Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms19030776
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dc.titleEmerging roles of p53 family members in glucose metabolism
dc.contributor.authorItahana, Y
dc.contributor.authorItahana, K
dc.date.accessioned2020-10-30T02:08:58Z
dc.date.available2020-10-30T02:08:58Z
dc.date.issued2018
dc.identifier.citationItahana, Y, Itahana, K (2018). Emerging roles of p53 family members in glucose metabolism. International Journal of Molecular Sciences 19 (3) : 776. ScholarBank@NUS Repository. https://doi.org/10.3390/ijms19030776
dc.identifier.issn16616596
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/182088
dc.description.abstractGlucose is the key source for most organisms to provide energy, as well as the key source for metabolites to generate building blocks in cells. The deregulation of glucose homeostasis occurs in various diseases, including the enhanced aerobic glycolysis that is observed in cancers, and insulin resistance in diabetes. Although p53 is thought to suppress tumorigenesis primarily by inducing cell cycle arrest, apoptosis, and senescence in response to stress, the non-canonical functions of p53 in cellular energy homeostasis and metabolism are also emerging as critical factors for tumor suppression. Increasing evidence suggests that p53 plays a significant role in regulating glucose homeostasis. Furthermore, the p53 family members p63 and p73, as well as gain-of-function p53 mutants, are also involved in glucose metabolism. Indeed, how this protein family regulates cellular energy levels is complicated and difficult to disentangle. This review discusses the roles of the p53 family in multiple metabolic processes, such as glycolysis, gluconeogenesis, aerobic respiration, and autophagy. We also discuss how the dysregulation of the p53 family in these processes leads to diseases such as cancer and diabetes. Elucidating the complexities of the p53 family members in glucose homeostasis will improve our understanding of these diseases. © 2018 by the authors. Licensee MDPI, Basel, Switzerland.
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectglucose transporter 3
dc.subjectglucose transporter 4
dc.subjectmitochondrial transcription factor A
dc.subjectmonocarboxylate transporter 1
dc.subjectprotein p53
dc.subjectprotein p63
dc.subjectsirtuin 1
dc.subjectglucose
dc.subjectprotein p53
dc.subjectTP63 protein, human
dc.subjecttranscription factor
dc.subjecttumor protein p73
dc.subjecttumor suppressor protein
dc.subjectautophagy
dc.subjectdephosphorylation
dc.subjectdiabetes mellitus
dc.subjectelectron transport
dc.subjectepigenetics
dc.subjectgluconeogenesis
dc.subjectglucose metabolism
dc.subjectglucose transport
dc.subjectglycolysis
dc.subjecthuman
dc.subjectinsulin release
dc.subjectinsulin resistance
dc.subjectmitochondrial respiration
dc.subjectnonhuman
dc.subjectoxidative phosphorylation
dc.subjectpentose phosphate cycle
dc.subjectprotein expression
dc.subjectReview
dc.subjecttranscription regulation
dc.subjectanimal
dc.subjectgenetics
dc.subjectglycolysis
dc.subjectmetabolism
dc.subjectmutation
dc.subjectAnimals
dc.subjectGlucose
dc.subjectGlycolysis
dc.subjectHumans
dc.subjectMutation
dc.subjectTranscription Factors
dc.subjectTumor Protein p73
dc.subjectTumor Suppressor Protein p53
dc.subjectTumor Suppressor Proteins
dc.typeReview
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.3390/ijms19030776
dc.description.sourcetitleInternational Journal of Molecular Sciences
dc.description.volume19
dc.description.issue3
dc.description.page776
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