Prolyl endopeptidase is involved in cellular signalling in human neuroblastoma SH-SY5Y cells.

Prolyl endopeptidase (PREP), probably acting through the inositol cycle, has been implicated in memory and learning. However, the physiological role of PREP is unknown. It has been shown that PREP expression, regulated in cerebellar granule cells, has probably a role in cell proliferation and differentiation.

Prolyl oligopeptidase induces angiogenesis both in vitro and in vivo in a novel regulatory manner.

BACKGROUND AND PURPOSE A serine protease, prolyl oligopeptidase (POP) has been reported to be involved in the release of the pro-angiogenic tetrapeptide acetyl-N-Ser-Asp-Lys-Pro (Ac-SDKP) from its precursor, 43-mer thymosin β4 (Tβ4). Recently, it was shown that both POP activity and the levels of Ac-SDKP are increased in malignant tumours. The aim of this study was to clarify the release of Ac-SDKP, and test if POP and a POP inhibitor, 4-phenyl-butanoyl-L-prolyl-2(S)-cyanopyrrolidine (KYP-2047), can affect angiogenesis.

Expression and traffic of cellular prolyl oligopeptidase are regulated during cerebellar granule cell differentiation, maturation, and aging.

Prolyl oligopeptidase (POP) is an endopeptidase which cleaves short proline-containing neuropeptides, and it is involved in memory and learning. POP also has an intercellular function mediated through the inositol pathway, and has been involved in cell death. POP has been early considered as a housekeeping enzyme, but the recent research indicates that POP expression is regulated across tissues and intracellularly.

Polymerase chain reaction detection of BK virus and monitoring of BK nephropathy in renal transplant recipients at the University Hospital La Fe.

Introduction: Reactivation of BK infection occurs in immunocompromised hosts causing tubulointerstitial nephropathy (BKVN). Approximately 5% of kidney transplant recipients (KTR) develop BKVN, special half of whom lose their grafts. However, BKVN morphologic diagnosis on a renal biopsy is complicated, because the cytopathic changes can sometimes mimic rejection.

LT, VP1 and TCR-BKV sequence analysis in a patient with post-transplant BKV nephropathy associated with EBV-related PTLD.

A 10-year-old boy kidney transplant recipient (KTR) developed an abdominal post-transplant lymphoproliferative syndrome (PTLD) followed by BK virus nephropathy (BKVN). BK virus (BKV) and Epstein-Barr virus (EBV) were studied in renal and PTLD tissue by polymerase chain reaction (PCR) assay. Afterwards, the patient was monitored in relation to BKV in urine and serum; transcription control region (TCR)-BK polymorphism sequence analysis was also performed.

A risk model for non-small cell lung cancer using clinicopathological variables, angiogenesis and oncoprotein expression.

Background: The aim of this study was to investigate new prognostic factors, by using a prognostic model, that could help to identify the patient group with the greatest probability of death.

Patients And Methods: First, the clinicopathological variables were analyzed. Second, microvessels were immunohistochemically (IHC) stained with factor VIII-related antibody and then counted in the most intense vascularization area or hotspot, using an automatic image analyzer.