Results 41 to 50 of about 119,425 (295)

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

The ubiquitin‐proteasome system and autophagy as guardians of the cellular proteome

open access: yesFEBS Letters, EarlyView.
This Perspective covers the three principles governing the crosstalk between the ubiquitin‐proteasome system and autophagy in cellular proteostasis: (1) a shared ubiquitin code routing substrates via shuttle factors or autophagy receptors; (2) spatial compartmentalization into phase‐separated degradation hubs and organelle‐specific modules (exemplified
Ivan Dikic
wiley   +1 more source

Formation and properties of C1‐inhibitor polymers [PDF]

open access: yesFEBS Letters, 1995
Heating of the serpin C1‐inhibitor above 55°C induced the formation of inactive polymers. Western blotting of non‐denaturing gels showed that the polymers bound to the conformation specific monoclonal antibody 4C3, suggesting that a similar conformational change to that occurring in complexed or cleaved inhibitor had taken place. N‐Terminal analysis of
Patston, Philip A.   +3 more
openaire   +2 more sources

Electron transfer between complexes III and IV in S. cerevisiae mitochondrial membranes

open access: yesFEBS Letters, EarlyView.
Mitochondrial oxidative phosphorylation in S. cerevisiae mitoplasts is limited by complex IV catalytic capacity, rather than two‐dimensional cytochrome c diffusion. At physiological cytochrome c : supercomplex ratios at salinity equivalent to that of 20 mm monovalent salt, activity is maximized, indicating that this low ionic strength accurately mimics
Ana Paula Lobez   +2 more
wiley   +1 more source

C1-inhibitor protects against brain ischemia–reperfusion injury via inhibition of cell recruitment and inflammation

open access: yesNeurobiology of Disease, 2005
Previous studies demonstrated that C1-inhibitor (C1-INH), a complement and contact-kinin systems inhibitor, is neuroprotective in cerebral ischemia.
Claudio Storini   +7 more
doaj   +1 more source

C1-esterase inhibitor reduces reperfusion injury after lung transplantation

open access: yes, 2002
BACKGROUND: Activation of the complement system and polymorphonuclear neutrophilic leukocytes plays a major role in mediating reperfusion injury after lung transplantation.
Schäfers, Hans-Joachim   +9 more
core   +1 more source

Structural insights and therapeutic targets in Acinetobacter baumannii capsule biosynthesis

open access: yesFEBS Letters, EarlyView.
Hypervirulent KL49 A. baumannii's capsular polysaccharide contains the nonulosonic acid 8‐epi‐Leg5,7Ac2, synthesized by epimerization via ElaA, ElaB, and ElaC. Crystal structures of ElaA, ElaB, and ElaC reveal their role in CMP‐Leg5,7Ac2 synthesis and regioselective C8 epimerization.
Woo Cheol Lee   +7 more
wiley   +1 more source

C1 Inhibitor Autoantibodies

open access: yes, 2014
Autoantibodies to C1 inhibitor (C1-INH) bind to epitopes on the reactive center of the C1-INH molecule. As a consequence of this binding, C1-INH is converted into an inactive substrate that can be cleaved by proteases.
Suffritti, C   +8 more
core   +1 more source

Hijacking emergency granulopoiesis: Neutrophil ontogeny and reprogramming in cancer

open access: yesMolecular Oncology, EarlyView.
Neutrophils are highly plastic innate immune cells; their functions in cancer extend beyond the tumour microenvironment. This Review summarises current understanding of neutrophil maturation and heterogeneity and highlights tumour‐induced granulopoiesis as a systemic programme that expands immature, immunosuppressive neutrophils via tumour‐derived ...
Gabriela Marinescu, Yi Feng
wiley   +1 more source

Monocyte C1-Inhibitor Synthesis [PDF]

open access: yes, 1987
C1-inhibitor is the major control protein of the classical pathway of complement. In man, its hereditary deficiency results in the clinical condition of hereditary angio-oedema (HAE).
Jones, Linda Margaret
core  

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