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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Glutaminyl-peptide cyclotransferase

glutaminyl cyclase, QPCT, glutaminyl-peptide cyclotransferase
This gene encodes human pituitary glutaminyl cyclase, which is responsible for the presence of pyroglutamyl residues in many neuroendocrine peptides. The amino acid sequence of this enzyme is 86% identical to that of bovine glutaminyl cyclase. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: ACID, CAN, V1a, fibrillin-1, APP
Papers on glutaminyl cyclase
IsoQC (QPCTL) knock-out mice suggest differential substrate conversion by glutaminyl cyclase isoenzymes.
Schilling et al., In Biol Chem, Feb 2016
This modification is catalyzed by the glutaminyl cyclases QC and isoQC.
Common Polymorphisms Within QPCT Gene Are Associated with the Susceptibility of Schizophrenia in a Han Chinese Population.
Zhang et al., Nanjing, China. In Mol Neurobiol, Dec 2015
UNASSIGNED: A recent genome-wide association study conducted in Caucasians has identified glutaminyl-peptide cyclotransferase (QPCT) gene as a susceptibility gene for schizophrenia, as its common single nucleotide polymorphism (SNP) rs2373000 was significantly associated with the risk of this disease.
Hypothesis: glutaminyl cyclase inhibitors decrease risks of Alzheimer's disease and related dementias.
Gaziano et al., Boca Raton, United States. In Expert Rev Neurother, Nov 2015
In this context, glutaminyl cyclase (QC) inhibitors have shown some early possible evidence of efficacy with a reassuring safety profile.
Common variants in QPCT gene confer risk of schizophrenia in the Han Chinese population.
Ji et al., Shanghai, China. In Am J Med Genet B Neuropsychiatr Genet, Nov 2015
The QPCT gene encodes Glutaminyl cyclase (QC), an enzyme which is involved in the post translational modification by converting N-terminal glutamate of protein to pyroglutamate, which is resistant to protease degradation, more hydrophobic, and prone to aggregation and neurotoxic.
Identification of Genes Expressed in Hyperpigmented Skin Using Meta-Analysis of Microarray Data Sets.
Hearing et al., Bethesda, United States. In J Invest Dermatol, Oct 2015
Immunohistochemistry was used to validate two of these markers at the protein level (TRIM63 and QPCT), and we discuss the possible functions of these genes in regulating skin physiology.
The soluble Y115E-Y117E variant of human glutaminyl cyclase is a valid target for X-ray and NMR screening of inhibitors against Alzheimer disease.
Mangani et al., Siena, Italy. In Acta Crystallogr Sect F Struct Biol Commun, Aug 2015
Recent developments in molecular pathology and genetics have allowed the identification of human glutaminyl cyclase (hQC) among the abnormal proteins involved in many neurodegenerative disorders.
Synthesis and evaluation of [(11)C]PBD150, a radiolabeled glutaminyl cyclase inhibitor for the potential detection of Alzheimer's disease prior to amyloid β aggregation.
Scott et al., Ann Arbor, United States. In Medchemcomm, Jul 2015
Evaluation of [(11)C]PBD150 by small animal PET imaging (mouse and rat) determined it does not permeate the blood brain barrier, indicating previously described therapeutic effect in transgenic mice was likely not the result of inhibiting central nervous system glutaminyl cyclase.
Phosphate ions and glutaminyl cyclases catalyze the cyclization of glutaminyl residues by facilitating synchronized proton transfers.
Schilling et al., Göttingen, Germany. In Bioorg Chem, Jun 2015
Phosphate ions and glutaminyl cyclase (QC) both catalyze the formation of pyroglutamate (pE, pGlu) from N-terminal glutamine residues of peptides and proteins.
Arsenic Trioxide Activate Transcription of Heme Oxygenase-1 by Promoting Nuclear Translocation of NFE2L2.
Wang et al., Changchun, China. In Int J Med Sci, 2014
First, using RT-QPCT and Western-blot, we found that ATO strongly induced the expression of heme oxygenase-1 (HO-1) in these human osteosarcoma cells.
A New Quantum Calibrated Force Field for Zinc-Protein Complex.
Zhang et al., Shanghai, China. In J Chem Theory Comput, 2013
A quantum calibrated polarizable-charge transfer force field (QPCT) has been proposed to accurately describe the interaction dynamics of zinc-protein complexes.
Pyroglutamate amyloid-β (Aβ): a hatchet man in Alzheimer disease.
Bayer et al., Göttingen, Germany. In J Biol Chem, 2011
Recent in vitro and in vivo experiments have proven that the enzyme glutaminyl cyclase catalyzes the formation of Aβ(pE3).
Structures of glycosylated mammalian glutaminyl cyclases reveal conformational variability near the active center.
Demuth et al., Halle, Germany. In Biochemistry, 2011
This study presents a first comparison of two mammalian QCs (human and mouse) containing typical, conserved post-translational modifications.
Glutaminyl cyclase contributes to the formation of focal and diffuse pyroglutamate (pGlu)-Aβ deposits in hippocampus via distinct cellular mechanisms.
Rossner et al., Leipzig, Germany. In Acta Neuropathol, 2011
The resilts of this studt provided histopathological evidence for QC being a prerequisite for pE-Abeta pathology in vivo and further underline the therapeutic potential of QC inhibition in Alzheimer Disease.
Structures of human Golgi-resident glutaminyl cyclase and its complexes with inhibitors reveal a large loop movement upon inhibitor binding.
Wang et al., Taipei, Taiwan. In J Biol Chem, 2011
Upon binding to PBD150, a large loop movement in gQC allows the inhibitor to be tightly held in its active site primarily by hydrophobic interactions.
Distinct glutaminyl cyclase expression in Edinger-Westphal nucleus, locus coeruleus and nucleus basalis Meynert contributes to pGlu-Abeta pathology in Alzheimer's disease.
Rossner et al., Leipzig, Germany. In Acta Neuropathol, 2010
This study demonstrated that glutaminyl cyclase expression and pE-Abeta formation in subcortical brain regions( Edinger-Westphal nucleus, locus coeruleus and nucleus basalis Meynert) affected in Alzheimer's disease.
Plucking, pillaging and plundering proteomes with combinatorial peptide ligand libraries.
Citterio et al., Milano, Italy. In J Chromatogr A, 2010
In particular, in the case of venom proteins, where essentially all components had been detected and fully described by conventional means, the application of the ligand library technology allowed the discovery of two, previously unreported, trace enzymes necessary for the maintenance of the native structure of venom components, namely peroxiredoxin and glutaminyl cyclase.
Mammalian glutaminyl cyclases and their isoenzymes have identical enzymatic characteristics.
Schilling et al., Halle, Germany. In Febs J, 2009
Human isoQC proteins displayed a broad substrate specificity and preference for hydrophobic substrates, similar to the related QC.
Glutaminyl cyclase inhibition attenuates pyroglutamate Abeta and Alzheimer's disease-like pathology.
Rossner et al., Halle, Germany. In Nat Med, 2008
We found that the N-terminal pE-formation is catalyzed by glutaminyl cyclase in vivo.
Alternative pathways for production of beta-amyloid peptides of Alzheimer's disease.
Hook et al., San Diego, United States. In Biol Chem, 2008
Furthermore, cyclization of N-terminal Glu by glutaminyl cyclase generates highly amyloidogenic pGluAbeta(3-40/42).
Meta-analysis and meta-review of thyroid cancer gene expression profiling studies identifies important diagnostic biomarkers.
Wiseman et al., Vancouver, Canada. In J Clin Oncol, 2006
A review of the top 12 candidates revealed well known thyroid cancer markers such as MET, TFF3, SERPINA1, TIMP1, FN1, and TPO as well as relatively novel or uncharacterized genes such as TGFA, QPCT, CRABP1, FCGBP, EPS8 and PROS1.
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