Results 1 to 10 of about 89,193 (109)

Myeloid differentiation factor 88 signaling in donor T cells accelerates graft-versus-host disease [PDF]

open access: yesHaematologica, 2020
Myeloid differentiation factor 88 (MyD88) signaling has a crucial role in activation of both innate and adoptive immunity. MyD88 transduces signals via Toll-like receptor and interleukin-1 receptor superfamily to the NFκB pathway and inflammasome by ...
Satomi Matsuoka   +14 more
doaj   +2 more sources

Inflammation Induced by Lipopolysaccharide and Palmitic Acid Increases Cholesterol Accumulation via Enhancing Myeloid Differentiation Factor 88 Expression in HepG2 Cells [PDF]

open access: yesPharmaceuticals, 2022
Recently, multiple studies have shown that chronic inflammation disturbs cholesterol homeostasis and promotes its accumulation in the liver. The underlying molecular mechanism remains to be revealed.
Junbin Chen   +10 more
doaj   +2 more sources

Identification and function of myeloid differentiation factor 88 (MyD88) in Litopenaeus vannamei. [PDF]

open access: yesPLoS ONE, 2012
Myeloid differentiation factor 88 (MyD88) is a universal and essential signaling protein in Toll-like receptor/interleukin-1 receptor-induced activation of nuclear factor-kappa B.
Shuang Zhang   +7 more
doaj   +2 more sources

Interleukin-1α Mediates Ozone-Induced Myeloid Differentiation Factor-88-Dependent Epithelial Tissue Injury and Inflammation [PDF]

open access: yesFrontiers in Immunology, 2018
Air pollution associated with ozone exposure represents a major inducer of respiratory disease in man. In mice, a single ozone exposure causes lung injury with disruption of the respiratory barrier and inflammation.
Chloé Michaudel   +9 more
doaj   +2 more sources

TcpC inhibits toll-like receptor signaling pathway by serving as an E3 ubiquitin ligase that promotes degradation of myeloid differentiation factor 88. [PDF]

open access: yesPLoS Pathogens, 2021
TcpC is a virulence factor of uropathogenic E. coli (UPEC). It was found that TIR domain of TcpC impedes TLR signaling by direct association with MyD88.
Jia-Qi Fang   +13 more
doaj   +2 more sources

Myeloid differentiation factor 88 (MyD88)-deficiency increases risk of diabetes in mice. [PDF]

open access: yesPLoS ONE, 2010
BACKGROUND: Multiple lines of evidence suggest innate immune response pathways to be involved in the development of obesity-associated diabetes although the molecular mechanism underling the disease is unknown.
Toru Hosoi   +4 more
doaj   +2 more sources

Grape seed-derived procyanidins decreases neuropathic pain and nerve regeneration by suppression of toll-like receptor 4-myeloid differentiation factor-88 signaling [PDF]

open access: yesMolecular Pain
Background: Recent studies have shown that peripheral nerve regeneration process is closely related to neuropathic pain. Toll-like receptor 4 (TLR4) signaling was involved in different types of pain and nerve regeneration. TLR4 induced the recruitment of
Li Hu   +6 more
doaj   +2 more sources

Inhibition of Myeloid Differentiation Factor 88 Reduces Human and Mouse T-Cell Interleukin-17 and IFNγ Production and Ameliorates Experimental Autoimmune Encephalomyelitis Induced in Mice [PDF]

open access: yesFrontiers in Immunology, 2017
Myeloid differentiation factor 88 (MyD88) recruits signaling proteins to the intracellular domain of receptors belonging to the toll-like/interleukin-1 (IL-1) receptor superfamily.
Shira Dishon   +4 more
doaj   +2 more sources

Expression of myeloid differentiation factor 88 in neurons is not requisite for the induction of sickness behavior by interleukin-1β [PDF]

open access: yesJournal of Neuroinflammation, 2012
Background Animals respond to inflammation by suppressing normal high-energy activities, including feeding and locomotion, in favor of diverting resources to the immune response.
Braun Theodore P   +6 more
doaj   +2 more sources

Effects of the co-administration of morphine and lipopolysaccharide on toll-like receptor-4/nuclear factor kappa β signaling pathway of MDA-MB-231 breast cancer cells

open access: yesAdvanced Biomedical Research, 2023
Background: The Toll-like receptor 4 (TLR4) gene promotes migration in adenocarcinoma cells. Morphine is an agonist for TLR4 that has a dual role in cancer development.
Marzieh Kafami   +6 more
doaj   +1 more source

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