ArticleThe Journal of biological chemistry2011
Protein kinase C (PKC) delta suppresses keratinocyte proliferation by increasing p21(Cip1) level by a KLF4 transcription factor-dependent mechanism.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Distinct senotypes in p16- and p21-positive cells across human and mouse aging tissues.The EMBO journal · 2025Article
- Aloe polysaccharide promotes keratinocyte proliferation, migration, and differentiation by upregulating the EGFR/PKC-dependent signaling pathways.Scientific reports · 2025Article
- Epidermal growth factor receptor-dependent stimulation of differentiation by human papillomavirus type 16 E5.Virology · 2024Article
- KLF4 regulates skeletal muscle development and regeneration by directly targeting P57 and Myomixer.Cell death & disease · 2023Article
- Mesothelioma cancer cells are glutamine addicted and glutamine restriction reduces YAP1 signaling to attenuate tumor formation.Molecular carcinogenesis · 2023Article
- Selective targeting of α7 nicotinic acetylcholine receptor by synthetic peptide mimicking loop I of human SLURP-1 provides efficient and prolonged therapy of epidermoid carcinomaFrontiers in cell and developmental biology · 2023Article
- Review
- Transglutaminase 2 enhances hepatocyte growth factor signaling to drive the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2022Article
- Transglutaminase 2 Maintains Hepatocyte Growth Factor Signaling to Enhance the Cancer Cell Phenotype.Molecular cancer research : MCR · 2021Article
- Sulforaphane inhibits PRMT5 and MEP50 function to suppress the mesothelioma cancer cell phenotype.Molecular carcinogenesis · 2021Article
- C1q/TNF-Related Protein 9 Attenuates Atherosclerosis by Inhibiting Hyperglycemia-Induced Endothelial Cell Senescence Through the AMPKα/KLF4 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Kruppel-like factor 4 upregulates matrix metalloproteinase 13 expression in chondrocytes via mRNA stabilization.Cell and tissue research · 2020Article
- Zebrafish Klf4 maintains the ionocyte progenitor population by regulating epidermal stem cell proliferation and lateral inhibition.PLoS genetics · 2019Article
- Role of FGFR2b expression and signaling in keratinocyte differentiation: sequential involvement of PKCδ and PKCα.Cell death & disease · 2018Article
- Embryonic AP1 Transcription Factor Deficiency Causes a Collodion Baby-Like Phenotype.The Journal of investigative dermatology · 2017Article
- K48-linked KLF4 ubiquitination by E3 ligase Mule controls T-cell proliferation and cell cycle progression.Nature communications · 2017Article
- Inhibition of apoptosis signal-regulating kinase 1 alters the wound epidermis and enhances auricular cartilage regeneration.PloS one · 2017Article
- MicroRNA-346 regulates neural stem cell proliferation and differentiation by targeting KLF4.American journal of translational research · 2017Article
- DNMT1 Regulates Epithelial-Mesenchymal Transition and Cancer Stem Cells, Which Promotes Prostate Cancer Metastasis.Neoplasia (New York, N.Y.) · 2016Article
- Lipin-1 expression is critical for keratinocyte differentiation.Journal of lipid research · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
PKCδ increases keratinocyte differentiation and suppresses keratinocyte proliferation and survival. However, the mechanism of proliferation suppression is not well understood. The present studies show that PKCδ overexpression increases p21(Cip1) mRNA and protein level and promoter activity and that treatment with dominant-negative PKCδ, PKCδ-siRNA, or rottlerin inhibits promoter activation. Analysis of the p21(Cip1) promoter upstream regulatory region reveals three DNA segments that mediate PKCδ-dependent promoter activation. The PKCδ response element most proximal to the transcription start site encodes six GC-rich DNA elements. Mutation of these sites results in a loss of PKCδ-dependent promoter activation. Gel mobility supershift and chromatin immunoprecipitation reveal that these DNA elements bind the Kruppel-like transcription factor KLF4. PKCδ increases KLF4 mRNA and protein level and KLF4 binding to the GC-rich elements in the p21(Cip1) proximal promoter. In addition, KLF4-siRNA inhibits PKCδ-dependent p21(Cip1) promoter activity. PKCδ increases KLF4 expression leading to enhanced KLF4 interaction with the GC-rich elements in the p21(Cip1) promoter to activate transcription.
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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.