ArticleThe Biochemical journal2004
B-Myb acts as a repressor of human COL1A1 collagen gene expression by interacting with Sp1 and CBF factors in scleroderma fibroblasts.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 0 citations in OpenAlex.
- Probe Sequencing Analysis of Regenerating Lizard Tails Indicates Crosstalk Among Osteoclasts, Epidermal Cells, and Fibroblasts.Journal of developmental biology · 2025Article
- COL1A1 proximal promoter topology regulates its transcriptional response to transforming growth factor β.Connective tissue research · 2024Article
- Significant Biomarkers Identification Associated with Cutaneous Squamous Cell Carcinoma Progression.International journal of general medicine · 2022Article
- Testis-specific protein, Y-linked 1 activates PI3K/AKT and RAS signaling pathways through suppressing IGFBP3 expression during tumor progression.Cancer science · 2019Article
- MYBL2, a link between proliferation and differentiation in maturing colon epithelial cells.Journal of cellular physiology · 2011Article
- Interactions of two transcriptional repressors and two transcriptional activators in modulating gibberellin signaling in aleurone cells.Plant physiology · 2008Article
- Scleroderma, fibroblasts, signaling, and excessive extracellular matrix.Current rheumatology reports · 2005Review
- Antifibrotic therapy in scleroderma: extracellular or intracellular targeting of activated fibroblasts?Current rheumatology reports · 2004Review
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
We investigated the role of B-Myb, a cell-cycle-regulated transcription factor, in the expression of the alpha1 (I) pro-collagen gene (COL1A1) in scleroderma fibroblasts. Scleroderma or SSc (systemic sclerosis) is a fibrotic disease characterized by excessive production of extracellular matrix components, especially type I collagen. Northern-blot analysis showed an inverse relationship between COL1A1 mRNA expression and that of B-Myb during exponential cell growth and during quiescence in human SSc fibroblasts. Overexpression of B-Myb in SSc fibroblasts was correlated with decreased COL1A1 mRNA expression. Transient transfections localized the down-regulatory effect of B-Myb to a region containing the proximal 174 bp of the COL1A1 promoter that does not contain B-Myb consensus binding sites. Gel-shift analysis, using nuclear extracts from normal and SSc fibroblasts transfected with B-Myb, showed no differences in DNA-protein complex formation when compared with the nuclear extracts from mock-transfected cells. However, we found that B-Myb decreases Sp1 (specificity protein 1) and CBF (CCAAT-binding factor) binding for their specific sites localized in the 174 bp COL1A1 proximal promoter. These results were also confirmed using B-Myb-immunodepleted nuclear extracts. Furthermore, immunoprecipitation assays using SSc nuclear extracts demonstrated a physical interaction of B-Myb with Sp1 and CBF transcription factors, and also an interaction between Sp1 and CBF. In addition, by employing full-length or deleted B-Myb cDNA construct, we found that B-Myb down-regulates the COL1A1 proximal promoter through its C-terminal domain. Thus these results suggest that B-Myb may be an important factor in the pathway(s) regulating collagen production in SSc fibroblasts.
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