ArticleMolecular and cellular biology1997
Activation of an enhancer on the syndecan-1 gene is restricted to fibroblast growth factor family members in mesenchymal cells.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 53 citations in OpenAlex.
- Spatial and Functional Roles of Syndecans in Skin Wound Healing.International journal of molecular sciences · 2025Review
- Spatiotemporal diversity and regulation of glycosaminoglycans in cell homeostasis and human disease.American journal of physiology. Cell physiology · 2022Review
- Syndecan-1 (CD138), Carcinomas and EMT.International journal of molecular sciences · 2021Review
- Syndecan-1 induction in lung microenvironment supports the establishment of breast tumor metastases.Breast cancer research : BCR · 2018Article
- Syndecan promotes axon regeneration by stabilizing growth cone migration.Cell reports · 2014Article
- FRS2α is essential for the fibroblast growth factor to regulate the mTOR pathway and autophagy in mouse embryonic fibroblasts.International journal of biological sciences · 2011Article
- KGF and EGF signalling block hair follicle induction and promote interfollicular epidermal fate in developing mouse skin.Development (Cambridge, England) · 2009Article
- Decoupled syndecan 1 mRNA and protein expression is differentially regulated by angiotensin II in macrophages.Journal of cellular physiology · 2008Article
- Fibroblast growth factor receptor 1 (FGFR1) tyrosine phosphorylation regulates binding of FGFR substrate 2alpha (FRS2alpha) but not FRS2 to the receptor.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Heparan sulfate proteoglycans as regulators of fibroblast growth factor-2 receptor binding in breast carcinomas.The American journal of pathology · 2002Article
- Transcriptional targeting of adenoviral gene delivery into migrating wound keratinocytes using FiRE, a growth factor-inducible regulatory element.Gene therapy · 2000Article
- Involvement of protein kinase A in fibroblast growth factor-2-activated transcription.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factors (FGFs) induce a variety of biological effects on different cell types. They activate a number of genes, including immediate-early genes, such as the transcription factors Fos and Jun, which are also common targets for other tyrosine kinase receptor-activating growth factors. Here we describe a secondary far-upstream enhancer on the syndecan-1 gene that is activated only by members of the FGF family in NIH 3T3 cells, not by other receptor tyrosine kinase-activating growth factors (e.g., epidermal growth factor, platelet-derived growth factor, insulin-like growth factor, or serum). This FGF-inducible response element (FiRE) consists of a 170-bp array of five DNA motifs which bind two FGF-inducible Fos-Jun heterodimers, one inducible AP-2-related protein, a constitutively expressed upstream stimulatory factor, and one constitutive 46-kDa transcription factor. Mutational analysis showed that both AP-1 binding motifs are required, but not sufficient, for FiRE activation. Moreover, agents such as 12-O-tetradecanoylphorbol-13-acetate, okadaic acid, or forskolin, which are known to activate AP-1 complexes and AP-1-driven promoters, fail to activate FiRE. However, FiRE can be activated by the tyrosine kinase phosphatase inhibitor orthovanadate. Taken together, this data implies a differential activation of growth factor-initiated signaling on AP-1-driven regulatory elements.
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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.