Systems biology of JAK-STAT signalling in human malignancies

被引：60

作者：

Vera, Julio ^{[1
]}

Rateitschak, Katja ^{[1
]}

Lange, Falko ^{[1
,2
]}

Kossow, Christina ^{[1
]}

Wolkenhauer, Olaf ^{[1
]}

Jaster, Robert ^{[2
]}

机构：

[1] Univ Rostock, Dept Syst Biol & Bioinformat, D-18051 Rostock, Germany

[2] Univ Rostock, Fac Med, Div Gastroenterol, Dept Med 2, D-18057 Rostock, Germany

来源：

PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY | 2011年 / 106卷 / 02期

关键词：

JAK-STAT; Cell signalling; Interferon-gamma; Pancreatic stellate cell; STAT1; Mathematical modelling; CHRONIC MYELOGENOUS LEUKEMIA; ERYTHROPOIETIN RECEPTOR; MATHEMATICAL-MODEL; PANCREATIC-CANCER; LYMPHOMA; MUTATION; GENE; HEMATOPOIESIS; TRANSDUCTION; ACTIVATION;

D O I：

10.1016/j.pbiomolbio.2011.06.013

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Originally implicated in the regulation of survival, proliferation and differentiation of haematopoietic cells, the JAK-STAT pathway has also been linked to developmental processes, growth control and maintenance of homeostasis in a variety of other cells and tissues. Although it remains a complex system, its relative simplicity and the availability of molecular data makes it particularly attractive for modelling approaches. In this review, we will focus on JAK-STAT signalling in the context of cancer and present efforts to investigate signalling dynamics with the help of mathematical models. We describe the modelling workflow that realises a systems biology approach and give an example for interferon-gamma signalling in pancreatic stellate cells. (C) 2011 Elsevier Ltd. All rights reserved.

引用

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页码：426 / 434

页数：9

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