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Journal articles on the topic 'STAT. Inhibitor'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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1

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

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

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2

Hu, Cheng-Ping, Jun-Tao Feng, Yu-Ling Tang, Jin-Qi Zhu, Min-Juan Lin, and Ming-En Yu. "LIF Upregulates Expression of NK-1R in NHBE Cells." Mediators of Inflammation 2006 (2006): 1–8. http://dx.doi.org/10.1155/mi/2006/84829.

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Leukemia inhibitory factor (LIF), a cytokine at the interface between neurobiology and immunology, is mainly mediated through JAK/STAT pathway and MAPK/ERK pathway. Evidence suggested LIF is related to the higher expression of neurokinin-1 receptor (NK-1R) in asthma. In this study, the immunohistochemistry stain showed the expressions of NK-1R, LIF, p-STAT3, and p-ERK1/2 in the lung tissues of allergic rats were increased compared with the controls, and the main positive cell type was airway epithelial cell. Normal human bronchial epithelial cells were treated with LIF in the presence or absen

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3

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

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

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5

Kim, Byung-Su, Chansu Lee, Juwon Park, et al. "Inactivation of JAK/STAT Cell Signaling by SK-7041, a Novel HDAC Inhibitor, Effectively Inhibits Growth of Acute Myeloid Leukemia Cells." Blood 112, no. 11 (2008): 4005. http://dx.doi.org/10.1182/blood.v112.11.4005.4005.

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Abstract Activation of the JAK/STAT pathway appears common in AML, occurring in up to 70% of AML patients. Therefore, JAK/STAT signal inhibitors are promising as candidate anti-cancer agents in AML. Recently, we reported that SK-7041, an HDAC inhibitor, inhibited the growth of AML cells via activation of caspase-3 and down-regulation of cyclin D1. These findings lead us to further examine whether SK-7041 inhibits the growth of KG1 AML cells via inactivation of JAK/STAT signals. Multi-immunoblotting technique (Kinetworks™ analysis) showed that expression of p-STAT-3, p-STAT-5, and p-Erk was dow

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Barclay, J. L., T. Wonisch, S. T. Anderson, M. J. Waters, and J. D. Curlewis. "124. Regulation of SOCS3 expression by prostaglandin, prolactin and growth hormone: challenging the Jak/STAT signalling dogma." Reproduction, Fertility and Development 17, no. 9 (2005): 74. http://dx.doi.org/10.1071/srb05abs124.

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SOCS3 is an inhibitor of various cytokine-receptor signalling pathways and is therefore involved in suppression of cellular responsiveness to these critical regulators. SOCS3 expression is thought to be regulated by a STAT responsive element (SRE). However, our research suggests the involvement of other signalling pathways. In T-47D breast cancer cells, we found that PGE2 induces a 3–5 fold increase in SOCS3 mRNA, as determined by real-time PCR. This effect was not due to phosphorylation of STATs, or inhibited by the Jak2 inhibitor, AG490, but was inhibited by the PI3Kinase inhibitor, LY294002

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Kitanaga, Yukihiro, Emiko Imamura, Yutaka Nakahara, et al. "In vitro pharmacological effects of peficitinib on lymphocyte activation: a potential treatment for systemic sclerosis with JAK inhibitors." Rheumatology 59, no. 8 (2019): 1957–68. http://dx.doi.org/10.1093/rheumatology/kez526.

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Abstract Objectives Peficitinib, a novel Janus kinase (JAK) inhibitor, demonstrated promising results in treating RA in phase 3 clinical trials. This in vitro study was undertaken to characterize the pharmacological properties of peficitinib and investigate the involvement of JAK and signal transducer and activator of transcription (STAT) pathways in the pathological processes of SSc, which is also an autoimmune disease. Methods Phosphorylation levels of STAT molecules were assessed in peripheral blood mononuclear cells collected from patients with RA or SSc and healthy subjects, and in skin s

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8

Zhou, Jianbiao, Chonglei Bi, Lai Fong Poon, et al. "Overactivation of STAT Pathways and Overexpression of Survivin Confer Resistance to FLT3 Inhibitors and Could Be Therapeutic Targets in AML." Blood 110, no. 11 (2007): 2367. http://dx.doi.org/10.1182/blood.v110.11.2367.2367.

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Abstract Internal tandem duplication (ITD) of fms-like tyrosine kinase 3 (FLT3) receptor plays an important role in the pathogenesis of acute myeloid leukemia (AML). A number of small molecule kinase inhibitors are currently proceeding in different phases of clinical trials. As with imatinib in CML, leukemic cells could develop resistance to these RTK inhibitors when used as monotherapy. Mutations in the ATP-binding pocket have been identified through PCR-based mutagenesis screening in Ba/F3-FLT3-ITD cells and selected for growth in the presence of PKC412, or in a resistant Ba/F3-FLT3-ITD cell

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9

Banes, Amy K., Séan Shaw, John Jenkins, et al. "Angiotensin II blockade prevents hyperglycemia-induced activation of JAK and STAT proteins in diabetic rat kidney glomeruli." American Journal of Physiology-Renal Physiology 286, no. 4 (2004): F653—F659. http://dx.doi.org/10.1152/ajprenal.00163.2003.

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Clinical and animal studies show that treatment with angiotensin-converting enzyme (ACE) inhibitors or ANG II-receptor antagonists slows progression of nephropathy in diabetes, indicating ANG II plays an important role in its development. We previously reported that hyperglycemia augments both ANG II-induced growth and activation of Janus kinase (JAK)2 and signal transducers and activators of transcription (STAT) proteins in cultured rat mesangial cells. Furthermore, we demonstrated that the tyrosine kinase enzyme JAK2 plays a key role in both ANG II- and hyperglycemia-induced growth in these

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

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

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Kim, Dong Wook, Young Suk Jo, Hye Sook Jung, et al. "An Orally Administered Multitarget Tyrosine Kinase Inhibitor, SU11248, Is a Novel Potent Inhibitor of Thyroid Oncogenic RET/Papillary Thyroid Cancer Kinases." Journal of Clinical Endocrinology & Metabolism 91, no. 10 (2006): 4070–76. http://dx.doi.org/10.1210/jc.2005-2845.

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Abstract Context: The oncogenic RET/PTC tyrosine kinase causes papillary thyroid cancer (PTC). The use of inhibitors specific for RET/PTC may be useful for targeted therapy of PTC. Objective: The objective of the study was to evaluate the efficacies of the recently developed kinase inhibitors SU11248, SU5416, and SU6668 in inhibition of RET/PTC. Design: SU11248, SU5416, and SU6668 were synthesized, and their inhibitory potencies were evaluated using an in vitro RET/PTC kinase assay. The inhibitory effects of the compounds on RET/PTC were evaluated by quantifying the autophosphorylation of RET/

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Shen, Yang, Linyi Meng, Huajun Sun, Yizhun Zhu, and Hongrui Liu. "Cochinchina MomordicaSeed Suppresses Proliferation and Metastasis in Human Lung Cancer Cells by Regulating Multiple Molecular Targets." American Journal of Chinese Medicine 43, no. 01 (2015): 149–66. http://dx.doi.org/10.1142/s0192415x1550010x.

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Cochinchina Momordica Seed, which is the dried ripe seed of Momordica cochinchinensis (Lour.) Spreng, has been used as a mainly anticancer ingredient for many years in China. This study aims at investigating the roles of an ethanol-soluble extract of Cochinchina Momordica Seed (ECMS) in suppressing the proliferation and metastasis of human lung cancer cells, and further elucidating underlying molecular mechanisms. Our researches suggest that ECMS dose-dependently decreased the survival rates of A549 and H1299 cells, and inhibited the migration and invasion in A549 cells. ECMS-induced apoptosis

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SHEN, Xuening, Zhigang TIAN, Michael J. HOLTZMAN та Bin GAO. "Cross-talk between interleukin 1β (IL-1β) and IL-6 signalling pathways: IL-1β selectively inhibits IL-6-activated signal transducer and activator of transcription factor 1 (STAT1) by a proteasome-dependent mechanism". Biochemical Journal 352, № 3 (2000): 913–19. http://dx.doi.org/10.1042/bj3520913.

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Interleukin 1β (IL-1β) suppresses the IL-6-dependent induction of type II acute-phase response genes, but the underlying mechanism for this suppression remains uncertain. Here we report that treatment of human hepatocullular carcinoma HepG2 cells with IL-1β inhibited the IL-6-dependent binding of signal transducer and activator of transcription factor (STAT)1, but not that of STAT3, to the high-affinity serum-inducible element (‘SIE’). Furthermore, IL-1β selectively down-regulated the IL-6-induced tyrosine phosphorylation of STAT1 without affecting the level of STAT1 or tyrosine phosphorylatio

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

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

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15

Suzuki, Asuka, Toshikatsu Hanada, Keiichi Mitsuyama, et al. "Cis3/Socs3/Ssi3 Plays a Negative Regulatory Role in Stat3 Activation and Intestinal Inflammation." Journal of Experimental Medicine 193, no. 4 (2001): 471–82. http://dx.doi.org/10.1084/jem.193.4.471.

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Immune and inflammatory systems are controlled by multiple cytokines, including interleukins (ILs) and interferons. These cytokines exert their biological functions through Janus tyrosine kinases and signal transducer and activator of transcription (STAT) transcription factors. We recently identified two intrinsic Janus kinase (JAK) inhibitors, JAK binding protein (JAB; also referred to as suppressor of cytokine signaling [SOCS1]/STAT-induced STAT inhibitor [SSI1]) and cytokine-inducible SH2 protein (CIS)3 (or SOCS3/SSI3), which play an essential role in the negative regulation of cytokine sig

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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.

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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

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Kuusanmäki, Heikki, Hanna Rajala, Arjan van Adrichem, et al. "Drug Sensitivity Profiling Identifies Drugs for Targeting Constitutively Active Mutant STAT3 and Mutant STAT5B Positive Malignancies." Blood 124, no. 21 (2014): 1771. http://dx.doi.org/10.1182/blood.v124.21.1771.1771.

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Abstract Introduction: Constitutive hyperactivation of the STAT3 and STAT5B transcription factors is often observed in cancer. Lately, activating STAT3 mutations have been identified in hematological malignancies including large granular lymphocytic (LGL) leukemia (prevalence 40%), aplastic anemia (7%) and CD30+ T-cell lymphoma (17%). Furthermore, recent studies highlight the importance of STAT5B mutations in the pathogenesis and prognosis of T-cell malignancies such as T-cell prolymphocytic leukemia (36%), T-cell acute lymphoblastic leukemia (8%) and hepatosplenic T-cell lymphoma (33%). While

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18

Koppikar, Priya, Omar Abdel-Wahab, Cyrus Hedvat, et al. "Efficacy of the JAK2 inhibitor INCB16562 in a murine model of MPLW515L-induced thrombocytosis and myelofibrosis." Blood 115, no. 14 (2010): 2919–27. http://dx.doi.org/10.1182/blood-2009-04-218842.

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Abstract The discovery of JAK2 and MPL mutations in patients with myeloproliferative neoplasms (MPNs) provided important insight into the genetic basis of these disorders and led to the development of JAK2 kinase inhibitors for MPN therapy. Although recent studies have shown that JAK2 kinase inhibitors demonstrate efficacy in a JAK2V617F murine bone marrow transplantation model, the effects of JAK2 inhibitors on MPLW515L-mediated myeloproliferation have not been investigated. In this report, we describe the in vitro and in vivo effects of INCB16562, a small-molecule JAK2 inhibitor. INCB16562 i

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Holloway, Gavan, Vi T. Dang, David A. Jans та Barbara S. Coulson. "Rotavirus inhibits IFN-induced STAT nuclear translocation by a mechanism that acts after STAT binding to importin-α". Journal of General Virology 95, № 8 (2014): 1723–33. http://dx.doi.org/10.1099/vir.0.064063-0.

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The importance of innate immunity to rotaviruses is exemplified by the range of strategies evolved by rotaviruses to interfere with the IFN response. We showed previously that rotaviruses block gene expression induced by type I and II IFNs, through a mechanism allowing activation of signal transducer and activator of transcription (STAT) 1 and STAT2 but preventing their nuclear accumulation. This normally occurs through activated STAT1/2 dimerization, enabling an interaction with importin α5 that mediates transport into the nucleus. In rotavirus-infected cells, STAT1/2 inhibition may limit the

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Ansell, Stephen M., Deanna Grote, Sherine F. Elsawa, et al. "Inhibition of the Jak/Stat Pathway Downregulates Immunoglobulin Production and Induces Cell Death in Waldenström Macroglobulinemia." Blood 114, no. 22 (2009): 1691. http://dx.doi.org/10.1182/blood.v114.22.1691.1691.

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Abstract Abstract 1691 Poster Board I-717 Waldenström macroglobulinemia (WM) is a B-cell malignancy that is characterized by the production of a monoclonal IgM protein and a lymphoplasmacytic infiltrate in the bone marrow. The aberrant production of the monoclonal IgM can result in serum hyperviscosity that can cause significant morbidity in patients with this disease. In previous work, we have shown that IL-6 significantly upregulates IgM secretion by WM cells and that IL-6 secretion is regulated by CCL5 (Rantes). We have also shown that IL-6 mediated IgM secretion in WM requires phosphoryla

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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.

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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

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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.

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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

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Croucher, Danielle C., Victor H. Jimenez-Zepeda, Zhi Hua Li, et al. "The Potent STAT3/5 Inhibitor, BP-1-102 Demonstrates Significant Anti-Tumor Activity Against Waldenström Macroglobulinemia." Blood 118, no. 21 (2011): 5101. http://dx.doi.org/10.1182/blood.v118.21.5101.5101.

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Abstract Abstract 5101 STAT3 is a cytoplasmic transcription factor, transiently activated in response to external stimuli such as growth factors and cytokines. As a transcription factor, STAT3 induces the expression of genes known to be involved in tumorigenesis, implicating STAT3 dysregulation in a number of hallmark oncogenic processes including tumor cell survival, proliferation, angiogenesis, metastasis, and drug resistance. Aberrant STAT3 signaling is prevalent in hematologic malignancies including Waldenstrom Macroglobulinemia (WM), a rare form of B cell non-Hodgkin lymphoma that is char

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Zoumpoulidou, Georgia, Marius C. Jones, Silvia Fernandez de Mattos та ін. "Convergence of Interferon-γ and Progesterone Signaling Pathways in Human Endometrium: Role of PIASy (Protein Inhibitor of Activated Signal Transducer and Activator of Transcription-y)". Molecular Endocrinology 18, № 8 (2004): 1988–99. http://dx.doi.org/10.1210/me.2003-0467.

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Abstract All cardinal events during the reproductive cycle, including ovulation, implantation, and menstruation, are characterized by a profound tissue remodeling and an associated local inflammatory response. The ovarian hormone progesterone is a key modulator of inflammatory signals in reproductive tissues, but the underlying mechanisms are not well understood. In this study, we report that differentiating human endometrial stromal cells (ESCs) acquire resistance to interferon-γ (IFNγ)-dependent signal transducers and activators of transcription (STAT) 1 signaling, although phosphorylation,

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HUANG, Jau-Shyang, Jinn-Yuh GUH, Wen-Chun HUNG, et al. "Role of the Janus kinase (JAK)/signal transducters and activators of transcription (STAT) cascade in advanced glycation end-product-induced cellular mitogenesis in NRK-49F cells." Biochemical Journal 342, no. 1 (1999): 231–38. http://dx.doi.org/10.1042/bj3420231.

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Advanced glycation end product (AGE) is important in the pathogenesis of diabetic nephropathy, which is characterized by cellular hypertrophy/hyperplasia leading to renal fibrosis. However, the signal transduction pathways of AGE remain poorly understood. The Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway has been associated with cellular proliferation in some extra-renal cells. Because interstitial fibroblast proliferation might be important in renal fibrosis, we studied the role of the JAK/STAT pathway in NRK-49F (normal rat kidney fibroblast) cells cult

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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.

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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

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Ma, Frank Y., Greg M. Anderson, Travis D. Gunn, Vincent Goffin, David R. Grattan, and Stephen J. Bunn. "Prolactin Specifically Activates Signal Transducer and Activator of Transcription 5b in Neuroendocrine Dopaminergic Neurons." Endocrinology 146, no. 12 (2005): 5112–19. http://dx.doi.org/10.1210/en.2005-0770.

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The hypothalamic neuroendocrine dopaminergic (NEDA) neurons are crucial in regulating prolactin secretion from the anterior pituitary. Rising prolactin concentrations stimulate these neurons to secrete dopamine, which acts via the pituitary portal vasculature to inhibit additional prolactin release. Prolactin is known to activate Janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathways in other cell types, including neurons. The possible role of JAK-STAT signaling in NEDA neurons has therefore been examined in this study using fetal rat mediobasal hypothala

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Kim, Lee, Song, et al. "Development of Oxadiazole-Based ODZ10117 as a Small-Molecule Inhibitor of STAT3 for Targeted Cancer Therapy." Journal of Clinical Medicine 8, no. 11 (2019): 1847. http://dx.doi.org/10.3390/jcm8111847.

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Persistently activated STAT3 is a promising target for a new class of anticancer drug development and cancer therapy, as it is associated with tumor initiation, progression, malignancy, drug resistance, cancer stem cell properties, and recurrence. Here, we discovered 3-(2,4-dichloro-phenoxymethyl)-5-trichloromethyl-[1,2,4]oxadiazole (ODZ10117) as a small-molecule inhibitor of STAT3 to be used in STAT3-targeted cancer therapy. ODZ10117 targeted the SH2 domain of STAT3 regardless of other STAT family proteins and upstream regulators of STAT3, leading to inhibition of the tyrosine phosphorylation

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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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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.

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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

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Ishida-Takahashi, Ryoko, Shigeo Uotani, Takahiro Abe, et al. "Rapid Inhibition of Leptin Signaling by Glucocorticoidsin Vitroandin Vivo." Journal of Biological Chemistry 279, no. 19 (2004): 19658–64. http://dx.doi.org/10.1074/jbc.m310864200.

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Elevated secretion of glucocorticoids (GCs) or hypersensitivity to GCs has a permissive effect on the development of obesity and leads to abnormalities of body fat distribution. Recent studies demonstrated GCs act as antagonists of leptin in rodents. However, little is known about the interaction between GCs and leptin signaling. In the present study, we investigated the effects of GCs on leptin actionin vitroandin vivo. GCs rapidly inhibited the leptin-induced STAT3 phosphorylation in a dose- and time-dependent manner, as assayed by Western blotting using anti-phosphospecific-STAT3 in human h

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Fiskus, Warren, Rekha Rao Manepalli, Ramesh Balusu, and Kapil N. Bhalla. "Synergistic Activity of Combinations of JAK2 Kinase Inhibitor with PI3K/mTOR, MEK or PIM Kinase Inhibitor Against Human Myeloproliferative Neoplasm Cells Expressing JAK2V617F." Blood 116, no. 21 (2010): 798. http://dx.doi.org/10.1182/blood.v116.21.798.798.

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Abstract Abstract 798 The mutant JAK2-V617F tyrosine kinase (TK) is present in the majority of patients with BCR-ABL negative myeloproliferative neoplasms (MPNs). JAK2-V617F activates downstream signaling through the STAT, RAS/MAPK and PI3/AKT pathways, conferring proliferative and survival advantages in the MPN hematopoietic progenitor cells (HPCs). We have previously reported that pan-histone deacetylase (HDAC) inhibitors e.g. panobinostat (PS) (Novartis Pharmaceuticals), depleted mRNA expression of JAK2-V617F, and disrupted the chaperone association of with hsp90 with JAK2-V617F, thereby pr

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Piairo, Paulina, Rute S. Moura, Maria João Baptista, Jorge Correia-Pinto, and Cristina Nogueira-Silva. "STATs in Lung Development: Distinct Early and Late Expression, Growth Modulation and Signaling Dysregulation in Congenital Diaphragmatic Hernia." Cellular Physiology and Biochemistry 45, no. 1 (2017): 1–14. http://dx.doi.org/10.1159/000486218.

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Background: Congenital diaphragmatic hernia (CDH) is a life-threatening developmental anomaly, intrinsically combining severe pulmonary hypoplasia and hypertension. During development, signal transducers and activators of transcription (STAT) are utilized to elicit cell growth, differentiation, and survival. Methods: We used the nitrofen-induced CDH rat model. At selected gestational time points, lungs were divided into two experimental groups, i.e., control or CDH. We performed immunohistochemistry and western blotting analysis to investigate the developmental expression profile of the comple

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Rosengren, Sanna, Maripat Corr, Gary S. Firestein, and David L. Boyle. "The JAK inhibitor CP-690,550 (tofacitinib) inhibits TNF-induced chemokine expression in fibroblast-like synoviocytes: autocrine role of type I interferon." Annals of the Rheumatic Diseases 71, no. 3 (2011): 440–47. http://dx.doi.org/10.1136/ard.2011.150284.

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ObjectivesThe objective of this study was to investigate the effect of the novel Janus kinase inhibitor CP-690,550 in fibroblast-like synoviocytes (FLSs) from patients with rheumatoid arthritis (RA).MethodsRA FLSs were isolated from tissue obtained by arthroplasty, cultured and serum-starved 48 h prior to stimulation. Messenger RNA and protein levels were determined by quantitative PCR and ELISA or multiplex bead assay, respectively. Phosphorylation of STAT (signal transducers and activators of transcription) proteins was determined by western blot.ResultsInterleukin-6-induced phosphorylation

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Dennis, Robyn M., Brandon Ballard, David John Tweardy, and Karen Rabin. "A Small Molecule Stat Inhibitor Blocks Stat3 and Stat5 Phosphorylation and Demonstrates Cytotoxicity In Acute Lymphoblastic Leukemia." Blood 116, no. 21 (2010): 2904. http://dx.doi.org/10.1182/blood.v116.21.2904.2904.

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Abstract Abstract 2904 Survival has improved dramatically in acute lymphoblastic leukemia (ALL), but further gains are unlikely using conventional chemotherapy alone. Several recently discovered, novel cytogenetic lesions with adverse prognostic impact, JAK2 activating mutations and CRLF2 rearrangements, occur in up to 15% of adult and pediatric ALL. These lesions are associated with activation of Jak2 and Stat5, and hold promise as targets for novel therapies affecting these signaling pathways. We performed in vitro testing of a novel small molecule Stat inhibitor, C188-9, in B-lineage ALL ce

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

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

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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.

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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

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Zhu, Shiguo, Cecele J. Denman, and Dean A. Lee. "Valproic Acid Selectively Inhibits STAT3 Phosphorylation." Blood 114, no. 22 (2009): 1720. http://dx.doi.org/10.1182/blood.v114.22.1720.1720.

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Abstract Abstract 1720 Poster Board I-746 Valproic acid (VPA), a histone deacetylase (HDAC) inhibitor (1), was found to enhance NK cell mediated antitumor activity by upregulating the surface expression of NKG2D ligands MICA and MICB on hepatoma cells (2). In contrast, VPA was found to impair NK cell antitumor activity by downregulating the surface expression of NKp30 and NKp46 on NK cells by blocking NFkB activation (3). Recently, we also found that VPA efficiently upregulates the surface expression of MICA, MICB, and ULBP family ligands on human osteosarcoma and neuroblastoma cells, but down

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Kiper, Hatice Demet, Burcin Tezcanli Kaymaz, Ozlem Purclutepe, et al. "The Potential Role of STAT's in Anti-Leukemic Therapy with Different Drugs." Blood 120, no. 21 (2012): 5120. http://dx.doi.org/10.1182/blood.v120.21.5120.5120.

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Abstract Abstract 5120 STAT pathways play a pivotal role in oncogenesis and leukemogenesis, thus targeting STAT signalling appears to be an effective anticancer treatment strategy. It has been described that constitutive activation of STAT3 and STAT5 plays a pro-oncogenic role both in acute and chronic myeloid neoplasms. In this study, we aimed to clarify the potential relationship between drug-induced apoptosis with different agents and STAT pathway. A third-generation bisphosphonate; zoledronate, an angiotensin-converting enzyme inhibitor (ACE-I); enalapril, a proteasome inhibitor which is u

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Xu, Bo, Ashish Bhattacharjee, Biswajit Roy, et al. "Interleukin-13 Induction of 15-Lipoxygenase Gene Expression Requires p38 Mitogen-Activated Protein Kinase-Mediated Serine 727 Phosphorylation of Stat1 and Stat3." Molecular and Cellular Biology 23, no. 11 (2003): 3918–28. http://dx.doi.org/10.1128/mcb.23.11.3918-3928.2003.

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ABSTRACT Interleukin-13 (IL-13) is a cytokine secreted by Th2 lymphocytes that is capable of inducing expression of 15-lipoxygenase (15-LO) in primary human monocytes. We recently demonstrated that induction of 15-LO requires the activation of Jak2 and Tyk2 kinases and Stats 1, 3, 5, and 6. Since IL-13-induced 15-LO expression was inhibited by H7 (a serine-threonine kinase inhibitor), we predicted that Stat serine phosphorylation may also be crucial for 15-LO expression. In this study, we present evidence indicating that IL-13-induced 15-LO mRNA expression was detectable as early as 1 h by rea

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Jamaluddin, Mohammad, Sanjeev Choudhary, Shaofei Wang та ін. "Respiratory Syncytial Virus-Inducible BCL-3 Expression Antagonizes the STAT/IRF and NF-κB Signaling Pathways by Inducing Histone Deacetylase 1 Recruitment to the Interleukin-8 Promoter". Journal of Virology 79, № 24 (2005): 15302–13. http://dx.doi.org/10.1128/jvi.79.24.15302-15313.2005.

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ABSTRACT Respiratory syncytial virus (RSV) is a paramyxovirus that produces airway inflammation, in part by inducing interleukin-8 (IL-8) expression, a CXC-type chemokine, via the NF-κB/RelA and STAT/IRF signaling pathways. In RSV-infected A549 cells, IL-8 transcription attenuates after 24 h in spite of ongoing viral replication and persistence of nuclear RelA, suggesting a mechanism for transcriptional attenuation. RSV infection induces B-cell lymphoma protein -3 (Bcl-3) expression 6 to 12 h after viral infection, at times when IL-8 transcription is inhibited. By contrast, 293 cells, deficien

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Naka, Tetsuji, Minoru Fujimoto, and Tadamitsu Kishimoto. "Negative regulation of cytokine signaling: STAT-induced STAT inhibitor." Trends in Biochemical Sciences 24, no. 10 (1999): 394–98. http://dx.doi.org/10.1016/s0968-0004(99)01454-1.

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Demosthenous, Christos, Guangzhen Hu, Thomas E. Witzig, and Mamta Gupta. "Loss-of-Function Missense Mutations in Tyrosine Phosphatase PTPN6 Deregulate STAT3 Signaling in Diffuse Large B-Cell Lymphoma." Blood 124, no. 21 (2014): 707. http://dx.doi.org/10.1182/blood.v124.21.707.707.

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Abstract Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin Lymphoma and is characterized by deregulation of several signal transduction pathways. Approximately 50% patients with DLBCL are shown to have aberrant activation of the signal transducer and activator of transcription (STAT) pathway. However, mechanism of aberrant STAT3 signaling in DLBCL is not well understood. Protein tyrosine phosphatases (PTPs) are important enzymes that control the activity of multiple signaling pathways downstream of tyrosine kinases; mutations in PTPN11 have been found associated with

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Jia, Lili, Wenli Yu, Hongli Yu, and Yiqi Weng. "Electroacupuncture Pretreatment Attenuates Intestinal Injury after Autogenous Orthotopic Liver Transplantation in Rats via the JAK/STAT Pathway." Oxidative Medicine and Cellular Longevity 2020 (August 4, 2020): 1–11. http://dx.doi.org/10.1155/2020/9187406.

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Background. Liver transplantation induces self-injury and affects remote organs, such as the lung, kidney, and intestine. Postoperative intestinal dysfunction has been associated with prolonged hospitalization and affects a patient’s health and quality of life. Electroacupuncture (EA) has been proven effective in multiple organ protection. However, the potential mechanism underlying the protective effects of EA on intestinal injury after liver transplantation remains unclear. Methods. After establishing an autogenous orthotopic liver transplantation (AOLT) model, we studied the effects of EA p

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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.

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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

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Banes-Berceli, Amy K. L., Pimonrat Ketsawatsomkron, Safia Ogbi, Bela Patel, David M. Pollock, and Mario B. Marrero. "Angiotensin II and endothelin-1 augment the vascular complications of diabetes via JAK2 activation." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 2 (2007): H1291—H1299. http://dx.doi.org/10.1152/ajpheart.00181.2007.

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The JAK/STAT pathway is activated in vitro by angiotensin II (ANG II) and endothelin-1 (ET-1), which are implicated in the development of diabetic complications. We hypothesized that ANG II and ET-1 activate the JAK/STAT pathway in vivo to participate in the development of diabetic vascular complications. Using male Sprague-Dawley rats, we performed a time course study [ days 7, 14, and 28 after streptozotocin (STZ) injection] to determine changes in phosphorylation of JAK2, STAT1, and STAT3 in thoracic aorta using standard Western blot techniques. On day 7 there was no change in phosphorylati

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Shi, Ce, Lina Han, Yoko Tabe, et al. "Dual Targeting of JAK2 Signaling with a Type II JAK2 Inhibitor and of mTOR with a TOR Kinase Inhibitor Induces Apoptosis in CRLF2-Rearranged Ph-like Acute Lymphoblastic Leukemia." Blood 124, no. 21 (2014): 3706. http://dx.doi.org/10.1182/blood.v124.21.3706.3706.

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Abstract Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a subtype of high-risk B-precursor ALL (B-ALL) that carries a high risk of relapse after conventional chemotherapy (Mullighan et al, N Engl J Med. 2009). Rearrangements in CRLF2, leading to overexpression of the receptor for the cytokine thymic stromal lymphopoietin (TSLP), are present in approximately 50% of Ph-like ALLs and are associated with hyperactive JAK/STAT and PI3K/mTOR signaling (Harvey et al, Blood 2010; Tasian et al, Blood 2014). Previous studies established that combining a tyrosine kinase inhib

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Buglio, Daniela, Manuela Lemoine, Sattva S. Neelapu, Francisco Vega, Donald Berry, and Anas Younes. "NVP-BEZ235, A Dual Inhibitor of Phosphoinositol-3-Kinase (PI3K) and Mammalian Target of Rapamycin (mTOR), Is a Potent Inhibitor of Lymphoma Cell Growth and Survival." Blood 118, no. 21 (2011): 4965. http://dx.doi.org/10.1182/blood.v118.21.4965.4965.

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Abstract Abstract 4965 The Phosphatidylinositol-3-kinase (PI3K)/AKT/mTOR pathway is frequently deregulated in Hodgkin (HL) and non-Hodgkin lymphoma (NHL), and has been linked with tumor cell growth and survival. Although several proteins/enzymes in this pathway can be targeted by a variety of small molecules in vitro and in vivo, it remains unclear which protein target is the ideal for clinical testing. Previous studies demonstrated that the clinical activity of mTOR inhibitors may be attenuated by a negative feedback loop that involves activation of AKT, suggesting that a dual inhibition of A

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Shi, Ce, Lina Han, Qi Zhang, et al. "Combined Targeting of JAK2 with a Type II JAK2 Inhibitor and mTOR with a TOR Kinase Inhibitor Constitutes Synthetic Activity in JAK2-Driven Ph-like Acute Lymphoblastic Leukemia." Blood 126, no. 23 (2015): 2529. http://dx.doi.org/10.1182/blood.v126.23.2529.2529.

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Abstract Background and rationale: Philadelphia chromosome-like acute lymphoblastic leukemia ("Ph-like ALL") is a subtype of high-risk B-precursor ALL (B-ALL), which carries a high risk of relapse with conventional chemotherapy(Roberts et al, N Engl J Med. 2014). Rearrangements in CRLF2, leading to overexpression of cytokine receptor for thymic stromal lymphopoietin (TSLP), are present in approximately 50% of Ph-like ALL and are associated with hyperactive JAK/STAT and PI3K/mTOR signaling (Harvey et al, Blood 2010;Tasian et al, Blood 2014).In addition,JAK2 fusion proteins, such as PAX5-JAK2 re

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