Results 21 to 30 of about 1,135,361 (222)

Profiling gene expression induced by protease-activated receptor 2 (PAR2) activation in human kidney cells.

open access: yesPLoS ONE, 2010
Protease-Activated Receptor-2 (PAR2) has been implicated through genetic knockout mice with cytokine regulation and arthritis development. Many studies have associated PAR2 with inflammatory conditions (arthritis, airways inflammation, IBD) and key ...
Jacky Y Suen   +3 more
doaj   +1 more source

Complement-Activating Immune Deposits in Systemic Lupus Erythematosus Skin [PDF]

open access: yes, 1983
Immune deposits at the cutaneous basement membrane zone are a characteristic feature of systemic lupus erythematosus. Previous studies using immunofluorescent methods to detect complement components have provided evidence that some deposits contain ...
Merritt, Carolyn C.   +5 more
core   +1 more source

COMPLEMENT-MEDIATED ADIPOCYTE LYSIS BY NEPHRITIC FACTOR SERA [PDF]

open access: yes, 1993
Recent data indicate a previously unsuspected link between the complement system and adipocyte biology. Murine adipocytes produce key components of the alternative pathway of complement and are able to activate this pathway.
Lachmann, PJ   +10 more
core   +1 more source

Engineering novel complement activity into a pulmonary surfactant protein [PDF]

open access: yes, 2010
Complement neutralizes invading pathogens, stimulates inflammatory and adaptive immune responses, and targets non- or altered-self structures for clearance.
Toth, Julia   +20 more
core   +1 more source

Hyperosmotic stress induces PARP1‐mediated HPF1‐dependent mono(ADP‐ribosyl)ation

open access: yesFEBS Letters, EarlyView.
Sorbitol‐induced hyperosmotic stress rapidly induces reversible mono(ADP‐ribosyl)ation (MARylation) on PARP1 without the signs of genotoxic signaling. We show that PARP1 autoMARylation is HPF1 dependent and forms hydroxylamine‐resistant O‐glycosidic linkages.
Anna Georgina Kopasz   +11 more
wiley   +1 more source

An isoform of 14‐3‐3 protein regulates transbilayer lipid movement at the plasma membrane

open access: yesFEBS Letters, EarlyView.
Loss of 14‐3‐3ζ in CHO cells confers resistance to exogenous phosphatidylserine (PS) and impairs endocytosis‐independent inward flip‐flop of fluorescent PS at the plasma membrane. RNAi‐mediated knockdown reproduces this defect, while no additive effect is seen in ATP11C‐deficient cells.
Akiko Yamaji‐Hasegawa   +3 more
wiley   +1 more source

Salmonella lipopolysaccharide‐containing supported lipid bilayers as platforms to study bacteriophage interactions

open access: yesFEBS Letters, EarlyView.
We present robust protocols for the preparation of supported lipid bilayers (SLBs) incorporating either Salmonella smooth LPS or outer membrane vesicles (OMVs). We use a combination of quartz crystal microbalance with dissipation (QCM‐D) and fluorescence microscopy to both characterize the SLBs of various compositions and to probe their interactions ...
Hudson P. Pace   +6 more
wiley   +1 more source

The Role of Complement in Tumors

open access: yes, 2020
The complement system is an essential part of the innate immune system that is responsible for regulating inflammation, facilitating immune defense mechanisms, and maintaining tissue homeostasis.

core   +1 more source

Microbiome−host proteostasis crosstalk—An emerging perspective on mechanisms and interventions toward healthy longevity

open access: yesFEBS Letters, EarlyView.
Proteostasis and the gut microbiota play a key role in shaping host physiology. Microbiota‐derived metabolites, vitamins, and RNA modulate host proteostasis. Findings from model systems, including C. elegans, indicate microbes can either stabilize or disrupt host proteostasis.
Abhishek Anil Dubey, Maria Ermolaeva
wiley   +1 more source

Complement Factor H: solution structures and interactions with ligands [PDF]

open access: yes, 2009
Factor H (FH) is a plasma glycoprotein that plays a central role in regulating the alternative pathway of complement. It is composed of 20 short complement regulator (SCR) domains.
Okemefuna, A.I.
core  

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