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Literature summary for 2.3.2.5 extracted from

  • Bridel, C.; Hoffmann, T.; Meyer, A.; Durieux, S.; Koel-Simmelink, M.A.; Orth, M.; Scheltens, P.; Lues, I.; Teunissen, C.E.
    Glutaminyl cyclase activity correlates with levels of Abeta peptides and mediators of angiogenesis in cerebrospinal fluid of Alzheimers disease patients (2017), Alzheimers Res. Ther., 9, 38 .
    View publication on PubMedView publication on EuropePMC

Application

Application Comment Organism
pharmacology Abeta38, Abeta40 and angiogenesis mediators Flt1, Tie2, VEGFD, CAM-1 and ICAM-1 are potential pharmacodynamic markers of glutaminyl cyclase (QC) inhibition, because their levels closely correlate with QC activity in Alzheimer's disease patients. The addition of QC activity to core diagnostic cerebrospinal fluid (CSF) biomarkers may be of specific interest in clinical cases with discordant imaging and biochemical biomarker results. Core CSF diagnostic biomarkers (Abeta42, tau and p-tau) are not part of the diagnostic workup Homo sapiens

Natural Substrates/ Products (Substrates)

Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
L-glutaminyl-peptide Homo sapiens
-
5-oxoprolyl-peptide + NH3
-
?

Organism

Organism UniProt Comment Textmining
Homo sapiens Q16769
-
-

Source Tissue

Source Tissue Comment Organism Textmining
cerebrospinal fluid
-
Homo sapiens
-

Substrates and Products (Substrate)

Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
L-glutaminyl-peptide
-
Homo sapiens 5-oxoprolyl-peptide + NH3
-
?

Synonyms

Synonyms Comment Organism
glutaminyl cyclase
-
Homo sapiens

General Information

General Information Comment Organism
physiological function glutaminyl cyclase activity correlates with levels of Abeta38, Abeta40 and angiogenesis mediators Flt1, Tie2, VEGFD, CAM-1 and ICAM-1 in cerebrospinal fluid of Alzheimers disease patients, core CSF diagnostic biomarkers (Abeta42, tau and p-tau) are not part of the diagnostic workup, detailed overview. Pyroglutamylation of truncated Abeta peptides, which is catalysed by enzyme glutaminyl cyclase (QC), generates pE-Abeta species with enhanced aggregation propensities and resistance to most amino-peptidases and endo-peptidases. pE-Abeta species have been identified as major constituents of Abeta plaques and reduction of pE-Abeta species is associated with improvement of cognitive tasks in animal models of Alzheimer's disease (AD). Some inflammatory or angiogenesis mediators are potential QC substrates Homo sapiens