Notes

These mitotic cells will slip through this forced mitosis, leading to gross micronucleation and apoptotic cell death. This is consistent with my observations, given that p downregulation was able to enhance micronuclei formation and also support precocious GM transition, giving rise to CIN.However, I could not detect an increase in gammaHAX foci to prove my hypothesis that decrease in p levels can result in inefficient DNA damage repair in preceding interphase leading to enhanced micronuclei formation in my system. There are two theoretically possible mechanisms by which a decrease in the activity of the cGASSTINGTBKIRF pathway might downregulate p.One is that the decrease in p levels is a consequence of transcriptional changes that would otherwise be controlled by cGASSTING pathway, which is now depleted, a possibility based on the fact that p levels are mainly regulated at the transcriptional level via various mechanisms.This mechanism predicts the possible involvement of IRF andor NFB transcriptional activity.The second possible mechanism is that changes in p levels that occur after depletion of the cGASSTING pathway are attributable to posttranslational changes.The halflife of p in actively dividing cells has been reported to be min. These observations suggest the need for additional studies on the possible association between the cGASSTINGTBKIRF axis and posttranslational modification of p protein.My ongoing efforts are focused on deciphering the precise mechanism underlying cGASSTING pathwaydependent regulation of p levels.Thus, proposing for the first time another previously unknown role of cGASSTINGTBKIRF innate immunity pathway during cellcycle progression.I have provided reproducible and tangible results supporting the fact that cGASSTING pathway regulates p levels that are otherwise necessary for proper cellcycle progression.Irradiation induces cancer lung metastasis through activation of the cGASSTINGCCL pathway in mesenchymal stromal cells.DNA damage enhancement by radiotherapyactivated hafnium oxide nanoparticles improves cGASSTING pathway activation in human colorectal cancer cells.The emerging links between chromosomal instability, metastasis, inflammation and tumour immunity.Chromosomal instability drives metastasis through a cytosolic DNA response.Tank binding kinase is a centrosomeassociated kinase necessary for microtubule dynamics and mitosis.Interferon regulatory factor activates pdependent cell growth inhibition.Molecular mechanisms of micronucleus, nucleoplasmic bridge and nuclear bud formation in mammalian and human cells.Geldanamycin promotes premature mitotic entry and micronucleation in irradiated pp deficient colon carcinoma cells.Oncogenic potential of a dominant negative mutant of interferon regulatory factor. Chk is a wee kinase in the G DNA damage checkpoint inhibiting cdc by Y phosphorylation.Cell Death Differ. T he prevalence of systemic allergic reactions seems to be higher in highly exposed populations such as beekeepers and individuals receiving live bee acupuncture. H owever, there are a very few of studies on venom allergy in these populations.Weperformed two observational studies to describe the characteristics and risk factors of venom allergy in beekeepers and the L population.M ethods: A total of beekeepers and individuals receiving live bee acupuncture were interviewed.S kin prick tests were performed on subjects with suspected bee venom allergy.R esults: T he prevalence of bee venom allergy was stings per year and. in the L population.of the L population, and. fold sting per year group.C onversely, in the L stings per week and population, compared to L stings per week, the adjusted O of venom allergy was. T he knowledge of adrenaline and venom immunotherapy was limited in both beekeepers and traditional doctors.