, Boudesco et al show that heat shock protein HSP110 (HSPH1) stabilizes wild-type and mutant MYD88, facilitating NF-κB activation in diffuse large B-cell lymphoma (DLBCL ...
openaire   +2 more sources

Lipopolysaccharide uptake is augmented in lipopolysaccharide‐tolerant mouse macrophage‐like cells via increased CD14 expression

open access: yesFEBS Open Bio, EarlyView.
In normal (nontolerant) cells, CD14 is crucial for both LPS uptake and LPS signaling. In LPS‐tolerant cells, in which LPS‐induced TNF‐α and IFN‐β production is suppressed, there is a dramatic increase in surface CD14 expression. The overexpressed CD14 in LPS‐tolerant cells is responsible for the enhanced LPS uptake without inducing pro‐inflammatory ...
Saeka Nishihara   +3 more
wiley   +1 more source

MyD88-Dependent and MyD88-Independent Pathways in Synergy, Priming, and Tolerance between TLR Agonists [PDF]

open access: yesThe Journal of Immunology, 2007
Abstract TLRs sense components of microorganisms and are critical host mediators of inflammation during infection. Different TLR agonists can profoundly alter inflammatory effects of one another, and studies suggest that the sequence of exposure to TLR agonists may importantly impact on responses during infection.
Aranya, Bagchi   +6 more
openaire   +2 more sources

Aging Is a Key Driver for Adult Acute Myeloid Leukemia

open access: yesAging and Cancer, EarlyView.
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley   +1 more source

MyD88 and its divergent toll in carcinogenesis [PDF]

open access: yesTrends in Immunology, 2013
Toll-like and interleukin-1 (IL-1) family receptors recognize microbial or endogenous ligands and inflammatory mediators, respectively, and with the exception of Toll-like receptor 3 (TLR3), signal via the adaptor molecule myeloid differentiation factor 88 (MyD88).
Rosalba, Salcedo   +4 more
openaire   +2 more sources

rWTC‐MBTA Vaccine, Alone and Enhanced with Anti‐PD1, Elicits Immune Responses against CNS and Peripheral B‐Cell Lymphoma

open access: yesAdvanced Science, EarlyView.
An autologous whole‐tumor‐cell vaccine (rWTC‐MBTA) is evaluated in murine CNS lymphoma. Subcutaneous vaccination activates dendritic cells, broadens T‐cell priming, and drives lymphocyte trafficking to brain tumors, producing durable tumor control. Longitudinal bioluminescence and adoptive‐transfer assays verify CNS engagement. Combination with anti‐PD‐
Yaping Zhang   +10 more
wiley   +1 more source

Two Human MYD88 Variants, S34Y and R98C, Interfere with MyD88-IRAK4-Myddosome Assembly [PDF]

open access: yesJournal of Biological Chemistry, 2011
Innate immune receptors detect microbial pathogens and subsequently activate adaptive immune responses to combat pathogen invasion. MyD88 is a key adaptor molecule in both Toll-like receptor (TLR) and IL-1 receptor superfamily signaling pathways. This is illustrated by the fact that human individuals carrying rare, naturally occurring MYD88 point ...
George, J   +8 more
openaire   +3 more sources

Improved Systemic Immunochemotherapy Employing an Oxaliplatin‐TLR7/8 Agonist Prodrug Strategy

open access: yesAdvanced Science, EarlyView.
A platinum(IV) prodrug is developed to systemically deliver the TLR7/8 agonist gardiquimod. Tumor‐targeting is mediated by an albumin‐binding maleimide, which limits premature complex activation. Ox‐Gardi‐Mal accumulates specifically in the tumor, where it activates the immune system.
Michael Gutmann   +15 more
wiley   +1 more source

A MyD88 meddles with survival [PDF]

open access: yesThe Journal of Experimental Medicine, 2007
In the MyD88 family of cytosolic adaptor proteins, the newest member is the group's black sheep, according to Kim et al. (page 2063). Whereas most MyD88 proteins turn on antipathogen responses within myeloid cells, the rebel, MyD88-5, instigates cell death within neurons.
openaire   +1 more source

Unresponsiveness of MyD88-Deficient Mice to Endotoxin [PDF]

open access: yesImmunity, 1999
MyD88 is a general adaptor protein that plays an important role in the Toll/IL-1 receptor family signalings. Recently, Toll-like receptors 2 and 4 (TLR2 and TLR4) have been suggested to be the signaling receptors for lipopolysaccharide (LPS). In this study, we demonstrate that MyD88 knockout mice lack the ability to respond to LPS as measured by shock ...
Kawai, Taro   +4 more
openaire   +2 more sources

Home - About - Disclaimer - Privacy