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Jak-STAT Pathways and Transcriptional Activation in Response to IFNs and Other Extracellular Signaling Proteins
Abstract
Through the study of transcriptional activation in response to interferon alpha (IFN-alpha) and interferon gamma (IFN-gamma), a previously unrecognized direct signal transduction pathway to the nucleus has been uncovered: IFN-receptor interaction at the cell surface leads to the activation of kinases of the Jak family that then phosphorylate substrate proteins called STATs (signal transducers and activators of transcription). The phosphorylated STAT proteins move to the nucleus, bind specific DNA elements, and direct transcription. Recognition of the molecules involved in the IFN-alpha and IFN-gamma pathway has led to discoveries that a number of STAT family members exist and that other polypeptide ligands also use the Jak-STAT molecules in signal transduction.
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“Signal transducer and activator of transcription 3 (STAT3) belongs to the family of STAT transcription factors which mediate the cellular response to a variety of cytokines and growth factors including IL-6 (6-8”
From STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration (2002) · cites this paper as [6]
In the citing paper
“Specifically, STAT1 and IRF5 have been shown to be involved in polarization and maintenance of an M1 phenotype while STAT6, IRF4, CREB-C/EBPβ, and PPARγ are involved in polarization and maintenance of an M2 phenotype [23–30].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [23]
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“Tumor cells could escape the effects of type II IFN (IFN-γ) by downregulating or mutating molecules involved in the IFNs signaling pathway, which goes by the IFN receptor chains Jak1/ Jak2 and STATs [107].”
BackgroundChromium genotoxicity: A double-edged sword
Nickens, K. P., Patierno, S. R., & Ceryak, S. M. (2010) · Chemico-Biological Interactions · doi:10.1016/j.cbi.2010.04.018 · Cited by 379
Regulating IRFs in IFN Driven Disease
Jefferies, C. A. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00325 · Cited by 364
“This results in activation of two cytoplasmic kinases JAK1 and TYK2, which subsequently phosphorylate the associated transcription factors STAT1 and STAT2 (55).”
Influential“Do We Know Jack” About JAK? A Closer Look at JAK/STAT Signaling Pathway
Bousoik, E., & Aliabadi, H. M. (2018) · Frontiers in Oncology · doi:10.3389/fonc.2018.00287 · Cited by 396
“Among STATs, STAT1 and STAT2 are known as the targets of interferon activation (165).”
BackgroundStrategies and Approaches of Targeting STAT3 for Cancer Treatment
Furtek, S. L., Backos, D. S., Matheson, C. J., & Reigan, P. (2016) · ACS Chemical Biology · doi:10.1021/acschembio.5b00945 · Cited by 356
Flanagan, M. E., Blumenkopf, T. A., Brissette, W. H., Brown, M. F., Casavant, J. M., Shang-Poa, C., Doty, J. L., Elliott, E. A., Fisher, M. B., Hines, M. H., et al. (2010) · Journal of Medicinal Chemistry · doi:10.1021/jm1004286 · Cited by 338
Kern, L., Mittenbühler, M., Vesting, A., Ostermann, A., Wunderlich, C., & Wunderlich, F. (2018) · Cancers · doi:10.3390/cancers11010024 · Cited by 331
The role of STAT3 in leading the crosstalk between human cancers and the immune system
Wang, Y., Shen, Y., Wang, S., Shen, Q., & Zhou, X. (2017) · Cancer Letters · doi:10.1016/j.canlet.2017.12.003 · Cited by 343
Ghilardi, N., & Skoda, R. C. (1997) · Molecular Endocrinology · doi:10.1210/mend.11.4.9907 · Cited by 326
Fensterl, V., & Sen, G. C. (2010) · Journal of Interferon & Cytokine Research · doi:10.1089/jir.2010.0101 · Cited by 288
Macrophage polarization and meta-inflammation
Li, C., Xu, M. M., Wang, K., Adler, A. J., Vella, A. T., & Zhou, B. (2017) · Translational research · doi:10.1016/j.trsl.2017.10.004 · Cited by 376
Protein tyrosine phosphatases in the JAK/STAT pathway
Xu, D. (2008) · Frontiers in bioscience · doi:10.2741/3051 · Cited by 314
“Darnell JE Jr, Kerr IM, Stark GR. Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins.”
BackgroundInfluentialBellucci, R., Martin, A., Bommarito, D., Wang, K., Hansen, S. H., Freeman, G. J., & Ritz, J. (2015) · OncoImmunology · doi:10.1080/2162402x.2015.1008824 · Cited by 307
“JAK kinases are associated with cytokine receptors and ligand binding of these receptors rapidly induces JAK phosphorylation, which in turn activates STAT transcription factors.(11) JAK kinases have also been reported to activate other kinases such as PI3K/AKT and ERK.”
BackgroundHaspel, R. L., Salditt‐Georgieff, M., & Darnell, J. E. (1996) · The EMBO Journal · doi:10.1002/j.1460-2075.1996.tb01016.x · Cited by 312
Dehkhoda, F., Lee, C. M. M., Medina, J., & Brooks, A. J. (2018) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00035 · Cited by 304
Toxoplasma Effectors Targeting Host Signaling and Transcription
Hakimi, M., Olias, P., & Sibley, L. D. (2017) · Clinical Microbiology Reviews · doi:10.1128/cmr.00005-17 · Cited by 342
“IFN- signaling proceeds through STAT1 phosphorylation and translocation to the nucleus to induce a set of interferon-stimulated genes (ISGs) (154, 155).”
BackgroundSTAT‐mediated EGFR signaling in cancer
Quesnelle, K. M., Boehm, A. L., & Grandis, J. R. (2007) · Journal of Cellular Biochemistry · doi:10.1002/jcb.21475 · Cited by 300
“Activated STATs form dimers and multiprotein complexes that translocate into the nucleus where target gene expression is initiated [Darnell et al., 1994].”
BackgroundStructural Bases of Unphosphorylated STAT1 Association and Receptor Binding
Mao, X., Ren, Z., Parker, G. N., Sondermann, H., Pastorello, M. A., Wang, W., McMurray, J. S., Demeler, B., Darnell, J. E., Jr., & Chen, X. (2005) · Molecular Cell · doi:10.1016/j.molcel.2005.02.021 · Cited by 309
Self-citationTranscriptional regulation by STAT1 and STAT2 in the interferon JAK-STAT pathway
Au-Yeung, N., Mandhana, R., & Horvath, C. M. (2013) · JAK-STAT · doi:10.4161/jkst.23931 · Cited by 307
“The sole type II IFN, IFNγ, represents the canonical JAK-STAT signaling paradigm, resulting in an SH2-phosphotyrosine-mediated homodimeric STAT1 transcription factor known as the gamma-IFN activated factor (GAF).(1) In addition to type I IFN, ISGF3 can be activated by type III IFNs, consisting of IFNλ1, IFNλ2, and IFN…”
BackgroundInfluentialThe Jak/STAT pathway.Preprint
Harrison, D. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a011205 · Cited by 308
“They were functionally linked to STATs and interferon signaling in powerful somatic cell genetic screens (Darnell et al. 1994; Schindler and Plumlee 2008).”
STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration
Li, W., Liang, X., Kellendonk, C., Poli, V., & Taub, R. (2002) · Journal of Biological Chemistry · doi:10.1074/jbc.m202807200 · Cited by 307
Insights into Cytokine–Receptor Interactions from Cytokine Engineering
Spangler, J. B., Moraga, I., Mendoza, J. L., & Garcia, K. C. (2015) · Annual Review of Immunology · doi:10.1146/annurev-immunol-032713-120211 · Cited by 304
ICSBP Directs Bipotential Myeloid Progenitor Cells to Differentiate into Mature Macrophages
Tamura, T., Nagamura-Inoue, T., Shmeltzer, Z., Kuwata, T., & Ozato, K. (2000) · Immunity · doi:10.1016/s1074-7613(00)00016-9 · Cited by 305
Human TRIM Gene Expression in Response to Interferons
Carthagéna, L., Bergamaschi, A., Luna, J. M., David, A., Uchil, P. D., Margottin-Goguet, F., Mothes, W., Hazan, U., Transy, C., Pancino, G., et al. (2009) · PLoS ONE · doi:10.1371/journal.pone.0004894 · Cited by 279
Mechanisms of Cancer Resistance to Immunotherapy
Bai, R., Chen, N., Li, L., Du, N., Bai, L., Lv, Z., Tian, H., & Cui, J. (2020) · Frontiers in Oncology · doi:10.3389/fonc.2020.01290 · Cited by 375
“In patients receiving immunotherapy, tumor cells can downregulate or alter IFNγ signaling pathways such as loss-of-function alleles of genes encoding for JAK1/2 and changes in STAT1 to escape the influence of IFN-γ (37), resulting in resistance.”
BackgroundSekrecka, A., Błaszczyk, K., Wesoły, J., & Bluyssen, H. A. R. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01135 · Cited by 333
Kershaw, N. J., Murphy, J. M., Liau, N. P. D., Varghese, L. N., Laktyushin, A., Whitlock, E. L., Lucet, I. S., Nicola, N. A., & Babon, J. J. (2013) · Nature Structural & Molecular Biology · doi:10.1038/nsmb.2519 · Cited by 301
“Mouse JAK2 JH1 domain (residues 836–1132) was coexpressed with the phosphatase PTP1B (residues 2–321) in Sf21 insect cells to obtain activation loop–dephosphorylated JAK2 JH1.”
MethodInfluentialInterferon-induced guanylate-binding proteins: Guardians of host defense in health and disease
Tretina, K., Park, E., Mamińska, A., & MacMicking, J. D. (2019) · The Journal of Experimental Medicine · doi:10.1084/jem.20182031 · Cited by 332
“Pioneering work by the Darnell group showed that GAS elements were occupied by STAT1 homodimers following IFN-γ treatment, for example, in the human GBP1 promoter (Darnell et al., 1994).”
BackgroundInfluentialPaun, A., & Pitha, P. M. (2007) · Biochimie · doi:10.1016/j.biochi.2007.01.014 · Cited by 277
Targeting STAT3 affects melanoma on multiple fronts
Kortylewski, M., Jove, R., & Yu, H. (2005) · Cancer and Metastasis Reviews · doi:10.1007/s10555-005-1580-1 · Cited by 286
Dengue Virus Inhibits Alpha Interferon Signaling by Reducing STAT2 Expression
Jones, M., Davidson, A., Hibbert, L., Gruenwald, P., Schlaak, J., Ball, S., Foster, G., & Jacobs, M. (2005) · Journal of Virology · doi:10.1128/jvi.79.9.5414-5420.2005 · Cited by 294
“The binding of IFN- / to IFNAR leads to the activation of Jak1 and Tyk2 kinases via tyrosine phosphorylation (4).”
BackgroundCell migration during morphogenesis
Aman, A. J., & Piotrowski, T. (2009) · Developmental Biology · doi:10.1016/j.ydbio.2009.11.014 · Cited by 298
Molecular mechanisms underlying chronic inflammation-associated cancers
Wu, Y., Antony, S., Meitzler, J. L., & Doroshow, J. H. (2013) · Cancer Letters · doi:10.1016/j.canlet.2013.08.014 · Cited by 312
Targeting Nuclear Factor-Kappa B to Overcome Resistance to Chemotherapy
Godwin, P., Baird, A., Heavey, S., Barr, M. P., O'Byrne, K. J., & Gately, K. A. (2013) · Frontiers in Oncology · doi:10.3389/fonc.2013.00120 · Cited by 312
“Upon binding to their cognate receptors, receptor associated Janus Kinases (JAKs) phosphorylate ligand-bound receptors resulting in the recruitment and activation of Signal Transducers and Activators of Transcription (STATs) (Darnell et al., 1994).”
BackgroundThe Multifaced Role of STAT3 in Cancer and Its Implication for Anticancer Therapy
Tolomeo, M., & Cascio, A. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22020603 · Cited by 329
“STATs are activated in the cytoplasm by Janus kinases (JAKs), a family composed of four different intracellular non-receptor tyrosine kinases, that transduce cytokine-mediated signals [7,8].”
BackgroundIdentification of a PTEN-regulated STAT3 brain tumor suppressor pathway
de la Iglesia, N., Konopka, G., Puram, S. V., Chan, J. A., Bachoo, R. M., You, M. J., Levy, D. E., DePinho, R. A., & Bonni, A. (2008) · Genes & Development · doi:10.1101/gad.1606508 · Cited by 336
“…RTKs is thought to recruit STAT3 to the RTK at the plasma membrane followed by induction of STAT3 phosphorylation at the key regulatory sites Tyr705 and Ser727 and consequent translocation of STAT3 to the nucleus (Zhong et al. 1994; Leaman et al. 1996; Vignais et al. 1996; Decker and Kovarik 2000).”
STAT1 as a key modulator of cell death
Kim, H. S., & Lee, M. (2006) · Cellular Signalling · doi:10.1016/j.cellsig.2006.09.003 · Cited by 283
Steatosis as a Risk Factor in Liver Surgery
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Innate and adaptive immune responses in HCV infections
Heim, M. H., & Thimme, R. (2014) · Journal of Hepatology · doi:10.1016/j.jhep.2014.06.035 · Cited by 313
“Type I and III IFNs additionally induce the heterotrimeric transcription factor IFN stimulated gene factor 3 (ISGF3) that consists of STAT1, STAT2, and IRF9 and binds to IFN-stimulated response elements (ISRE) [23,25,26] (Fig.”
BackgroundBoisson‐Dupuis, S., Kong, X., Okada, S., Cypowyj, S., Puel, A., Abel, L., & Casanova, J. (2012) · Current Opinion in Immunology · doi:10.1016/j.coi.2012.04.011 · Cited by 293
Kruppel-like Factor 4 Is a Mediator of Proinflammatory Signaling in Macrophages
Feinberg, M. W., Cao, Z., Wara, A. K., Lebedeva, M. A., SenBanerjee, S., & Jain, M. K. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m509378200 · Cited by 298
Transcription Factor STAT3 as a Novel Molecular Target for Cancer Prevention
Xiong, A., Yang, Z., Shen, Y., Zhou, J., & Shen, Q. (2014) · Cancers · doi:10.3390/cancers6020926 · Cited by 288
“STATs, a family of transcription factors first identified in 1994 [1], play a fundamental role in the regulation of growth, survival and differentiation of various cells.”
BackgroundCancer Prevention With Natural Compounds
Gullett, N. P., Amin, A. R. M. R., Bayraktar, S., Pezzuto, J. M., Shin, D. M., Khuri, F. R., Aggarwal, B. B., Surh, Y., & Küçük, Ö. (2010) · Seminars in Oncology · doi:10.1053/j.seminoncol.2010.06.014 · Cited by 496
Peterson, W. M., Wang, Q., Tzekova, R., & Wiegand, S. J. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-11-04081.2000 · Cited by 267
STAT proteins in cancer: orchestration of metabolism
Li, Y., Zhang, C., Martincuks, A., Herrmann, A., & Yu, H. (2023) · Nature reviews. Cancer · doi:10.1038/s41568-022-00537-3 · Cited by 305
Kim, S. Y., Kang, J. W., Song, X., Kim, B. K., Yoo, Y. D., Kwon, Y. T., & Lee, Y. J. (2013) · Cellular Signalling · doi:10.1016/j.cellsig.2013.01.007 · Cited by 306
Castrop, H., Höcherl, K., Kurtz, A., Schweda, F., Todorov, V., & Wagner, C. (2010) · Physiological Reviews · doi:10.1152/physrev.00011.2009 · Cited by 265
Lo, H., Cao, X., Zhu, H., & Ali‐Osman, F. (2008) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-07-4923 · Cited by 257
Holzinger, D., Jorns, C., Stertz, S., Boisson‐Dupuis, S., Thimme, R., Weidmann, M., Casanova, J., Haller, O., & Kochs, G. (2007) · Journal of Virology · doi:10.1128/jvi.00546-06 · Cited by 241
“Type I and type III IFNs are induced by viral infection and act through the JAK/STAT pathway (17, 74).”
BackgroundThe IRF family of transcription factors: Inception, impact and implications in oncogenesis
Yanai, H., Negishi, H., & Taniguchi, T. (2012) · OncoImmunology · doi:10.4161/onci.22475 · Cited by 261
Kotenko, S. V., Izotova, L. S., Mirochnitchenko, O. V., Esterova, E., Dickensheets, H., Donnelly, R. P., & Pestka, S. (2001) · The Journal of Immunology · doi:10.4049/jimmunol.166.12.7096 · Cited by 260
Impaired interferon signaling is a common immune defect in human cancer
Critchley-Thorne, R. J., Simons, D. L., Yan, N., Miyahira, A. K., Dirbas, F. M., Johnson, D. L., Swetter, S. M., Carlson, R. W., Fisher, G. A., Koong, A. C., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0901329106 · Cited by 249
Targeting transcription factor STAT3 for cancer prevention and therapy
Chai, E. Z. P., Shanmugam, M. K., Arfuso, F., Dharmarajan, A., Wang, C., Kumar, A. P., Samy, R. P., Lim, L. H. K., Wang, L., Goh, B. C., et al. (2016) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2015.10.004 · Cited by 272
“2) (Darnell et al., 1994; Aittomaki & Pesu, 2014;Mohan et al., 2014; Siveen, Sikka, et al., 2014; Dai et al., 2015; Lee et al., 2015).”
Molecular mechanisms in the pathogenesis of diabetic nephropathy: An update
Arora, M. K., & Singh, U. K. (2013) · Vascular Pharmacology · doi:10.1016/j.vph.2013.01.001 · Cited by 241
Mediator Condensates Localize Signaling Factors to Key Cell Identity Genes
Zamudio, A. V., Dall’Agnese, A., Henninger, J. E., Manteiga, J. C., Afeyan, L. K., Hannett, N. M., Coffey, E. L., Li, C. H., Oksuz, O., Sabari, B. R., et al. (2019) · Molecular Cell · doi:10.1016/j.molcel.2019.08.016 · Cited by 281
“3D) Representative images of in vitro droplet assays of signaling factors with purified Mediator showing the ability of β-catenin, STAT3 and SMAD3 to interact and partition into intact Mediator droplets.”
BackgroundInfluentialInterferon gamma: A master regulator of atherosclerosis
McLaren, J. E., & Ramji, D. P. (2008) · Cytokine & Growth Factor Reviews · doi:10.1016/j.cytogfr.2008.11.003 · Cited by 243
“Each STAT1 monomer becomes tyrosine phosphorylated at tyrosine 701 by the JAKs, dissociates from the receptor to form a STAT1:STAT1 homodimer which translocates to the nucleus and binds to g-activated sequence (GAS) elements in the promoters of IFN-g responsive genes [12,19,20,25].”
BackgroundYamamoto, T., Sekine, Y., Kashima, K., Kubota, A., Sato, N., Aoki, N., & Matsuda, T. (2002) · Biochemical and Biophysical Research Communications · doi:10.1016/s0006-291x(02)02291-x · Cited by 250
Current and future status of JAK inhibitors
McLornan, D. P., Pope, J. E., Gotlib, J. R., & Harrison, C. N. (2021) · The Lancet · doi:10.1016/s0140-6736(21)00438-4 · Cited by 336
EGFR Phosphorylates Tumor-Derived EGFRvIII Driving STAT3/5 and Progression in Glioblastoma
Fan, Q.-W., Cheng, C. K., Gustafson, W. C., Charron, E. M., Zipper, P., Wong, R. A., Chen, J., Lau, J., Knobbe-Thomsen, C. B., Weller, M., et al. (2013) · Cancer Cell · doi:10.1016/j.ccr.2013.09.004 · Cited by 259
“STAT signals downstream of EGFR are activated in 60% of glioblastoma patients, drives progression in animal models of glioma, and correlates inversely with survival (Birner et al., 2010; Darnell et al., 1994; Doucette et al., 2012; Shao et al., 2003), prompting us to analyze this pathway.”
Lo, H., Hsu, S.-C., & Hung, M. (2005) · Breast Cancer Research and Treatment · doi:10.1007/s10549-005-9011-0 · Cited by 240
“Other known receptor/transcription factor modules include IL receptors/STATs, HER2/STATs, and TGF-bRI/Smads [64,104,110,129].”
BackgroundResistance to Checkpoint Inhibition in Cancer Immunotherapy
Barrueto, L., Caminero, F., Cash, L., Makris, C., Lamichhane, P., & Deshmukh, R. R. (2020) · Translational Oncology · doi:10.1016/j.tranon.2019.12.010 · Cited by 296
Mumphrey, S. M., Changotra, H., Moore, T., Heimann-Nichols, E., Wobus, C., Reilly, M. J., Moghadamfalahi, M., Shukla, D., & Karst, S. M. (2007) · Journal of Virology · doi:10.1128/jvi.02096-06 · Cited by 239
“control of viral infections, and deficiencies in the absence of STAT-1 are most likely indicative of a loss of IFN signaling (9, 12, 29).”
BackgroundSTAT3 as a therapeutic target in head and neck cancer
Leeman‐Neill, R. J., Lui, V. W. Y., & Grandis, J. R. (2006) · Expert Opinion on Biological Therapy · doi:10.1517/14712598.6.3.231 · Cited by 225
“STATs were originally discovered in the context of cytokine signalling [1-3].”
BackgroundInfluentialSTAT3, stem cells, cancer stem cells and p63
Galoczová, M., Coates, P. J., & Vojtěšek, B. (2018) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-018-0078-0 · Cited by 272
Wang, Z. W., Sarmento, L., Wang, Y., Li, X.-Q., Dhingra, V., Tseggai, T., Jiang, B., & Fu, Z. F. (2005) · Journal of Virology · doi:10.1128/jvi.79.19.12554-12565.2005 · Cited by 235
“Phosphorylated STATs form specific multimeric complexes that translocate to the nucleus and initiate transcription (13).”
BackgroundResultLung adenocarcinoma distally rewires hepatic circadian homeostasis
Masri, S., Papagiannakopoulos, T., Kinouchi, K., Liu, Y., Cervantes, M., Baldi, P., Jacks, T., & Sassone-Corsi, P. (2016) · Cell · doi:10.1016/j.cell.2016.04.039 · Cited by 234
“Specifically, significant elevation of IL-6 was observed in TB mouse serum, along with a clear, though statistically non-significant, increase in IL-1α, TNFα, LIF and IFNγ (Figure 5A and Figure S7).”
Influential
Metadata
- Authors
- Darnell, J. E., Kerr, L. M., & Stark, G. R.
- Affiliations
- Rockefeller University (US)
- Case Comprehensive Cancer Center (US)
- ORCID
- Stark, George R.
- Venue
- Science
- Published
- 1994-06-03
- Volume
- 264
- Issue
- 5164
- Pages
- 1415-1421
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2029275361
- Cited by
- 6,080
- References
- 85
- Citations by year
- 2026: 84 · 2025: 139 · 2024: 175 · 2023: 170 · 2022: 183 · 2021: 177 · 2020: 162 · 2019: 155 · 2018: 121 · 2017: 166 · 2016: 148 · 2015: 152 · 2014: 160 · 2013: 207 · 2012: 188
- FWCI
- 28.59
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- JAK/STAT signaling, interferon-alpha, interferon-gamma, signal transduction, STAT proteins, transcriptional activation, JAK kinases, interferon receptor, nuclear translocation, DNA binding
- MeSH terms
- Amino Acid Sequence, Animals, Base Sequence, Cell Line, DNA-Binding Proteins, Genes, Genetic Complementation Test, Humans, Interferon-gamma, Molecular Sequence Data, Mutation, Protein-Tyrosine Kinases, Regulatory Sequences, Nucleic Acid, Transcription Factors, Signal Transduction, Transcriptional Activation, Interferon-alpha, Interferon-Stimulated Gene Factor 3, Interferon-Stimulated Gene Factor 3, gamma Subunit
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