www.med.uoc.gr Department  of  Biochemistry - Division of Basic Sciences - University  of  Crete
  I N F O


HOMEPAGE
 

 

C O U R S E S


Undergraduate

Graduate
 

 
| Info - Contact | Research Directions | Research Group | Publications |


Papakonstanti Evangelia

Ast Professor of Biochemistry, Department of Biochemistry
Faculty of Medicine, University of Crete

E-mailepapak@med.uoc.gr
Phone +30.2810.39.4554
Fax+30.2810.39.4530
Address

Medical School,
Vassilika Vouton,
GR-71110,
Heraklion-Crete,
Greece

Papakonstanti Evangelia

Current Research Interests:

  • role of PI3K isoforms in the nucleus
    Until recently it was thought that PI3Ks exert their effects mainly in the cytoplasm. Over the past few years, it has been shown that PI3Ks are also localized and/or translocated to the nucleus. Using cells from genetic modified mice for the PI3K isoforms (in collaboration with Dr. Vanhaesebroeck's lab in London) we attempt to understand the individual roles that distinct PI3K isoforms play in the nucleus as well as the mechanism of PI3Ks activation in the nuclear compartment. We are also interested in understanding the mechanism that controls the translocation of p110s into the nucleus and to identify the nuclear import/export sequences in the p110s sequence.
  • potential link between PI3K isoforms in the nucleus with cytosolic signalling in the context of the Rho small GTPases
    The cyclin-dependent kinase inhibitors (CKIs) when located in the nucleus function as inhibitors of cyclin-CDK activity. However, in addition to their anti-proliferative function in the nucleus members of the Cip/Kip family (p27, p21, p57) play an oncogenic role in the cytoplasm by inhibiting the Rho GTPase's pathway at distinct points promoting thus migration. p27 and p21 are localized in the cytoplasm after their phosphorylation by Akt a downstream effector of PI3Ks. We are investigating a potential PI3K-isoform specific regulation of cross-talk between CKIs and Rho GTPases that bridges the nuclear with cytosolic signalling. This will contribute to exploiting therapeutic strategies which by targeting one molecule will co-ordinately regulate both, cell proliferation and metastasis.
  • role of p110d?RhoA?PTEN feedback mechanism in cancer cells growth and metastasis
    Inactivation of PI 3-kinase signalling by PTEN was thought to be a unidirectional relationship in which PTEN degrades the lipids produced by PI3Ks. We showed for the first time that this relationship is in fact bidirectional, whereby p110d PI3K reciprocally regulates its regulator PTEN through a feedback mechanism involving inhibition of RhoA activity. Using in vitro and in vivo models we are investigating the role of this pathway in tumour growth and metastasis.
 



Powered And Designed by: Virtual Medical Lab