ArticleThe Biochemical journal1999
Transcription factor Sp1 activates involucrin promoter activity in non-epithelial cell types.
Article in The Biochemical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 49 citations in OpenAlex.
- GATA3 regulates FLG and FLG2 expression in human primary keratinocytes.Scientific reports · 2017Article
- MEP50/PRMT5 Reduces Gene Expression by Histone Arginine Methylation and this Is Reversed by PKCδ/p38δ Signaling.The Journal of investigative dermatology · 2016Article
- Methylosome Protein 50 and PKCδ/p38δ Protein Signaling Control Keratinocyte Proliferation via Opposing Effects on p21Cip1 Gene Expression.The Journal of biological chemistry · 2015Article
- Protein kinase C δ increases Kruppel-like factor 4 protein, which drives involucrin gene transcription in differentiating keratinocytes.The Journal of biological chemistry · 2013Article
- Article
- AP1 transcription factors in epidermal differentiation and skin cancer.Journal of skin cancer · 2013Article
- Sulforaphane induction of p21(Cip1) cyclin-dependent kinase inhibitor expression requires p53 and Sp1 transcription factors and is p53-dependent.The Journal of biological chemistry · 2012Article
- Effect of the HIV nucleoside reverse transcriptase inhibitor zidovudine on the growth and differentiation of primary gingival epithelium.HIV medicine · 2012Article
- Protein kinase C (PKC) delta suppresses keratinocyte proliferation by increasing p21(Cip1) level by a KLF4 transcription factor-dependent mechanism.The Journal of biological chemistry · 2011Article
- Synergistic activation of human involucrin gene expression by Fra-1 and p300--evidence for the presence of a multiprotein complex.The Journal of investigative dermatology · 2008Article
- A distal region of the human TGM1 promoter is required for expression in transgenic mice and cultured keratinocytes.BMC dermatology · 2004Article
- Durable and stratum-specific gene expression in epidermis.Gene therapy · 2002Article
- Article
- Thapsigargin suppresses phorbol ester-dependent human involucrin promoter activity by suppressing CCAAT-enhancer-binding protein alpha (C/EBPalpha) DNA binding.The Biochemical journal · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The gene for human involucrin (hINV) is selectively expressed in stratifying epithelial cells lining external body surfaces. Previously, we characterized the hINV promoter 5' distal regulatory region (DRR) located between nt -2473 and -2088 upstream of the transcription start site. This region is required for optimal hINV gene expression. The DRR contains weak and strong activator elements. The strong activator comprises AP1- and Sp1-binding sites that combine to drive high-level promoter expression in human keratinocytes. Here we show that the hINV promoter is expressed in a cell-specific manner in vitro and that the DRR contains elements that are partly responsible for cell-type-specific expression of hINV. hINV promoter activity is barely detectable in 3T3 fibroblasts or HEK-293 human embryonic kidney cells. Reporter plasmids containing the full-length promoter or the isolated DRR can, however, be activated in 3T3 and HEK-293 cells by co-transfection with a plasmid encoding the transcription factor Sp1. Consistently with the lower hINV promoter activity, immunoblotting studies indicate that Sp1 protein levels are lower in 3T3 and HEK-293 cells than in human epidermal keratinocytes. Increased Sp1 protein in transfected 3T3 cells and HEK-293 cells correlates with increased promoter activity. In addition, Sp1 transfection activates the expression of the endogenous gene for hINV in HEK-293 cells. These studies suggest that Sp1 might have a role in cell-specific expression of hINV.
Indexed as
Identifiers
9895295PMC1220003W2093076728What OpenQuestion holds
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.