ArticleThe Journal of cell biology2000
Protein kinase C signaling mediates a program of cell cycle withdrawal in the intestinal epithelium.
Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 113 citations in OpenAlex.
- [Calcium, Vitamin D, and Colorectal Cancer].The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi · 2023Review
- PROTEIN KINASE C ALPHA IS A CENTRAL NODE FOR TUMORIGENIC TRANSCRIPTIONAL NETWORKS IN HUMAN PROSTATE CANCER.Cancer research communications · 2022Article
- The complexities of PKCα signaling in cancer.Advances in biological regulation · 2021Review
- Diacylglycerol-evoked activation of PKC and PKD isoforms in regulation of glucose and lipid metabolism: a review.Lipids in health and disease · 2020Review
- Article
- Dual Role of Bile Acids on the Biliary Epithelium: Friend or Foe?International journal of molecular sciences · 2019Review
- Crosstalk between PKCα and PI3K/AKT Signaling Is Tumor Suppressive in the Endometrium.Cell reports · 2018Article
- Lgr5The Journal of cell biology · 2018Article
- Protein Kinase Cα (PKCα) Is Resistant to Long Term Desensitization/Down-regulation by Prolonged Diacylglycerol Stimulation.The Journal of biological chemistry · 2016Article
- Review
- Differential regulation of cyclin D1 expression by protein kinase C α and ϵ signaling in intestinal epithelial cells.The Journal of biological chemistry · 2014Article
- miR-26a plays an important role in cell cycle regulation in ACTH-secreting pituitary adenomas by modulating protein kinase Cδ.Endocrinology · 2013Article
- C1B domain peptide of protein kinase Cγ significantly suppresses growth of human colon cancer cells in vitro and in an in vivo mouse xenograft model through induction of cell cycle arrest and apoptosis.Cancer biology & therapy · 2012Article
- Protein kinase C signaling and cell cycle regulation.Frontiers in immunology · 2012Article
- Protein kinase Cα signaling regulates inhibitor of DNA binding 1 in the intestinal epithelium.The Journal of biological chemistry · 2011Article
- Protein kinases and phosphatases in the control of cell fate.Enzyme research · 2011Article
- Protein kinase Cgamma in colon cancer cells: expression, Thr514 phosphorylation and sensitivity to butyrate-mediated upregulation as related to the degree of differentiation.Chemico-biological interactions · 2010Article
- Berberine suppresses intestinal disaccharidases with beneficial metabolic effects in diabetic states, evidences from in vivo and in vitro study.Naunyn-Schmiedeberg's archives of pharmacology · 2010Article
- Protein kinase C alpha-dependent signaling mediates endometrial cancer cell growth and tumorigenesis.International journal of cancer · 2009Article
- Stimulation of protein kinase C-alpha suppresses colon cancer cell proliferation by down-regulation of beta-catenin.Journal of cellular and molecular medicine · 2009Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Members of the protein kinase C (PKC) family of signal transduction molecules have been widely implicated in regulation of cell growth and differentiation, although the underlying molecular mechanisms involved remain poorly defined. Using combined in vitro and in vivo intestinal epithelial model systems, we demonstrate that PKC signaling can trigger a coordinated program of molecular events leading to cell cycle withdrawal into G(0). PKC activation in the IEC-18 intestinal crypt cell line resulted in rapid downregulation of D-type cyclins and differential induction of p21(waf1/cip1) and p27(kip1), thus targeting all of the major G(1)/S cyclin-dependent kinase complexes. These events were associated with coordinated alterations in expression and phosphorylation of the pocket proteins p107, pRb, and p130 that drive cells to exit the cell cycle into G(0) as indicated by concomitant downregulation of the DNA licensing factor cdc6. Manipulation of PKC isozyme levels in IEC-18 cells demonstrated that PKCalpha alone can trigger hallmark events of cell cycle withdrawal in intestinal epithelial cells. Notably, analysis of the developmental control of cell cycle regulatory molecules along the crypt-villus axis revealed that PKCalpha activation is appropriately positioned within intestinal crypts to trigger this program of cell cycle exit-specific events in situ. Together, these data point to PKCalpha as a key regulator of cell cycle withdrawal in the intestinal epithelium.
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Registered trials
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.