The DOI matches its Crossref record; 14 of the 14 references it cites were found in a registry or an index.
STAT proteins: From normal control of cellular events to tumorigenesis
Abstract
Signal transducers and activators of transcription (STAT) proteins comprise a family of transcription factors latent in the cytoplasm that participate in normal cellular events, such as differentiation, proliferation, cell survival, apoptosis, and angiogenesis following cytokine, growth factor, and hormone signaling. STATs are activated by tyrosine phosphorylation, which is normally a transient and tightly regulates process. Nevertheless, several constitutively activated STATs have been observed in a wide number of human cancer cell lines and primary tumors, including blood malignancies and solid neoplasias. STATs can be divided into two groups according to their specific functions. One is made up of STAT2, STAT4, and STAT6, which are activated by a small number of cytokines and play a distinct role in the development of T‐cells and in IFNγ signaling. The other group includes STAT1, STAT3, and STAT5, activated in different tissues by means of a series of ligands and involved in IFN signaling, development of the mammary gland, response to GH, and embriogenesis. This latter group of STATS plays an important role in controlling cell‐cycle progression and apoptosis and thus contributes to oncogenesis. Although an increased expression of STAT1 has been observed in many human neoplasias, this molecule can be considered a potential tumor suppressor, since it plays an important role in growth arrest and in promoting apoptosis. On the other hand, STAT3 and 5 are considered as oncogenes, since they bring about the activation of cyclin D1, c‐Myc, and bcl‐xl expression, and are involved in promoting cell‐cycle progression, cellular transformation, and in preventing apoptosis. J. Cell. Physiol. 197: 157–168, 2003© 2003 Wiley‐Liss, Inc.
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Cites
STATs: transcriptional control and biological impact
Levy, D. E., & Darnell, J. E. (2002) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm909 · Cited by 3,201
Bowman, T., Garcia, R., Turkson, J., & Jove, R. (2000) · Oncogene · doi:10.1038/sj.onc.1203527 · Cited by 1,743
Demonstration of an interferon γ-dependent tumor surveillance system in immunocompetent mice
Kaplan, D. H., Shankaran, V., Dighe, A. S., Stockert, E., Aguet, M., Old, L. J., & Schreiber, R. D. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.13.7556 · Cited by 1,465
Constitutive Stat3 activity up-regulates VEGF expression and tumor angiogenesis
Niu, G., Wright, K. L., Huang, M., Song, L., Haura, E., Turkson, J., Zhang, S., Wang, T., Sinibaldi, D., Coppola, D., et al. (2002) · Oncogene · doi:10.1038/sj.onc.1205260 · Cited by 1,207
The role of STATs in transcriptional control and their impact on cellular function
Bromberg, J., & Darnell, J. E. (2000) · Oncogene · doi:10.1038/sj.onc.1203476 · Cited by 1,201
Specific Inhibition of Stat3 Signal Transduction by PIAS3
Chung, C. D., Liao, J., Liu, B., Rao, X., Jay, P., Berta, P., & Shuai, K. (1997) · Science · doi:10.1126/science.278.5344.1803 · Cited by 980
Serine phosphorylation of STATs
Decker, T., & Kovarik, P. (2000) · Oncogene · doi:10.1038/sj.onc.1203481 · Cited by 887
Levy, D. E., & Lee, C.-K. (2002) · Journal of Clinical Investigation · doi:10.1172/jci0215650 · Cited by 734
Epling-Burnette, P. K., Liu, J. H., Catlett-Falcone, R., Turkson, J., Oshiro, M., Kothapalli, R., Li, Y., Wang, J.-M., Yang-Yen, H.-F., Karras, J., et al. (2001) · Journal of Clinical Investigation · doi:10.1172/jci9940 · Cited by 633
Imada, K., & Leonard, W. J. (2000) · Molecular Immunology · doi:10.1016/s0161-5890(00)00018-3 · Cited by 610 · cited 2×
“STAT 1 and 3 with this altered serine have a transcriptional capacity reduced by 20% (Imada and Leonard, 2000).”
Background
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The potential and controversy of targeting STAT family members in cancer
Verhoeven, Y., Tilborghs, S., Jacobs, J., De Waele, J., Quatannens, D., Deben, C., Prenen, H., Pauwels, P., Trinh, X. B., Wouters, A., et al. (2020) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2019.10.002 · Cited by 409
Pasutto, F., Sticht, H., Hammersen, G., Gillessen-Kaesbach, G., FitzPatrick, D. R., Nürnberg, G., Brasch, F., Schirmer-Zimmermann, H., Tolmie, J. L., Chitayat, D., et al. (2007) · The American Journal of Human Genetics · doi:10.1086/512203 · Cited by 361
Lam, L. T., Wright, G., Davis, R. E., Lenz, G., Farinha, P., Dang, L., Chan, J. W., Rosenwald, A., Gascoyne, R. D., & Staudt, L. M. (2008) · Blood · doi:10.1182/blood-2007-09-111948 · Cited by 353
Endocrine disruptors in marine organisms: Approaches and perspectives
Porte, C., Janer, G., Lorusso, L. C., Ortiz-Zarragoitia, M., Cajaraville, M. P., Fossi, M. C., & Canesi, L. (2006) · Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology · doi:10.1016/j.cbpc.2006.03.004 · Cited by 310
The BET family in immunity and disease
Wang, N., Wu, R., Tang, D., & Kang, R. (2021) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00384-4 · Cited by 295
Metadata
- Authors
- Calò, V., Migliavacca, M., Bazan, V., Macaluso, M., Buscemi, M., Gebbia, N., & Russo, A.
- Venue
- Journal of Cellular Physiology
- Publisher
- Wiley
- Published
- 2003-07-31
- Volume
- 197
- Issue
- 2
- Pages
- 157-168
- ISSN
- 0021-9541 (ISSN-L)
- 1097-4652
- OpenAlex
- W1988719795
- Cited by
- 610
- References
- 14
- FWCI
- 19.10
- Type
- journal article
- Language
- en
- Open access
- closed
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