Gene expression profiles of MCF7 cells treated with NB001
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE198111 | GEO | 2022/03/08
REPOSITORIES: GEO
Similar Datasets
Project description:Nociceptive neuropeptide CGRP acts directly on HSCs via the its receptor RAMP1/CALCRL, to promote egress by activating Gαs/Adenylyl cyclase/cAMP pathway.
2020-10-12 | GSE156449 | GEO
Project description:Cyclic nucleotides are important signalling molecules across evolution, but their roles in malaria parasites are poorly understood. We have investigated the role of cAMP in asexual blood stage development of Plasmodium falciparum through conditional disruption of adenylyl cyclase (ACβ) and its downstream effector, cAMP-dependent protein kinase (PKA). We show that both production of cAMP and activity of PKA are critical for erythrocyte invasion, whilst key developmental steps that precede invasion still take place in the absence of cAMP-dependent signalling. We also show that another protein with putative cyclic nucleotide binding sites, PfEpac, does not play an essential role in cyclic nucleotide signalling in blood stages. We identify over 2,000 sites whose phosphorylation is dependent on cAMP signalling and we provide mechanistic insight as to how cAMP-dependent phosphorylation of the cytoplasmic domain of the essential invasion adhesin apical membrane antigen 1 (AMA1) controls erythrocyte invasion.
2019-05-14 | PXD012143 | Pride
Project description:Human infertility has become a medical and social health problem globally. Mice deficient in type 3 adenylyl cyclase (AC3), a key enzyme that synthesizes cyclic adenosine monophosphate (cAMP), develop male infertility but its underlying molecular mechanisms are still unknown. Here, we performed label-free quantitative (LFQ) proteomics study to identify testicular differentially expressed proteins (DEPs) and their respective biological processes.
2021-07-19 | PXD027382 |
Project description:Astrocytes contain the majority of the brain’s supply of glycogen which has been suggested to play an important role in neuronal synaptic plasticity. This may be mediated by release of glycogen-derived lactate or glutamine supporting neuronal metabolism or via induction of neuronal signaling pathways. The second messenger cyclic AMP (cAMP) can induce glycogen breakdown and activation of cytosolic soluble adenylyl cyclase (sAC) in astrocytes has been suggested to be the link between neuronal depolarization and glycogen breakdown. However, recent studies have revealed that sAC residing in the mitochondria rather than the cytosol is regulating mitochondrial bioenergetics, and that employing pharmacological inhibitors of sAC significantly alters cellular energy metabolism. This effect on energy metabolism could influence the interpretation of previous studies employing pharmacological inhibition of sAC. Here, we show that pharmacological inhibition of sAC lowers mitochondrial respiration, induces phosphorylation of the metabolic master switch AMPK, and decreases glycogen stores in cultured astrocytes. In light of this, we discuss the pharmacological challenges of investigating the functional and metabolic roles of sAC in astrocytes.
2021-08-13 | PXD027901 | Pride
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.
2005-01-01 | MODEL1006230118 | BioModels
Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT) Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment.
2009-08-25 | GSE17777 | GEO
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.
2009-09-26 | GSE17338 | GEO
Project description:Human microvascular endothelial cells (HMVEC) treated with vascular endothelial growth factor (VEGF), Antrhax Edema Toxin (ET), or the Epac activator, 8-pCPT-2'-O-Me-cAMP (8CPT); Human microvascular endothelial cells (HMVEC) were treated with VEGF alone or VEGF in combination with either the the Epac-specific cAMP-mimetic, 8-pCPT-2'-O-Me-cAMP (8CPT), or anthrax edema toxin (ET), an adenylyl cyclase. ET or 8CPT can inhibit VEGF-mediated chemotaxis and angiogenesis. The goal of the study was to identify genes regulated by cAMP production (ET) or by activation of Epac/Rap (8CPT) that may mitigate the effects of VEGF treatment. Experiment Overall Design: Gene expression was measured 4 hours after treatment with VEGF, VEGF + 8CPT, VEGF + ET or mock treatment. Each sample contained one replicate.
2009-09-13 | E-GEOD-17777 | biostudies-arrayexpress
Project description:The whooping cough agent, Bordetella pertussis, subverts dendritic cell (DCs) functions through powerful immunomodulatory activities of its toxins. Here we focused on the signaling action of the adenylate cyclase toxin (CyaA) that targets myeloid cells expressing the αMβ2 integrin CD11b/CD18 (known as complement receptor 3 (CR3) or Mac-1). CyaA delivers an extremely catalytically potent adenylyl cyclase enzyme domain into the cytosol of phagocytes and disrupts their innate and adaptive immune functions through unregulated production of the key signaling molecule cAMP. Here we describe the global phosphoproteomic analysis of cAMP signaling in murine bone marrow-derived DCs exposed to CyaA. Gathered data reveal toxin-triggered alternations of phosphorylation status of proteins regulating actin cytoskeleton, chromatin remodeling, mTOR activity and IL-10 gene expression. The reported findings highlight the complexity of subversive physiological manipulation that is exerted on myeloid phagocytes by the cAMP-generating adenylate cyclase toxin of Bordetellae.
2017-11-29 | PXD004733 | Pride
Project description:Here we report the gene expression profile of in vitro cultured human endometrial stromal cells treated with siRNA targeting FOXO1 piror to eutherian differentiation media exposure. The eutherian differentiation media contains cyclic AMP (cAMP) analogue 8-Br-cAMP and the progesterone (P4) analogue medroxyprogesterone acetate (MPA).
2018-06-21 | GSE115832 | GEO