Log in

Relevant bibliographies by topics / JAK/STAT Signaling Pathway / Journal articles

To see the other types of publications on this topic, follow the link: JAK/STAT Signaling Pathway.

Journal articles on the topic 'JAK/STAT Signaling Pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 9 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'JAK/STAT Signaling Pathway.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

3

Raivola, Juuli, Teemu Haikarainen, and Olli Silvennoinen. "Characterization of JAK1 Pseudokinase Domain in Cytokine Signaling." Cancers 12, no. 1 (2019): 78. http://dx.doi.org/10.3390/cancers12010078.

Full text

Abstract:

The Janus kinase-signal transducer and activator of transcription protein (JAK-STAT) pathway mediates essential biological functions from immune responses to haematopoiesis. Deregulated JAK-STAT signaling causes myeloproliferative neoplasms, leukaemia, and lymphomas, as well as autoimmune diseases. Thereby JAKs have gained significant relevance as therapeutic targets. However, there is still a clinical need for better JAK inhibitors and novel strategies targeting regions outside the conserved kinase domain have gained interest. In-depth knowledge about the molecular details of JAK activation i

APA, Harvard, Vancouver, ISO, and other styles

4

Malemud, Charles J. "The role of the JAK/STAT signal pathway in rheumatoid arthritis." Therapeutic Advances in Musculoskeletal Disease 10, no. 5-6 (2018): 117–27. http://dx.doi.org/10.1177/1759720x18776224.

Full text

Abstract:

Proinflammatory cytokine activation of the Janus kinase/signal transducers and activators of transcription (JAK/STAT) signal transduction pathway is a critical event in the pathogenesis and progression of rheumatoid arthritis. Under normal conditions, JAK/STAT signaling reflects the influence of negative regulators of JAK/STAT, exemplified by the suppressor of cytokine signaling and protein inhibitor of activated STAT. However, in rheumatoid arthritis (RA) both of these regulators are dysfunctional. Thus, continuous activation of JAK/STAT signaling in RA synovial joints results in the elevated

APA, Harvard, Vancouver, ISO, and other styles

5

Sonkin, Dmitriy, Catherine Regnier, Xianhui Rong, et al. "Identification of pSTAT5 gene signature in hematologic malignancy." Journal of Clinical Oncology 31, no. 15_suppl (2013): 7111. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.7111.

Full text

Abstract:

7111 Background: The JAK/STAT pathway is an important signaling pathway downstream of multiple cytokine and growth factor receptors. Receptor-associated JAKs are activated following receptor-ligand binding. Activated JAKs phosphorylate STAT proteins, which then dimerize and translocate to the nucleus where they modulate the expression of target genes. Dysregulated JAK/STAT signaling has been implicated in the pathogenesis of multiple human malignancies. Activating mutations in JAK2 and the associated activation of STAT5 in myeloproliferative neoplasia is one example of the involvement of this

APA, Harvard, Vancouver, ISO, and other styles

6

Andl, Claudia D., Takaaki Mizushima, Kenji Oyama, Mark Bowser, Hiroshi Nakagawa, and Anil K. Rustgi. "EGFR-induced cell migration is mediated predominantly by the JAK-STAT pathway in primary esophageal keratinocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 6 (2004): G1227—G1237. http://dx.doi.org/10.1152/ajpgi.00253.2004.

Full text

Abstract:

The epidermal growth factor receptor (EGFR) activates several signaling cascades in response to epidermal growth factor stimulation. One of these signaling events involves tyrosine phosphorylation of signal transducer and activator of transcription (STAT), whereas another involves activation of the phosphatidylinositol 3-OH kinase pathway. Two possibilities for STAT activation exist: a janus kinase (JAK)-dependent and a JAK-independent mechanism. Herein, we demonstrate that EGFR overexpression in primary esophageal keratinocytes activates STAT in a JAK-dependent fashion with the functional con

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

8

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

10

Zheng, Ying, Hongwei Qin, Stuart J. Frank, et al. "A CK2-dependent mechanism for activation of the JAK-STAT signaling pathway." Blood 118, no. 1 (2011): 156–66. http://dx.doi.org/10.1182/blood-2010-01-266320.

Full text

Abstract:

Abstract JAK-STAT signaling is involved in the regulation of cell survival, proliferation, and differentiation. JAK tyrosine kinases can be transiently activated by cytokines or growth factors in normal cells, whereas they become constitutively activated as a result of mutations that affect their function in tumors. Specifically, the JAK2V617F mutation is present in the majority of patients with myeloproliferative disorders (MPDs) and is implicated in the pathogenesis of these diseases. In the present study, we report that the kinase CK2 is a novel interaction partner of JAKs and is essential

APA, Harvard, Vancouver, ISO, and other styles

11

Banes, Amy K. L., Seán M. Shaw, Amany Tawfik, et al. "Activation of the JAK/STAT pathway in vascular smooth muscle by serotonin." American Journal of Physiology-Cell Physiology 288, no. 4 (2005): C805—C812. http://dx.doi.org/10.1152/ajpcell.00385.2004.

Full text

Abstract:

Serotonin (5-hydroxytryptamine, 5-HT) is a vasoconstrictor and mitogen whose levels are elevated in diabetes. Previous studies have shown the presence of 5-HT2A, 5-HT2B, and 5-HT1B receptors in vascular smooth muscle cells (VSMCs). There are currently no data regarding 5-HT2B and 5-HT1B receptor activation of the JAK/STAT pathway in VSMCs and resultant potential alterations in 5-HT signaling in diabetes. Therefore, we tested the hypothesis that 5-HT differentially activates the JAK/STAT pathway in VSMCs under conditions of normal (5 mM) and high (25 mM) glucose. Treatment of rat VSMCs with 5-H

APA, Harvard, Vancouver, ISO, and other styles

12

Rawlings, J. S. "The JAK/STAT signaling pathway." Journal of Cell Science 117, no. 8 (2004): 1281–83. http://dx.doi.org/10.1242/jcs.00963.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

Pfeifer, Andrea C., Jens Timmer, and Ursula Klingmüller. "Systems biology of JAK/STAT signalling." Essays in Biochemistry 45 (September 30, 2008): 109–20. http://dx.doi.org/10.1042/bse0450109.

Full text

Abstract:

Signalling in multicellular organisms is mediated by complex networks that integrate extracellular and intracellular signals to generate appropriate responses regulating cell proliferation, differentiation and survival. Downstream of many cytokine and growth hormone receptors, receptor-associated JAKs (Janus kinases) activate transcription factors of the STAT (signal transducer and activator of transcription) protein family and thereby mediate signal transduction from the plasma membrane to the nucleus. The JAK/STAT pathway has been shown to be constitutively activated in a wide array of human

APA, Harvard, Vancouver, ISO, and other styles

14

Moser, Bernhard, Sophie Edtmayer, Agnieszka Witalisz-Siepracka, and Dagmar Stoiber. "The Ups and Downs of STAT Inhibition in Acute Myeloid Leukemia." Biomedicines 9, no. 8 (2021): 1051. http://dx.doi.org/10.3390/biomedicines9081051.

Full text

Abstract:

Aberrant Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling is implicated in the pathogenesis of acute myeloid leukemia (AML), a highly heterogeneous hematopoietic malignancy. The management of AML is complex and despite impressive efforts into better understanding its underlying molecular mechanisms, survival rates in the elderly have not shown a substantial improvement over the past decades. This is particularly due to the heterogeneity of AML and the need for personalized approaches. Due to the crucial role of the deregulated JAK-STAT signaling in AML, select

APA, Harvard, Vancouver, ISO, and other styles

15

Pérez, Cristina, Julia Gonzalez-Rincon, Carmen Almaraz, et al. "A Role of JAK/STAT Pathway in Cutaneous T-Cell Lymphomas: Exploring Its Effects for Targeted Therapy." Blood 124, no. 21 (2014): 4498. http://dx.doi.org/10.1182/blood.v124.21.4498.4498.

Full text

Abstract:

Abstract INTRODUCTION Development of targeted therapy in Cutaneous T-Cell Lymphoma (CTCL) patients still requires actionable mutated genes and deregulated pathways to be identified. We have recently published the mutational status of a number of human CTCL lesions, and found JAK/STAT signaling pathway to frequently harbor somatic mutations (Vaqué et al 2014). In this line of evidence, activating mutations in JAK kinases have been reported in human hematological malignancies (Kameda T1 2010) and may serve as indicators for targeted therapy. Therefore, we decided to analyze the mutational status

APA, Harvard, Vancouver, ISO, and other styles

16

Khan, Muhammad Zahoor, Adnan Khan, Jianxin Xiao, et al. "Role of the JAK-STAT Pathway in Bovine Mastitis and Milk Production." Animals 10, no. 11 (2020): 2107. http://dx.doi.org/10.3390/ani10112107.

Full text

Abstract:

The cytokine-activated Janus kinase (JAK)—signal transducer and activator of transcription (STAT) pathway is a sequence of communications between proteins in a cell, and it is associated with various processes such as cell division, apoptosis, mammary gland development, lactation, anti-inflammation, and immunity. The pathway is involved in transferring information from receptors on the cell surface to the cell nucleus, resulting in the regulation of genes through transcription. The Janus kinase 2 (JAK2), signal transducer and activator of transcription A and B (STAT5 A & B), STAT1, and cyt

APA, Harvard, Vancouver, ISO, and other styles

17

Thomas, Sally J., Katherine Fisher, Stephen Brown, John A. Snowden, Sarah Danson, and Martin Zeidler. "Methotrexate Is a Suppressor of JAK/STAT Pathway Activation Which Inhibits JAK2V617F Induced Signalling." Blood 124, no. 21 (2014): 4577. http://dx.doi.org/10.1182/blood.v124.21.4577.4577.

Full text

Abstract:

Abstract The classical myeloproliferative neoplasms (MPNs) are a group of disorders characterised by activation of the JAK/STAT signalling pathway. A large proportion of patients with MPNs have an acquired mutation, JAK2V617F, which causes constitutive kinase activity. Patients with wild-type JAK2 show gene expression patterns characteristic of JAK/STAT activation, and the majority have mutations in other genes associated with increased pathway activation. Inhibition of JAK/STAT activation represents an attractive therapeutic approach for these disorders. In myelofibrosis, treatment with a JAK

APA, Harvard, Vancouver, ISO, and other styles

18

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

19

Gonzalez-Traves, P., B. Murray, F. Campigotto, A. Meng, and J. A. DI Paolo. "THU0067 JAK SELECTIVITY AND THE IMPACT ON CYTOKINE SIGNALING INHIBITION AT CLINICAL RHEUMATOID ARTHRITIS DOSES." Annals of the Rheumatic Diseases 79, Suppl 1 (2020): 246.1–246. http://dx.doi.org/10.1136/annrheumdis-2020-eular.2074.

Full text

Abstract:

Background:Janus kinase 1 (JAK1) inhibitors are efficacious in rheumatoid arthritis (RA). Despite having similar efficacy, in vitro studies have shown differences in JAK selectivity profiles for the small-molecule JAK inhibitors (JAKi) baricitinib (BARI), tofacitinib (TOFA), and upadacitinib (UPA).1For example, BARI and UPA are JAK1/JAK2 selective, while TOFA is JAK1/JAK3 selective, but each JAKi has some activity against other JAKs. As JAKs form signaling pairs, differences in selectivity could lead to distinct pharmacologic profiles that may impact clinical efficacy and safety.Objectives:As

APA, Harvard, Vancouver, ISO, and other styles

20

Xu, FenLan, Liying Xu, Xiaoyan Xu, Zhenhua Huang, and Liang Su. "Dexmedetomidine Inhibited Proliferation and Invasion of Cervical Cancer Cells by Inhibiting the Janus Tyrosine Kinase/Signal Transducer and Activator of Transcription Signaling Pathway." Journal of Biomaterials and Tissue Engineering 11, no. 7 (2021): 1293–304. http://dx.doi.org/10.1166/jbt.2021.2702.

Full text

Abstract:

The role of anesthetics in the treatment of cancer has been reported, but the role of Dexmedetomidine (Dex) in the treatment of cervical cancer (CC) has not been reported.In this study, cell viability and proliferation were determined by MTT and cloning formation assay. The expression of proliferation-related proteins ki67 and PCNA was detected by western blot. Wound healing and transwell detected cell migration and invasion, and western blot detected the expression of migration and invasion related proteins MMP4 and MMP9, and epithelial-mesenchymal transformation (ETM)-related proteins N-cadh

APA, Harvard, Vancouver, ISO, and other styles

21

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

22

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

23

Frost, E. R., E. A. Ford, A. E. Peters, et al. "Signal transducer and activator of transcription (STAT) 1 and STAT3 are expressed in the human ovary and have Janus kinase 1-independent functions in the COV434 human granulosa cell line." Reproduction, Fertility and Development 32, no. 12 (2020): 1027. http://dx.doi.org/10.1071/rd20098.

Full text

Abstract:

Ovarian granulosa cells are fundamental for oocyte maintenance and maturation. Recent studies have demonstrated the importance of members of the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signalling pathway in the granulosa cell population of mouse and horse ovaries, with perturbation of JAK1 signalling in the mouse shown to impair oocyte maintenance and accelerate primordial follicle activation. The presence and role of the JAK/STAT pathway in human granulosa cells has yet to be elucidated. In this study, expression of JAK1, STAT1 and STAT3 was detected in oocy

APA, Harvard, Vancouver, ISO, and other styles

24

Brizzi, Maria Felice, Paola Defilippi, Arturo Rosso, et al. "Integrin-mediated Adhesion of Endothelial Cells Induces JAK2 and STAT5A Activation: Role in the Control of c-fos Gene Expression." Molecular Biology of the Cell 10, no. 10 (1999): 3463–71. http://dx.doi.org/10.1091/mbc.10.10.3463.

Full text

Abstract:

Integrin-mediated adhesion induces several signaling pathways leading to regulation of gene transcription, control of cell cycle entry and survival from apoptosis. Here we investigate the involvement of the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway in integrin-mediated signaling. Plating primary human endothelial cells from umbilical cord and the human endothelial cell line ECV304 on matrix proteins or on antibody to β1- or αv-integrin subunits induces transient tyrosine phosphorylation of JAK2 and STAT5A. Consistent with a role for the JAK/STAT pathw

APA, Harvard, Vancouver, ISO, and other styles

25

Bellucci, Roberto, Allison Martin, Marc Buren, Hong-Nam Nguyen, Davide Bommarito та Jerome Ritz. "JAK1 and JAK2 Modulate Myeloma Cell Susceptibility to NK Cells Through the Interferon Gamma (IFN-γ) Pathway",. Blood 118, № 21 (2011): 3960. http://dx.doi.org/10.1182/blood.v118.21.3960.3960.

Full text

Abstract:

Abstract Abstract 3960 Multiple myeloma (MM) is a B cell neoplasm characterized by clonal expansion of malignant plasma cells in the bone marrow. Despite the use of new drugs such as lenalidomide and bortezomib, MM remains an incurable disease. Successful treatment of MM with allogeneic stem cell transplantation suggests that MM is susceptible to immunologic approaches. NK cells are the primary effectors of the innate immune response against infectious pathogens and malignant transformation. Unlike T and B cells, NK cells do not recognize antigens in the context of classical major histocompati

APA, Harvard, Vancouver, ISO, and other styles

26

O'Connell, Danielle, Belaid Bouazza, Blerina Kokalari та ін. "IFN-γ-induced JAK/STAT, but not NF-κB, signaling pathway is insensitive to glucocorticoid in airway epithelial cells". American Journal of Physiology-Lung Cellular and Molecular Physiology 309, № 4 (2015): L348—L359. http://dx.doi.org/10.1152/ajplung.00099.2015.

Full text

Abstract:

Although the majority of patients with asthma are well controlled by inhaled glucocorticoids (GCs), patients with severe asthma are poorly responsive to GCs. This latter group is responsible for a disproportionate share of health care costs associated with asthma. Recent studies in immune cells have incriminated interferon-γ (IFN-γ) as a possible trigger of GC insensitivity in severe asthma; however, little is known about the role of IFN-γ in modulating GC effects in other clinically relevant nonimmune cells, such as airway epithelial cells. We hypothesized that IFN-γ-induced JAK/STAT-associat

APA, Harvard, Vancouver, ISO, and other styles

27

Li, Willis X., Herve Agaisse, Bernard Mathey-Prevot, and Norbert Perrimon. "Differential requirement for STAT by gain-of-function and wild-type receptor tyrosine kinase Torso in Drosophila." Development 129, no. 18 (2002): 4241–48. http://dx.doi.org/10.1242/dev.129.18.4241.

Full text

Abstract:

Malignant transformation frequently involves aberrant signaling from receptor tyrosine kinases (RTKs). These receptors commonly activate Ras/Raf/MEK/MAPK signaling but when overactivated can also induce the JAK/STAT pathway, originally identified as the signaling cascade downstream of cytokine receptors. Inappropriate activation of STAT has been found in many human cancers. However, the contribution of the JAK/STAT pathway in RTK signaling remains unclear. We have investigated the requirement of the JAK/STAT pathway for signaling by wild-type and mutant forms of the RTK Torso (Tor) using a gen

APA, Harvard, Vancouver, ISO, and other styles

28

Damerau, Alexandra, Timo Gaber, Sarah Ohrndorf, and Paula Hoff. "JAK/STAT Activation: A General Mechanism for Bone Development, Homeostasis, and Regeneration." International Journal of Molecular Sciences 21, no. 23 (2020): 9004. http://dx.doi.org/10.3390/ijms21239004.

Full text

Abstract:

The Janus kinase (JAK) signal transducer and activator of transcription (STAT) signaling pathway serves as an important downstream mediator for a variety of cytokines, hormones, and growth factors. Emerging evidence suggests JAK/STAT signaling pathway plays an important role in bone development, metabolism, and healing. In this light, pro-inflammatory cytokines are now clearly implicated in these processes as they can perturb normal bone remodeling through their action on osteoclasts and osteoblasts at both intra- and extra-articular skeletal sites. Here, we summarize the role of JAK/STAT path

APA, Harvard, Vancouver, ISO, and other styles

29

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

30

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.

Full text

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 the Stat fa

APA, Harvard, Vancouver, ISO, and other styles

31

Callus, Bernard A., and Bernard Mathey-Prevot. "Interleukin-3–Induced Activation of the JAK/STAT Pathway Is Prolonged by Proteasome Inhibitors." Blood 91, no. 9 (1998): 3182–92. http://dx.doi.org/10.1182/blood.v91.9.3182.

Full text

Abstract:

Abstract One facet of cytokine receptor signaling involves the activation of signal transducers and activators of transcription (STATs). STATs are rapidly activated via tyrosine phosphorylation by Janus kinase (JAK) family members and subsequently inactivated within a short period. We investigated the effect of proteasome inhibition on interleukin-3 (IL-3) activation of the JAK/STAT pathway following stimulation of Ba/F3 cells. Treatment of Ba/F3 cells with the proteasome inhibitor,N-acetyl-l-leucinyl-l-leucinyl-norleucinal (LLnL), led to stable tyrosine phosphorylation of the IL-3 receptor, b

APA, Harvard, Vancouver, ISO, and other styles

32

Callus, Bernard A., and Bernard Mathey-Prevot. "Interleukin-3–Induced Activation of the JAK/STAT Pathway Is Prolonged by Proteasome Inhibitors." Blood 91, no. 9 (1998): 3182–92. http://dx.doi.org/10.1182/blood.v91.9.3182.3182_3182_3192.

Full text

Abstract:

One facet of cytokine receptor signaling involves the activation of signal transducers and activators of transcription (STATs). STATs are rapidly activated via tyrosine phosphorylation by Janus kinase (JAK) family members and subsequently inactivated within a short period. We investigated the effect of proteasome inhibition on interleukin-3 (IL-3) activation of the JAK/STAT pathway following stimulation of Ba/F3 cells. Treatment of Ba/F3 cells with the proteasome inhibitor,N-acetyl-l-leucinyl-l-leucinyl-norleucinal (LLnL), led to stable tyrosine phosphorylation of the IL-3 receptor, beta commo

APA, Harvard, Vancouver, ISO, and other styles

33

Gorre, M., I. Jilani, H. Kantarjian, F. Giles, A. Hannah, and M. Albitar. "Novel Quantitative Flow Cytometry-Based Signaling Assays Reveal a Potential Role for HSP90 Inhibitors in the Treatment of JAK2 Mutant-Positive Diseases." Blood 106, no. 11 (2005): 3526. http://dx.doi.org/10.1182/blood.v106.11.3526.3526.

Full text

Abstract:

Abstract The V617F mutation in the JAK2 tyrosine kinase, recently described in a majority of patients with myeloproliferative disorders (MPDs), confers growth factor independence in vitro and oncogenicity in mice. Therefore, targeted inhibition of mutant JAK2 kinase activity may be an effective strategy for treatment of MPD patients with this mutation. The ability to measure the activation status of JAK2 in patient samples will thus be of substantial value for monitoring therapeutic efficacy. We have developed quantitative flow cytometry-based assays for rapid and reproducible measurement of i

APA, Harvard, Vancouver, ISO, and other styles

34

Carlesso, N., D. A. Frank, and J. D. Griffin. "Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl." Journal of Experimental Medicine 183, no. 3 (1996): 811–20. http://dx.doi.org/10.1084/jem.183.3.811.

Full text

Abstract:

Bcr/Abl is a chimeric oncogene that can cause both acute and chronic human leukemias. Bcr/Abl-encoded proteins exhibit elevated kinase activity compared to c-Abl, but the mechanisms of transformation are largely unknown. Some of the biological effects of Bcr/Abl overlap with those of hematopoietic cytokines, particularly interleukin 3 (IL-3). Such effects include mitogenesis, enhanced survival, and enhanced basophilic differentiation. Therefore, it has been suggested that p210Bcr/Abl and the IL-3 receptor may activate some common signal transduction pathways. An important pathway for IL-3 sign

APA, Harvard, Vancouver, ISO, and other styles

35

David, M., H. E. Chen, S. Goelz, A. C. Larner, and B. G. Neel. "Differential regulation of the alpha/beta interferon-stimulated Jak/Stat pathway by the SH2 domain-containing tyrosine phosphatase SHPTP1." Molecular and Cellular Biology 15, no. 12 (1995): 7050–58. http://dx.doi.org/10.1128/mcb.15.12.7050.

Full text

Abstract:

Interferons (IFNs) induce early-response genes by stimulating Janus family (Jak) tyrosine kinases, leading to tyrosine phosphorylation of Stat transcription factors. Previous studies implicated protein-tyrosine phosphatase (PTP) activity in the control of IFN-regulated Jak/Stat signaling, but the specific PTPs responsible remained unidentified. We have found that SH2 domain-containing PTP1 (SHPTP1; also called PTP1C, HCP, or SHP) reversibly associates with the IFN-alpha receptor complex upon IFN addition. Compared with macrophages from normal littermate controls, macrophages from motheaten mic

APA, Harvard, Vancouver, ISO, and other styles

36

Jung, Ji Hoon, Tae-Rin Kwon, Soo-Jin Jeong, et al. "Apoptosis Induced by Tanshinone IIA and Cryptotanshinone Is Mediated by Distinct JAK/STAT3/5 and SHP1/2 Signaling in Chronic Myeloid Leukemia K562 Cells." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/805639.

Full text

Abstract:

Though tanshinone IIA and cryptotanshinone possess a variety of biological effects such as anti-inflammatory, antioxidative, antimetabolic, and anticancer effects, the precise molecular targets or pathways responsible for anticancer activities of tanshinone IIA and cryptotanshinone in chronic myeloid leukemia (CML) still remain unclear. In the present study, we investigated the effect of tanshinone IIA and cryptotanshinone on the Janus activated kinase (JAK)/signal transducer and activator of transcription (STAT) signaling during apoptotic process. We found that both tanshinone IIA and cryptot

APA, Harvard, Vancouver, ISO, and other styles

37

Trivedi, Sunny, and Michelle Starz-Gaiano. "Drosophila Jak/STAT Signaling: Regulation and Relevance in Human Cancer and Metastasis." International Journal of Molecular Sciences 19, no. 12 (2018): 4056. http://dx.doi.org/10.3390/ijms19124056.

Full text

Abstract:

Over the past three-decades, Janus kinase (Jak) and signal transducer and activator of transcription (STAT) signaling has emerged as a paradigm to understand the involvement of signal transduction in development and disease pathology. At the molecular level, cytokines and interleukins steer Jak/STAT signaling to transcriptional regulation of target genes, which are involved in cell differentiation, migration, and proliferation. Jak/STAT signaling is involved in various types of blood cell disorders and cancers in humans, and its activation is associated with carcinomas that are more invasive o

APA, Harvard, Vancouver, ISO, and other styles

38

Sriram, Krishnan, Stanley A. Benkovic, Meleik A. Hebert, Diane B. Miller, and James P. O'Callaghan. "Induction of gp130-related Cytokines and Activation of JAK2/STAT3 Pathway in Astrocytes Precedes Up-regulation of Glial Fibrillary Acidic Protein in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Neurodegeneration." Journal of Biological Chemistry 279, no. 19 (2004): 19936–47. http://dx.doi.org/10.1074/jbc.m309304200.

Full text

Abstract:

Reactive gliosis is a hallmark of disease-, trauma-, and chemical-induced damage to the central nervous system. The signaling pathways associated with this response to neural injury remain to be elucidated, but recent evidence implicates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway. Here, we used the known dopaminergic neurotoxicant, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), to selectively damage striatal dopaminergic nerve terminals and elicit a glial response. We then analyzed changes in gene expression and protein phosphorylation,in vivo,

APA, Harvard, Vancouver, ISO, and other styles

39

Gupta, Rohit, Jason H. Rogers, Xin Long, et al. "Targeting Activated Signaling Pathways for the Treatment of IKZF1-Deleted B Lymphoblastic Leukemia." Blood 134, Supplement_1 (2019): 3789. http://dx.doi.org/10.1182/blood-2019-127209.

Full text

Abstract:

In B lymphoblastic leukemia (B-ALL), genome-wide association studies have revealed that deletions and mutations of the gene IKAROS family zinc finger 1 (IKZF1) are present in nearly 30% of patients. These lesions are most prevalent in high-risk subsets, including greater than 60% of patients with Philadelphia chromosome positive (Ph+) and Ph-like ALL. IKZF1 deletions are associated with an increased risk of relapse, therapy resistance, and inferior survival. It is therefore imperative to devise new treatment strategies for this poor-prognosis subset of patients. To this regard, using novel CRI

APA, Harvard, Vancouver, ISO, and other styles

40

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.

Full text

Abstract:

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

APA, Harvard, Vancouver, ISO, and other styles

41

Goodman, Michael D., Sheryl E. Koch, Geraldine A. Fuller-Bicer, and Karyn L. Butler. "Regulating RISK: a role for JAK-STAT signaling in postconditioning?" American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (2008): H1649—H1656. http://dx.doi.org/10.1152/ajpheart.00692.2008.

Full text

Abstract:

Postconditioning (POC), a novel strategy of cardioprotection against ischemia-reperfusion injury, is clinically attractive because of its therapeutic application at the predictable onset of reperfusion. POC activates several intracellular kinase signaling pathways, including phosphatidylinositol 3-kinase (PI3K)-Akt (RISK). The regulation of POC-induced survival kinase signaling, however, has not been fully characterized. JAK-STAT activation is integral to cardiac ischemic tolerance and may provide upstream regulation of RISK. We hypothesized that POC requires the activation of both JAK-STAT an

APA, Harvard, Vancouver, ISO, and other styles

42

Westfall, Matt, Rachael E. Hawtin, Diane Longo, et al. "Functional Pathway Analysis Of JAK2 Mutated and Wild Type Myeloproliferative Neoplasms As a Tool For Patient Stratification and Therapeutic Selection." Blood 122, no. 21 (2013): 5263. http://dx.doi.org/10.1182/blood.v122.21.5263.5263.

Full text

Abstract:

Abstract Background JAK2 signaling is essential for normal development of multiple hematopoietic cell lineages. A JAK2 (V617F) gain of function mutation has been identified in 95% of polycythemia vera (PV) and 50-60% of essential thrombocythemia (ET) patients, providing a rationale for the development of small molecule JAK2 inhibitors. Clinically, JAK2 inhibitors have been shown to be effective in controlling hyperproliferation of hematopoietic cells in PV and ET in patients with (JAK2+) and without (JAK2 WT) the JAK2 V617F mutation. This suggests that deregulation of the JAK/STAT pathway is a

APA, Harvard, Vancouver, ISO, and other styles

43

Chen, Xing-Yuan. "JAK-STAT signaling pathway and acute pancreatitis." World Chinese Journal of Digestology 23, no. 6 (2015): 932. http://dx.doi.org/10.11569/wcjd.v23.i6.932.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Sutherland, J. M., R. Keightley, R. L. Robker, D. L. Russell, and E. A. McLaughlin. "126. JAK/STAT SIGNALLING IN FOLLICULOGENESIS." Reproduction, Fertility and Development 22, no. 9 (2010): 44. http://dx.doi.org/10.1071/srb10abs126.

Full text

Abstract:

Primordial follicle activation marks the first stage of pre-pubertal ovarian folliculogenesis, and is therefore fundamental to female fertility. Entry into development is initiated by a group of pleiotropic cytokines and growth factors, originating in and acting upon both the oocyte and granulosa support cells of the ovarian follicle through the Janus Kinase/Signal Transducer and Activator of Transcription (JAK/STAT) signalling pathway. Pivotal to this process is the transcriptional regulation of target genes via STAT complexes and negative regulation by the Suppressors of Cytokine Signalling

APA, Harvard, Vancouver, ISO, and other styles

45

Meng, Lingkai, Ling Ding, Yue Yu, Wang Li, and Tao Huang. "JAK3 and TYK2 Serve as Prognostic Biomarkers and Are Associated with Immune Infiltration in Stomach Adenocarcinoma." BioMed Research International 2020 (September 19, 2020): 1–15. http://dx.doi.org/10.1155/2020/7973568.

Full text

Abstract:

Background. Stomach adenocarcinoma (STAD) is one of the most common malignant tumors. The Janus kinases (JAKs) play a significant part in cellular biological process, inflammation, and immunity. The roles of JAKs in STAD are still not systematically described. Methods. A series of bioinformatics tools were used to clarify the role of JAKs in STAD. Results. JAK3/TYK2 levels were significantly increased in STAD during subgroup analyses based on gender, tumor grade, cancer stages, and nodal metastasis status. STAD patients with high levels of JAK3/TYK2 had poor overall survival, postprogression s

APA, Harvard, Vancouver, ISO, and other styles

46

Lacronique, Virginie, Anthony Boureux, Richard Monni, et al. "Transforming properties of chimeric TEL-JAK proteins in Ba/F3 cells." Blood 95, no. 6 (2000): 2076–83. http://dx.doi.org/10.1182/blood.v95.6.2076.

Full text

Abstract:

Abstract The involvement of the cytokine signaling pathway in oncogenesis has long been postulated. Recently, rearrangements of the gene encoding the tyrosine Janus kinase 2 (JAK2) have been reported in human leukemias indicating a direct JAK-signal transduction and activator of transcription (STAT)-mediated leukemic process. The leukemia-associated TEL-JAK2 fusion protein is formed by the oligomerization domain of the translocated ets leukemia (TEL) protein fused to the catalytic domain of JAK2. TEL-mediated oligomerization results in a constitutive tyrosine kinase activity that, in turn, is

APA, Harvard, Vancouver, ISO, and other styles

47

Shariq, Aisha S., Elisa Brietzke, Joshua D. Rosenblat, et al. "Therapeutic potential of JAK/STAT pathway modulation in mood disorders." Reviews in the Neurosciences 30, no. 1 (2018): 1–7. http://dx.doi.org/10.1515/revneuro-2018-0027.

Full text

Abstract:

Abstract Convergent evidence demonstrates that immune dysfunction (e.g. chronic low-grade inflammatory activation) plays an important role in the development and progression of mood disorders. The Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway is a pleiotropic cellular cascade that transduces numerous signals, including signals from the release of cytokines and growth factors. The JAK/STAT signaling pathway is involved in mediating several functions of the central nervous system, including neurogenesis, synaptic plasticity, gliogenesis, and microgl

APA, Harvard, Vancouver, ISO, and other styles

48

Lee, Annah, Gabriela Cardoso Dal Pont, Michele Battaglia, Ryan J. Arsenault, and Michael H. Kogut. "Role of JAK-STAT Pathway in Broiler Chicks Fed with Chestnut Tannins." Animals 11, no. 2 (2021): 337. http://dx.doi.org/10.3390/ani11020337.

Full text

Abstract:

The objective of this study was to identify the phosphorylation events associated with host immunity with the inclusion of chestnut tannins (ChT) in the diet. A total of 200 male day-of-hatch Cobb 500 chicks were randomly assigned to two treatment groups, totaling 50 chicks per pen per experiment (this study was repeated two times). The treatments were as follows: (1) control feed—normal starter feed (n = 50), and (2) 1% ChT inclusion feed (n = 50). The ceca were collected on each necropsy day for analysis via (1) a peptide array to provide tissue immunometabolism information from the host, an

APA, Harvard, Vancouver, ISO, and other styles

49

Ptacek, Jason, Rachael E. Hawtin, Dongmei Sun, et al. "Diminished cytokine-induced Jak/STAT signaling is associated with rheumatoid arthritis and disease activity." PLOS ONE 16, no. 1 (2021): e0244187. http://dx.doi.org/10.1371/journal.pone.0244187.

Full text

Abstract:

Rheumatoid arthritis (RA) is a systemic and incurable autoimmune disease characterized by chronic inflammation in synovial lining of joints. To identify the signaling pathways involved in RA, its disease activity, and treatment response, we adapted a systems immunology approach to simultaneously quantify 42 signaling nodes in 21 immune cell subsets (e.g., IFNα→p-STAT5 in B cells) in peripheral blood mononuclear cells (PBMC) from 194 patients with longstanding RA (including 98 patients before and after treatment), and 41 healthy controls (HC). We found multiple differences between patients with

APA, Harvard, Vancouver, ISO, and other styles

50

Park, Ju-won, Kwang-Sung Ahn, Young-Ju Kim, et al. "Blockage of IL-6 Mediated JAK2/STAT3 Cell Signaling Pathway by sIL-6R Effectively Inhibited the Growth of Multiple Myeloma Cell." Blood 108, no. 11 (2006): 5083. http://dx.doi.org/10.1182/blood.v108.11.5083.5083.

Full text

Abstract:

Abstract Interleukin-6 (IL-6) is a key growth factor and thus plays a pivotal role in the pathogenesis of multiple myeloma. IL-6 is absolutely necessary for the cellular signalling cascade via JAK/STAT and RAS/MAPK pathways involved in proliferation and viability. We found interleukin (IL)-6 induced JAK-2 phosphorylation and induced proliferation of multiple myeloma cell line. Also phosphorylation of Stat1 and Stat3 was increased by IL-6 stimulation. Silencing JAK2 expression by small interfering RNA (siRNA) abrogated IL-6 induced phosphorylation of STAT3. In addition, soluble interleukin-6 re

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!