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Artículos de revistas sobre el tema "Jak2-Stat3"

Autor: Grafiati

Publicado: 9 de noviembre de 2024

Última modificación: 31 de julio de 2025

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1

Zhou, Zehua, Ying Chen, Wenmin Dong, Rui An, Kun Liang, and Xinhong Wang. "Da Cheng Qi Decoction Alleviates Cerulein-Stimulated AR42J Pancreatic Acinar Cell Injury via the JAK2/STAT3 Signaling Pathway." Evidence-Based Complementary and Alternative Medicine 2021 (April 9, 2021): 1–13. http://dx.doi.org/10.1155/2021/6657036.

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Background. Acute pancreatitis (AP) is a common acute abdomen inflammation, characterized by the dysregulation of digestive enzyme production and secretion. Many studies have shown that Da Cheng Qi Decoction (DCQD) is a secure, effective prescription on AP. In this study, cerulein-stimulated AR42J cells damage model was established to further explore the feasibility and underlying mechanism of DCQD as a potential inhibitor of JAK2/STAT3 pathway for the treatment of AP. Methods. Cell viability of DCQD was measured using a cell counting Kit-8 assay. Pancreatic biochemical markers such as amylase

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Jin, Wenyin, and Yinfeng Shen. "Da-Cheng-Qi Decoction Alleviates Intestinal Injury in Rats with Severe Acute Pancreatitis by Inhibiting the JAK2-STAT3 Signaling Pathway." Evidence-Based Complementary and Alternative Medicine 2019 (August 14, 2019): 1–12. http://dx.doi.org/10.1155/2019/3909468.

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Objective. To investigate the effect of Da-Cheng-Qi decoction (DCQD) on treating intestinal injury in rats with severe acute pancreatitis (SAP), based on the Janus kinase 2 (JAK2)/signal transducers and transcription 3 (STAT3) signaling pathway. Methods. Rats were randomly divided into the SAP group, SAP + ruxolitinib (JAK2 inhibitor) group, SAP + Stattic (STAT3 inhibitor) group, SAP + DCQD group, and sham operation group. They were further divided into 3-hour, 6-hour, 12-hour, and 18-hour subgroups. Levels of amylase and the inflammatory cytokines tumor necrosis factor-α, interleukin 6, inter

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Hofmann, Hans-Dieter, and Matthias Kirsch. "JAK2-STAT3 signaling." JAK-STAT 1, no. 3 (2012): 191–93. http://dx.doi.org/10.4161/jkst.20446.

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4

Kim, Hyunkyung, Dongha Kim, Seon Ah Choi, et al. "KDM3A histone demethylase functions as an essential factor for activation of JAK2−STAT3 signaling pathway." Proceedings of the National Academy of Sciences 115, no. 46 (2018): 11766–71. http://dx.doi.org/10.1073/pnas.1805662115.

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Janus tyrosine kinase 2 (JAK2)−signal transducer and activator of transcription 3 (STAT3) signaling pathway is essential for modulating cellular development, differentiation, and homeostasis. Thus, dysregulation of JAK2−STAT3 signaling pathway is frequently associated with human malignancies. Here, we provide evidence that lysine-specific demethylase 3A (KDM3A) functions as an essential epigenetic enzyme for the activation of JAK2−STAT3 signaling pathway. KDM3A is tyrosine-phosphorylated by JAK2 in the nucleus and functions as a STAT3-dependent transcriptional coactivator. JAK2−KDM3A signaling

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5

Bouaouiche, Sarra, Silvia Ghione, Randa Sghaier, et al. "Nitric Oxide-Releasing Drug Glyceryl Trinitrate Targets JAK2/STAT3 Signaling, Migration and Invasion of Triple-Negative Breast Cancer Cells." International Journal of Molecular Sciences 22, no. 16 (2021): 8449. http://dx.doi.org/10.3390/ijms22168449.

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Triple-negative breast cancer (TNBC) is a highly aggressive disease with invasive and metastasizing properties associated with a poor prognosis. The STAT3 signaling pathway has shown a pivotal role in cancer cell migration, invasion, metastasis and drug resistance of TNBC cells. IL-6 is a main upstream activator of the JAK2/STAT3 pathway. In the present study we examined the impact of the NO-donor glyceryl trinitrate (GTN) on the activation of the JAK2/STAT3 signaling pathway and subsequent migration, invasion and metastasis ability of TNBC cells through in vitro and in vivo experiments. We us

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6

Barber, Ruth, Jenny Zobel, Daniel Beck, et al. "JAK2 Is a Direct BCL6 Target Gene: Implications for Therapy in Diffuse Large B-Cell Lymphoma." Blood 124, no. 21 (2014): 3112. http://dx.doi.org/10.1182/blood.v124.21.3112.3112.

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Abstract Increased STAT3 signalling is a factor in driving ~50% of diffuse large B-cell lymphoma. In some cases increased cytokine production by the lymphoma is responsible for activation of JAK2 and STAT3 but the regulation of signalling through this pathway is not clear. We constructed a conditional BCL6 deficient cell line through disruption of the endogenous BCL6 loci of a genetically tractable human B-cell lymphoma by homologous recombination, and insertion of a tetracycline regulatable BCL6 transgene. On induction of BCL6 deficiency growth of the cell line slowed by 3 to 4-fold. A synthe

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7

Li, Yun-Qing. "Down-Regulation of Insulin Signaling Is Involved in Painful Diabetic Neuropathy in Type 2 Diabetes." Pain Physician 2;16, no. 2;3 (2013): E71—E83. http://dx.doi.org/10.36076/ppj.2013/16/e71.

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Background: Previous theories considered that the main cause of painful diabetic neuropathy (PDN) was due to hyperglycemia. However, recent evidence indicated that hyperinsulinemia plays a greater role in type 2 diabetic metabolisms (T2DM). Objectives: Our aim was to explore insulin signaling to determine the molecular mechanism involved in the pathogenesis of PDN in T2DM. Study Design: A randomized, double blind, controlled animal trial. Methods: We observed the localization of insulin receptor (IR) and phosphorylated insulin receptor substrate 1 (IRS-1) in the spinal cord using in situ hybri

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8

Lei, Bo, Ju Bai, Wanggang Zhang, et al. "Acute Monocytic Leukemia Associated Antigen MLAA-34 up-Regulates JAK2/STAT3 Expression and JAK2/STAT3 Enhances MLAA-34 Activation in a Positive Feedback Loop." Blood 126, no. 23 (2015): 1393. http://dx.doi.org/10.1182/blood.v126.23.1393.1393.

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Abstract Backgroud: The MLAA-34 gene (GenBank no. AY288977.2) was first discovered in acute monocytic leukemia (M5) in an effort to identify monocytic leukemia-associated antigens by serologic analysis of a recombinant cDNA expression library (SEREX). Previous study showed that high MLAA-34 levels were independently associated with a poorer relapse-free survival and overall survival in AML patients. The MLAA-34 is located on 13q14.2 and has been confirmed to be a novel splice variant of CAB39L (calcium binding protein 39-like). Both mRNA and protein levels of MLAA-34 were found to be higher in

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9

Zhang, Xuekang, Jun Zhou, Qian Hu, et al. "The Role of Janus Kinase/Signal Transducer and Activator of Transcription Signalling on Preventing Intestinal Ischemia/Reperfusion Injury with Dexmedetomidine." Journal of Nanoscience and Nanotechnology 20, no. 5 (2020): 3295–302. http://dx.doi.org/10.1166/jnn.2020.16416.

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Dexmedetomidine (Dex) works as a crucial agent for the treatment of intestinal ischemia/reperfusion (I/R), but its mechanism remains unclear. Recent articles demonstrated the pivotal role of Janus kinase/signal transducer and activator of transcription (JAK2/STAT3) signalling in I/R. Therefore, it is reasonable to explore the associated mechanism of JAK2/STAT3 signalling in Dex treatment. The study purpose was to evaluate the JAK2/STAT3 signalling regulatory mechanisms of Dex in preventing I/R. Anaesthetized rats were subjected to superior mesenteric artery occlusion consisting of 1 h of ische

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10

Liu, Fa-Yu, Jawad Safdar, Zhen-Ning Li, et al. "CCR7 Regulates Cell Migration and Invasion through JAK2/STAT3 in Metastatic Squamous Cell Carcinoma of the Head and Neck." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/415375.

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Squamous cell carcinoma of the head and neck (SCCHN) frequently involves metastasis at diagnosis. Our previous research has demonstrated that CCR7 plays a key role in regulating SCCHN metastasis, and this process involves several molecules, such as PI3K/cdc42, pyk2, and Src. In this study, the goals are to identify whether JAK2/STAT3 also participates in CCR7’s signal network, its relationship with other signal pathways, and its role in SCCHN cell invasion and migration. The results showed that stimulation of CCL19 could induce JAK2/STAT3 phosphorylation, which can be blocked by Src and pyk2 i

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11

Rong, Jing, Lizhong Li, Li Jing, Haiqin Fang, and Shuangqing Peng. "JAK2/STAT3 Pathway Mediates Protection of Metallothionein Against Doxorubicin-Induced Cytotoxicity in Mouse Cardiomyocytes." International Journal of Toxicology 35, no. 3 (2015): 317–26. http://dx.doi.org/10.1177/1091581815614261.

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Doxorubicin (Dox) is one of the most important anticancer agents; however, its clinical application is limited by its severe cardiotoxicity. In our previous study, we found that the gene expression levels of the Janus-activated kinase/signal transducer and activator of transcription 3 (JAK2/STAT3) pathway were different between MT−/− cardiomyocytes and MT+/+ cardiomyocytes when they were treated with Dox. Thus, this study was intended to investigate the role of JAK2/STAT3 pathway in metallothionein (MT) protection of Dox-induced cardiotoxicity. Tyrphostin AG490 (α-cyano-(3,4-dihydroxy)-N-benzy

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Koh, Jin Sung, Jong-Jae Park, Moon Kyung Joo, et al. "Antitumorigenic effect of plumbagin by induction of SHP1 in human gastric carcinoma cell lines." Journal of Clinical Oncology 33, no. 3_suppl (2015): 74. http://dx.doi.org/10.1200/jco.2015.33.3_suppl.74.

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74 Background: Plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) is a plant-drived natural agent extracted from the root of Plumbago zeylanic. A recent study reported that plumbagin down-regulated the activity of Janus kinase 2 (JAK2)-signal transducer and activator of transcription 3 (STAT3) pathway to show various anti-tumor effects. We aimed in this in vitrostudy to demonstrate the inhibition of JAK2-STAT3 pathway by plumbagin through inducing SH2-containing protein tyrosine phosphatase 1 (SHP1) expression in gastric cancer cell line. Methods: We performed Wetern blot to measure SHP1, phosp

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13

Mao, Ying, Yang Yao, and Li Liu. "Small molecule inhibitor azd1480 reverses radiotherapy resistance in NSCLC by targeting JAK2/STAT3 pathway." Tropical Journal of Pharmaceutical Research 23, no. 1 (2024): 45–50. http://dx.doi.org/10.4314/tjpr.v23i1.6.

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Purpose: To investigate the effect of small molecule inhibitor AZD1480 on radiotherapy resistance in non-small cell lung cancer (NSCLC), and the involvement of Janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway in the process. Methods: Radiation-resistant cell lines A549-20F, A549-30F, A549-40F and H460, H46040F, H460- 40F, and H460-40F were established, and expressions of proteins related to JAK/STAT pathway, mitogen-activated protein (MAPK) pathway and transforming growth factor-β (TGF- β) were assayed. The JAK2V617FH460 overexpression cell line and JAK2

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14

Zhu, Mingming, Min Yang, Quanyu Yang, et al. "Chronic Hypoxia-Induced Microvessel Proliferation and Basal Membrane Degradation in the Bone Marrow of Rats Regulated through the IL-6/JAK2/STAT3/MMP-9 Pathway." BioMed Research International 2020 (January 25, 2020): 1–10. http://dx.doi.org/10.1155/2020/9204708.

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Chronic hypoxia (CH) is characterized by long-term hypoxia that is associated with microvessel proliferation and basal membrane (BM) degradation in tissues. The IL-6/JAK2/STAT3/MMP-9 pathway has been described in a variety of human cancers and plays an essential role in microvessel proliferation and BM degradation. Therefore, this study investigated the role of the IL-6/JAK2/STAT3/MMP-9 pathway in hypoxia-mediated microvessel proliferation and BM degradation in the rat bone marrow. Eighty pathogen-free Sprague Dawley male rats were randomly divided into four groups (20 per group)—control group

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Morgan, Ethan L., and Andrew Macdonald. "JAK2 Inhibition Impairs Proliferation and Sensitises Cervical Cancer Cells to Cisplatin-Induced Cell Death." Cancers 11, no. 12 (2019): 1934. http://dx.doi.org/10.3390/cancers11121934.

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Persistent infection with high-risk human papillomavirus (HPV) is the underlying cause of ~5% of all human cancers, including the majority of cervical carcinomas and many other ano-genital and oral cancers. A major challenge remains to identify key host targets of HPV and to reveal how they contribute to virus-mediated malignancy. The HPV E6 oncoprotein aberrantly activates the signal transducer and activator of transcription 3 (STAT3) transcription factor and this is achieved by a virus-driven increase in the levels of the pro-inflammatory cytokine interleukin-6 (IL-6) in HPV positive cervica

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16

Yu, Xin, Zhi Li, Qilong Wan, et al. "Inhibition of JAK2/STAT3 signaling suppresses bone marrow stromal cells proliferation and osteogenic differentiation, and impairs bone defect healing." Biological Chemistry 399, no. 11 (2018): 1313–23. http://dx.doi.org/10.1515/hsz-2018-0253.

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Abstract Mesenchymal stem cells (MSCs) undergo osteogenic differentiation during bone defect healing. However, the role of JAK2/STAT3 in the osteogenic differentiation of MSCs and bone defect healing is still not fully understood. In this study, we aimed to analyze the effect of AG490, a JAK2-specific inhibitor, on MSCs proliferation and osteogenic differentiation as well as in bone defect healing. We used AG490 to inhibit the JAK2/STAT3 signaling in a mice bone marrow stromal cells (BMSCs) culture. AG490 inhibited BMSCs proliferation and osteogenic differentiation markers, i.e. Col1α, Alp and

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Hu, Yue, Hailong Chen, Lijuan Jin, Xiumei Chi, Jian Zhao, and Qinying Cao. "Hypomethylation of IL6ST promotes development of endometriosis by activating JAK2/STAT3 signaling pathway." PLOS ONE 20, no. 1 (2025): e0317569. https://doi.org/10.1371/journal.pone.0317569.

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Endometriosis is a chronic inflammatory disorder characterized by presence of endometrial tissue outside the uterine cavity. Immunohistochemical analysis (IHC) revealed markedly elevated expression of IL6ST in endometrial tissue of patients with ovarian endometriosis. Level of methylation of IL6ST is diminished in patients with endometriosis, whereas level of mRNA expression is markedly elevated by RT-PCR. Cell Counting Kit-8, Transwell, Terminal deoxynucleotidyl transferase dUTP nick end labeling assays substantiated endometrial stromal cells stably transfected with 3*FLAG-IL6ST plasmid exhib

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Kapuria, Vaibhav, Geoffrey Bartholomeusz, William Bornmann, Ling Y. Kong, Moshe Talpaz, and Nicholas J. Donato. "Inhibition of JAK2/STAT Signaling by Degrasyn through a Novel Mechanism." Blood 108, no. 11 (2006): 3423. http://dx.doi.org/10.1182/blood.v108.11.3423.3423.

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Abstract Janus Kinase 2 (JAK2) is a cytokine receptor associated tyrosine kinase. Cytokine stimulation results in JAK2 activation and tyrosine phosphorylation of the cytokine receptor. Cytosolic SH2 domain containing proteins, such as the signal transducer and activator of transcription 3 (STAT3) are recruited to phospho-tyrosine residues on the activated cytokine receptor, and phosphorylated by JAK2 to form stable dimers, followed by their translocation to the nucleus where they function as transcription factors. Deregulation of the JAK-STAT pathway is seen in several epithelial tumors and ma

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Perrone, Giulia, Elisabetta Calabrese, Teru Hideshima, et al. "Panobinostat Inhibits JAK2/STAT3 Pathway in Multiple Myeloma." Blood 114, no. 22 (2009): 2849. http://dx.doi.org/10.1182/blood.v114.22.2849.2849.

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Abstract Abstract 2849 Poster Board II-825 Histone deacetylase inhibitors (HDACi) are emerging as a potential therapy for Multiple Myeloma (MM). Their antineoplastic activity depends not only on nucleosomal histone acetylation, but also on direct modulation of non-histone proteins, including p53 or HSP90. Previous studies suggest that histone deacetylases inhibitors modulate Jak2/Stat3 signaling pathway, a cascade mediating tumor cell survival. Here we examine how Panobinostat, a class I-HDAC inhibitor currently in phase I/II clinical trial, can modulate the function of the Jak2/ Stat3 pathway

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Severin, Filippo, Federica Frezzato, Veronica Martini, et al. "Three Different Jak2/Stat3-Related Pathways Favor the Survival of Chronic Lymphocytic Leukemia Neoplastic Clone." Blood 132, Supplement 1 (2018): 4405. http://dx.doi.org/10.1182/blood-2018-99-114591.

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Abstract INTRODUCTION Chronic lymphoproliferative disorders are characterized by the expansion of malignant lymphocytes, the most common form being Chronic Lymphocytic Leukemia (CLL). Besides intrinsic abnormalities, the acquisition of the transformed phenotype and the diffusion of disease are related to the favorable cross-talking tumor cell-microenvironment. Furthermore, it has been demonstrated that CLL cells own an amplified mitochondrial respiration leading to an increased Reactive Oxygen Species (ROS) production and intrinsic oxidative stress. Several molecules released by microenvironme

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Grisouard, Jean, Takafumi Shimizu, Adrian Duek, et al. "Deletion of Stat3 in hematopoietic cells enhances thrombocytosis and shortens survival in a JAK2-V617F mouse model of MPN." Blood 125, no. 13 (2015): 2131–40. http://dx.doi.org/10.1182/blood-2014-08-594572.

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Key Points Loss of Stat3 in hematopoietic cells enhances JAK2-V617F–driven thrombopoiesis and negatively impacts survival in mouse models. The phenotypic changes of Stat3-deficient JAK2-V617F mice could in part be mediated by increased Stat1 expression and activation.

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Nicholson, SE, U. Novak, SF Ziegler, and JE Layton. "Distinct regions of the granulocyte colony-stimulating factor receptor are required for tyrosine phosphorylation of the signaling molecules JAK2, Stat3, and p42, p44MAPK." Blood 86, no. 10 (1995): 3698–704. http://dx.doi.org/10.1182/blood.v86.10.3698.bloodjournal86103698.

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The protein tyrosine kinases JAK1 and JAK2 are phosphorylated tyrosine after the interaction of granulocyte colony-stimulating factor (G-CSF) with its transmembrane receptor. So too is Stat3, a member of the STAT family of transcriptional activators thought to be activated by the JAK kinases. Truncated G-CSF receptor (G-CSF-R) mutants were used to determine the different regions of the cytoplasmic domain necessary for tyrosine phosphorylation of the signaling molecules JAK2, Stat3, and p42, p44MAPK. We have shown that G-CSF-induced tyrosine phosphorylation and kinase activation of JAK2 require

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Wu, Yi-Hong, Hsing-Yu Chen, Wei-Chin Hong, Chen-Ying Wei, and Jong-Hwei Su Pang. "Carboplatin-Induced Thrombocytopenia through JAK2 Downregulation, S-Phase Cell Cycle Arrest, and Apoptosis in Megakaryocytes." International Journal of Molecular Sciences 23, no. 11 (2022): 6290. http://dx.doi.org/10.3390/ijms23116290.

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Chemotherapy-induced thrombocytopenia (CIT) is a common complication when treating malignancies with cytotoxic agents wherein carboplatin is one of the most typical agents causing CIT. Janus kinase 2 (JAK2) is one of the critical enzymes to megakaryocyte proliferation and differentiation. However, the role of the JAK2 in CIT remains unclear. In this study, we used both carboplatin-induced CIT mice and MEG-01 cell line to examine the expression of JAK2 and signal transducer and activator of transcription 3 (STAT3) pathway. Under CIT, the expression of JAK2 was significantly reduced in vivo and

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Wu, Yang, Tan Yuan, Wei-Wei Wang, et al. "Long Noncoding RNA HOST2 Promotes Epithelial-Mesenchymal Transition, Proliferation, Invasion and Migration of Hepatocellular Carcinoma Cells by Activating the JAK2-STAT3 Signaling Pathway." Cellular Physiology and Biochemistry 51, no. 1 (2018): 301–14. http://dx.doi.org/10.1159/000495231.

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Background/Aims: This study aims to examine the effect of long noncoding RNA HOST2 (LncRNA HOST2) on epithelial-mesenchymal transition (EMT), proliferation, invasion and migration of hepatocellular carcinoma (HCC) cells via activation of the JAK2-STAT3 signaling pathway. Methods: HCC and para-cancerous tissues were collected from 136 HCC patients. Immunohistochemistry was used to detect the expression of JAK2 and STAT3. HCC SMMC7721 cells were grouped into blank, negative control (NC), HOST2 mimic and HOST2 inhibitor groups. The mRNA and protein expression levels of HOST2, JAK2, STAT3, E-cadhe

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You, Kyu Sic, Tae-Sung Kim, Su Min Back, et al. "JAK2 Inhibition Augments the Anti-Proliferation Effects by AKT and MEK Inhibition in Triple-Negative Breast Cancer Cells." International Journal of Molecular Sciences 26, no. 13 (2025): 6139. https://doi.org/10.3390/ijms26136139.

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Janus kinase 2 (JAK2) inhibitors have gained regulatory approval for treating various human diseases. While the JAK2/signal tranducer and activator of transcription 3 (STAT3) pathway plays a role in tumorigenesis, JAK2/STAT3 inhibitors have shown limited therapeutic efficacy in triple-negative breast cancer (TNBC). In this study, we assessed the antiproliferative effects of clinically approved JAK2 inhibitors in TNBC cell lines (MDA-MB-231 and HS578T) using the MTT assay. Among the four JAK2 inhibitors evaluated (fedratinib, cerdulatinib, peficitinib, and filgotinib), fedratinib significantly

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Xu, Hong, Ya-min Zhang, Hua Sun, Su-hui Chen, and Ying-kui Si. "Electroacupuncture at GV20 and ST36 Exerts Neuroprotective Effects via the EPO-Mediated JAK2/STAT3 Pathway in Cerebral Ischemic Rats." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/6027421.

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Background. While electroacupuncture (EA) in cerebral ischemia has been used to promote functional recovery, the underlying mechanism of its protective effect remains poorly understood.Objective. We investigated the effects of EA stimulation at GV20 and ST36 to observe the changes in erythropoietin- (EPO-) mediated Janus family tyrosine kinases 2 (JAK2) signal transducers and activators of the transcription 3 (STAT3) cell pathway.Methods. Thirty-six specific pathogen-free Sprague-Dawley (SD) male rats were randomly assigned to three groups: the sham-operated group (S group), the middle cerebra

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Alanazi, Ahmed Z., and Michelle A. Clark. "Angiotensin III Induces JAK2/STAT3 Leading to IL-6 Production in Rat Vascular Smooth Muscle Cells." International Journal of Molecular Sciences 20, no. 22 (2019): 5551. http://dx.doi.org/10.3390/ijms20225551.

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The Janus kinase-2/ signal transducer and activators of transcription-3 (JAK2/STAT3) pathway and interleukin-6 (IL-6) are pleiotropic signal transduction systems that are responsible for induction of many cytokines and growth factors. It is unknown whether the renin angiotensin aldosterone system (RAAS) peptide, angiotensin (Ang) III induces JAK2/STAT3 and IL-6 in vascular smooth muscle cells (VSMCs). Thus, the purpose of this study was to investigate whether Ang III induces the JAK2/STAT3 pathway leading to IL-6 production in cultured VSMCs isolated from Wistar rats and determine whether diff

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Zhang, Zuo, Hongli Zhou, and Jiyin Zhou. "Neuritin inhibits astrogliosis to ameliorate diabetic cognitive dysfunction." Journal of Molecular Endocrinology 66, no. 4 (2021): 259–72. http://dx.doi.org/10.1530/jme-20-0321.

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Earlier, it was shown that reversing the downregulation of neuritin expression in the brain improves central neuropathy in diabetic rats. We investigated the protective mechanism of neuritin in diabetic cognitive dysfunction via astrocytes. Further, the impact of the overexpression of neuritin in the cortex and the hippocampus on diabetic cognitive dysfunction and astrogliosis in type 2 diabetic (db/db) mice was assessed. Antagonists were used to inhibit the JAK2/STAT3 signaling pathway in U-118MG, an astrocyte cell line. Immunofluorescence, Western blotting, and real-time PCR were performed.

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Ji, Hongyun, Hui Lu, Feng Li, Ying Qu, Qing Hu, and Xiaoran Li. "MiR-189 Exerts Anticancer Activity Through Janus Kinase 2/Signal Transducer and Activator of Transcription 3 (JAK2/STAT3) Pathway in Non-Small Cell Lung Cancer." Journal of Biomaterials and Tissue Engineering 11, no. 12 (2021): 2421–26. http://dx.doi.org/10.1166/jbt.2021.2846.

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Non-small cell lung cancer (NSCLC) remains a threat to human health but its etiology remains unclear. MicroRNAs (miRNAs) are involved in NSCLC progression. This study aims to elucidate the mechanism by how exosomal miR-189 functions in NSCLC. After identification, BMSCs were co-cultured with NSCLC cells which were then transfected with miR-189 mimics followed by analysis of the expression of JAK2/Stat3 proteins and miR-189, cell migration and invasion by Transwell assay, cell viability by MTT assay, apoptosis by flow cytometry. miR-189 is downregulated in NSCLC cells and tissues. miR-189 overe

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Auer, Franziska, Minhui Lin, Karin Nebral, et al. "Novel Recurrent Germline JAK2 G571S Variant in Childhood Acute B-Lymphoblastic Leukemia: A Double Hit One Pathway Scenario." Blood 132, Supplement 1 (2018): 387. http://dx.doi.org/10.1182/blood-2018-99-115293.

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Abstract Introduction: Current studies demonstrate an involvement of germline predispositions in the development of approximately 5% of childhood leukemias (Zhang J et al.,N Engl J Med, 2015), although their actual contribution is believed to be much higher. Being able to understand tumor evolution starting from a predisposed cell, opens up a new avenue in the form of disease prevention rather than treatment. Here, we present a novel finding of a double hit - one pathway scenario, in which a rare (MAF<0.01) germline JAK2 variant (G571S), inherited paternally, and a newly described germline

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Wu, Jianjiang, Jin Yu, Peng Xie, et al. "Sevoflurane postconditioning protects the myocardium against ischemia/reperfusion injury via activation of the JAK2–STAT3 pathway." PeerJ 5 (April 4, 2017): e3196. http://dx.doi.org/10.7717/peerj.3196.

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BackgroundSevoflurane postconditioning (S-post) has similar cardioprotective effects as ischemic preconditioning. However, the underlying mechanism of S-post has not been fully elucidated. Janus kinase signaling transduction/transcription activator (JAK2–STAT3) plays an important role in cardioprotection. The purpose of this study was to determine whether the cardioprotective effects of S-post are associated with activation of the JAK2–STAT3 signal pathway.MethodsAn adult male Sprague–Dawley (SD) rat model of myocardial ischemia/reperfusion (I/R) injury was established using the Langendorff is

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Kim, Ji-Hyang, Hack Sun Choi, Su-Lim Kim, and Dong-Sun Lee. "The PAK1-Stat3 Signaling Pathway Activates IL-6 Gene Transcription and Human Breast Cancer Stem Cell Formation." Cancers 11, no. 10 (2019): 1527. http://dx.doi.org/10.3390/cancers11101527.

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Cancer stem cells (CSCs) have unique properties, including self-renewal, differentiation, and chemoresistance. In this study, we found that p21-activated kinase (PAK1) inhibitor (Group I, PAK inhibitor, IPA-3) and inactivator (ivermectin) treatments inhibit cell proliferation and that tumor growth of PAK1-knockout cells in a mouse model is significantly reduced. IPA-3 and ivermectin inhibit CSC formation. PAK1 physically interacts with Janus Kinase 2 (JAK2), and JAK2 inhibitor (TG101209) treatment inhibits mammosphere formation and reduces the nuclear PAK1 protein level. PAK1 interacts with si

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Lee, Jennifer K., Jung-Heun Ha, Do-Kyun Kim, JaeHee Kwon, Young-Eun Cho, and In-Sook Kwun. "Depletion of Zinc Causes Osteoblast Apoptosis with Elevation of Leptin Secretion and Phosphorylation of JAK2/STAT3." Nutrients 15, no. 1 (2022): 77. http://dx.doi.org/10.3390/nu15010077.

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Zinc (Zn) has been reported to mediate leptin secretion, and thus leptin can be an important candidate molecule linking Zn with bone formation. The present study investigated whether zinc deficiency induces leptin secretion by activating a JAK2/STAT3 signaling pathway and leads to osteoblastic apoptosis. MC3T3-E1 cells were incubated for 24 h in normal osteogenic differentiation medium (OSM) or OSM treated with either 1 μM (Low Zn) or 15 μM (High Zn) of ZnCl2 containing 5 μM TPEN (Zn chelator). Our results demonstrated that low Zn stimulated extracellular leptin secretion and increased mRNA an

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Li, Xiangzi, Liangtong Li, Xuanchen Liu, et al. "Attenuation of Cardiac Ischaemia-reperfusion Injury by Treatment with Hydrogen-rich Water." Current Molecular Medicine 19, no. 4 (2019): 294–302. http://dx.doi.org/10.2174/1566524019666190321113544.

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Background: Hydrogen has been shown to exert a bioactive effect on the myocardium. This study examined the signalling pathways for hydrogen attenuating ischaemia-reperfusion injury. Methods: In total, 20 male Wistar rats were evaluated for the effects of hydrogen-rich water on ischaemia-reperfusion in hearts. Left ventricular tissue was taken for screening and analysis of active protein factors by protein chip technology. The enrichment of the KEGG pathway was obtained by using the Gene Ontology (GO) enrichment principle. The expression of JAK2, STAT1, STAT3, p-STAT1, p-JAK2, p-STAT3 in rat my

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Sun, Yueyue, Huan Tong, Lingyu Zeng, Kailin Xu, and Jianlin Qiao. "Notch1 Regulates Hepatic Thrombopoietin Production." Blood 142, Supplement 1 (2023): 281. http://dx.doi.org/10.1182/blood-2023-177812.

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Notch signaling is highly conserved and regulates cell-fate decisions in several developmental processes and cell functions. However, a role for Notch in hepatic thrombopoietin (TPO) production has not been described. We noted that mice with a deficiency in hepatic Notch1 had thrombocytopenia, and so investigated TPO production and other features of platelets in these mice. We found that the liver ultrastructure and hepatocyte function were comparable between control mice and Notch1-deficient mice. However, the Notch1-deficient mice had significantly lower plasma TPO and hepatic TPO mRNA level

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Wulansari, Noviana, Yanuar Alan Sulistio, Wahyu Handoko Wibowo Darsono, Chang-Hoon Kim, and Sang-Hun Lee. "LIF maintains mouse embryonic stem cells pluripotency by modulating TET1 and JMJD2 activity in a JAK2-dependent manner." Stem Cells 39, no. 6 (2021): 750–60. http://dx.doi.org/10.1002/stem.3345.

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Abstract The LIF-JAK2-STAT3 pathway is the central signal transducer that maintains undifferentiated mouse embryonic stem cells (mESCs), which is achieved by the recruitment of activated STAT3 to the master pluripotency genes and activation of the gene transcriptions. It remains unclear, however, how the epigenetic status required for the master gene transcriptions is built into LIF-treated mESC cultures. In this study, Jak2, but not Stat3, in the LIF canonical pathway, establishes an open epigenetic status in the pluripotency gene promoter regions. Upon LIF activation, cytosolic JAK2 was tran

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Chatterjee, Prodyot K., Yousef Al-Abed, Barbara Sherry, and Christine N. Metz. "Cholinergic agonists regulate JAK2/STAT3 signaling to suppress endothelial cell activation." American Journal of Physiology-Cell Physiology 297, no. 5 (2009): C1294—C1306. http://dx.doi.org/10.1152/ajpcell.00160.2009.

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The cholinergic anti-inflammatory pathway is a physiological mechanism that inhibits cytokine production and minimizes tissue injury during inflammation. Previous investigations revealed that cholinergic stimulation (via cholinergic agonists and vagus nerve stimulation) suppresses endothelial cell activation and leukocyte recruitment. The purpose of this study was to investigate the mechanisms by which cholinergic agonists (e.g., nicotine and GTS-21) regulate endothelial cell activation. Specifically, we examined the effects of cholinergic agonists on IL-6-mediated endothelial cell activation

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Severin, Frezzato, Visentin, et al. "In Chronic Lymphocytic Leukemia the JAK2/STAT3 Pathway Is Constitutively Activated and Its Inhibition Leads to CLL Cell Death Unaffected by the Protective Bone Marrow Microenvironment." Cancers 11, no. 12 (2019): 1939. http://dx.doi.org/10.3390/cancers11121939.

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The bone marrow microenvironment promotes proliferation and drug resistance in chronic lymphocytic leukemia (CLL). Although ibrutinib is active in CLL, it is rarely able to clear leukemic cells protected by bone marrow mesenchymal stromal cells (BMSCs) within the marrow niche. We investigated the modulation of JAK2/STAT3 pathway in CLL by BMSCs and its targeting with AG490 (JAK2 inhibitor) or Stattic (STAT3 inhibitor). B cells collected from controls and CLL patients, were treated with medium alone, ibrutinib, JAK/Signal Transducer and Activator of Transcription (STAT) inhibitors, or both drug

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Ni, Chih-Wen, Hsyue-Jen Hsieh, Yuen-Jen Chao, and Danny Ling Wang. "Interleukin-6-induced JAK2/STAT3 signaling pathway in endothelial cells is suppressed by hemodynamic flow." American Journal of Physiology-Cell Physiology 287, no. 3 (2004): C771—C780. http://dx.doi.org/10.1152/ajpcell.00532.2003.

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Endothelial cells (ECs) are constantly exposed to shear stress, the action of which triggers signaling pathways and cellular responses. During inflammation, cytokines such as IL-6 increase in plasma. In this study, we examined the effects of steady flow on IL-6-induced endothelial responses. ECs exposed to IL-6 exhibited STAT3 activation via phosphorylation of Tyr705. However, when ECs were subjected to shear stress, shear force-dependent suppression of IL-6-induced STAT3 phosphorylation was observed. IL-6 treatment increased the phosphorylation of JAK2, an upstream activator of STAT3. Consist

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Zhang, Le, Bing-Hui Wu, Ting-Ting Liang, et al. "Leptin activates the JAK/STAT pathway to promote angiogenesis in RF/6A cells in vitro." International Journal of Ophthalmology 15, no. 4 (2022): 554–59. http://dx.doi.org/10.18240/ijo.2022.04.05.

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AIM: To investigate the effect of leptin on the angiogenesis of RF/6A cells (monkey retinal choroidal endothelial cells) in vitro and test the cellular signaling in the mechanism. METHODS: RF/6A cells were cultured in vitro and randomly divided into four groups: normal control, with leptin at 50, 100, 200 ng/mL for cell counting kit-8 (CCK8). RF/6A cell proliferation and migration were examined by Transwell assays, while RF/6A cell tube formation by Matrigel assay. JAK2, p-JAK2, STAT3, and p-STAT3 protein expression was measured by Western blotting. Cells were then divided into the following t

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Yu, Yechen, Xu Wang, Fan Yang, Ke Xing, Lihong Ren, and Guangfei Xu. "Effect of Jiawei Tangzhiqing granules on JAK2/STAT3 signal pathway and Th17/Treg ratio in diabetic nephropathy mice." Tropical Journal of Pharmaceutical Research 23, no. 2 (2024): 279–89. http://dx.doi.org/10.4314/tjpr.v23i2.7.

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Purpose: To investigate the effect of Jiawei Tangzhiqing granules on JAK2/STAT3 signaling pathway and Th17/Treg ratio in diabetic nephropathy (DN) mice.  Methods: Selected 60 male SPF C57BL/6N mice, divided into control group and DN model group; the latter was further further split into model control, Western medicine group, and three Jiawei Tangzhiqing granule groups (high, medium, and low doses). Treatments were administered orally for 12 weeks. Key health indicators and renal tissue pathology were analyzed. Th17 and Treg levels in CD4+ T cells were quantified, and JAK2 and STAT3 prote

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Xu, Yefang, Jingjing Zhang, Jing Wu, Sheng Zhong, and Hongxia Li. "Inhibition of JAK2 Reverses Paclitaxel Resistance in Human Ovarian Cancer Cells." International Journal of Gynecologic Cancer 25, no. 9 (2015): 1557–64. http://dx.doi.org/10.1097/igc.0000000000000550.

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ObjectiveResistance to chemotherapy is a major factor that limits the postsurgical survival of ovarian cancer patients. Janus-activated kinase 2 (JAK2) has been implicated in cancer cell survival and the development of drug resistance in ovarian cancers. In the present study, we sought to determine whether inhibition of JAK2 reverses drug resistance in OC3/TAX300 cells, a paclitaxel-resistant human ovarian cancer cell line previously established in our laboratory.MethodsOC3/TAX300 cells were transduced with lentivirus expressing small interference RNA (siRNA) against JAK2 and treated with JAK2

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Mellado, M., J. M. Rodríguez-Frade, A. Aragay, et al. "The Chemokine Monocyte Chemotactic Protein 1 Triggers Janus Kinase 2 Activation and Tyrosine Phosphorylation of the CCR2B Receptor." Journal of Immunology 161, no. 2 (1998): 805–13. http://dx.doi.org/10.4049/jimmunol.161.2.805.

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Abstract The chemokines are a growing family of low m.w., 70- to 80-residue proinflammatory cytokines that operate by interacting with G protein-coupled receptors. Chemokines are involved in cell migration and in the activation of specific leukocyte subsets. Using the Mono Mac 1 monocytic cell line, we show that monocyte chemotactic protein 1 (MCP-1) triggers activation of the Janus kinase 2 (JAK2)/STAT3 pathway and CCR2 receptor tyrosine phosphorylation. Both Ca2+ mobilization and cell migration are blocked in Mono Mac 1 cells by tyrphostin B42, a specific JAK2 kinase inhibitor. Within second

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Regua, Angelina T., Dongqin Zhu, Daniel L. Doheny, et al. "Abstract 1039: TrkA and JAK2-STAT3 pathway crosstalk promotes breast cancer stem cells in HER2-enriched and triple-negative breast cancers." Cancer Research 82, no. 12_Supplement (2022): 1039. http://dx.doi.org/10.1158/1538-7445.am2022-1039.

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Abstract Breast cancer is the most commonly diagnosed cancer in American women and accounts for ~15% of cancer-related deaths. Despite the current standard of care, metastatic HER2-enriched breast cancer and triple-negative breast cancer remain difficult to treat due to poor response to treatment, lack of actionable targets, or eventual acquired resistance. The high mortality rate of metastatic HER2-enriched breast cancers and triple-negative breast cancers highlights the need for novel actionable targets for improved response to therapeutic intervention. Through datamining of publicly availab

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Bao, Yan, Wei Liang, Yingchun Ye, and Bo Yi. "PERK-Dependent Activation of the JAK2/STAT3 Pathway Contributes to High Glucose-Induced Extracellular Matrix Deposition in Renal Tubular Epithelial Cells." International Journal of Endocrinology 2021 (July 19, 2021): 1–9. http://dx.doi.org/10.1155/2021/8475868.

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Background. Although the deposition of extracellular matrix (ECM) is critical leading to tubular damage in diabetic kidney disease (DKD), the mechanism still remains unclear. The purpose of this study was to demonstrate a role for protein kinase R-like endoplasmic reticulum kinase (PERK) (a protein located in the endoplasmic reticulum membrane) in this pathologic process. Methods. NRK-52E cells were grown in the media containing different concentrations of glucose or thapsigargin for different durations. Cells were subsequently incubated with or without AG490, a selective inhibitor of Janus ki

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Wang, Kun, Yong-Gui Wu, Jing Su, Jing-Jing Zhang, Pei Zhang, and Xiang-Ming Qi. "Total Glucosides of Paeony Regulates JAK2/STAT3 Activation and Macrophage Proliferation in Diabetic Rat Kidneys." American Journal of Chinese Medicine 40, no. 03 (2012): 521–36. http://dx.doi.org/10.1142/s0192415x12500401.

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Total glucosides of paeony (TGP) is the major active constituent of Paeonia lactiflora Pall., which has shown renoprotection in experimental diabetic nephropathy. Activation of Janus kinase/signal transducers and activators of transcription (JAK/STAT) is an important mechanism by which hyperglycemia contributes to renal damage. Macrophages also play an essential role in the pathogenesis of diabetic nephropathy. Herein, we investigated the ability of TGP to modulate JAK2/STAT3 activation and macrophage proliferation in rats with streptozotocin (STZ)-induced diabetes. TGP (50, 100, and 200 mg/kg

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Proietti, Cecilia, Mariana Salatino, Cinthia Rosemblit, et al. "Progestins Induce Transcriptional Activation of Signal Transducer and Activator of Transcription 3 (Stat3) via a Jak- and Src-Dependent Mechanism in Breast Cancer Cells." Molecular and Cellular Biology 25, no. 12 (2005): 4826–40. http://dx.doi.org/10.1128/mcb.25.12.4826-4840.2005.

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ABSTRACT Interactions between steroid hormone receptors and signal transducer and activator of transcription (Stat)-mediated signaling pathways have already been described. In the present study, we explored the capacity of progestins to modulate Stat3 transcriptional activation in an experimental model of hormonal carcinogenesis in which the synthetic progestin medroxyprogesterone acetate (MPA) induced mammary adenocarcinomas in BALB/c mice and in the human breast cancer cell line T47D. We found that C4HD epithelial cells, from the MPA-induced mammary tumor model, expressed Stat3 and that MPA

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Chao, Angel, Min-Jie Liao, Shun-Hua Chen, et al. "JAK2-Mediated Phosphorylation of Stress-Induced Phosphoprotein-1 (STIP1) in Human Cells." International Journal of Molecular Sciences 23, no. 5 (2022): 2420. http://dx.doi.org/10.3390/ijms23052420.

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Stress-induced phosphoprotein-1 (STIP1)—a heat shock protein (HSP)70/HSP90 adaptor protein—is commonly overexpressed in malignant cells, where it controls proliferation via multiple signaling pathways, including JAK2/STAT3. We have previously shown that STIP1 stabilizes the protein tyrosine kinase JAK2 in cancer cells via HSP90 binding. In this study, we demonstrate that STIP1 may act as a substrate for JAK2 and that phosphorylation of tyrosine residues 134 and 152 promoted STIP1 protein stability, induced its nuclear-cytoplasmic shuttling, and promoted its secretion into the extracellular spa

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Lian, Mengqiao, Yuchao Sun, Yuan Lin, et al. "p-JAK2 plays a key role in catalpol-induced protection against rat intestinal ischemia/reperfusion injury." RSC Advances 7, no. 86 (2017): 54369–78. http://dx.doi.org/10.1039/c7ra10506a.

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Wang, MingJun, Jian Wu, Jing Cao, et al. "Action of Tofacitinib in a Rat Model of Synovitis." Journal of Biomaterials and Tissue Engineering 12, no. 10 (2022): 1981–87. http://dx.doi.org/10.1166/jbt.2022.3130.

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Purpose: To evaluate effects and mechanism of tofacitinib in treatment of rheumatoid arthritis (RA) model rats. Materials and Methods: Dividing 27 rats into 3 groups: NC (normal control), Model (RA model) and Tofacitinib (RA model rats treated with tofacitinib) groups. Observation joint swelling and articular synovium pathology by HE staining, IL-1β, IL-6, IL-10 and TNF-α levels by ELISA assay, JAK2, STAT3 and NF-κB(p65) proteins by IHC and WB assay. Results: Compared with NC group, joint swelling, histopathological score IL-1β, IL-6, IL-10 and TNF-α significantly deteriorated (P < 0.001, r

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