Results 11 to 20 of about 537,344 (241)

Antagonizing Neuronal Toll-like Receptor 2 Prevents Synucleinopathy by Activating Autophagy

open access: yesCell Reports, 2015
Impaired autophagy has been implicated in many neurodegenerative diseases, such as Parkinson’s disease (PD), and might be responsible for deposition of aggregated proteins in neurons. However, little is known about how neuronal autophagy and clearance of
Changyoun Kim   +9 more
doaj   +2 more sources

N-terminal and C-terminal domains of calmodulin mediate FADD and TRADD interaction [PDF]

open access: yes, 2015
FADD (Fas–associated death domain) and TRADD (Tumor Necrosis Factor Receptor 1-associated death domain) proteins are important regulators of cell fate in mammalian cells. They are both involved in death receptors mediated signaling pathways and have been
Balog, Edward M.   +7 more
core   +18 more sources

How Toll-like receptors influence Parkinson’s disease in the microbiome–gut–brain axis

open access: yesFrontiers in Immunology, 2023
Recently, a large number of experimenters have found that the pathogenesis of Parkinson’s disease may be related to the gut microbiome and proposed the microbiome–gut–brain axis.
Ziyi Zhang   +4 more
doaj   +1 more source

Response of Human Toll–Like Receptor 2 During the Infection of Leptospirosis

open access: yesInternational Journal of Infectious Diseases, 2022
Purpose: Since Toll-like receptor2 (TLR2) plays a key role in mediating the innate immune responses in mice models against leptospirosis, we aimed to determine the response of human TLR2 during the infection of pathogenic Leptospira spp.
C. Kappagoda   +5 more
doaj   +1 more source

Immunological study of orthodontically treated patients recovering from COVID-19 in Babylon Province, Iraq

open access: yesMedical Journal of Babylon, 2023
Background and Objectives: This study aimed to examine the levels of the toll-like receptors TLR4 and TLR2 in the blood and saliva of patients with coronavirus disease-2019 (COVID-19) receiving orthodontic care in Babylon Province. Materials and Methods:
Basma Abdel Khaleq Eidan   +2 more
doaj   +1 more source

Toll-like Receptor 2 in Autoimmune Inflammation

open access: yesImmune Network, 2021
TLR signaling is critical for broad scale immune recognition of pathogens and/or danger molecules. TLRs are particularly important for the activation and the maturation of cells comprising the innate immune response. In recent years it has become apparent that several different TLRs regulate the function of lymphocytes as well, albeit to a lesser ...
Kathryne E. Marks   +3 more
openaire   +2 more sources

Toll-like receptor 2 signalling and inflammation [PDF]

open access: yesAnnals of the Rheumatic Diseases, 2005
Toll-like receptors (TLRs) are a family of proteins that are involved in the initial phase of host defence against invading pathogens. TLRs act as primary sensors of microbial products and activate signalling pathways that lead to the induction of immune and inflammatory genes.1 TLRs belong to a broader family of proteins, which include receptors for ...
F Y, Liew, M, Patel, D, Xu
openaire   +2 more sources

Involvement of Toll-Like Receptor 4 in Decreased Vasopressor Response Following Trauma/Hemorrhagic Shock

open access: yesCritical Care Explorations, 2021
OBJECTIVES:. Refractory vascular failure due to the inability of vascular smooth muscle to respond to vasoconstrictors such as phenylephrine is a final common pathway for severe circulatory shock of any cause, including trauma/hemorrhagic shock ...
Rafi Mazor, PhD   +5 more
doaj   +1 more source

Herpesviral infection and Toll-like receptor 2 [PDF]

open access: yesProtein & Cell, 2012
In the last decade, substantial progress has been made in understanding the molecular mechanisms involved in the initial host responses to viral infections. Herpesviral infections can provoke an inflammatory cytokine response, however, the innate pathogen-sensing mechanisms that transduce the signal for this response are poorly understood.
Ming-sheng, Cai   +2 more
openaire   +2 more sources

Home - About - Disclaimer - Privacy