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Journal articles on the topic 'Inhibiteurs de JAK/STAT'

Author: Grafiati

Published: 22 June 2024

Last updated: 31 July 2025

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1

El Jammal, Thomas, Mathieu Gerfaud-Valentin, Pascal Seve, and Yvan Jamilloux. "Inhibiteurs de la signalisation JAK/STAT au cours des maladies rhumatologiques : un spectre grandissant." Revue du Rhumatisme 87, no. 4 (2020): 261–72. http://dx.doi.org/10.1016/j.rhum.2020.01.032.

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Sagez, F., M. Sawaf, J. Sibilia, H. Dumortier, F. Monneaux, and J. E. Gottenberg. "Nouveau mécanisme d’action des inhibiteurs de la voie JAK/STAT : l’inhibition de la différenciation et de la fonction des lymphocytes T folliculaires auxiliaires." Revue du Rhumatisme 83 (November 2016): A215. http://dx.doi.org/10.1016/s1169-8330(16)30522-1.

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3

Colonne, Punsiri M., Marina E. Eremeeva, and Sanjeev K. Sahni. "Beta Interferon-Mediated Activation of Signal Transducer and Activator of Transcription Protein 1 Interferes with Rickettsia conorii Replication in Human Endothelial Cells." Infection and Immunity 79, no. 9 (2011): 3733–43. http://dx.doi.org/10.1128/iai.05008-11.

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ABSTRACTInfection of the endothelial cell lining of blood vessels withRickettsia conorii, the causative agent of Mediterranean spotted fever, results in endothelial activation. We investigated the effects ofR. conoriiinfection on the status of the Janus kinase (JAK)-signal transducer and activator of transcription protein (STAT) signaling pathway in human microvascular endothelial cells (HMECs), the most relevant host cell type, in light of rickettsial tropism for microvascular endotheliumin vivo.R. conoriiinfection induced phosphorylation of STAT1 on tyrosine 701 and serine 727 at 24, 48, and

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4

Barry, Sean P. "JAK-STAT." JAK-STAT 1, no. 2 (2012): 90–91. http://dx.doi.org/10.4161/jkst.20939.

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5

Galli Sanchez, Ana Paula, Tatiane Ester Aidar Fernandes, and Gustavo Martelli Palomino. "The JAK-STAT Pathway and the JAK Inhibitors." Journal of Clinical Research in Dermatology 7, no. 5 (2020): 1–6. http://dx.doi.org/10.15226/2378-1726/7/5/001128.

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Dozens of cytokines that bind Type I and Type II receptors use the Janus Kinases (JAK) and the Signal Transducer and Activator of Transcription (STAT) proteins pathway for intracellular signaling, orchestrating hematopoiesis, inducing inflammation, and controlling the immune response. Currently, oral JAK inhibitors are being used to treat many inflammatory and myeloproliferative diseases and are also under investigation in several clinical trials for skin diseases. Thus, dermatologists should understand how the JAK-STAT pathway works as well as the mechanism of action of the JAK inhibitors whi

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6

Liu, Jia, Faping Wang, and Fengming Luo. "The Role of JAK/STAT Pathway in Fibrotic Diseases: Molecular and Cellular Mechanisms." Biomolecules 13, no. 1 (2023): 119. http://dx.doi.org/10.3390/biom13010119.

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There are four members of the JAK family and seven of the STAT family in mammals. The JAK/STAT molecular pathway could be activated by broad hormones, cytokines, growth factors, and more. The JAK/STAT signaling pathway extensively mediates various biological processes such as cell proliferation, differentiation, migration, apoptosis, and immune regulation. JAK/STAT activation is closely related to growth and development, homeostasis, various solid tumors, inflammatory illness, and autoimmune diseases. Recently, with the deepening understanding of the JAK/STAT pathway, the relationship between

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7

Mirault, Tristan. "Risques cardiovasculaires des inhibiteurs de JAK." JMV-Journal de Médecine Vasculaire 47 (March 2022): S40. http://dx.doi.org/10.1016/j.jdmv.2022.01.015.

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8

Minaudo, Carla. "Vía JAK-STAT e inhibidores JAK." Dermatología Argentina 28, no. 2 (2022): 55–62. http://dx.doi.org/10.47196/da.v28i2.2324.

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La vía JAK-STAT (Janus Kinasas) es una cadena de traducción de señales intracelulares, que se activa a través de receptores de citoquinas I y II. Mediante esta vía, varias moléculas de importancia en dermatología ejercen sus efectos: IL2, IL4, IL7, IL5, IL6, IL9, IL12, IL13, IL15, IL21, IL23, INFa e INFb, entre otras. También es la señal intracelular de hormonas como la prolactina y la hormona de crecimiento. La inhibición de distintos componentes de esta vía es utilizada como terapéutica en enfermedades reumatológicas y un número cada vez mayor de patologías cutáneas. Los inhibidores JAK surg

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9

Schieler, Jarod M., and Jeffrey O. Henderson. "Treating a Dysregulated JAK/STAT Pathway in Cancer Cells." Journal of Student Research 5, no. 1 (2016): 11–17. http://dx.doi.org/10.47611/jsr.v5i1.282.

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The JAK/STAT pathway is induced by the binding of a cytokine to its cognate receptor. The receptor’s engagement with the cytokine recruits a JAK protein, which activates itself via auto/trans-phosphorylation. In turn, the activated JAKs recruit and phosphorylate STAT proteins. The phosphorylated STAT proteins form a dimer, translocate to the cell nucleus and acts as a transcription factor to induce gene expression. In this way, the JAK/STAT pathway can mediate a cell’s response to extracellular signals. The proteins ultimately induced by the JAK/STAT pathway contribute to processes such as inf

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10

Zhan, Xinliang, Yan Wang, and Jing Yang. "Janus Kinase/Signal Converters, and the Transcriptional Activator Signaling Pathway Promotes Lung Cancer Through Increasing M2 Macrophage." Journal of Biomaterials and Tissue Engineering 11, no. 4 (2021): 605–11. http://dx.doi.org/10.1166/jbt.2021.2566.

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Accumulating evidence highlights the salient function of JAK/STAT signaling pathway in tumorigenesis and development. But the mechanism of JAK/STAT signaling in lung cancer remains elusive. This study assessed the impact of JAK/STAT on lung tumorigenesis and its interaction with microenvironment. Mouse model of primary lung cancer was established and then treated with JAK/STAT inhibitor. Immunofluorescence was performed to analyze fluorescent labels. Transwell assay determined the cell migration ability, and Western blot, immunohistochemistry, and immunofluorescence to detect the expression of

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11

Valle-Mendiola, Arturo, Adriana Gutiérrez-Hoya, and Isabel Soto-Cruz. "JAK/STAT Signaling and Cervical Cancer: From the Cell Surface to the Nucleus." Genes 14, no. 6 (2023): 1141. http://dx.doi.org/10.3390/genes14061141.

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The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway constitutes a rapid signaling module from the cell surface to the nucleus, and activates different cellular responses, such as proliferation, survival, migration, invasion, and inflammation. When the JAK/STAT pathway is altered, it contributes to cancer progression and metastasis. STAT proteins play a central role in developing cervical cancer, and inhibiting the JAK/STAT signaling may be necessary to induce tumor cell death. Several cancers show continuous activation of different STATs, including

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12

Rodriguez, Irasema, and Kate J. F. Carnevale. "Systematic Review: JAK-STAT Regulation and Its Impact on Inflammation Response in ARDS from COVID-19." Immuno 4, no. 2 (2024): 147–58. http://dx.doi.org/10.3390/immuno4020010.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has had a global impact and resulted in millions of deaths worldwide. The course of the Janus kinase signaling transducers and activators (JAK-STAT) pathway is an important molecular pathway that is involved in the cellular response to various cytokines and growth factors promoting an inflammatory response. The overactivation of the JAK-STAT signaling pathway in coronavirus disease 2019 (COVID-19) and its effect on acute respiratory distress syndrome (ARDS)-induced inflammatory processes was observed in various clinical art

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13

Park, Hyunjung, Sangjik Lee, Jaehun Lee, Hyuk Moon, and Simon Weonsang Ro. "Exploring the JAK/STAT Signaling Pathway in Hepatocellular Carcinoma: Unraveling Signaling Complexity and Therapeutic Implications." International Journal of Molecular Sciences 24, no. 18 (2023): 13764. http://dx.doi.org/10.3390/ijms241813764.

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Hepatocellular Carcinoma (HCC) continues to pose a substantial global health challenge due to its high incidence and limited therapeutic options. In recent years, the Janus Kinase (JAK) and Signal Transducer and Activator of Transcription (STAT) pathway has emerged as a critical signaling cascade in HCC pathogenesis. The review commences with an overview of the JAK/STAT pathway, delving into the dynamic interplay between the JAK/STAT pathway and its numerous upstream activators, such as cytokines and growth factors enriched in pathogenic livers afflicted with chronic inflammation and cirrhosis

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14

Montero, Paula, Javier Milara, Inés Roger, and Julio Cortijo. "Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms." International Journal of Molecular Sciences 22, no. 12 (2021): 6211. http://dx.doi.org/10.3390/ijms22126211.

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Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical p

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15

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.

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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

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16

Neeli, Indira, Zhimin Liu, Nagadhara Dronadula, Z. Alex Ma, and Gadiparthi N. Rao. "An Essential Role of the Jak-2/STAT-3/Cytosolic Phospholipase A2Axis in Platelet-derived Growth Factor BB-induced Vascular Smooth Muscle Cell Motility." Journal of Biological Chemistry 279, no. 44 (2004): 46122–28. http://dx.doi.org/10.1074/jbc.m406922200.

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Platelet-derived growth factor-BB (PDGF-BB) is a potent motogen for vascular smooth muscle cells (VSMCs). To understand its motogenic signaling events, we have studied the role of the Janus-activated kinase/signal transducers and activators of transcription (Jak/STAT) pathway and cytosolic phospholipase A2(cPLA2). PDGF-BB stimulated tyrosine phosphorylation of Jak-2 and STAT-3 in a time-dependent manner in VSMCs. In addition, AG490 and Jak-2KEpRK5, a selective pharmacological inhibitor and a dominant negative mutant, respectively, of Jak-2, attenuated PDGF-BB-induced STAT-3 tyrosine phosphoryl

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17

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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18

Grange, L., F. Barde, C. Montardi, and K. Chevalier. "Tout savoir sur les inhibiteurs de JAK." La Revue de Médecine Interne 45, no. 9 (2024): S9—S12. http://dx.doi.org/10.1016/s0248-8663(24)00775-6.

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19

Gouverneur, A., J. Avouac, C. Prati, et al. "Inhibiteurs de JAK et risque de cancer." Revue du Rhumatisme 89 (December 2022): A69—A70. http://dx.doi.org/10.1016/j.rhum.2022.10.094.

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20

Gerds, Aaron T. "Beyond JAK-STAT: novel therapeutic targets in Ph-negative MPN." Hematology 2019, no. 1 (2019): 407–14. http://dx.doi.org/10.1182/hematology.2019000048.

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Abstract The Philadelphia chromosome-negative myeloproliferative neoplasms (MPNs) share a common pathobiology of constitutive activation of the JAK and STAT pathway, despite having the 3 distinct phenotypes of essential thrombocythemia, polycythemia vera, and primary myelofibrosis. Targeting the JAK-STAT pathway has led to remarkable clinical benefit, including reduction in splenomegaly, amelioration of cytokine-driven symptoms, improvement in quality of life, and even some improvement in survival. However, targeting this pathway has not resulted in consistent disease modification by current m

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21

Jain, Mayank, Mukul Kumar Singh, Hari Shyam, et al. "Role of JAK/STAT in the Neuroinflammation and its Association with Neurological Disorders." Annals of Neurosciences 28, no. 3-4 (2021): 191–200. http://dx.doi.org/10.1177/09727531211070532.

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Background: Innate immunity is mediated by a variety of cell types, including microglia, macrophages, and neutrophils, and serves as the immune system's first line of defense. There are numerous pathways involved in innate immunity, including the interferon (IFN) pathway, TRK pathway, mitogen-activated protein kinase (MAPK) pathway, Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway, interleukin (IL) pathways, chemokine pathways (CCR5), GSK signaling, and Fas signaling. Summary: JAK/STAT is one of these important signaling pathways and this review focused on JAK/S

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22

Harrison, D. A. "The JAK/STAT Pathway." Cold Spring Harbor Perspectives in Biology 4, no. 3 (2012): a011205. http://dx.doi.org/10.1101/cshperspect.a011205.

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23

Wells, William A. "A JAK/STAT invasion." Journal of Cell Biology 156, no. 3 (2002): 413. http://dx.doi.org/10.1083/jcb1563rr2.

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24

Aaronson, D. S., and C. M. Horvath. "The JAK-STAT Pathway." Science Signaling 2003, no. 197 (2003): cm11. http://dx.doi.org/10.1126/stke.2003.197.cm11.

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25

Myllymäki, H., and M. Rämet. "JAK/STAT Pathway inDrosophilaImmunity." Scandinavian Journal of Immunology 79, no. 6 (2014): 377–85. http://dx.doi.org/10.1111/sji.12170.

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26

Imada, Kazuroni, and Warren J. Leonard. "The Jak-STAT pathway." Molecular Immunology 37, no. 1-2 (2000): 1–11. http://dx.doi.org/10.1016/s0161-5890(00)00018-3.

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27

Ladyman, Sharon R., and David R. Grattan. "JAK-STAT and feeding." JAK-STAT 2, no. 2 (2013): e23675. http://dx.doi.org/10.4161/jkst.23675.

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28

Hombría, James Castelli-Gair, and Sol Sotillos. "JAK-STAT pathway inDrosophilamorphogenesis." JAK-STAT 2, no. 3 (2013): e26089. http://dx.doi.org/10.4161/jkst.26089.

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29

Mertens, Claudia, and James E. Darnell. "SnapShot: JAK-STAT Signaling." Cell 131, no. 3 (2007): 612–612. http://dx.doi.org/10.1016/j.cell.2007.10.033.

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30

Karati, Dipanjan, Kakasaheb Ramoo Mahadik, Piyush Trivedi, and Dileep Kumar. "The Emerging Role of Janus Kinase Inhibitors in the Treatment of Cancer." Current Cancer Drug Targets 22, no. 3 (2022): 221–33. http://dx.doi.org/10.2174/1568009622666220301105214.

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Abstract: Cancer is a leading cause of death worldwide. The Janus kinase (JAK) signal transducer and activator of transcription (STAT) signalling pathway are activated abnormally, which promotes carcinogenesis. Several cytokines are important cancer drivers. These proteins bind to receptors and use the Janus kinase (JAK) and STAT pathways to communicate their responses. Cancer risks are linked to genetic differences in the JAK-STAT system. JAK inhibitors have been shown to reduce STAT initiation, tissue propagation, and cell existence in preclinical investigations involving solid tumour cell l

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31

Wahnschaffe, Linus, Till Braun, Sanna Timonen, et al. "JAK/STAT-Activating Genomic Alterations Are a Hallmark of T-PLL." Cancers 11, no. 12 (2019): 1833. http://dx.doi.org/10.3390/cancers11121833.

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T-cell prolymphocytic leukemia (T-PLL) is a rare and poor-prognostic mature T-cell leukemia. Recent studies detected genomic aberrations affecting JAK and STAT genes in T-PLL. Due to the limited number of primary patient samples available, genomic analyses of the JAK/STAT pathway have been performed in rather small cohorts. Therefore, we conducted—via a primary-data based pipeline—a meta-analysis that re-evaluated the genomic landscape of T-PLL. It included all available data sets with sequence information on JAK or STAT gene loci in 275 T-PLL. We eliminated overlapping cases and determined a

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32

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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Gutiérrez-Hoya, Adriana, and Isabel Soto-Cruz. "Role of the JAK/STAT Pathway in Cervical Cancer: Its Relationship with HPV E6/E7 Oncoproteins." Cells 9, no. 10 (2020): 2297. http://dx.doi.org/10.3390/cells9102297.

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The janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway is associated with the regulation of essential cellular mechanisms, such as proliferation, invasion, survival, inflammation, and immunity. Aberrant JAK/STAT signaling contributes to cancer progression and metastatic development. STAT proteins play an essential role in the development of cervical cancer, and the inhibition of the JAK/STAT pathway may be essential for enhancing tumor cell death. Persistent activation of different STATs is present in a variety of cancers, including cervical cancer, an

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34

Pazdrak, K., S. Stafford, and R. Alam. "The activation of the Jak-STAT 1 signaling pathway by IL-5 in eosinophils." Journal of Immunology 155, no. 1 (1995): 397–402. http://dx.doi.org/10.4049/jimmunol.155.1.397.

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Abstract The intracellular signal transduction of IL-5 in eosinophils is unknown. The objective of this study was to investigate the involvement of the newly discovered Jak-STAT pathway in the IL-5 signal transduction mechanism. Eosinophils were purified from peripheral blood by discontinuous Percoll gradients and stimulated with IL-5. The involvement of Jak 2 was investigated by immunoprecipitation followed by immunoblotting for tyrosine phosphorylation. The activation of Jak 2 was studied by autophosphorylation of the immunoprecipitated kinase. Jak 2 was tyrosine phosphorylated within 1 to 3

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35

Li, Boheng, Qin Wan, Zhubo Li, and Wee-Joo Chng. "Janus Kinase Signaling: Oncogenic Criminal of Lymphoid Cancers." Cancers 13, no. 20 (2021): 5147. http://dx.doi.org/10.3390/cancers13205147.

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The Janus kinase (JAK) family are known to respond to extracellular cytokine stimuli and to phosphorylate and activate signal transducers and activators of transcription (STAT), thereby modulating gene expression profiles. Recent studies have highlighted JAK abnormality in inducing over-activation of the JAK/STAT pathway, and that the cytoplasmic JAK tyrosine kinases may also have a nuclear role. A couple of anti-JAK therapeutics have been developed, which effectively harness lymphoid cancer cells. Here we discuss mutations and fusions leading to JAK deregulations, how upstream nodes drive JAK

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Li, Boheng, Qin Wan, Zhubo Li, and Wee-Joo Chng. "Janus Kinase Signaling: Oncogenic Criminal of Lymphoid Cancers." Cancers 13, no. 20 (2021): 5147. http://dx.doi.org/10.3390/cancers13205147.

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The Janus kinase (JAK) family are known to respond to extracellular cytokine stimuli and to phosphorylate and activate signal transducers and activators of transcription (STAT), thereby modulating gene expression profiles. Recent studies have highlighted JAK abnormality in inducing over-activation of the JAK/STAT pathway, and that the cytoplasmic JAK tyrosine kinases may also have a nuclear role. A couple of anti-JAK therapeutics have been developed, which effectively harness lymphoid cancer cells. Here we discuss mutations and fusions leading to JAK deregulations, how upstream nodes drive JAK

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Serbina, Inessa Mykhailivna, and Yu S. Ovcharenko. "JANUS KINASE INHIBITORS IN DERMATOLOGY: PRESENT AND FUTURE." International Medical Journal, no. 4(108) (December 10, 2021): 70–76. http://dx.doi.org/10.37436/2308-5274-2021-4-13.

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New facts about the importance of the JAK−STAT signaling system in development of a number of inflammatory and autoimmune diseases are now emerging. The JAK−STAT system, or pathway consisting of Janus kinase (JAK) and signal transducer protein as well as transcription activator (STAT), transmits information from extracellular polypeptide signals through transmembrane receptors directly to target gene promoters in the nucleus without the involvement of secondary messengers. The JAK−STAT system plays an important role in the implementation of immunological processes and is considered a therapeut

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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.

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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

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Roger, Inés, Javier Milara, Paula Montero, and Julio Cortijo. "The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension." International Journal of Molecular Sciences 22, no. 9 (2021): 4980. http://dx.doi.org/10.3390/ijms22094980.

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Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a

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40

Conzelmann, Michael, Elena Rodionova, Michael Hess, et al. "Complementary JAK/STAT Signalling Is Required for the Pro-Inflammatory Effects of CD40 Ligation: Differential Effects in Human Myeloid and B Cells." Blood 110, no. 11 (2007): 2413. http://dx.doi.org/10.1182/blood.v110.11.2413.2413.

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Abstract CD40L represents a strong endogenous danger signal that induces pro-inflammatory activation of CD40-expressing cells such as dendritic cells (DC), monocytes, and B cells. However, since CD40 activation alone is insufficient to induce pro-inflammatory cytokines such as IL-12p70, we studied whether CD40-mediated pro-inflammatory activity might be dependent on co-signalling pathways involving JAK/STAT. Using quantitative Western blotting, we demonstrate that JAK/STAT signalling is induced by cytokines such as IL-4, GM-CSF and IFNg, whereas CD40 activation mediates NFkB signalling. CD40L-

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41

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.

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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

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42

Chen, Pei-Chi, Chen-Hsun Ho, Chia-Kwung Fan, Shih-Ping Liu, and Po-Ching Cheng. "Antimicrobial Peptide LCN2 Inhibited Uropathogenic Escherichia coli Infection in Bladder Cells in a High-Glucose Environment through JAK/STAT Signaling Pathway." International Journal of Molecular Sciences 23, no. 24 (2022): 15763. http://dx.doi.org/10.3390/ijms232415763.

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JAK/STAT plays a key role in regulating uropathogenic Escherichia coli (UPEC) infection in urothelial cells, probably via antimicrobial peptide (AMP) production, in diabetic patients with urinary tract infections. Whether multiple pathways regulate AMPs, especially lipid-carrying protein-2 (LCN2), to achieve a vital effect is unknown. We investigated the effects of an LCN2 pretreatment on the regulation of the JAK/STAT pathway in a high-glucose environment using a bladder cell model with GFP-UPEC and phycoerythrin-labeled TLR-4, STAT1, and STAT3. Pretreatment with 5 or 25 μg/mL LCN2 for 24 h d

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Godoi, Mariely A., Angelo C. Camilli, Karen G. A. Gonzales, et al. "JAK/STAT as a Potential Therapeutic Target for Osteolytic Diseases." International Journal of Molecular Sciences 24, no. 12 (2023): 10290. http://dx.doi.org/10.3390/ijms241210290.

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Several cytokines with major biological functions in inflammatory diseases exert their functions through the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signal transduction pathway. JAKs phosphorylate the cytoplasmic domain of the receptor, inducing the activation of its substrates, mainly the proteins known as STATs. STATs bind to these phosphorylated tyrosine residues and translocate from the cytoplasm to the nucleus, further regulating the transcription of several genes that regulate the inflammatory response. The JAK/STAT signaling pathway plays a critical ro

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Bright, J. J., L. D. Kerr, and S. Sriram. "TGF-beta inhibits IL-2-induced tyrosine phosphorylation and activation of Jak-1 and Stat 5 in T lymphocytes." Journal of Immunology 159, no. 1 (1997): 175–83. http://dx.doi.org/10.4049/jimmunol.159.1.175.

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Abstract Signaling through IL-2R, IL-2 induces tyrosine phosphorylation and activation of Jak-1 and Jak-3 kinases and Stat 3 and Stat 5 transcription factors leading to cell cycle progression of activated T cells from G1 to S phase. TGF-beta is an immunosuppressive cytokine, which inhibits T cell proliferation at G1 to S phase transition. We examined the effect of TGF-beta on IL-2R signal transduction pathway in activated T cells. We show here that treatment of activated T cells with TGF-beta inhibited IL-2-induced tyrosine phosphorylation and activation of Jak-1 and Stat 5 but not Jak-3 and S

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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.

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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

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Macrì, Federica, Ilaria Vigorito, Stefania Castiglione, et al. "High Phosphate-Induced JAK-STAT Signalling Sustains Vascular Smooth Muscle Cell Inflammation and Limits Calcification." Biomolecules 14, no. 1 (2023): 29. http://dx.doi.org/10.3390/biom14010029.

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Vascular calcification (VC) is an age-related complication characterised by calcium-phosphate deposition in the arterial wall driven by the osteogenic transformation of vascular smooth muscle cells (VSMCs). The JAK-STAT pathway is an emerging target in inflammation. Considering the relationship between VC and inflammation, we investigated the role of JAK-STAT signalling during VSMC calcification. Human aortic smooth muscle cells (HASMCs) were cultured in high-inorganic phosphate (Pi) medium for up to 7 days; calcium deposition was determined via Alizarin staining and colorimetric assay. Inflam

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López-Mejía, José A., Jessica C. Mantilla-Ollarves, and Leticia Rocha-Zavaleta. "Modulation of JAK-STAT Signaling by LNK: A Forgotten Oncogenic Pathway in Hormone Receptor-Positive Breast Cancer." International Journal of Molecular Sciences 24, no. 19 (2023): 14777. http://dx.doi.org/10.3390/ijms241914777.

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Breast cancer remains the most frequently diagnosed cancer in women worldwide. Tumors that express hormone receptors account for 75% of all cases. Understanding alternative signaling cascades is important for finding new therapeutic targets for hormone receptor-positive breast cancer patients. JAK-STAT signaling is commonly activated in hormone receptor-positive breast tumors, inducing inflammation, proliferation, migration, and treatment resistance in cancer cells. In hormone receptor-positive breast cancer, the JAK-STAT cascade is stimulated by hormones and cytokines, such as prolactin and I

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Zhang, Yan, Bo-Xue Li, Qian-Zhuo Mao, et al. "The JAK-STAT pathway promotes persistent viral infection by activating apoptosis in insect vectors." PLOS Pathogens 19, no. 3 (2023): e1011266. http://dx.doi.org/10.1371/journal.ppat.1011266.

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The Janus kinase-signal transducer and activator of transcription (JAK-STAT) pathway is an evolutionarily conserved signaling pathway that can regulate various biological processes. However, the role of JAK-STAT pathway in the persistent viral infection in insect vectors has rarely been investigated. Here, using a system that comprised two different plant viruses, Rice stripe virus (RSV) and Rice black-streaked dwarf virus (RBSDV), as well as their insect vector small brown planthopper, we elucidated the regulatory mechanism of JAK-STAT pathway in persistent viral infection. Both RSV and RBSDV

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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.

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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

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Liu, Jia Bin, Ying Qian, Ren Yu Xue, Guang Li Cao, and Cheng Liang Gong. "Prediction of Genes Regulated by JAK-STAT Signal Pathway." Advanced Materials Research 796 (September 2013): 25–35. http://dx.doi.org/10.4028/www.scientific.net/amr.796.25.

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JAK-STAT signaling pathway shared by a variety of cytokines was discovered in recent years. It plays an important role in growth and development, cell apoptosis and immune response. In general, activated STAT dimer binds to a palindromic sequence (TTCN2-4GAA) located at the upstream promoter region to activate gene transcription. Some signal pathways including Toll and Imd in silkworm Bombyx mori, a model of Lepidopteran insect, have been well studied. However, little is known regarding JAK-STAT signal pathway. In the present study, the genes regulated by JAK-STAT signal pathway were predicted

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