Transcription factors regulate gene expression by cooperating with the RNA polymerase II enzyme to synthesize messenger RNA molecules (mRNA) that are then used to produce proteins. Because they control the protein repertoire expressed by a cell, transcription factors critically regulate all physiologic processes. Not surprisingly, alterations in transcription factors have significant impact on diseases and their treatment. This article reviews basic concepts about the functions and regulation of transcription factors that are important for better understanding cell physiology, pathophysiology, and molecular medicine. A particular focus of our discussion will be the implications of this knowledge in the fields of surgery and transplantation. Better understanding of the functions of transcription factors will facilitate the design of novel therapies for some human diseases, and the control of biologic responses after surgery and transplantation.
To read this article in full you will need to make a payment
Purchase one-time access:Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
One-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:Subscribe to Surgery
Already a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
- The organization of replication and transcription.Science. 1999; 284: 1790-1795
- An integrated model of the transcription complex in elongation, termination, and editing.Science. 1998; 281: 660-665
- Initiation of protein synthesis in eukaryotic cells.Eur J Biochem. 1996; 236: 747-771
- Protein sorting by transport vesicles.Science. 1996; 272: 227-234
- Protein traffic in the yeast endocytic and vacuolar protein sorting pathways.Curr Opin Cell Biol. 1998; 10: 513-522
- Association of distinct yeast Not2 functional domains with components of Gcn5 histone acetylase and Ccr4 transcriptional regulatory complexes.EMBO J. 1998; 17: 6714-6722
- Acetylation of general transcription factors by histone acetyltransferases.Curr Biol. 1997; 7: 689-692
- Multiple roles for the Wilms' tumour suppressor gene, WT1 in genitourinary development.Mol Cell Endocrinol. 1998; 140: 65-69
- A transformed view of cyclosporine.Nature. 1999; 397: 471-472
- Cyclosporine induces cancer progression by a cell-autonomous mechanism.Nature. 1999; 397: 530-534
- Regulation of immune responses by TGF-beta.Annu Rev Immunol. 1998; 16: 137-161
- Transcription factor EGR-1 suppresses the growth and transformation of human HT-1080 fibrosarcoma cells by induction of transforming growth factor beta 1.Proc Natl Acad Sci U S A. 1996; 93: 11831-11836
- EGR-1, the reluctant suppression factor: EGF-1 is known to function in the regulation of growth, differentiation, and also has significant tumor suppressor activity and a mechanism involving the induction of TGF-beta1 is postulated to account for this suppressor activity.Crit Rev Oncol. 1996; 7: 101-125
- The transcription factor EGF-1 suppresses transformation of human fibrosarcoma HT1080 cells by coordinated induction of transforming growth factor-β1, fibronectin, and plasminogen activator inhibitor-1.J Biol Chem. 1999; 274: 4400-4411
- The IE2 regulatory protein of human cytomegalovirus induces expression of the human transforming growth factor beta 1 gene through an Egr-1 binding site.J Virol. 1996; 70: 7062-7070
- Coactivation of AP-1 activity and TGF-beta-1 gene expression in the stress response of normal skin cells to ionizing radiation.Oncogene. 1997; 15: 981-989
- The transcription factor E2F-1 modulates TGF-beta-1 RNA expression in glial cells.Oncogene. 1997; 14: 2959-2969
- Retinoic acid induces secretion of transforming growth factors by PC12 pheochromocytoma cells.Oncogene. 1997; 14: 579-587
- Modulation of chemokine expression during ischemia/reperfusion in transgenic mice overproducing human glutathione peroxidases.J Immunol. 1999; 163: 5666-5677
- Redox gene therapy for ischemia/reperfusion injury of the liver reduces AP-1 and NF-κB activation.Nat Med. 1998; 4: 698-704
- Ischemia/reperfusion injury in the liver of BALB/c mice activates AP-1 and nuclear factor kappa B independently of IkappaB degradation.Hepatology. 1998; 28: 1022-1030
- Overexpression of human glutathione perioxidase protects transgenic mice against focal cerebral ischemia/reperfusion damage.Brain Res Mol Brain Res. 1998; 53: 333-338
- Transgenic mice overexpressing glutathione peroxidase are resistant to myocardial ischemia/reperfusion injury.J Mol Cell Cardiol. 1996; 28: 1759-1767
- Tyrosine phosphorylation of I kappa B-alpha activates NF-kappa B without proteolytic degradation of I kappa B-alpha.Cell. 1996; 86: 787-798
- Involvement of regulatory and catalytic subunits of phosphoinositide 3-kinase in NF-kappa B activation.Proc Natl Acad Sci U S A. 1999; 96: 429-434
- Inhibition of interleukin-1-stimulated NF-kappaB RelA/p65 phosphorylation by mesalamine is accompanied by decreased transcriptional activity.J Biol Chem. 1999; 274: 26448-26453
- Chemokines, lymphocytes and viruses: what goes around, comes around.Curr Opin Immunol. 1998; 10: 265-270
- Chemokines, lymphocytes, and viruses: what goes around, comes around.Curr Opin Immunol. 1998; 10: 265-270
Accepted: February 8, 2000
*Supported by the Mayo Foundation and the National Institutes of Health grants GM59763 to K. H. and DK52912 to R. U.
**Reprint requests: Dr Raul Urrutia, Gastroenterology Research Unit, 2-445A Alfred Building, 200 First St SW, Mayo Clinic, Rochester, MN 55905.
© 2000 Mosby, Inc. Published by Elsevier Inc. All rights reserved.