Sp1 Transcription Factor
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Subject Areas on Research
- A high expression level of insulin-like growth factor I receptor is associated with increased expression of transcription factor Sp1 and regional lymph node metastasis of human gastric cancer.
- A human gamma globin gene variant binds SP1.
- A naturally occurring gamma globin gene mutation enhances SP1 binding activity.
- A role for Pin1 in mammalian germ cell development and spermatogenesis.
- A variant in the CHEK2 promoter at a methylation site relieves transcriptional repression and confers reduced risk of lung cancer.
- ALOX5 polymorphism associates with increased leukotriene production and reduced lung function and asthma control in children with poorly controlled asthma.
- Activin induces hepatocyte cell growth arrest through induction of the cyclin-dependent kinase inhibitor p15INK4B and Sp1.
- An HMGA2-IGF2BP2 axis regulates myoblast proliferation and myogenesis.
- Celecoxib inhibits vascular endothelial growth factor expression in and reduces angiogenesis and metastasis of human pancreatic cancer via suppression of Sp1 transcription factor activity.
- Chromatin accessibility reveals insights into androgen receptor activation and transcriptional specificity.
- Collaborative interactions between MEF-2 and Sp1 in muscle-specific gene regulation.
- Constitutive Sp1 activity is essential for differential constitutive expression of vascular endothelial growth factor in human pancreatic adenocarcinoma.
- Cooperation of Sp1 and p300 in the induction of the CDK inhibitor p21WAF1/CIP1 during NGF-mediated neuronal differentiation.
- Functional similarities between HIV-1 Tat and DNA sequence-specific transcriptional activators.
- Glutamine enhances heat shock protein 70 expression via increased hexosamine biosynthetic pathway activity.
- HIF-1alpha induces genetic instability by transcriptionally downregulating MutSalpha expression.
- Histone Deacetylase Inhibitors Inhibit Rhabdomyosarcoma by Reactive Oxygen Species-Dependent Targeting of Specificity Protein Transcription Factors.
- Hyperosmotic stress stimulates promoter activity and regulates cellular utilization of the serum- and glucocorticoid-inducible protein kinase (Sgk) by a p38 MAPK-dependent pathway.
- RB regulates transcription of the p21/WAF1/CIP1 gene.
- Ras induces p21Cip1/Waf1 cyclin kinase inhibitor transcriptionally through Sp1-binding sites.
- Regulation of vascular endothelial growth factor receptor-1 expression by specificity proteins 1, 3, and 4 in pancreatic cancer cells.
- Sp and GATA factors are critical for Apolipoprotein AI downstream enhancer activity in human HepG2 cells.
- Sp1 activation of a TATA-less promoter requires a species-specific interaction involving transcription factor IID.
- Sp1 regulates osteopontin expression in SW480 human colon adenocarcinoma cells.
- Sp1 transcription factor is required for in vitro basal and Tat-activated transcription from the human immunodeficiency virus type 1 long terminal repeat.
- Sp1, but not Sp3, functions to mediate promoter activation by TGF-beta through canonical Sp1 binding sites.
- The carboxyl-terminal repeat domain of RNA polymerase II is not required for transcription factor Sp1 to function in vitro.
- Tolfenamic acid and pancreatic cancer growth, angiogenesis, and Sp protein degradation.
- Transcriptional activation of p21(waf1/cip1) by alkylphospholipids: role of the mitogen-activated protein kinase pathway in the transactivation of the human p21(waf1/cip1) promoter by Sp1.
- Transcriptional regulation of N-acetylglutamate synthase.
- Transcriptional regulation of the human alpha1a-adrenergic receptor gene. Characterization Of the 5'-regulatory and promoter region.
- Transforming growth factor beta activates the promoter of cyclin-dependent kinase inhibitor p15INK4B through an Sp1 consensus site.
- Truncation of Sp1 transcription factor by myeloblastin in undifferentiated HL60 cells.
- UV radiation is a transcriptional inducer of p21(Cip1/Waf1) cyclin-kinase inhibitor in a p53-independent manner.
- c-Myc creates an activation loop by transcriptionally repressing its own functional inhibitor, hMad4, in young fibroblasts, a loop lost in replicatively senescent fibroblasts.