Results 41 to 50 of about 3,979 (154)

The complement receptor C3AR constitutes a novel therapeutic target in NPM1-mutated AML [Elektronisk resurs]

open access: yes, 2023
Mutated Nucleophosmin 1 (NPM1) is the most common genetic alteration in acute myeloid leukemia (AML), found in approximately 30% of cases. Although mutations in this gene are considered favorable according to current risk stratification guidelines, a ...
Thorsson, Hanna,   +18 more
core   +2 more sources

Roles for NHERF1 and NHERF2 on the regulation of C3a receptor signaling in human mast cells. [PDF]

open access: yesPLoS ONE, 2012
The anaphylatoxin C3a binds to the G protein coupled receptor (GPCR, C3aR) and activates divergent signaling pathways to induce degranulation and cytokine production in human mast cells. Adapter proteins such as the Na(+)/H(+) exchange regulatory factor (
Hariharan Subramanian   +2 more
doaj   +1 more source

Protective Role of C3aR (C3a Anaphylatoxin Receptor) Against Atherosclerosis in Atherosclerosis-Prone Mice

open access: yes, 2020
OBJECTIVE: Emerging evidence suggests that C3aR (C3a anaphylatoxin receptor) signaling has protective roles in various inflammatory-related diseases. However, its role in atherosclerosis has been unknown.
Li, Zong Fang   +11 more
core   +1 more source

Complement C3a treatment accelerates recovery after stroke via modulation of astrocyte reactivity and cortical connectivity

open access: yesThe Journal of Clinical Investigation, 2023
Despite advances in acute care, ischemic stroke remains a major cause of long-term disability. Approaches targeting both neuronal and glial responses are needed to enhance recovery and improve long-term outcome.
Anna Stokowska   +18 more
doaj   +1 more source

Monitoring C3aR Expression Using a Floxed tdTomato-C3aR Reporter Knock-in Mouse

open access: yes, 2017
C3a exerts multiple biologic functions through activation of its cognate C3a receptor. C3−/− and C3aR−/− mice have been instrumental in defining important roles of the C3a/C3aR axis in the regulation of acute and chronic inflammatory diseases, including ...
Christian M. Karsten   +15 more
core   +1 more source

C3aR signaling is essential for adipocyte differentiation.

open access: yes, 2016
(A) Knockdown of C3aR inhibits adipocyte differentiation. C3H10T1/2 cells were infected with virus harboring two independent shRNAs against C3aR or scrambled shRNA (scr) and stable cells were selected with puromycin (2 μg/ml) for 2 weeks.
Ui Jeong Yun (3111426)   +9 more
core   +1 more source

Loss of C3a and C5a receptors promotes adipocyte browning and attenuates diet-induced obesity via activating inosine/A2aR pathway

open access: yesCell Reports, 2023
Summary: Complement activation is thought to underline the pathologic progression of obesity-related metabolic disorders; however, its role in adaptive thermogenesis has scarcely been explored.
Ling-Ran Kong   +9 more
doaj   +1 more source

Characterization of phosphorylation sites in C3aR.

open access: yes, 2013
(A) Schematic representation of the carboxyl-terminal domain of C3aR (WT) and mutants MT1–MT7 used for phosphorylation studies. (B) HEK293 cells transiently expressing HA-tagged C3aR or mutants were labeled with 32P and exposed to buffer or C3a (100 nM ...
Andreas Klos (71279)   +3 more
core   +1 more source

C5aR and C3aR antagonists each inhibit diet-induced obesity, metabolic dysfunction, and adipocyte and macrophage signaling

open access: yes, 2013
Mammalian survival depends on metabolizing nutrients, storing energy, and combating infection. Complement activation in blood triggers energy-depleting immune responses to fight infections.
Fairlie, David P.   +7 more
core   +1 more source

C3a/C3aR Affects the Propagation of Cryptosporidium parvum in the Ileum Tissues of Mice by Regulating the Gut Barrier, Cell Proliferation, and CD4+ T Cell Main Effectors

open access: yesAnimals, 2023
Cryptosporidium parvum is an important zoonotic protozoon that threatens the health of humans and animals, but the interaction mechanisms between C. parvum and hosts are poorly understood.
Xin Yang   +7 more
doaj   +1 more source

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