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Journal articles on the topic 'STAT'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Ebersbach, Celina, Alicia-Marie K. Beier, Christian Thomas, and Holger H. H. Erb. "Impact of STAT Proteins in Tumor Progress and Therapy Resistance in Advanced and Metastasized Prostate Cancer." Cancers 13, no. 19 (2021): 4854. http://dx.doi.org/10.3390/cancers13194854.

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Signal transducers and activators of transcription (STATs) are a family of transcription factors involved in several biological processes such as immune response, cell survival, and cell growth. However, they have also been implicated in the development and progression of several cancers, including prostate cancer (PCa). Although the members of the STAT protein family are structurally similar, they convey different functions in PCa. STAT1, STAT3, and STAT5 are associated with therapy resistance. STAT1 and STAT3 are involved in docetaxel resistance, while STAT3 and STAT5 are involved in antiand

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2

Konjevic, Gordana. "STAT proteins in cancerogenesis and therapy of malignancies." Srpski arhiv za celokupno lekarstvo 137, no. 1-2 (2009): 98–105. http://dx.doi.org/10.2298/sarh0902098k.

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Signal transducers and activators of transcription (STAT) proteins are a 7-member family of cytoplasmic transcription fators that participate in signal transduction by cytokines, hormones, and growth factors. STAT proteins control the most important cellular processes, including survival, proliferation and differentiation. A great number of cytokines and other factors in different cell types activate STAT1, STAT3 and STAT5 and in this manner regulate processes such as cellular proliferation, differentiation and survival. STATs such as STAT4 and STAT6 have a more specific effect and are engaged

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3

de Haas, Nienke, Coco de Koning, Stefania di Blasio, Georgina Flórez-Grau, I. Jolanda M. de Vries, and Stanleyson V. Hato. "STAT Family Protein Expression and Phosphorylation State during moDC Development Is Altered by Platinum-Based Chemotherapeutics." Journal of Immunology Research 2019 (June 11, 2019): 1–12. http://dx.doi.org/10.1155/2019/7458238.

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The STAT signaling pathway is important in dendritic cell (DC) development and function. Tumor cells can induce STAT signaling, thereby inhibiting DC maturation and immunostimulatory functions, leading to hampered efficacy of DC-based immunotherapies. Platinum-based chemotherapeutics can inhibit STAT signaling, thereby making them an interesting tool to improve DC development and function. In this study, we provide a comprehensive overview of STAT expression and phosphorylation during DC differentiation and maturation and investigate the effects of platinum drugs on STAT signaling during these

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4

Lee, Hyun-Ku, Gita Singh, and Sujay Singh. "STAT reporter cell line systems as a tool for cancer therapeutic target screening." Journal of Immunology 200, no. 1_Supplement (2018): 169.8. http://dx.doi.org/10.4049/jimmunol.200.supp.169.8.

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Abstract Signal transducer and activator of transcription (STAT) proteins as cytoplasmic transcription factors respond to cytokines and growth factors that mediate downstream signaling. STATs are closely related with cancers as they are frequently found to be dysregulated in primary tumors, leading to enhanced survival of tumors and increased angiogenesis. Among seven STAT family members, STAT3, STAT4 and STAT5 are considered to primarily promote cancer development and progression, while STAT1 may function either as a tumor suppressor or tumor promoter. STAT3, 4 and 5 are persistently activate

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5

Gorissen, Marnix, Erik de Vrieze, Gert Flik, and Mark O. Huising. "STAT genes display differential evolutionary rates that correlate with their roles in the endocrine and immune system." Journal of Endocrinology 209, no. 2 (2011): 175–84. http://dx.doi.org/10.1530/joe-11-0033.

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We identified orthologues of all mammalian Janus kinase (JAK) and signal transducer and activator of transcription (STAT) genes in teleostean fishes, indicating that these protein families were already largely complete before the teleost tetrapod split, 450 million years ago. In mammals, the STAT repertoire consists of seven genes (STAT1, -2, -3, -4, -5a, -5b, and -6). Our phylogenetic analyses show that STAT proteins that are recruited downstream of endocrine hormones (STAT3 and STAT5a and -5b) show a markedly higher primary sequence conservation compared with STATs that convey immune signals

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6

Tian, SS, P. Tapley, C. Sincich, RB Stein, J. Rosen, and P. Lamb. "Multiple signaling pathways induced by granulocyte colony-stimulating factor involving activation of JAKs, STAT5, and/or STAT3 are required for regulation of three distinct classes of immediate early genes." Blood 88, no. 12 (1996): 4435–44. http://dx.doi.org/10.1182/blood.v88.12.4435.bloodjournal88124435.

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Granulocyte colony-stimulating factor (G-CSF) is the major regulator of proliferation and differentiation of neutrophilic granulocyte precursor cells. G-CSF activates multiple signaling molecules, including the JAK1 and JAK2 kinases and the STAT transcription factors. To investigate G-CSF signaling events regulated by the JAK-STAT pathway, we have generated UT7-epo cells stably expressing either wild-type (wt) G-CSF receptor or a series of C-terminal deletion mutants. Gel mobility shift and immunoprecipitation/Western analysis showed that STAT5 is rapidly activated by G-CSF in cells expressing

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7

Chen, Honglin, Lindsey Hutt-Fletcher, Liang Cao, and S. Diane Hayward. "A Positive Autoregulatory Loop of LMP1 Expression and STAT Activation in Epithelial Cells Latently Infected with Epstein-Barr Virus." Journal of Virology 77, no. 7 (2003): 4139–48. http://dx.doi.org/10.1128/jvi.77.7.4139-4148.2003.

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ABSTRACT STAT3 and STAT5 are constitutively activated and nuclear in nasopharyngeal carcinoma (NPC) cells. In normal signaling, STATs are only transiently activated. To investigate whether Epstein-Barr virus (EBV), and in particular the protein LMP1, contributes to sustained STAT phosphorylation and activation in epithelial cells, we examined STAT activity in two sets of paired cell lines, HeLa, an EBV-converted HeLa cell line, HeLa-Bx1, the NPC-derived cell line CNE2-LNSX, and an LMP1-expressing derivative, CNE2-LMP1. EBV infection was associated with a significant increase in the tyrosine-ph

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8

Murphy, Theresa L., Erik D. Geissal, J. David Farrar, and Kenneth M. Murphy. "Role of the Stat4 N Domain in Receptor Proximal Tyrosine Phosphorylation." Molecular and Cellular Biology 20, no. 19 (2000): 7121–31. http://dx.doi.org/10.1128/mcb.20.19.7121-7131.2000.

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ABSTRACT Stat4 is activated by the cytokines interleukin 12 and alpha interferon (IFN-α) and plays a significant role in directing development of naı̈ve CD4+ T cells to the Th1 phenotype. Signal transducers and activators of transcription (STAT) proteins undergo phosphorylation on a conserved tyrosine residue, resulting in homo- and heterodimerization, nuclear translocation, and DNA binding. Stat4 can bind to single IFN-γ-activated sites (GASs) as a dimer or bind two tandem GASs as a pair of STAT dimers, or tetramer, stabilized through N-terminal domain (N domain) interactions between dimers.

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9

Guo, DanQun, James D. Dunbar, Chuan He Yang, Lawrence M. Pfeffer, and David B. Donner. "Induction of Jak/STAT Signaling by Activation of the Type 1 TNF Receptor." Journal of Immunology 160, no. 6 (1998): 2742–50. http://dx.doi.org/10.4049/jimmunol.160.6.2742.

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Abstract Cellular responses to TNF are initiated by either of two cell surface receptors, the type 1 TNF receptor (TNFR1) and the type 2 TNF receptor (TNFR2). Although neither receptor contains an intrinsic protein tyrosine kinase, such activity has been implicated in TNF action. In this study, we show that murine TNF induces the tyrosine phosphorylation and activation of the intracellular Janus tyrosine kinases Jak1, Jak2, and Tyk2 in murine 3T3-L1 adipocytes. Activation of Jak kinases by TNF was associated with tyrosine phosphorylation of STAT1, STAT3, STAT5, and STAT6, but not STAT2 or STAT

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10

Morgan, Ethan L., and Andrew Macdonald. "Manipulation of JAK/STAT Signalling by High-Risk HPVs: Potential Therapeutic Targets for HPV-Associated Malignancies." Viruses 12, no. 9 (2020): 977. http://dx.doi.org/10.3390/v12090977.

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Human papillomaviruses (HPVs) are small, DNA viruses that cause around 5% of all cancers in humans, including almost all cervical cancer cases and a significant proportion of anogenital and oral cancers. The HPV oncoproteins E5, E6 and E7 manipulate cellular signalling pathways to evade the immune response and promote virus persistence. The Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) pathway has emerged as a key mediator in a wide range of important biological signalling pathways, including cell proliferation, cell survival and the immune response. While STAT1 and

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11

Miyakawa, Y., A. Oda, BJ Druker, et al. "Thrombopoietin induces tyrosine phosphorylation of Stat3 and Stat5 in human blood platelets." Blood 87, no. 2 (1996): 439–46. http://dx.doi.org/10.1182/blood.v87.2.439.bloodjournal872439.

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Thrombopoietin is known to be essential for megakaryocytopoiesis and thrombopoiesis. Recently, we and others have shown that thrombopoietin induces rapid tyrosine phosphorylation of Jak2 and other proteins in human platelets and BaF3 cells, genetically engineered to express c- Mpl, a receptor for thrombopoietin. The Jak family of tyrosine kinases are known to mediate some of the effects of cytokines or hematopoietic growth factors by recruitment and tyrosine phosphorylation of a variety of Stat (signal transducers and activators of transcription) proteins. Hence, we have investigated whether S

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12

Mirza, Noweeda, Soraya Zorro Manrique, Skylar Cohen, Ana Dominguez, Peter Cohen, and Sandra Gendler. "Aging subverts immune function by dictating alternative STAT responses to cytokine signaling (P5078)." Journal of Immunology 190, no. 1_Supplement (2013): 180.22. http://dx.doi.org/10.4049/jimmunol.190.supp.180.22.

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Abstract Chronic inflammation in the aged closely resembles tumor-induced immune suppression, manifested as a progressive T1→T2 shift and an increased presence of MDSCs. We hypothesize that reversing these age-related phenomena should reduce the elderly’s heightened susceptibility to malignancy. We have now optimized real-time analyses of phosphorylated STATs in murine T cells and MDSCs in order to correlate STAT activation with immune suppression. Both young and old T cells responded to IL-4 stimulation with STAT6 activation and to IFN-γ stimulation with STAT1 activation. Uniquely, however, y

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Demirci Yildirim, T., A. Kahraman Akkalp, A. Köken Avşar, F. Onen, S. Akar, and İ. Sari. "AB1480 EXPRESSION OF JAK-STAT SIGNALING PATHWAY IN HIDRADENITIS SUPPURATIVA PATHOLOGICAL BIOPSY SPECIMENS." Annals of the Rheumatic Diseases 82, Suppl 1 (2023): 1969.2–1969. http://dx.doi.org/10.1136/annrheumdis-2023-eular.993.

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BackgroundHidradenitis suppurativa (HS) is inflammatory skin disease with an unknown etiology. JAK-STAT pathway may be implicated in its pathogenesis. Considering the unmet need in the treatment of inflammatory skin diseases, assessment of the JAK/STAT pathway could provide new understanding in the pathogenesis of these disorders. Therefore, in this study we primarily intended to investigate this pathway in patients with HS.ObjectivesHerein we aimed to investigate the JAK/STAT signaling pathway in the skin biopsies of HS patients and compared with psoriasis (PSO) and healthy subject.MethodsThi

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14

Jones, Dan, Justin Windham, Brian Stewart, Luis Fayad, Alma Rodriguez, and Fredrick B. Hagemeister. "Differential JAK-STAT Pathway Activation in Primary Mediastinal Large B-Cell Lymphoma: Two Subgroups with Differential Cytokine Activation Patterns and Predicted Responses to Kinase Inhibitors." Blood 114, no. 22 (2009): 968. http://dx.doi.org/10.1182/blood.v114.22.968.968.

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Abstract Abstract 968 Background: Primary mediastinal large B-cell lymphoma (PMBCL) is a specialized type of diffuse large B-cell lymphoma which shows diagnostic and pathogenetic overlap with mediastinal classical Hodgkin lymphoma. Approximately 60% of patients with PMBCL have good response to conventional chemoradiotherapy with the rest often showing distant relapses. Microarray studies of PMBCL have revealed overexpression of components and targets of the JAK-STAT signaling pathways including upregulation of IL13 receptor and STAT1; a subset of PMBCL have genome amplification of JAK2 or dele

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15

Liu, Shasha, Feng Qiu, Rongrong Gu, and Erying Xu. "Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus." International Journal of Molecular Sciences 25, no. 24 (2024): 13589. https://doi.org/10.3390/ijms252413589.

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Signal transducers and activators of transcription (STATs) function both as signal transducers and transcription regulators. STAT proteins are involved in the signaling pathways of cytokines and growth factors; thus, they participate in various life activities and play especially critical roles in antiviral immunity. Convincing evidence suggests that STATs can establish innate immune status through multiple mechanisms, efficiently eliminating pathogens. STAT1 and STAT2 can activate the antiviral status by regulating the interferon (IFN) signal. In turn, suppressor of cytokine signaling-1 (SOCS

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16

Kirito, Keita, Koichi Nakajima, Tomoko Watanabe, et al. "Identification of the human erythropoietin receptor region required for Stat1 and Stat3 activation." Blood 99, no. 1 (2002): 102–10. http://dx.doi.org/10.1182/blood.v99.1.102.

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Signal transducers and activators of transcription (Stat) proteins play important roles in the regulation of hematopoiesis as downstream molecules of cytokine signal transduction. It was previously demonstrated that erythropoietin (EPO), a major regulator of erythropoiesis, activates 3 different Stat members, Stat1, Stat3, and Stat5, in a human EPO-dependent cell line, UT-7/EPO. To clarify the mechanism by which EPO activates Stat1 and Stat3 via the EPO receptor (EPOR), a series of chimeric receptors was constructed bearing the extracellular domain of the granulocyte colony-stimulating factor

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Alunno, Alessia, Ivan Padjen, Antonis Fanouriakis, and Dimitrios T. Boumpas. "Pathogenic and Therapeutic Relevance of JAK/STAT Signaling in Systemic Lupus Erythematosus: Integration of Distinct Inflammatory Pathways and the Prospect of Their Inhibition with an Oral Agent." Cells 8, no. 8 (2019): 898. http://dx.doi.org/10.3390/cells8080898.

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Four Janus kinases (JAKs) (JAK1, JAK2, JAK3, TYK2) and seven signal transducers and activators of transcription (STATs) (STAT1, STAT2, STAT3, STAT4, STAT5A, STAT5B, STAT6) mediate the signal transduction of more than 50 cytokines and growth factors in many different cell types. Located intracellularly and downstream of cytokine receptors, JAKs integrate and balance the actions of various signaling pathways. With distinct panels of STAT-sensitive genes in different tissues, this highly heterogeneous system has broad in vivo functions playing a crucial role in the immune system. Thus, the JAK/ST

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Gupta, Sanjay, Man Jiang та Alessandra B. Pernis. "IFN-α Activates Stat6 and Leads to the Formation of Stat2:Stat6 Complexes in B Cells". Journal of Immunology 163, № 7 (1999): 3834–41. http://dx.doi.org/10.4049/jimmunol.163.7.3834.

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Abstract IFN-α consists of a family of highly homologous proteins, which exert pleiotropic effects on a wide variety of cell types. The biologic activities of IFN-α are mediated by its binding to a multicomponent receptor complex resulting in the activation of the Janus kinase-STAT signaling pathway. In most cell types, activation of Stat1 and Stat2 by IFN-α leads to the formation of either STAT homo-/heterodimers or of the IFN-stimulated gene factor 3 complex composed of Stat1, Stat2, and p48, a non-STAT protein. These distinct transcriptional complexes then target two different sets of cis-e

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Roby, Justin Alexander, Brian C. Keller, Hilario J. Ramos, Michael S. Diamond, and Michael J. Gale. "The JAK/STAT signaling cascades of multiple cytokines are dysregulated during West Nile virus infection." Journal of Immunology 196, no. 1_Supplement (2016): 217.38. http://dx.doi.org/10.4049/jimmunol.196.supp.217.38.

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Abstract The neurotropic arthropod-borne flavivirus West Nile virus (WNV) is responsible for sporadic outbreaks of fever and encephalitis in infected humans, with an almost global distribution of circulating strains. During WNV infection in mammals Interferon-α/β (IFN-α/β) drives signaling through JAK/STAT pathways to enhance the expression of antiviral genes with an overall protective effect against WNV infection. However, WNV strains have been demonstrated to be able to antagonize IFN-α/β signaling within infected cells, interrupting this JAK/STAT cascade and promoting viral replication. We

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Mukaddam, Khaled, Sabrina Ruggiero, Steffen M. Berger, et al. "Cytokines Activate JAK–STAT Signaling Pathway in MG-63 Cells on Titanium and Zirconia." Materials 15, no. 16 (2022): 5621. http://dx.doi.org/10.3390/ma15165621.

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Although titanium has been traditionally used as the gold standard for dental implants, recent years have seen the widespread application of zirconia implants given their superiority with regards to reduced bacterial adhesion, inflammation and cellular-interaction in terms of bio-compatibility. The JAK–STAT signaling pathway plays an important role in bone remodeling and formation. The aim of the study was to investigate the activation of the JAK–STAT pathway through different cytokines in osteoblast-like cells (MG-63) on zirconia in comparison to titanium discs. IFN-γ induced the very strong

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Ociepa, Kamila, Marian Danilewicz, Małgorzata Wągrowska-Danilewicz, et al. "Expression of the Selected Proteins of JAK/STAT Signaling Pathway in Diseases with Oral Mucosa Involvement." International Journal of Molecular Sciences 24, no. 1 (2022): 323. http://dx.doi.org/10.3390/ijms24010323.

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Background: The JAK/STAT signal pathway is a system of intracellular proteins used by many cytokines and growth factors to express genes responsible for the process of cell activation, proliferation and differentiation. There has been numerous inflammatory and autoimmune diseases identified where the JAK/STAT signaling is disrupted; however, there are only a few papers concerning autoimmune bullous diseases published. The aim of this study was to evaluate the expression of proteins: JAK3, STAT2, STAT4 and STAT6 in epithelium lesions in patients with pemphigus vulgaris (PV), bullous pemphigoid

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Saharinen, Pipsa, Niklas Ekman, Krista Sarvas, Peter Parker, Kari Alitalo та Olli Silvennoinen. "The Bmx Tyrosine Kinase Induces Activation of the Stat Signaling Pathway, Which Is Specifically Inhibited by Protein Kinase Cδ". Blood 90, № 11 (1997): 4341–53. http://dx.doi.org/10.1182/blood.v90.11.4341.

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Abstract Members of the hematopoietically expressed Tec tyrosine kinase family have an important role in hematopoietic signal transduction, as exemplified by the crucial role of Btk for B-cell differentiation and activation. Although a variety of cell surface receptors have been found to activate Tec tyrosine kinases, the specific signaling pathways and substrate molecules used by Tec kinases are still largely unknown. In this study a Tec family kinase, Bmx, was found to induce activation of the Stat signaling pathway. Bmx induced the tyrosine phosphorylation and DNA binding activity of all th

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Saharinen, Pipsa, Niklas Ekman, Krista Sarvas, Peter Parker, Kari Alitalo та Olli Silvennoinen. "The Bmx Tyrosine Kinase Induces Activation of the Stat Signaling Pathway, Which Is Specifically Inhibited by Protein Kinase Cδ". Blood 90, № 11 (1997): 4341–53. http://dx.doi.org/10.1182/blood.v90.11.4341.4341_4341_4353.

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Members of the hematopoietically expressed Tec tyrosine kinase family have an important role in hematopoietic signal transduction, as exemplified by the crucial role of Btk for B-cell differentiation and activation. Although a variety of cell surface receptors have been found to activate Tec tyrosine kinases, the specific signaling pathways and substrate molecules used by Tec kinases are still largely unknown. In this study a Tec family kinase, Bmx, was found to induce activation of the Stat signaling pathway. Bmx induced the tyrosine phosphorylation and DNA binding activity of all the Stat fa

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Parisien, Jean-Patrick, Joe F. Lau, Jason J. Rodriguez, Christina M. Ulane, and Curt M. Horvath. "Selective STAT Protein Degradation Induced by Paramyxoviruses Requires both STAT1 and STAT2 but Is Independent of Alpha/Beta Interferon Signal Transduction." Journal of Virology 76, no. 9 (2002): 4190–98. http://dx.doi.org/10.1128/jvi.76.9.4190-4198.2002.

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ABSTRACT The alpha/beta interferon (IFN-α/β)-induced STAT signal transduction pathway leading to activation of the ISGF3 transcription complex and subsequent antiviral responses is the target of viral pathogenesis strategies. Members of the Rubulavirus genus of the Paramyxovirus family of RNA viruses have acquired the ability to specifically target either STAT1 or STAT2 for proteolytic degradation as a countermeasure for evading IFN responses. While type II human parainfluenza virus induces STAT2 degradation, simian virus 5 induces STAT1 degradation. The components of the IFN signaling system

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Palmroth, M., K. Kuuliala, R. Peltomaa, et al. "AB0250 TOFACITINIB SUPPRESSES SEVERAL JAK-STAT PATHWAYS IN RHEUMATOID ARTHRITIS AND BASELINE SIGNALING PROFILE ASSOCIATES WITH TREATMENT RESPONSE." Annals of the Rheumatic Diseases 80, Suppl 1 (2021): 1150.2–1151. http://dx.doi.org/10.1136/annrheumdis-2021-eular.448.

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Background:Cytokines are important mediators of inflammation and tissue destruction in rheumatoid arthritis (RA) 1. Several cytokines involved in RA pathogenesis act through Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway 2. The effects of JAK-inhibitor tofacitinib on cytokine signaling in vitro are well established, while in vivo evidence in patients remains scarce.Objectives:To investigate in vivo in rheumatoid arthritis patients i) which JAK-STAT pathways are inhibited by tofacitinib and ii) if baseline signaling profile is associated with the treatment re

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Ulane, Christina M., Alex Kentsis, Cristian D. Cruz, Jean-Patrick Parisien, Kristi L. Schneider, and Curt M. Horvath. "Composition and Assembly of STAT-Targeting Ubiquitin Ligase Complexes: Paramyxovirus V Protein Carboxyl Terminus Is an Oligomerization Domain." Journal of Virology 79, no. 16 (2005): 10180–89. http://dx.doi.org/10.1128/jvi.79.16.10180-10189.2005.

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ABSTRACT Transcription regulators STAT1 and STAT2 are key components of the interferon signaling system leading to innate antiviral immunity. The related STAT3 protein is a regulator of interleukin-6-type cytokine signals and can contribute to both cell growth and death important for cancer gene regulation and tumor survival. These three STAT proteins are targeted for proteasome-mediated degradation by RNA viruses in the Rubulavirus genus of the Paramyxoviridae. A single viral protein, the V protein, assembles STAT-specific ubiquitin ligase complexes from cellular components. Simian virus 5 (S

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Yu, C. R., J. X. Lin, D. W. Fink, S. Akira, E. T. Bloom, and A. Yamauchi. "Differential utilization of Janus kinase-signal transducer activator of transcription signaling pathways in the stimulation of human natural killer cells by IL-2, IL-12, and IFN-alpha." Journal of Immunology 157, no. 1 (1996): 126–37. http://dx.doi.org/10.4049/jimmunol.157.1.126.

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Abstract IL-2-, IL-12-, and IFN-alpha-mediated signaling pathways were analyzed in primary NK cells and in the NK3.3 cell line. Gel mobility shift and immunoprecipitation analyses revealed that in addition to activating STAT3 (signal transducer and activator of transcription-3) and STAT5, IL-2 induced tyrosine and serine phosphorylation of STAT1 alpha, which formed IFN-gamma-activated sequence-binding complexes by itself and with STAT3. Although IL-2 and IFN-alpha activated STAT1 alpha and STAT5, IL-2 predominantly activated STAT5, while IFN-alpha predominantly activated STAT1 alpha. IL-2 indu

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Weber-Nordt, RM, C. Egen, J. Wehinger, et al. "Constitutive activation of STAT proteins in primary lymphoid and myeloid leukemia cells and in Epstein-Barr virus (EBV)-related lymphoma cell lines." Blood 88, no. 3 (1996): 809–16. http://dx.doi.org/10.1182/blood.v88.3.809.809.

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Abstract Although various molecular mechanisms of STAT protein (signal transducers and activators of transcription) activation have been identified, little is known about the functional role of STAT-dependent transcriptional activation. Herein we report the constitutive nuclear localization, phosphorylation, and DNA-binding activity of STAT proteins in leukemia cells and lymphoma cell lines. With the use of oligonucleotide probes derived from the Fc gamma RI promoter, the beta- casein promoter and a STAT-binding element in the promoter of the Bci-2 gene constitutive activation of STAT proteins

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Weber-Nordt, RM, C. Egen, J. Wehinger, et al. "Constitutive activation of STAT proteins in primary lymphoid and myeloid leukemia cells and in Epstein-Barr virus (EBV)-related lymphoma cell lines." Blood 88, no. 3 (1996): 809–16. http://dx.doi.org/10.1182/blood.v88.3.809.bloodjournal883809.

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Although various molecular mechanisms of STAT protein (signal transducers and activators of transcription) activation have been identified, little is known about the functional role of STAT-dependent transcriptional activation. Herein we report the constitutive nuclear localization, phosphorylation, and DNA-binding activity of STAT proteins in leukemia cells and lymphoma cell lines. With the use of oligonucleotide probes derived from the Fc gamma RI promoter, the beta- casein promoter and a STAT-binding element in the promoter of the Bci-2 gene constitutive activation of STAT proteins was dete

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Gouilleux-Gruart, V., F. Gouilleux, C. Desaint, et al. "STAT-related transcription factors are constitutively activated in peripheral blood cells from acute leukemia patients." Blood 87, no. 5 (1996): 1692–97. http://dx.doi.org/10.1182/blood.v87.5.1692.1692.

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Abstract A signal transduction pathway activated by many cytokines has recently been elaborated. The JAK kinases and the signal transducers and activators of transcription (STAT) factors have been found to be essential components. In this report, we describe the presence of constitutively activated STAT factors in peripheral blood cells from patients with acute leukemia. We used oligonucleotide probes from the beta-casein and IRF-1 gene promoters and the ISRE probe to detect STAT proteins in nuclear extracts from acute leukemia cells in bandshift assays. Specific DNA protein complex formation

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Gouilleux-Gruart, V., F. Gouilleux, C. Desaint, et al. "STAT-related transcription factors are constitutively activated in peripheral blood cells from acute leukemia patients." Blood 87, no. 5 (1996): 1692–97. http://dx.doi.org/10.1182/blood.v87.5.1692.bloodjournal8751692.

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A signal transduction pathway activated by many cytokines has recently been elaborated. The JAK kinases and the signal transducers and activators of transcription (STAT) factors have been found to be essential components. In this report, we describe the presence of constitutively activated STAT factors in peripheral blood cells from patients with acute leukemia. We used oligonucleotide probes from the beta-casein and IRF-1 gene promoters and the ISRE probe to detect STAT proteins in nuclear extracts from acute leukemia cells in bandshift assays. Specific DNA protein complex formation was obser

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Palosaari, Heidi, Jean-Patrick Parisien, Jason J. Rodriguez, Christina M. Ulane, and Curt M. Horvath. "STAT Protein Interference and Suppression of Cytokine Signal Transduction by Measles Virus V Protein." Journal of Virology 77, no. 13 (2003): 7635–44. http://dx.doi.org/10.1128/jvi.77.13.7635-7644.2003.

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ABSTRACT Measles virus, a paramyxovirus of the Morbillivirus genus, is responsible for an acute childhood illness that infects over 40 million people and leads to the deaths of more than 1 million people annually (C. J. Murray and A. D. Lopez, Lancet 349:1269-1276, 1997). Measles virus infection is characterized by virus-induced immune suppression that creates susceptibility to opportunistic infections. Here we demonstrate that measles virus can inhibit cytokine responses by direct interference with host STAT protein-dependent signaling systems. Expression of the measles V protein prevents alp

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Zhao, Lan-Juan, Sheng-Fei He, Yuan Liu, Ping Zhao, Zhong-Qi Bian, and Zhong-Tian Qi. "Inhibition of STAT Pathway Impairs Anti-Hepatitis C Virus Effect of Interferon Alpha." Cellular Physiology and Biochemistry 40, no. 1-2 (2016): 77–90. http://dx.doi.org/10.1159/000452526.

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Background/Aims: Signal transducer and activator of transcription (STAT) pathway plays an important role in antiviral efficacy of interferon alpha (IFN-α). IFN-α is the main therapeutic against hepatitis C virus (HCV) infection. We explored effects of IFN-α on HCV replication and antiviral gene expression by targeting STAT. Methods: In response to IFN-α, STAT status, HCV replication, and antiviral gene expression were analyzed in human hepatoma Huh7.5.1 cells before and after cell culture-derived HCV infection. Results: IFN-α treatment induced expression and phosphorylation of STAT1 and STAT2

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Read, Kaitlin, Bharath Sreekumar, Michael Duane Powell, Devin Jones, and Kenneth J. Oestreich. "Ikaros zinc finger transcription factors as novel regulators of STAT factor activity." Journal of Immunology 202, no. 1_Supplement (2019): 64.3. http://dx.doi.org/10.4049/jimmunol.202.supp.64.3.

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Abstract Cytokine signaling is important for the differentiation and function of a number of cell types, including lymphocyte populations. One mechanism by which cytokine signals are propagated is via phosphorylation-mediated activation of Signal Transducer and Activator of Transcription (STAT) factors, which directly regulate cell type-specific gene programs. We recently identified novel regulatory modules composed of STAT and Ikaros Zinc Finger (IkZF) transcription factors in CD4+ T cell populations. Specifically, we found that IkZF/STAT modules composed of Aiolos/STAT3 and Eos/STAT5 directl

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Wang, Kathy S., Jerome Ritz, and David A. Frank. "IL-2 Induces STAT4 Activation in Primary NK Cells and NK Cell Lines, But Not in T Cells." Journal of Immunology 162, no. 1 (1999): 299–304. http://dx.doi.org/10.4049/jimmunol.162.1.299.

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Abstract IL-2 exerts potent but distinct functional effects on two critical cell populations of the immune system, T cells and NK cells. Whereas IL-2 leads to proliferation in both cell types, it enhances cytotoxicity primarily in NK cells. In both T cells and NK cells, IL-2 induces the activation of STAT1, STAT3, and STAT5. Given this similarity in intracellular signaling, the mechanism underlying the distinct response to IL-2 in T cells and NK cells is not clear. In this study, we show that in primary NK cells and NK cell lines, in addition to the activation of STAT1 and STAT5, IL-2 induces

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Higashi, Takehiro, Junichi Tsukada, Takamitsu Mizobe, et al. "Synergistic Transactivation of the Sis-Inducible Element by STAT4/STAT3 Heterodimer in Cytokine Signal Cascade." Blood 108, no. 11 (2006): 1119. http://dx.doi.org/10.1182/blood.v108.11.1119.1119.

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Abstract Signal transducer and activator of transcription (STAT) proteins are activated in response to cytokine stimulation. STAT3 is activated in response to interleukin (IL)-6 family of cytokines, following activation of Janus family of tyrosine kinases JAK1 and JAK2, which in turn phosphorylate STAT3 on tyrosine 705 (tyr-705). On the other hand, STAT4 is activated in response to IL-12 following activation of Janus family of tyrosine kinases JAK2 and Tyk2, which in turn phosphorylate STAT4 on tyrosine 693 (tyr-693). p38/MKK6 signaling pathway activated by IL-12 further phosphorylates STAT4 o

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37

de Koning, JP, F. Dong, L. Smith, et al. "The membrane-distal cytoplasmic region of human granulocyte colony- stimulating factor receptor is required for STAT3 but not STAT1 homodimer formation." Blood 87, no. 4 (1996): 1335–42. http://dx.doi.org/10.1182/blood.v87.4.1335.bloodjournal8741335.

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Signal transduction from the granulocyte colony-stimulating factor receptor (G-CSF-R) involves the activation of the Janus tyrosine kinase/signal transducer and activator of transcription (Jak/STAT) pathway. G-CSF induces tyrosine phosphorylation of Jak1, Jak2, STAT1, and STAT3. The membrane-proximal region of G-CSF-R is sufficient for activation of Jaks. It is still unclear how STAT proteins are activated by G-CSF-R. We investigated the possible involvement of the C-terminal region of G-CSF-R in the recruitment of STAT proteins using BAF3 cell transfectants expressing wild type (WT) G-CSF-R,

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38

Gowing, H., M. Lawler, A. Hagenbeek, et al. "Effect of ultraviolet-B light on lymphocyte activity at doses at which normal bone marrow stem cells are preserved." Blood 87, no. 4 (1996): 1635–43. http://dx.doi.org/10.1182/blood.v87.4.1635.bloodjournal8741635.

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Signal transduction from the granulocyte colony-stimulating factor receptor (G-CSF-R) involves the activation of the Janus tyrosine kinase/signal transducer and activator of transcription (Jak/STAT) pathway. G-CSF induces tyrosine phosphorylation of Jak1, Jak2, STAT1, and STAT3. The membrane-proximal region of G-CSF-R is sufficient for activation of Jaks. It is still unclear how STAT proteins are activated by G-CSF-R. We investigated the possible involvement of the C-terminal region of G-CSF-R in the recruitment of STAT proteins using BAF3 cell transfectants expressing wild type (WT) G-CSF-R,

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39

Standing, David, Emma Feess, Satvik Kodiyalam, et al. "The Role of STATs in Ovarian Cancer: Exploring Their Potential for Therapy." Cancers 15, no. 9 (2023): 2485. http://dx.doi.org/10.3390/cancers15092485.

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Ovarian cancer (OvCa) is a deadly gynecologic malignancy that presents many clinical challenges due to late-stage diagnoses and the development of acquired resistance to standard-of-care treatment protocols. There is an increasing body of evidence suggesting that STATs may play a critical role in OvCa progression, resistance, and disease recurrence, and thus we sought to compile a comprehensive review to summarize the current state of knowledge on the topic. We have examined peer reviewed literature to delineate the role of STATs in both cancer cells and cells within the tumor microenvironment

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Takeda, Takashi, Hirohisa Kurachi, Toshiya Yamamoto, et al. "Participation of JAK, STAT and unknown proteins in human placental lactogen-induced signaling: a unique signaling pathway different from prolactin and growth hormone." Journal of Endocrinology 153, no. 1 (1997): R1—R3. http://dx.doi.org/10.1677/joe.0.153r001.

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Abstract The signal transduction mechanism involved in human placental lactogen (hPL) was studied. We have identified that hPL rapidly stimulated the tyrosine phosphorylation of at least 7 proteins including Janus Kinases (JAK1 and JAK2) and a signal transducer and activator of transcription protein (Stat3). This is the first evidence that the JAK-STAT pathway is involved in the hPL signaling. Moreover, two unknown proteins which were different from STAT proteins (Stat1, 3 and 5) in sizes were predominantly tyrosine-phosphorylated. Because human growth hormone (hGH) activates Stat1, 3, 5 and h

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Owen, Katie L., Natasha K. Brockwell, and Belinda S. Parker. "JAK-STAT Signaling: A Double-Edged Sword of Immune Regulation and Cancer Progression." Cancers 11, no. 12 (2019): 2002. http://dx.doi.org/10.3390/cancers11122002.

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Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling mediates almost all immune regulatory processes, including those that are involved in tumor cell recognition and tumor-driven immune escape. Antitumor immune responses are largely driven by STAT1 and STAT2 induction of type I and II interferons (IFNs) and the downstream programs IFNs potentiate. Conversely, STAT3 has been widely linked to cancer cell survival, immunosuppression, and sustained inflammation in the tumor microenvironment. The discovery of JAK-STAT cross-regulatory mechanisms, post-translational con

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Polak, Chernosky, Smigiel, Tamagno, and Jackson. "Balancing STAT Activity as a Therapeutic Strategy." Cancers 11, no. 11 (2019): 1716. http://dx.doi.org/10.3390/cancers11111716.

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Driven by dysregulated IL-6 family member cytokine signaling in the tumor microenvironment (TME), aberrant signal transducer and activator of transcription (STAT3) and (STAT5) activation have been identified as key contributors to tumorigenesis. Following transformation, persistent STAT3 activation drives the emergence of mesenchymal/cancer-stem cell (CSC) properties, important determinants of metastatic potential and therapy failure. Moreover, STAT3 signaling within tumor-associated macrophages and neutrophils drives secretion of factors that facilitate metastasis and suppress immune cell fun

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Liang, Zengenni, Zhi-Hang Yuan, Yan Wang, et al. "New Mechanistic Insight into the Protective Effects of Ganoderma lucidum Polysaccharides Against Palmitic Acid-Induced Cell Damage in Porcine Intestinal Epithelial Cell Line IPEC-J2." Natural Product Communications 17, no. 11 (2022): 1934578X2211281. http://dx.doi.org/10.1177/1934578x221128103.

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Ganoderma lucidum ( G. lucidum) is one of the well-known mushrooms in China, which has G. lucidum polysaccharides (GLP) that have been widely studied for various biological activities, such as antioxidant, antitumor, antiinflammatory, antiviral, antidiabetes, and immunomodulatory activities. A signal transducer and activator of transcription (STAT) signaling pathway is related to cell proliferation and apoptosis. The relationship between STAT and intestinal protection of GLP is still unknown. We studied the inhibitors AG490 in the STAT pathway and its downstream molecules to analyze the unique

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Zare, F., M. Dehghan-Manshadi, and A. Mirshafiey. "The signal transducer and activator of transcription factors lodge in immunopathogenesis of rheumatoid arthritis." Reumatismo 67, no. 4 (2016): 127. http://dx.doi.org/10.4081/reumatismo.2015.851.

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Rheumatoid arthritisis (RA) is a chronic autoimmune disorder that affects ~1-2% of the world’s population and damages synovial joints. RA is characterized by inflammation, autoantibody production, cartilage and bone destruction and synovial hyperplasia. Inflammation induces systemic and articular synthesis of pro-inflammatory cytokines, such as tumor necrosis factor alpha and interleukin-6 that play essential roles in joint and other organ damage in this disease. Considering the role of signal transducer and activator of transcription factors (STATs) in signaling of these cytokines, these prot

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Komyod, Waraporn, Uta-Maria Bauer, Peter C. Heinrich, Serge Haan, and Iris Behrmann. "Are STATS Arginine-methylated?" Journal of Biological Chemistry 280, no. 23 (2005): 21700–21705. http://dx.doi.org/10.1074/jbc.c400606200.

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Transcription factors of the STAT (signal transducer and activator of transcription) family are important in signal transduction of cytokines. They are subject to post-translational modification by phosphorylation on tyrosine and serine residues. Recent evidence suggested that STATs are methylated on a conserved arginine residue within the N-terminal region. STAT arginine methylation has been described to be important for STAT function and loss of arginine methylation was discussed to be involved in interferon resistance of cancer cells. Here we provide several independent lines of evidence in

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Matikainen, Sampsa, Timo Sareneva, Tapani Ronni, Anne Lehtonen, Päivi J. Koskinen, and Ilkka Julkunen. "Interferon- Activates Multiple STAT Proteins and Upregulates Proliferation-Associated IL-2R, c-myc, and pim-1 Genes in Human T Cells." Blood 93, no. 6 (1999): 1980–91. http://dx.doi.org/10.1182/blood.v93.6.1980.406k20_1980_1991.

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Interferon- (IFN-) is a pleiotropic cytokine that has antiviral, antiproliferative, and immunoregulatory functions. There is increasing evidence that IFN- has an important role in T-cell biology. We have analyzed the expression ofIL-2R, c-myc, and pim-1 genes in anti-CD3–activated human T lymphocytes. The induction of these genes is associated with interleukin-2 (IL-2)–induced T-cell proliferation. Treatment of T lymphocytes with IFN-, IL-2, IL-12, and IL-15 upregulated IL-2R, c-myc, andpim-1 gene expression. IFN- also sensitized T cells to IL-2–induced proliferation, further suggesting

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Bagby, Grover, Winifred Keeble, Tara Koretsky, et al. "Oxidative Stress Induces Binding of FANCD2 to STAT5 and Facilitates STAT5-Dependent Survival Signals." Blood 104, no. 11 (2004): 33. http://dx.doi.org/10.1182/blood.v104.11.33.33.

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Abstract Fanconi anemia (FA) cells are hypersensitive to oxidative stress and exhibit aberrant STAT activation responses to defined extracellular proteins but whether these abnormalities are linked is unclear. Because oxidative stress is known to induce STAT activation, we hypothesized that proper STAT signaling responses in normal cells exposed to H2O2 require intact FA proteins. In fact, we found that FA-C, FA-G, and FA-D2 cells (fibroblasts) showed a significant increase in apoptosis after H2O2-exposure compared to retrovirally-complemented cells. H2O2 induced higher phospho-STAT5 (P-STAT5)

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Giang, Nguyen Hoang, Nguyen Thanh Huyen, and Nguyen Thi Xuan. "Expression of genes involved in immune regulation in chronic myeloid leukemia." Vietnam Journal of Biotechnology 19, no. 1 (2021): 51–60. http://dx.doi.org/10.15625/1811-4989/14672.

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Chronic myeloid leukemia (CML) is a blood cancer involved in abnormal proliferation of myeloid cells at all stages of differentiation. Translocation of regions of the BCR and ABL genes, leading to the fusion gene BCR-ABL, which forms the Philadelphia (Ph) chromosome, is the cause of more than 90% of CML. The BCR-ABL protein shows abnormal tyrosine kinase activity, leading to changes in proliferation signals including signal transducer and activator of transcriptions (STATs) and nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) and resulting in uncontrolled proliferation of myelo

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Tuyt, Leonore M. L., Krista Bregman, Chantal Lummen, Wim H. A. Dokter, and Edo Vellenga. "Differential Binding Activity of the Transcription Factor LIL-Stat in Immature and Differentiated Normal and Leukemic Myeloid Cells." Blood 92, no. 4 (1998): 1364–73. http://dx.doi.org/10.1182/blood.v92.4.1364.

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Abstract Cytokines and growth factors induce activation of the family of signal transducers and activators of transcription (Stats) that directly activate gene expression. Recently, constitutively activated Stat1, Stat3, and Stat5 were identified in nuclear extracts of acute myeloid leukemia (AML) patients, suggesting involvement of constitutive Stat activity in the events of leukemogenesis. In the present study, blasts of nine AML cases were investigated for the constitutive binding activity of the recently identified transcription factor LIL-Stat (LPS- and IL-1-inducible Stat). Band-shift as

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50

Tuyt, Leonore M. L., Krista Bregman, Chantal Lummen, Wim H. A. Dokter, and Edo Vellenga. "Differential Binding Activity of the Transcription Factor LIL-Stat in Immature and Differentiated Normal and Leukemic Myeloid Cells." Blood 92, no. 4 (1998): 1364–73. http://dx.doi.org/10.1182/blood.v92.4.1364.416k34_1364_1373.

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Cytokines and growth factors induce activation of the family of signal transducers and activators of transcription (Stats) that directly activate gene expression. Recently, constitutively activated Stat1, Stat3, and Stat5 were identified in nuclear extracts of acute myeloid leukemia (AML) patients, suggesting involvement of constitutive Stat activity in the events of leukemogenesis. In the present study, blasts of nine AML cases were investigated for the constitutive binding activity of the recently identified transcription factor LIL-Stat (LPS- and IL-1-inducible Stat). Band-shift assays were

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