Results 221 to 230 of about 2,358,049 (278)

Molecular mechanism of naturally-encoded signaling-bias at the complement anaphylatoxin receptors

open access: yes
Tiwari D   +28 more
europepmc   +1 more source

Inhibiting the C5–C5a receptor axis

Molecular Immunology, 2011
Activation of the complement system is a major pathogenic event that drives various inflammatory responses in numerous diseases. All pathways of complement activation lead to cleavage of the C5 molecule generating the anaphylatoxin C5a and, C5b that subsequently forms the terminal complement complex (C5b-9).
Woodruff, Trent M.   +2 more
openaire   +4 more sources

The Alternative C5a Receptor Function

Advances in Experimental Medicine and Biology, 2012
When acute inflammatory states are induced by treatment with chemical mediators in C5-deficient mice, neutrophil influxes are commonly decreased. Therefore, the neutrophil C5a receptor (C5aR) is believed to be a member of the pro-inflammatory receptors.
H. Nishiura
openaire   +3 more sources

Development of Potent and Selective Agonists for Complement C5a Receptor 1 with In Vivo Activity.

Journal of Medicinal Chemistry, 2021
The anaphylatoxin C5a is a complement peptide associated with immune-related disorders. C5a binds with equal potency to two GPCRs, C5aR1 and C5aR2. Multiple C5a peptide agonists have been developed to interrogate the C5a receptor function but none show ...
Declan M. Gorman   +8 more
semanticscholar   +1 more source

Human C5a and C5a analogs as probes of the neutrophil C5a receptor

Molecular Immunology, 1980
Abstract Quantitative assessment of the human neutrophil chemotactic response and immunologic evidence demonstrate that human C5a and/or its physiological equivalent, C5a des Arg' serves as the predominant chemotactic factor in complement activated serum.
D E, Chenoweth, T E, Hugli
openaire   +2 more sources

Distribution of Rat C5a Anaphylatoxin Receptor

Microbiology and Immunology, 2002
AbstractThe anaphylatoxin, complement 5a (C5a), plays a key role in mediating various inflammatory reactions following complement activation. Several investigators have reported that C5a receptor (C5aR) is expressed in non‐myeloid cells under certain conditions or in different cell lines.
Hiroyasu, Akatsu   +7 more
openaire   +2 more sources

Mapping the Ligand-Binding Site on the C5a Receptor:  Arginine74 of C5a Contacts Aspartate282 of the C5a Receptor

Biochemistry, 2001
The interaction between the anaphylatoxin C5a and its receptor involves two distinct sites. One site is formed by acidic residues at the receptor N-terminus and contributes to only ligand binding. The second site, responsible for activation, is less well defined.
Cain, S. A., Coughlan, T., Monk, P. N.
openaire   +2 more sources

Human T Cells Express the C5a Receptor and Are Chemoattracted to C5a

The Journal of Immunology, 1999
AbstractThe anaphylatoxin C5a is a potent mediator of inflammation that exerts a broad range of activity on cells of the myeloid lineage. In this study, we present the first evidence that human T cells express the C5a receptor (C5aR) and are chemotactic to C5a.
S, Nataf   +3 more
openaire   +2 more sources

ChemInform Abstract: C5a Receptor Antagonists

ChemInform, 2000
AbstractChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
Theodore C. Pellas, Lawrence P. Wennogle
openaire   +1 more source

The chemotactic receptor for human C5a anaphylatoxin

Nature, 1991
Host defence and inflammatory responses are controlled and amplified by receptor-mediated events often initiated by a chemotactic factor that directs the approach of phagocytic cells. Complement receptors CR1 and CR3 are responsible for the phagocytic and adhesive properties of neutrophils, whereas the C5a receptor mediates the pro-inflammatory and ...
N P, Gerard, C, Gerard
openaire   +2 more sources

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