• Institut für Biomedizinische Alternsforschung

IBA Publikation

Bild






IBA Publikation


Verlag der Österreichischen Akademie der Wissenschaften
Austrian Academy of Sciences Press
A-1011 Wien, Dr. Ignaz Seipel-Platz 2
Tel. +43-1-515 81/DW 3420, Fax +43-1-515 81/DW 3400
https://verlag.oeaw.ac.at, e-mail: verlag@oeaw.ac.at

Bestellung/Order


Bild






IBA Publikation
IBA Publikation







Send or fax to your local bookseller or to:

Verlag der Österreichischen Akademie der Wissenschaften
Austrian Academy of Sciences Press
A-1011 Wien, Dr. Ignaz Seipel-Platz 2,
Tel. +43-1-515 81/DW 3420, Fax +43-1-515 81/DW 3400
https://verlag.oeaw.ac.at, e-mail: bestellung.verlag@oeaw.ac.at
UID-Nr.: ATU 16251605, FN 71839x Handelsgericht Wien, DVR: 0096385

Bitte senden Sie mir
Please send me
 
Exemplar(e) der genannten Publikation
copy(ies) of the publication overleaf


NAME


ADRESSE / ADDRESS


ORT / CITY


LAND / COUNTRY


ZAHLUNGSMETHODE / METHOD OF PAYMENT
    Visa     Euro / Master     American Express


NUMMER

Ablaufdatum / Expiry date:  

    I will send a cheque           Vorausrechnung / Send me a proforma invoice
 
DATUM, UNTERSCHRIFT / DATE, SIGNATURE

BANK AUSTRIA CREDITANSTALT, WIEN (IBAN AT04 1100 0006 2280 0100, BIC BKAUATWW), DEUTSCHE BANK MÜNCHEN (IBAN DE16 7007 0024 0238 8270 00, BIC DEUTDEDBMUC)
Bild






IBA Publikation

Age-dependent prosttranslational modifications of voltage-dependent anion channel 1

    Karlfried Groebe, Martina Klemm-Manns, Gerhard P. Schwall, Heiko Hübenthal, Herrmann Unterluggauer, Pidder Jansen-Dürr, Robert M. Tanguay, Geneviève Morrow, André Schrattenholz

IBA Publikation, pp. 632-637, 2010/02/26

doi: 10.1016/j.exger.2010.02.006


Object
X
BibTEX-Export:

X
EndNote/Zotero-Export:

X
RIS-Export:

X 
Researchgate-Export (COinS)

Permanent QR-Code

doi:10.1016/j.exger.2010.02.006

Abstract

The accumulation of oxidative damage in mitochondrial proteins, membranes and DNA during ageing is supposed to lead to mitochondrial inactivation, downstream molecular impairments and subsequent decline of biological systems.In a quantitative study investigating the age-related changes of mitochondrial proteins on the level of oxidative posttranslational modifications, we previously found a set of conserved biomarkers across ageing models in five species with consistent oxidative break-up of tryptophan residues and formation of N-formyl kynurenine. In an additional proteomic profiling of a long-living Drosophila mutant overexpressing mitochondrial Hsp22 and controls, we found age-related redundant isoforms of voltage-dependent anion channel 1 (VDAC-1). A re-examination of data from human umbilical vein endothelial cells (with normal and chemically accelerated in vitro ageing), revealed similar age-dependent alterations of voltage-dependent anion channel isoforms.Building on these results, we examined the expression of VDAC-1 in an in vitro model of excitotoxicity. We show that glutamate-induced calcium toxicity in neurons induces changes of voltage-dependent anion channel 1 related to downstream events of mitochondrial apoptosis like poly-ADP-ribosylation.

Keywords: Mitochondrial-permeability-transition-pore Voltage-dependent-anion-channel-1 Quantitative-proteomics Systems-biology Oxidative-posttranslational-modifications Ageing-model HSP-22 Longevity Mitochondrial-apoptosis PARP-1