Informacja

Drogi użytkowniku, aplikacja do prawidłowego działania wymaga obsługi JavaScript. Proszę włącz obsługę JavaScript w Twojej przeglądarce.

Wyszukujesz frazę "Mężyk-Kopeć, Renata" wg kryterium: Autor


Wyświetlanie 1-2 z 2
Tytuł:
Antibody-based antiangiogenic and antilymphangiogenic therapies to prevent tumor growth and progression
Autorzy:
Bzowska, Monika
Mężyk-Kopeć, Renata
Próchnicki, Tomasz
Kulesza, Małgorzata
Klaus, Tomasz
Bereta, Joanna
Powiązania:
https://bibliotekanauki.pl/articles/1039514.pdf
Data publikacji:
2013
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
monoclonal antibodies
antiangiogenic therapy
antilymphangiogenic therapy
VEGF- A
VEGF-C
VEGF-D
Opis:
Blood and lymphatic vessel formation is an indispensable factor for cancer progression and metastasis. Therefore, various strategies designed to block angiogenesis and lymphangiogenesis are being investigated in the hope to arrest and reverse tumor development. Monoclonal antibodies, owing to their unequalled diversity and specificity, might be applied to selectively inhibit the pathways that cancer cells utilize to build up a network of blood vessels and lymphatics. Among the possible targets of antibody-based therapies are proangiogenic and prolymphangiogenic growth factors from the VEGF family and the receptors to which they bind (VEGFRs). Here, we present molecular mechanisms of angiogenesis and lymphangiogenesis exploited by tumors to progress and metastasise, with examples of antibody-based therapeutic agents directed at interfering with these processes. The expanding knowledge of vascular biology helps to explain some of the problems encountered in such therapies, that arise due to the redundancy in signaling networks controlling the formation of blood and lymphatic vessels, and lead to tumor drug resistance. Nonetheless, combined treatments and treatments focused on newly discovered proangiogenic and prolymphangiogenic factors give hope that more prominent therapeutic effects might be achieved in the future.
Źródło:
Acta Biochimica Polonica; 2013, 60, 3; 263-275
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Exogenous nitric oxide inhibits shedding of ADAM17 substrates
Autorzy:
Bzowska, Monika
Stalińska, Krystyna
Mężyk-Kopeć, Renata
Wawro, Karolina
Duda, Katarzyna
Das, Sudipta
Bereta, Joanna
Powiązania:
https://bibliotekanauki.pl/articles/1040593.pdf
Data publikacji:
2009
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
shedding
ADAM17
TNF receptor 1
TNF
nitric oxide
Opis:
Both ADAM17, the secretase responsible for the shedding of ectodomains of numerous membrane proteins including TNF and its receptors, as well as nitric oxide synthesized by inducible nitric oxide synthase play regulatory roles in inflammation and tumor progression. We analyzed the effect of endogenous and exogenous nitric oxide on the expression and activity of ADAM17 in murine endothelial cells and a monocyte/macrophage cell line. We found that endogenous nitric oxide influenced neither ADAM17 mRNA level nor the shedding of two ADAM17 substrates, TNF and TNFR1. Exogenous NO significantly diminished the release of TNF and TNFR1 without affecting the ADAM17 transcript level. Our data seem contrary to a previous report that showed the activation of ADAM17 by nitric oxide (Zhang et al., 2000, J Biol Chem 275: 15839-15844). We discuss potential mechanisms of NO-mediated inhibition of ectodomain shedding and possible reasons of discrepancy between our results and the previous report.
Źródło:
Acta Biochimica Polonica; 2009, 56, 2; 325-335
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
    Wyświetlanie 1-2 z 2

    Ta witryna wykorzystuje pliki cookies do przechowywania informacji na Twoim komputerze. Pliki cookies stosujemy w celu świadczenia usług na najwyższym poziomie, w tym w sposób dostosowany do indywidualnych potrzeb. Korzystanie z witryny bez zmiany ustawień dotyczących cookies oznacza, że będą one zamieszczane w Twoim komputerze. W każdym momencie możesz dokonać zmiany ustawień dotyczących cookies