ArticleJournal of cellular biochemistry2003
Mammalian transcription factor LSF is a target of ERK signaling.
Article in Journal of cellular biochemistry, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- TFCP2 as a therapeutic nexus: unveiling molecular signatures in cancer.Cancer metastasis reviews · 2024Review
- TFCP2 Overcomes Senescence by Cooperating With SREBP2 to Activate Cholesterol Synthesis in Pancreatic Cancer.Frontiers in oncology · 2021Article
- Vasoactive intestinal peptide induces proliferation of human hepatocytes.Cell proliferation · 2018Article
- TFCP2 activates beta-catenin/TCF signaling in the progression of pancreatic cancer.Oncotarget · 2017Article
- Glucose Deficiency Elevates Acid-Sensing Ion Channel 2a Expression and Increases Seizure Susceptibility in Temporal Lobe Epilepsy.Scientific reports · 2017Article
- Transcription factor LSF (TFCP2) inhibits melanoma growth.Oncotarget · 2016Article
- Regulation of the g1/s transition in hepatocytes: involvement of the cyclin-dependent kinase cdk1 in the DNA replication.International journal of hepatology · 2012Article
- The transcription factor LSF: a novel oncogene for hepatocellular carcinoma.American journal of cancer research · 2012Article
- Cooperation of deregulated Notch signaling and Ras pathway in human hepatocarcinogenesis.Journal of molecular histology · 2011Article
- Late SV40 factor: a key mediator of Notch signaling in human hepatocarcinogenesis.World journal of gastroenterology · 2011Article
- Prolyl isomerase Pin1 regulates transcription factor LSF (TFCP2) by facilitating dephosphorylation at two serine-proline motifs.The Journal of biological chemistry · 2010Article
- Transcription factors LSF and E2Fs: tandem cyclists driving G0 to S?Cell cycle (Georgetown, Tex.) · 2009Article
- Phosphorylation by cyclin C/cyclin-dependent kinase 2 following mitogenic stimulation of murine fibroblasts inhibits transcriptional activity of LSF during G1 progression.Molecular and cellular biology · 2009Article
- PHB2 interacts with RNF2 and represses CP2c-stimulated transcription.Molecular and cellular biochemistry · 2008Article
- Erythroid cell-specific alpha-globin gene regulation by the CP2 transcription factor family.Molecular and cellular biology · 2005Article
- Mitogen-activated protein kinases regulate LSF occupancy at the human immunodeficiency virus type 1 promoter.Journal of virology · 2005Article
- Lineage-specific and ubiquitous biological roles of the mammalian transcription factor LSF.Gene · 2004Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
LSF is a mammalian transcription factor that is rapidly and quantitatively phosphorylated upon growth induction of resting, peripheral human T cells, as assayed by a reduction in its electrophoretic mobility. The DNA-binding activity of LSF in primary T cells is greatly increased after this phosphorylation event (Volker et al. [1997]: Genes Dev 11:1435-1446). We demonstrate here that LSF is also rapidly and quantitatively phosphorylated upon growth induction in NIH 3T3 cells, although its DNA-binding activity is not significantly altered. Three lines of experimentation established that ERK is responsible for phosphorylating LSF upon growth induction in both cell types. First, phosphorylation of LSF by ERK is sufficient to cause the reduced electrophoretic mobility of LSF. Second, the amount of ERK activity correlates with the extent of LSF phosphorylation in both primary human T cells and NIH 3T3 cells. Finally, specific inhibitors of the Ras/Raf/MEK/ERK pathway inhibit LSF modification in vivo. This phosphorylation by ERK is not sufficient for activation of LSF DNA-binding activity, as evidenced both in vitro and in mouse fibroblasts. Nonetheless, activation of ERK is a prerequisite for the substantial increase in LSF DNA-binding activity upon activation of resting T cells, indicating that ERK phosphorylation is necessary but not sufficient for activation of LSF in this cell type.
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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.