PuSH - Publication Server of Helmholtz Zentrum München: Modelling of intercellular induction of apoptosis in oncogenic transformed cells and radiation effects on the phenomenon.

Information

Clues to quality of journals

Open Access Policy of Helmholtz Association 2016

CC Licencences

Publication Metrics

Navigation

Home

Deutsch

EVA: Electronic Publishing

New EVA Application

Research

Advanced Search

Browse by ...

... HMGU-Authors/Consortia

... Organizational Structure

... Journal

... Publication Type

... Research Data

... Arbeitsgruppen

... Publication Year

Publication overview

Statistics

Statistics (last 5 years)

OA Publications

Publish

Submit Publication

Import publication from...

...EVA

Report missing publication

Highlights

Support & Contact

Contact persons

Help

Data protection

Helmholtz Open Science

JANE Journal Estimator

SHERPA/RoMEO

DOAJ

Export:

Text

Endnote (RIS) BIB

BibTeX

Kundrát, P. ; Friedland, W. ; Jacob, P.

Modelling of intercellular induction of apoptosis in oncogenic transformed cells and radiation effects on the phenomenon.

Radiat. Prot. Dosim. 143, 549-553 (2011)

DOI

PMC

Open Access Green as soon as Postprint is submitted to ZB.

Abstract
Metrics
Extra information

The removal of transformed cells via induction of apoptosis through intercellular signalling by surrounding cells is supposed to represent an important control mechanism limiting carcinogenesis. Low doses of radiation influence the efficiency of this anti-carcinogenesis process, indicating possible beneficial effects of low doses of radiation mediated by intercellular communication ('non-targeted effects'). To quantitatively understand the signalling system involved and the effects of radiation and to assess the role of this phenomenon in radiation-induced carcinogenesis, multi-scale modelling studies have been started. The proposed kinetic model takes into account (i) triggering of the effector function in cells in the vicinity of transformed cells, (ii) intercellular signalling between effector and transformed cells and (iii) execution of apoptosis in attacked cells. The systems model without radiation perturbance is reviewed. First results accounting for radiation-induced modulations of the signalling schemes are presented.

Impact Factor

Scopus SNIP

Web of Science
Times Cited

Scopus
Cited By

Altmetric

0.966

0.812