{"database":"BioModels","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Xml":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1812040001?filename=Model.xml"],"Other":["https://www.ebi.ac.uk/biomodels/model/download/MODEL1812040001?filename=V2.cps"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"submitter":["Sarubini Kananathan"],"curationStatus":["Non-curated"],"levelVersion":["L2V4"],"full_dataset_link":["https://www.ebi.ac.uk/biomodels/MODEL1812040001"],"publication_pubmed":["24345497"],"isPrivate":["false"],"repository":["BioModels"],"omics_type":["Models"],"modelFormat":["SBML"],"tokenised_name":["Bedessem2014   HiF 1 a  mediated response to hypoxia on the G1/S transition"],"publication_year":["2014"],"submissionId":["MODEL1812040001"],"publication_authors":["B Bedessem, Angélique Stéphanou"],"first_author":["B Bedessem"],"publication":["24345497,\n                            Hypoxia is known to influence the cell cycle by increasing the G1 phase duration or by inducing a quiescent state (arrest of cell proliferation). This entry into quiescence is a mean for the cell to escape from hypoxia-induced apoptosis. It is suggested that some cancer cells have gain the advantage over normal cells to easily enter into quiescence when environmental conditions, such as oxygen pressure, are unfavorable [43,1]. This ability contributes in the appearance of highly resistant and aggressive tumor phenotypes [2]. The HiF-1α factor is the key actor of the intracellular hypoxia pathway. As tumor cells undergo chronic hypoxic conditions, HiF-1α is present in higher level in cancer than in normal cells. Besides, it was shown that genetic mutations promoting overstabilization of HiF-1α are a feature of various types of cancers [7]. Finally, it is suggested that the intracellular level of HiF-1α can be related to the aggressiveness of the tumors [53,24,4,10]. However, up to now, mathematical models describing the G1/S transition under hypoxia, did not take into account the HiF-1α factor in the hypoxia pathway. Therefore, we propose a mathematical model of the G1/S transition under hypoxia, which explicitly integrates the HiF-1α pathway. The model reproduces the slowing down of G1 phase under moderate hypoxia, and the entry into quiescence of proliferating cells under severe hypoxia. We show how the inhibition of cyclin D by HiF-1α can induce quiescence; this result provides a theoretical explanation to the experimental observations of Wen et al. (2010) [50]. Thus, our model confirms that hypoxia-induced chemoresistance can be linked, for a part, to the negative regulation of cyclin D by HiF-1α.. null, 248.\n                            UJF-Grenoble 1, CNRS, Laboratory TIMC-IMAG/DyCTIM, UMR 5525, 38041 Grenoble, France. Electronic address: Baptiste.Bedessem@imag.fr."],"submitter_mail":["skananathan@ebi.ac.uk"],"submitter_affiliation":["EMBL-EBI"],"pubmed_abstract":["Hypoxia is known to influence the cell cycle by increasing the G1 phase duration or by inducing a quiescent state (arrest of cell proliferation). This entry into quiescence is a mean for the cell to escape from hypoxia-induced apoptosis. It is suggested that some cancer cells have gain the advantage over normal cells to easily enter into quiescence when environmental conditions, such as oxygen pressure, are unfavorable [43,1]. This ability contributes in the appearance of highly resistant and aggressive tumor phenotypes [2]. The HiF-1α factor is the key actor of the intracellular hypoxia pathway. As tumor cells undergo chronic hypoxic conditions, HiF-1α is present in higher level in cancer than in normal cells. Besides, it was shown that genetic mutations promoting overstabilization of HiF-1α are a feature of various types of cancers [7]. Finally, it is suggested that the intracellular level of HiF-1α can be related to the aggressiveness of the tumors [53,24,4,10]. However, up to now, mathematical models describing the G1/S transition under hypoxia, did not take into account the HiF-1α factor in the hypoxia pathway. Therefore, we propose a mathematical model of the G1/S transition under hypoxia, which explicitly integrates the HiF-1α pathway. The model reproduces the slowing down of G1 phase under moderate hypoxia, and the entry into quiescence of proliferating cells under severe hypoxia. We show how the inhibition of cyclin D by HiF-1α can induce quiescence; this result provides a theoretical explanation to the experimental observations of Wen et al. (2010) [50]. Thus, our model confirms that hypoxia-induced chemoresistance can be linked, for a part, to the negative regulation of cyclin D by HiF-1α."],"pubmed_title":["A mathematical model of HiF-1α-mediated response to hypoxia on the G1/S transition."],"pubmed_authors":["Bedessem B B, Stéphanou A A"],"additional_accession":[]},"is_claimable":false,"name":"Bedessem2014 - HiF-1 a -mediated response to hypoxia on the G1/S transition","description":"No description","dates":{"last_modification":"2018-12-04","publication":"2018-12-04","submission":"2018-12-04"},"accession":"MODEL1812040001","cross_references":{"pubmed":["24345497"],"biomodels__db":["MODEL1812040001"]}}