ArticleThe Journal of biological chemistry2008
G0 function of BCL2 and BCL-xL requires BAX, BAK, and p27 phosphorylation by Mirk, revealing a novel role of BAX and BAK in quiescence regulation.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 66 citations in OpenAlex.
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- The Effects of Resveratrol, Gallic Acid, and Piperine on the Expression of miR-17, miR-92b, miR-181a, miR-222, BAX, BCL-2, MCL-1, WT1, c-Kit, and CEBPA in Human Acute Myeloid Leukemia Cells and Their Roles in Apoptosis.Biochemical genetics · 2024Article
- Caloric Restriction Mitigates Kidney Fibrosis in an Aged and Obese Rat Model.Antioxidants (Basel, Switzerland) · 2023Article
- Expression and significance of cyclin D1, cyclin-dependent kinase 4 and cyclin-dependent kinase inhibitor P27 in patients with non-neoplastic epithelial disorders of the vulva.Experimental and therapeutic medicine · 2023Article
- Bcl-xL Enforces a Slow-Cycling State Necessary for Survival in the Nutrient-Deprived Microenvironment of Pancreatic Cancer.Cancer research · 2022Article
- Targeting DYRK1A/B kinases to modulate p21-cyclin D1-p27 signalling and induce anti-tumour activity in a model of human glioblastoma.Journal of cellular and molecular medicine · 2021Article
- A proteomic analysis of Bcl-2 regulation of cell cycle arrest: insight into the mechanisms.Journal of Zhejiang University. Science. B · 2021Article
- Serum deprivation initiates adaptation and survival to oxidative stress in prostate cancer cells.Scientific reports · 2020Article
- Delayed endometrial decidualisation in polycystic ovary syndrome; the role of AR-MAGEA11.Journal of molecular medicine (Berlin, Germany) · 2019Article
- Expression of Bcl-2 is a favorable prognostic biomarker in lung squamous cell carcinoma.Oncology letters · 2018Article
- When BAX doesn't kill.Cell cycle (Georgetown, Tex.) · 2018Article
- Bax, Bcl-2, and Bax/Bcl-2 as prognostic markers in acute myeloid leukemia: are we ready for Bcl-2-directed therapy?Cancer management and research · 2018Article
- Transcriptional Profiling of Quiescent Muscle Stem Cells In Vivo.Cell reports · 2017Article
- Article
- Bcl-2 delays cell cycle through mitochondrial ATP and ROS.Cell cycle (Georgetown, Tex.) · 2017Article
- Cell cycle progression dictates the requirement for BCL2 in natural killer cell survival.The Journal of experimental medicine · 2017Article
- The pro-apoptotic BAX protein influences cell growth and differentiation from the nucleus in healthy interphasic cells.Cell cycle (Georgetown, Tex.) · 2017Article
- Article
- Article
- BCL-xL/MCL-1 inhibition and RARγ antagonism work cooperatively in human HL60 leukemia cells.Experimental cell research · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
BCL2 and BCL-x(L) facilitate G(0) quiescence by decreasing RNA content and cell size and up-regulating p27 protein, but the precise mechanism is not understood. We investigated the relationship between cell cycle regulation and the anti-apoptosis function of BCL2 and BCL-x(L). Neither caspase inhibition nor abrogation of mitochondria-dependent apoptosis by BAX and BAK deletion fully recapitulated the G(0) effects of BCL2 or BCL-x(L), suggesting that mechanisms in addition to anti-apoptosis are involved in the cell cycle arrest function of BCL2 or BCL-x(L). We found that BCL2 and BCL-x(L) expression in bax(-/-) bak(-/-) cells did not confer cell cycle effects, consistent with the G(0) function of BCL2 and BCL-x(L) being mediated through BAX or BAK. Stabilization of p27 in G(0) in BCL2 or BCL-x(L) cells was due to phosphorylation of p27 at Ser(10) by the kinase Mirk. In bax(-/-) bak(-/-) cells, total p27 and p27 phosphorylated at Ser(10) were elevated. Re-expression of BAX in bax(-/-) bak(-/-) cells and silencing of BAX and BAK in wild type cells confirmed that endogenous BAX and BAK modulated p27. These data revealed a novel role for BAX and BAK in the regulation of G(0) quiescence.
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