Results 51 to 60 of about 93,626 (282)

Contribution of the infection-associated complement regulator-acquiring surface protein 4 (ErpC) to complement resistance of Borrelia burgdorferi [PDF]

open access: yes, 2012
Borrelia burgdorferi evades complement-mediated killing by interacting with complement regulators through distinct complement regulator-acquiring surface proteins (CRASPs).
Hallström, Teresia   +6 more
core   +4 more sources

The inflammatory process of gout and its treatment. [PDF]

open access: yes, 2006
Gouty arthritis is a characteristically intense acute inflammatory reaction that erupts in response to articular deposits of monosodium urate (MSU) crystals.
Cronstein, Bruce N, Terkeltaub, Robert
core   +2 more sources

Pathogenic Leptospira Secreted Proteases Target the Membrane Attack Complex: A Potential Role for Thermolysin in Complement Inhibition

open access: yesFrontiers in Microbiology, 2017
Leptospirosis is a zoonosis caused by spirochetes from the genus Leptospira. This disease is common in tropical and subtropical areas, constituting a serious public health problem.
T. Amamura   +4 more
semanticscholar   +1 more source

Immunophysical Evaluation of the Initiating Step in the Formation of the Membrane Attack Complex

open access: yesFrontiers in Physics, 2018
The complex between complement system proteins C5b and C6 is the cornerstone for the assembly of the membrane attack complex (MAC, also known as C5b6789n). MAC is the terminal product of three converging pathways of the complement system and functions as
Nehemiah Zewde   +2 more
doaj   +1 more source

Innate immune system activation in zebrafish and cellular models of Diamond Blackfan Anemia. [PDF]

open access: yes, 2018
Deficiency of ribosomal proteins (RPs) leads to Diamond Blackfan Anemia (DBA) associated with anemia, congenital defects, and cancer. While p53 activation is responsible for many features of DBA, the role of immune system is less defined.
Bibikova, Elena   +5 more
core   +2 more sources

The first transmembrane region of complement component-9 acts as a brake on its self-assembly

open access: yesNature Communications, 2018
The Complement component 9 (C9) is the pore-forming component of the Membrane Attack Complex which targets pathogens. Here authors use structural biology to compare monomeric C9 to C9 within the polymeric assembly and identify the element which inhibits ...
Bradley A. Spicer   +11 more
doaj   +1 more source

The role of proteases in pathologies of the synovial joint [PDF]

open access: yes, 2008
Synovial (diarthrodial) joints are employed within the body to provide skeletal mobility and have a characteristic structure adapted to provide a smooth almost frictionless surface for articulation.
Buttle, D, Jones, GC, Riley, GP
core   +1 more source

Structural biology of ferritin nanocages

open access: yesFEBS Letters, EarlyView.
Ferritin is a conserved iron‐storage protein that sequesters iron as a ferric mineral core within a nanocage, protecting cells from oxidative damage and maintaining iron homeostasis. This review discusses ferritin biology, structure, and function, and highlights recent cryo‐EM studies revealing mechanisms of ferritinophagy, cellular iron uptake, and ...
Eloise Mastrangelo, Flavio Di Pisa
wiley   +1 more source

Dynamics and Molecular Interactions of GPI-Anchored CD59

open access: yesToxins, 2023
CD59 is a GPI-anchored cell surface receptor that serves as a gatekeeper to controlling pore formation. It is the only membrane-bound inhibitor of the complement membrane attack complex (MAC), an immune pore that can damage human cells. While CD59 blocks
Tomas B. Voisin   +3 more
doaj   +1 more source

Organ‐specific redox imbalances in spinal muscular atrophy mice are partially rescued by SMN antisense oligonucleotides

open access: yesFEBS Letters, EarlyView.
We identified a systemic, progressive loss of protein S‐glutathionylation—detected by nonreducing western blotting—alongside dysregulation of glutathione‐cycle enzymes in both neuronal and peripheral tissues of Taiwanese SMA mice. These alterations were partially rescued by SMN antisense oligonucleotide therapy, revealing persistent redox imbalance as ...
Sofia Vrettou, Brunhilde Wirth
wiley   +1 more source

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