Gene expression profiles of MCF7 cells treated with NB001
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE198111 | GEO | 2022/03/08
REPOSITORIES: GEO
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Project description:This a model from the article:
Modeling beta-adrenergic control of cardiac myocyte contractility in silico.
Saucerman JJ, Brunton LL, Michailova AP, McCulloch AD. J Biol Chem
2003 Nov 28;278(48):47997-8003 12972422
,
Abstract:
The beta-adrenergic signaling pathway regulates cardiac myocyte contractility
through a combination of feedforward and feedback mechanisms. We used systems
analysis to investigate how the components and topology of this signaling
network permit neurohormonal control of excitation-contraction coupling in the
rat ventricular myocyte. A kinetic model integrating beta-adrenergic signaling
with excitation-contraction coupling was formulated, and each subsystem was
validated with independent biochemical and physiological measurements. Model
analysis was used to investigate quantitatively the effects of specific
molecular perturbations. 3-Fold overexpression of adenylyl cyclase in the model
allowed an 85% higher rate of cyclic AMP synthesis than an equivalent
overexpression of beta 1-adrenergic receptor, and manipulating the affinity of
Gs alpha for adenylyl cyclase was a more potent regulator of cyclic AMP
production. The model predicted that less than 40% of adenylyl cyclase molecules
may be stimulated under maximal receptor activation, and an experimental
protocol is suggested for validating this prediction. The model also predicted
that the endogenous heat-stable protein kinase inhibitor may enhance basal
cyclic AMP buffering by 68% and increasing the apparent Hill coefficient of
protein kinase A activation from 1.0 to 2.0. Finally, phosphorylation of the
L-type calcium channel and phospholamban were found sufficient to predict the
dominant changes in myocyte contractility, including a 2.6x increase in systolic
calcium (inotropy) and a 28% decrease in calcium half-relaxation time
(lusitropy). By performing systems analysis, the consequences of molecular
perturbations in the beta-adrenergic signaling network may be understood within
the context of integrative cellular physiology.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Saucerman JJ, Brunton LL, Michailova AP, McCulloch AD. (2003) - version=1.0
The original CellML model was created by:
Geoffrey Nunns
gnunns1@jhu.edu
The University of Auckland
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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Project description:The cAMP-pathway plays a central role in regulation of growth, differentiation, and virulence of human pathogenic fungi, including Cryptococcus neoformans. Three major upstream signaling regulators of the adenylyl cyclase (Cac1), Ras, Aca1 (Adenylyl cyclase-associated protein 1) and G-alpha subunit protein (Gpa1), have been identified to control the cAMP-pathway in C. neoformans, but their functional relationship remains elusive. Here we performed genome-wide transcriptome analysis with C. neoformans ras1, gpa1, cac1, aca1, and pka1 pka2 mutants by DNA microarray. The aca1, gpa1, cac1, and pka1 pka2 mutants displayed similar transcriptome patterns to each other whereas the ras1 mutant exhibited distinctive transcriptome patterns compared to WT and the cAMP mutants. Interestingly, a number of environmental stress response genes are differentially modulated in the ras1 and cAMP mutants. In fact, the Ras1-signaling pathway was found to be involved in osmotic and genotoxic stress response, and maintenance of cell wall integrity via the Cdc24-dependent signaling pathway. Through this microarray analysis, we have identified a number of cAMP-dependent genes, including GRE2, HSP12, ENA1, TCO2, PKP2, CAT1, in C. neoformans. Notably, a majority of ergosterol biosynthesis genes were found to be upregulated in the cAMP mutants. Interestingly, the gpa1, cac1, and pka1 mutants, but not the aca1 and pka2 mutants were hypersensitive to amphotericin B, but resistant to fluconazole. In conclusion, we demonstrated in this study that the Ras1- and cAMP-signaling pathways are involved in stress response and sterol biosynthesis of C. neoformans. There are more than 95% of genome homology between JEC21 and H99. Therefore 100 slides of JEC21 (cryptococcus neoformans var. neoformans serotype D) 70-mer oligo are used in this analysis, 3 biological replicate experiments are performed, total RNAs are extracted with 6 strains from H99 (H99 Wild type strain (Cryptococcus neoformans var. grubii serotype A), ras1Î, aca1Î, gpa1Î, cac1Î, pka1Îpka2Î), We use the mixed all of total RNAs from this experiment as a control RNA. We use Cy5 as Sample dye and Cy3 as a control dye. several sample are dye swaped.
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