ArticleGene expression1993
Expression of the carcinoma-associated keratin K6 and the role of AP-1 proto-oncoproteins.
Article in Gene expression, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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
15 citing papers in PubMed, 49 citations in OpenAlex.
- Keratins 6, 16, and 17 in Health and Disease: A Summary of Recent Findings.Current issues in molecular biology · 2024Review
- Keratin 6a reorganization for ubiquitin-proteasomal processing is a direct antimicrobial response.The Journal of cell biology · 2018Article
- Specific and shared targets of ephrin A signaling in epidermal keratinocytes.The Journal of biological chemistry · 2011Article
- The c-Jun NH2-terminal kinase is essential for epidermal growth factor expression during epidermal morphogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- Thyroid hormones and gamma interferon specifically increase K15 keratin gene transcription.Molecular and cellular biology · 2004Article
- Article
- CRE DNA binding proteins bind to the AP-1 target sequence and suppress AP-1 transcriptional activity in mouse keratinocytes.Oncogene · 1999Article
- Transcriptional control of K5, K6, K14, and K17 keratin genes by AP-1 and NF-kappaB family members.Gene expression · 1997Article
- Oncogenic regulation and function of keratins 8 and 18.Cancer metastasis reviews · 1996Review
- Transcription factor regulation of epidermal keratinocyte gene expression.Molecular biology reports · 1996Review
- A 5'-upstream region of a bovine keratin 6 gene confers tissue-specific expression and hyperproliferation-related induction in transgenic mice.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- An Sp1 binding site and the minimal promoter contribute to overexpression of the cytokeratin 18 gene in tumorigenic clones relative to that in nontumorigenic clones of a human carcinoma cell line.Molecular and cellular biology · 1995Article
- Disease-activated transcription factor: allergic reactions in human skin cause nuclear translocation of STAT-91 and induce synthesis of keratin K17.Molecular and cellular biology · 1994Article
- On the role of AP2 in epithelial-specific gene expression.Gene expression · 1993Article
- A cluster of five nuclear proteins regulates keratin gene transcription.Gene expression · 1993Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The normal pattern of keratin expression in epidermis is altered in carcinomas as well as in nonmalignant diseases such as psoriasis and wound healing. Under these circumstances, the transcription of differentiation-specific keratins K1 and K10 is suppressed, whereas the activation- and hyperproliferation-associated keratins K6 and K16 are induced. Very little is known regarding transcriptional regulators involved in this switch. To investigate the nuclear factors that participate in regulation of expression of the K6 gene, we have characterized the binding sites for nuclear proteins on the promoter DNA of the K6 gene by gel retardation assays and site-specific deletion mutagenesis. We found four nuclear protein binding sites in the K6 gene promoter. Two are near the TATA box, but their ability to bind HeLa or keratinocyte nuclear extracts is independent of the TATA box-binding protein complex. The third binding site is a large palindrome. The sequences of these three sites do not correspond to any described target sequences for characterized transcriptional factors. The fourth is an AP-1 site, the target sequence for the proto-oncoproteins fos and jun. All four sites are independent of the previously characterized epidermal growth factor-responsive element, EGF-RE. These findings suggest that there may be two parallel pathways of induction of K6 transcription. One proceeds through the EGF-RE, which may be involved in nonmalignant hyperproliferation processes; the other, through the AP-1 site and the fos-jun proto-oncoproteins, may be related to induction in malignant processes.
Indexed as
Identifiers
7505671PMC6081629W2415074568What 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.