He regulation of diverse vital metabolic processes which include cell division. Longterm jet leg impact can disrupt the circadian clock Actin Cytoskeleton Inhibitors MedChemExpress organization, hence, causing deregulated cellular proliferation and tumor growth. This study employed a variety of formal procedures which get started with model checking for the inference of logical parameters. These parameters are then utilised for the generation of a logical regulatory graph which is lastly converted to towards 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 one hand,Hassan et al. (2018), PeerJ, DOI 10.7717/peerj.20/it controls the expression of oncogenic protein MYC although however it suppresses proliferation of damaged cells by regulating the activation of p53. Maintaining in view the simulation results obtained just after modeling the effects of jet lag on circadian clock, it may be stated that alterations in sleep/wake and light/dark cycles trigger 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. As a result, it truly is concluded that a effectively functioning circadian clock is essential for making certain a tumor no cost technique.ACKNOWLEDGEMENTSWe would prefer to convey our gratitude to Mr. Resorufin methyl ether Cytochrome P450 Muhammad Tariq Saeed (Assistant Professor, RCMS, NUST) for delivering guidance with regards to qualitative modeling.Further Facts AND DECLARATIONSFundingThis study was supported by the Greater Education Commission of Pakistan (HEC), by way of award of research grant (Grant no. 20-4599/R D/HEC/14/138). The funders had no part in study design, data collection and analysis, selection to publish, or preparation in 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 you will discover no competing interests.Author ContributionsAzka Hassan performed the experiments, analyzed the information, ready figures and/or tables, authored or reviewed drafts of your paper, approved the final draft. Jamil Ahmad conceived and created the experiments, performed the experiments, analyzed the information, contributed reagents/materials/analysis tools, authored or reviewed drafts with the paper, authorized the final draft. Hufsah Ashraf and Amjad Ali analyzed the data, authored or reviewed drafts from the paper, authorized the final draft.Information AvailabilityThe following data was supplied relating to data availability: The raw data are incorporated within the Supplemental Files.Supplemental InformationSupplemental details for this article could be identified 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 harm checkpoint plus the spindle assembly checkpoint (SAC), manage the fidelity of chromosome segregation. The DNA damage checkpoint responds to various 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 towards the signal transduction network in budding.