Home > Search Results: Kupcová Skalníková, Helena
Search:
Search Tips :: Advanced Search
Search collections:
Sort by: Display results: Output format:
National Repository of Grey Literature 2 records found  Search took 0.00 seconds. 
Multiple forms of dipeptidyl peptidase IV and fibroblast activation protein in brain tumors
 Matrasová, Ivana ; Šedo, Aleksi (advisor) ; Kupcová Skalníková, Helena (referee) ; Modrianský, Martin (referee)
Proteolytic enzymes are known to contribute to the initiation, development and progression of a number of diseases. Dipeptidyl peptidase IV (DPP-IV) and fibroblast activation protein (FAP) are serine proteases with the unique ability to cleave dipeptides containing - highly evolutionarily conserved - proline at the penultimate position of the N- terminus of substrates/biologically active peptides. FAP also exhibits gelatinolytic activity, which it exerts during extracellular matrix remodeling processes. Glial brain tumors (gliomas) arise from resident transformed glial cells, whereas brain metastases originate from circulating transformed extracranial tumor cells. Our previous work has described an increased expression of DPP-IV and FAP in high-grade glioma tissues. The presence of DPP- IV and FAP in brain metastatic tissues has not been described to date. The aim of this thesis was to describe the multiple forms of DPP-IV and FAP, and to describe their cellular origin and possible regulation in brain tumors. DPP-IV and its molecular MW and pI forms were expressed predominantly by transformed glial cells, whereas FAP and its MW and pI forms were expressed by transformed and stromal cells present in GBM and brain metastatic tissues. The spectrum of multiple forms of DPP-IV and FAP in GBM tissues and...
Detailed record
Body fluid exosomes as potential carriers of Huntington’s disease biomarkers
 Kupcová Skalníková, Helena ; Červenka, Jakub ; Bohuslavová, Božena ; Turnovcová, Karolína ; Vodička, Petr
Huntington’s disease (HD) is a hereditary neurodegenerative disorder characterized by a progressive motor, behavioural, and cognitive decline, ending in death. The cause of HD is an abnormal expansion of CAG repeats in HTT gene resulting in prolonged polyglutamine (polyQ) sequence in huntingtin protein (HTT). Huntingtin is a large protein (348 kDa) expressed ubiquitously through the body, with highest expression in the brain and testes. To study HD pathophysiology and to test experimental therapies, a transgenic HD minipig (TgHD) model expressing N-terminal part (N548-124Q) of human mutated huntingtin (mHTT) under the control of human huntingtin promoter was created in Libechov. Beside the mild neurological impairment, the TgHD boars show decreased fertility after 13th month of age.
Detailed record

Interested in being notified about new results for this query?
Subscribe to the RSS feed.
Digital Repository :: Search :: Submit :: Personalize :: Help
Powered by Invenio v1.1.2
Maintained by admin.invenio@techlib.cz
This site is also available in the following languages:
Česky  English