Haller Martina, Mag.biol.

University / Clinic: Department of Visceral, Transplant and Thoracic Su
Institute: Daniel-Swarovski-Research Laboratory
 
Research Area: Molecular cell biology

Email: m.haller@-i-med.ac.at
Web: www.i-med.ac.at/tx-research/


Research Topic:
The RAS/RAF/MEK/ERK pathway controls important cellular processes including proliferation, differentiation and survival. We have shown recently that RAF assures the survival of growth factor-deprived cells by maintaining permissive levels of mitochondrial reactive oxygen species (ROS) and calcium (Ca2+). But how the absence of a growth factor translates into mitochondrial changes is still unclear. One candidate we are investigating now is the p66SHC protein, for which it has been shown recently that in response to cellular stress, p66SHC gets phosphorylated and translocates to mitochondria where it directly produces ROS.

Selected publications:
 
  Haller M, Khalid S, Kremser L, Fresser F, Furlan T, Hermann M, Guenther J, Drasche A, Leitges M, Giorgio M, Baier G, Lindner H, Troppmair J
Novel insights into the PKCβ-dependent regulation of the oxidoreductase p66Shc.
J Biol Chem. 2016 Sep 13. pii: jbc.M116.752766. [Epub ahead of print] PubMed PMID: 27624939.

  Ashraf M, Ebner M, Wallner C, Haller M, Khalid S, Schwelberger H, Koziel K, Enthammer M, Hermann M, Sickinger S, Soleiman A, Steger C, Vallant S, Sucher R, Brandacher G, Santer P, Dragun D, Troppmair
A p38MAPK/MK2 signaling pathway leading to redox stress, cell death and ischemia/reperfusion injury.
Cell Commun Signal. 2014 Jan 14;12:6

  Zebisch A, W├Âlfler A, Fried I, Wolf O, Lind K, Bodner C, Haller M, Drasche A, Pirkebner D, Matallanas D, Rath O, Blyth K, Delwel R, Taskesen E, Quehenberger F, Kolch W, Troppmair J, Sill H
Frequent loss of RAF kinase inhibitor protein expression in acute myeloid leukemia.
Leukemia. 2012 Aug;26(8):1842-9. doi: 10.1038/leu.2012.61. Epub 2012 Mar 5. PubMed PMID: 22388727.

  Zebisch A, Haller M, Hiden K, Goebel T, Hoefler G, Troppmair J, Sill H.
Loss of RAF kinase inhibitor protein is a somatic event in the pathogenesis of therapy-related acute myeloid leukemias with C-RAF germline mutations.
Leukemia. 2009 Jun;23(6):1049-1053.