1 – 10 of 13
- show: 10
- |
- sort: year (new to old)
Close
Embed this list
<iframe src=" "
width=" "
height=" "
allowtransparency="true"
frameborder="0">
</iframe>
- 2013
-
Mark
Exosomes reflect the hypoxic status of glioma cells and mediate hypoxia-dependent activation of vascular cells during tumor development.
(
- Contribution to journal › Article
- 2011
-
Mark
Heparan sulfate proteoglycan-mediated polyamine uptake.
(
- Contribution to journal › Article
- 2010
-
Mark
On the Role of Polyamines and Microvesicles in Tumour Development. Regulation by Hypoxia and Implications for Therapeutic Intervention of Cancer.
(
- Thesis › Doctoral thesis (compilation)
-
Mark
Cancer cell-derived microvesicles constitute a novel mediator of hypoxia dependent induction of pro-angiogenic signaling
2010) 35th Congress of the Federation-of-European-Biochemical-Societies In The FEBS Journal 277(Suppl. 1). p.132-132(
- Contribution to journal › Published meeting abstract
-
Mark
Ornithine decarboxylase and extracellular polyamines regulate microvascular sprouting and actin cytoskeleton dynamics in endothelial cells.
(
- Contribution to journal › Article
-
Mark
Establishment of heparan sulphate deficient primary endothelial cells from EXT-1(flox/flox) mouse lungs and sprouting aortas.
(
- Contribution to journal › Article
- 2009
-
Mark
ScFv antibody-induced translocation of cell-surface heparan sulfate proteoglycan to endocytic vesicles: Evidence for heparan sulfate epitope specificity and role of both syndecan and glypican.
(
- Contribution to journal › Article
-
Mark
The polyamines regulate endothelial cell survival during hypoxic stress through PI3K/AKT and MCL-1.
(
- Contribution to journal › Article
- 2008
-
Mark
Hypoxia-mediated induction of the polyamine system provides opportunities for tumor growth inhibition by combined targeting of vascular endothelial growth factor and ornithine decarboxylase.
(
- Contribution to journal › Article
- 2007
-
Mark
HIV-Tat protein transduction domain specifically attenuates growth of polyamine deprived tumor cells.
(
- Contribution to journal › Article