ArticleThe Journal of biological chemistry2015
Glucose deprivation triggers protein kinase C-dependent β-catenin proteasomal degradation.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 27 citations in OpenAlex.
- Impaired insulin secretion via the Wnt5a/β-catenin pathway contributes to diabetes development in pancreatic cancer.Experimental & molecular medicine · 2026Article
- Inhibiting autophagy enhances anti-cancer properties of sulforaphane.Scientific reports · 2026Article
- Regulation of LRRK2 activity by metabolic stress and heavy metal exposure.Brain research · 2025Article
- The Role of Protein Kinase C During the Differentiation of Stem and Precursor Cells into Tissue Cells.Biomedicines · 2024Review
- Muscle Proteome Analysis of Facioscapulohumeral Dystrophy Patients Reveals a Metabolic Rewiring Promoting Oxidative/Reductive Stress Contributing to the Loss of Muscle Function.Antioxidants (Basel, Switzerland) · 2024Article
- Glucose deprivation triggers DCAF1-mediated inactivation of Rheb-mTORC1 and promotes cancer cell survival.Cell death & disease · 2024Article
- BAMLET (Bovine α-lactalbumin made lethal to tumor cells) inhibits autophagy flux and induces apoptosis via down-regulation of protein kinase CK1α and attenuation of the AKT/p-ß-catenin (S552) pathway in RAS-mutated human colorectal HCT 116 cells.Iranian journal of basic medical sciences · 2023Article
- cPKCγ Deficiency Exacerbates Autophagy Impairment and Hyperphosphorylated Tau Buildup through the AMPK/mTOR Pathway in Mice with Type 1 Diabetes Mellitus.Neuroscience bulletin · 2022Article
- WNT/β-Catenin-Mediated Resistance to Glucose Deprivation in Glioblastoma Stem-like Cells.Cancers · 2022Article
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- Autophagy under glucose starvation enhances protein translation initiation in response to re-addition of glucose in C2C12 myotubes.FEBS open bio · 2020Article
- The roles of PKCs in regulating autophagy.Journal of cancer research and clinical oncology · 2018Review
- Developmental protein kinase C hyper-activation results in microcephaly and behavioral abnormalities in zebrafish.Translational psychiatry · 2018Article
- Protective effect of autophagy in neural ischemia and hypoxia: Negative regulation of the Wnt/β-catenin pathway.International journal of molecular medicine · 2017Article
- Phospholipid flippase ATP11C is endocytosed and downregulated following CaNature communications · 2017Article
- Protein kinase C ϵ stabilizes β-catenin and regulates its subcellular localization in podocytes.The Journal of biological chemistry · 2017Article
- The regulation of β-catenin activity and function in cancer: therapeutic opportunities.Oncotarget · 2017Review
- Galectin-3 supports stemness in ovarian cancer stem cells by activation of the Notch1 intracellular domain.Oncotarget · 2016Article
- Ablation of human telomerase reverse transcriptase (hTERT) induces cellular senescence in gastric cancer through a galectin-3 dependent mechanism.Oncotarget · 2016Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a conserved process that contributes to cell homeostasis. It is well known that induction mainly occurs in response to nutrient starvation, such as starvation of amino acids and insulin, and its mechanisms have been extensively characterized. However, the mechanisms behind cellular glucose deprivation-induced autophagy are as of now poorly understood. In the present study, we determined a mechanism by which glucose deprivation induced the PKC-dependent proteasomal degradation of β-catenin, leading to autophagy. Glucose deprivation was shown to cause a sub-G1 transition and enhancement of the LC3-II protein levels, whereas β-catenin protein underwent degradation in a proteasome-dependent manner. Moreover, the inhibition of GSK3β was unable to abolish the glucose deprivation-mediated β-catenin degradation or up-regulation of LC3-II protein levels, which suggested GSK3β-independent protein degradation. Intriguingly, the inhibition of PKCα using a pharmacological inhibitor and transfection of siRNA for PKCα was observed to effectively block glucose deprivation-induced β-catenin degradation as well as the increase in LC3-II levels and the accumulation of a sub-G1 population. Together, our results demonstrated a molecular mechanism by which glucose deprivation can induce the GSK3β-independent protein degradation of β-catenin, leading to autophagy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.