Expression data from PonA stimulated transfected U373 Cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE18798 | GEO | 2010/10/01
SECONDARY ACCESSION(S): PRJNA121207
REPOSITORIES: GEO
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Project description:The consitutive activation of the JAK/STAT signalling cascade is reponsible for the majority of meyoproliferative disorders in humans, a disease that is also conserved in Drosophila. A gain-of-function mutation in the Drosophila JAK kinase leads to blood cell (haemocyte) overproliferation which eventually is manifested as black melanotic tumors. Haemocyte-like Drosophila Kc167 cells were used to identify downstream target genes of the JAK/STAT pathway which may be responsible for tumour generation and progression. Experiment Overall Design: Kc167 cells were activated with the principal JAK/STAT pathway ligand Unpaired (UPD) in a time course manner. To this end, for each transcript profiling condition and time point, biological duplicates were activated with UPD or Mock conditioned media for 30 min, and total RNA was extracted 2, 4 or 10h after initial addition of conditioned media. 12 samples were used for hybridization to the arrays.
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Project description:NCBS Curation Comments:
This model shows the control mechanism of Jak-Stat pathway, here SOCS1 (Suppressor of cytokine signaling-I) was identified as the negative regulator of Jak and STAT signal transduction pathway. This is the knockout version of Jak-Stat pathway in this model the SOCS1 has been knocked out i.e it formation is not shown. The graphs are almost similar to the graphs as shown in the paper but STAT1n graph has some ambiguities. Thanks to Dr Satoshi Yamada for clarifying some of those ambiguities and providing the values used in simulations.
Biomodels Curation Comments:
The model reproduces the figures 2 (B,D,F,H,J,L,N) corresponding to JAK/STAT activation in SOCS1 knock out cells. The model was successfully tested on MathSBML
This model originates from BioModels Database: A Database of Annotated Published Models. It is copyright (c) 2005-2006 The BioModels Team.
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2007-01-26 | BIOMD0000000094 | BioModels