He regulation of distinct crucial metabolic processes for example cell division. Longterm jet leg impact can disrupt the circadian clock organization, as a result, causing deregulated cellular proliferation and tumor growth. This study employed many formal strategies which start off with model checking for the inference of logical parameters. These parameters are then employed for the generation of a logical regulatory graph which is ultimately converted to for the Petri net model to acquire deep insights in to the circadian technique and analyze its behavior in normal and jet lag conditions. The model presented within this study depicts that circadian clock plays a dual role in cell cycle progression. On a single hand,Hassan et al. (2018), PeerJ, DOI ten.7717/peerj.20/it controls the expression of oncogenic protein MYC while on the other hand it suppresses proliferation of damaged cells by regulating the activation of p53. Keeping in view the simulation outcomes obtained just after modeling the effects of jet lag on circadian clock, it could be stated that alterations in sleep/wake and light/dark cycles lead to circadian disruption. This disruption negatively impacts the expression of important cell cycle genes MYC and p53. The expression levels of p53 are suppressed resulting in persistently higher expression of MYC. This condition favors the proliferation of tumor cells. Hence, it’s concluded that a adequately functioning circadian clock is required for ensuring a tumor totally free method.ACKNOWLEDGEMENTSWe would like to convey our AQP Inhibitors Related Products gratitude to Mr. Muhammad Tariq Saeed (Assistant Professor, RCMS, NUST) for offering guidance with regards to qualitative modeling.Additional Info AND DECLARATIONSFundingThis study was supported by the Higher Education Commission of Pakistan (HEC), via award of investigation grant (Grant no. 20-4599/R D/HEC/14/138). The XY028-133 supplier funders had no part in study style, data collection and analysis, decision to publish, or preparation on the manuscript.Grant DisclosuresThe following grant facts was disclosed by the authors: Greater Education Commission of Pakistan (HEC): 20-4599/R D/HEC/14/138.Competing InterestsThe authors declare there are no competing interests.Author ContributionsAzka Hassan performed the experiments, analyzed the data, prepared figures and/or tables, authored or reviewed drafts of the paper, approved the final draft. Jamil Ahmad conceived and made the experiments, performed the experiments, analyzed the information, contributed reagents/materials/analysis tools, authored or reviewed drafts of the paper, approved the final draft. Hufsah Ashraf and Amjad Ali analyzed the information, authored or reviewed drafts of your paper, approved the final draft.Data AvailabilityThe following information was supplied with regards to data availability: The raw information are integrated within the Supplemental Files.Supplemental InformationSupplemental information for this short article could be found on line at http://dx.doi.org/10.7717/ peerj.4877#supplemental-information.Hassan et al. (2018), PeerJ, DOI 10.7717/peerj.21/Two evolutionarily conserved checkpoints, the DNA damage checkpoint and the spindle assembly checkpoint (SAC), control the fidelity of chromosome segregation. The DNA harm checkpoint responds to several different DNA lesions and controls entry into S phase, completion of S phase and entry into mitosis [1,2]. The DNA damage checkpoint can be a signal transduction network consisting of sensors, signal transducers and downstream effectors. Central for the signal transduction network in budding.
