He regulation of unique important metabolic processes which include cell division. Longterm jet leg impact can disrupt the circadian clock organization, hence, causing deregulated cellular proliferation and tumor growth. This study employed N-Acetyl-D-cysteine Autophagy several formal approaches which commence with model checking for the inference of logical parameters. These parameters are then applied for the generation of a logical regulatory graph which can be lastly converted to towards the Petri net model to acquire deep insights into the circadian program and analyze its behavior in standard and jet lag conditions. The model presented in this study depicts that circadian clock plays a dual role in cell cycle progression. On 1 hand,Hassan et al. (2018), PeerJ, DOI 10.7717/peerj.20/it controls the expression of oncogenic protein MYC whilst alternatively it suppresses proliferation of broken cells by regulating the activation of p53. Keeping in view the simulation outcomes obtained immediately after modeling the effects of jet lag on circadian clock, it may be stated that alterations in sleep/wake and light/dark cycles cause circadian disruption. This disruption negatively impacts the expression of essential cell cycle genes MYC and p53. The expression levels of p53 are suppressed resulting in persistently high expression of MYC. This condition favors the proliferation of tumor cells. Therefore, it’s concluded that a correctly functioning circadian clock is needed for ensuring a tumor free system.ACKNOWLEDGEMENTSWe would like to convey our gratitude to Mr. Muhammad Tariq Saeed (Assistant Professor, RCMS, NUST) for supplying guidance with regards to qualitative modeling.Additional Data AND DECLARATIONSFundingThis study was supported by the Larger Education Commission of Pakistan (HEC), via award of research grant (Grant no. 20-4599/R D/HEC/14/138). The funders had no role in study style, information collection and evaluation, selection to publish, or preparation of your manuscript.Grant DisclosuresThe following grant data was disclosed by the authors: Greater Education Commission of Pakistan (HEC): 20-4599/R D/HEC/14/138.Competing InterestsThe authors declare you can find no competing interests.Author ContributionsAzka Hassan performed the experiments, analyzed the data, prepared figures and/or tables, authored or reviewed drafts in the paper, authorized 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 on the paper, approved 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 facts was supplied regarding information availability: The raw information are incorporated in the Supplemental Files.Supplemental InformationSupplemental data for this short article might be discovered 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 plus the spindle assembly checkpoint (SAC), manage the fidelity of chromosome segregation. The DNA harm checkpoint responds to various DNA lesions and controls entry into S phase, completion of S phase and entry into mitosis [1,2]. The DNA harm checkpoint is a signal transduction network consisting of sensors, signal transducers and downstream effectors. Central towards the signal transduction network in budding.
