Results 101 to 110 of about 349,286 (299)

Deciphering transcriptional plasticity in pancreatic ductal adenocarcinoma reveals alterations in sensory neuron innervation

open access: yesMolecular Oncology, EarlyView.
Pancreatic sensory neurons innervating healthy and PDAC tissue were retrogradely labeled and profiled by single‐cell RNA sequencing. Tumor‐associated innervation showed a dominant neurofilament‐positive subtype, altered mitochondrial gene signatures, and reduced non‐peptidergic neurons.
Elena Genova   +14 more
wiley   +1 more source

Self-association of complement factor H in the presence and absence of metals

open access: yes, 2010
In the complement system of innate immunity, factor H (FH) is a major regulator of its activation, and is comprised of 20 short complement regulator (SCR) domains.
Nan, R.
core  

Elevated factor H-related protein 1 and factor H pathogenic variants decrease complement regulation in IgA nephropathy

open access: yes, 2017
IgA nephropathy (IgAN), a frequent cause of chronic kidney disease worldwide, is characterized by mesangial deposition of galactose-deficient IgA1-containing immune complexes.
Gutiérrez Tenorio, Josué   +5 more
core   +1 more source

Paths reunited: initiation of the classical and lectin pathways of complement activation [PDF]

open access: yes, 2010
Understanding the structural organisation and mode of action of the initiating complex of the classical pathway of complement activation (C1) has been a central goal in complement biology since its isolation almost 50 years ago.
Schmid, Ralf   +9 more
core   +1 more source

Complement Factor H-Related Protein 4A Is the Dominant Circulating Splice Variant of CFHR4

open access: yesFrontiers in Immunology, 2018
Recent research has elucidated circulating levels of almost all factor H-related (FHR) proteins. Some of these proteins are hypothesized to act as antagonists of the important complement regulator factor H (FH), fine-tuning complement regulation on human
Richard B. Pouw   +8 more
doaj   +1 more source

Heterozygous loss‐of‐function alleles associate the conserved 3′‐5′ exoribonuclease EXOSC10 with hypersensitivity to the anticancer drug 5‐fluorouracil

open access: yesMolecular Oncology, EarlyView.
EXOSC10, an essential nuclear RNA exosome‐associated 3′‐5′ exoribonuclease, is inhibited by the anticancer drug 5‐fluorouracil (5‐FU), and EXOSC10 depletion increases 5‐FU sensitivity. The colon‐cancer variant EXOSC10S402T, located in a proteolysis motif, is stable and nuclear but nonfunctional in vivo.
Radhika Sain   +10 more
wiley   +1 more source

Mechanism and function of complement factor H [PDF]

open access: yes, 2014
Factor H (FH) is a 155-kDa plasma protein that regulates the alternative pathway of the complement system. Its 20 CCP modules, of 51-62 amino acid residues each, are linked by short stretches (“linkers’) of three to eight residues.
McIntosh, Nicola
core  

Autoantibodies Against Factor B and Factor H Without Pathogenic Effects in a Patient with Immune Complex-Mediated Membranoproliferative Glomerulonephritis

open access: yesBiomedicines
Background: Membranoproliferative glomerulonephritis (MPGN) is an umbrella term for chronic disorders affecting the glomeruli. MPGN is often accompanied by the presence of autoantibodies against complement components.
Alexandra T. Matola   +6 more
doaj   +1 more source

Transcriptional profiling of circulating extracellular vesicles from prebiopsy prostate cancer patients

open access: yesMolecular Oncology, EarlyView.
RNA profiling of circulating extracellular vesicles (EVs) from blood samples of men undergoing prostate biopsy identifies transcripts associated with clinically significant prostate cancer. Integrative analysis with public tumor datasets links EV‐derived gene signatures to tumor stage and progression‐free survival, highlighting CASP3, XRCC2, and RIT1 ...
Stefan Werner   +14 more
wiley   +1 more source

The Role of von Willebrand Factor in the Pathogenesis of C3 Glomerulopathy

open access: yesKidney International Reports
Introduction: C3 glomerulopathy (C3G) is caused by dysregulation of complement activation. Our previous study found that patients with C3G showed rare variants in von Willebrand factor (vWF).
Zixin Hua   +7 more
doaj   +1 more source

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