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Gotowe bibliografie tematyczne / Jak2-Stat3

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Gotowa bibliografia na temat „Jak2-Stat3”

Autor: Grafiati

Data publikacji: 9 listopada 2024

Data aktualizacji: 31 lipca 2025

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Artykuły w czasopismach na temat "Jak2-Stat3"

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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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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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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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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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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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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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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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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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Rozprawy doktorskie na temat "Jak2-Stat3"

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Wang, Kepeng. "The involvement of JAK2/STAT2/STAT3 in myogenic differentiation /." View abstract or full-text, 2008. http://library.ust.hk/cgi/db/thesis.pl?BICH%202008%20WANGK.

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Studd, James. "The role of JAK2, STAT3 and ERBB2 in ovarian cancer." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24443.

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Background: Ovarian cancer is the most lethal gynaecological malignancy, accounting for an estimated 140,000 deaths per year worldwide. Five year survival rates have not increased significantly in the last 10 years and the acquisition of resistance to chemotherapy remains a significant barrier to improving patient survival. Isogenic cell line models of in vivo acquired resistance to chemotherapy were used to examine cellular responses to cisplatin and identify differences between sensitive and resistant pairs that might be exploited to sensitise cells to treatment. Results: Microarray analysis

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Poulot, Yiannis. "Hétérogénéité et régulation des astrocytes dans la maladie d'Alzheimer : vers des interventions ciblées sur les voies JAK2-STAT3 et NF-kB." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL060.

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La maladie d'Alzheimer (MA) est une maladie neurodégénérative et la première cause de démence à travers le monde. Au cours de la MA, les astrocytes développent un phénotype réactif et présentent des changements moléculaires, morphologiques et fonctionnels, pouvant induire des effets délétères et/ou bénéfiques sur le fonctionnement des neurones. Récemment, des données de séquençage ARN (RNAseq) de cellules/noyaux uniques ont révélé l'existence de sous-populations distinctes d'astrocytes dans des cerveaux de patients atteints de la MA et dans les modèles murins. Cependant, les cascades de signal

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Hernández, Ribes Gracia. "ESTUDIO DE LA RUTA CELULAR JAK2/STAT3 COMO POTENCIAL INHIBIDOR EN EL MODELO DE FIBROSIS PULMONAR." Doctoral thesis, Universitat Politècnica de València, 2016. http://hdl.handle.net/10251/64087.

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[EN] Idiopathic pulmonary fibrosis (IPF) is the pulmonary disease with higher incidence and worse prognosis. Recent evidence suggests that cucurbitaceae, selective inhibitors of the JAK2/STAT3 pathway, may improve the pathogenesis of IPF, as anti-inflammatory and antioxidative properties have been confirmed in other diseases. However the role in IPF is unknown. Two pharmacological models were investigated in the present study. In the preventive model, Wistar rats were instilled intratracheally with a single dose of bleomycin (BLM)(3.75 U/kg; n=12) to induce lung injury. CuI (20mg/kg/day; n=6)

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Jark, Paulo César [UNESP]. "Estudo da via jak2/stat3 e de seus inibidores em linfomas multicêntricos difusos de grandes células B caninos." Universidade Estadual Paulista (UNESP), 2016. http://hdl.handle.net/11449/146685.

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Jark, Paulo César. "Estudo da via jak2/stat3 e de seus inibidores em linfomas multicêntricos difusos de grandes células B caninos /." Jaboticabal, 2016. http://hdl.handle.net/11449/146685.

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Orientador: Mirela Tinucci Costa<br>Banca: Felipe Augusto Ruiz Sueiro<br>Banca: Lucas Campos de Sá Rodrigues<br>Banca: Andrigo Barboza De Nardi<br>Banca: Letícia Abrahão Anai<br>Resumo: A via Janus Kinase (JAK) e do transdutor de sinal e ativador de transcrição (STAT) desempenham papéis importantes na patogênese de neoplasias hematopoiéticas. A ativação da via JAK2/STAT3 promove o crescimento e sobrevivência celular em uma variedade de linfomas humanos. Há uma necessidade de compreender a participação da via JAK2/STAT3 em linfomas caninos difusos de grandes células B e do potencial terapêutico

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Ben, Haim Lucile. "Modulation of the JAK2/STAT3 pathway in vivo : understanding reactive astrocyte functional features and contribution to neurodegenerative diseases." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066534/document.

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Les astrocytes deviennent réactifs dans les maladies neurodégénératives (MND) comme la maladie d’Alzheimer (MA) et de Huntington (MH) mais les conséquences fonctionnelles de cette réactivité sont peu connues. Dans cette étude, nous avons évalué 1) les voies de signalisation impliquées dans la réactivité astrocytaire, 2) la contribution des astrocyte réactifs (AR) à la dysfonction neuronale dans des modèles de MND et 3) les caractéristiques fonctionnelles des AR.Nous avons montré que la voie JAK2/STAT3 est responsable de la réactivité astrocytaire dans des modèles murins de la MA et la MH. Nous

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Yerabolu, Naga Dinesh Reddy [Verfasser]. "Inhibition of the JAK2-STAT3 pathway using ruxolitinib as a therapeutic option for pulmonary hypertension / Naga Dinesh Reddy Yerabolu." Gießen : Universitätsbibliothek, 2020. http://d-nb.info/1223462145/34.

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Ceyzériat, Kelly. "Modulation de la réactivité astrocytaire par ciblage de la voie JAK2-STAT3 : conséquences dans des modèles murins de la maladie d’Alzheimer." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS556/document.

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Les astrocytes sont des éléments clés de la physiologie cérébrale. Dans les maladies neurodégénératives comme la maladie d’Alzheimer (MA), les astrocytes deviennent réactifs. Cette réactivité astrocytaire (RA) est essentiellement caractérisée par des changements morphologiques. En revanche, les effets de la réactivité sur les fonctions de support des astrocytes sont mal connus. De plus, les cascades de signalisation qui conduisent à la RA restent à déterminer. Les objectifs de ce projet étaient de : 1/ démontrer que la voie JAK2-STAT3 (Janus Kinase 2 - Signal Transducer and Activator of Transc

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Etter, Jonathan Parker. "Development of Inhibitors in the IL-6/GP130/JAK/STAT Pathway as Therapeutic Agents." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376525461.

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Części książek na temat "Jak2-Stat3"

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Wu, Ruifan, and Xinxia Wang. "SOCS3/JAK2/STAT3 pathway in iPSCs." In Molecular Players in iPSC Technology. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-90059-1.00009-9.

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Demir Çetinkaya, Büşra. "Targeting the SH2 Domain of STAT3 Proteins in Breast Cancer Treatment." In Current Researches in Health Sciences-II. Özgür Yayınları, 2023. http://dx.doi.org/10.58830/ozgur.pub128.c630.

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Stat proteins, transcription factors that convert extracellular stimuli into appropriate biological responses, are involved in many normal physiological cell processes, including proliferation, differentiation, apoptosis, angiogenesis, and immune system regulation. Irregular Stat activation is often associated with tumorigenesis. This situation has made the Stat pathway an interesting target for drug development studies in cancer treatment and has led to the development of various inhibitors targeting this pathway. Stat signal inhibitors are divided into two main groups as inhibitors with dire

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Nawwaf Al-Harithy, Rowyda. "Adipocytokines: Are They the Theory of Cancer Progression?" In Tumor Angiogenesis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.104581.

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Adipocytokines have gained significant attention in the scientific community over the past few decades. They are a family of enzymes, hormones, growth factors, proteins, and other bioactive molecules that are important regulators of many processes. Adipocytokines are predominantly produced by preadipocytes and mature adipocytes to act through a network of autocrine, paracrine, and endocrine pathways. Leptin (LEP) is the first adipocytokine discovered that has a role in modulating adiposity and has been shown to exert pleiotropic effects on many metabolic pathways through the leptin receptors (

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Centonze, Giorgia, Jennifer Chapelle, Costanza Angelini, et al. "The Scaffold Protein p140Cap as a Molecular Hub for Limiting Cancer Progression: A New Paradigm in Neuroblastoma." In Pheochromocytoma, Paraganglioma and Neuroblastoma. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96383.

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Neuroblastoma, the most common extra-cranial pediatric solid tumor, is responsible for 9–15% of all pediatric cancer deaths. Its intrinsic heterogeneity makes it difficult to successfully treat, resulting in overall survival of 50% for half of the patients. Here we analyze the role in neuroblastoma of the adaptor protein p140Cap, encoded by the SRCIN1 gene. RNA-Seq profiles of a large cohort of neuroblastoma patients show that SRCIN1 mRNA levels are an independent risk factor inversely correlated to disease aggressiveness. In high-risk patients, SRCIN1 was frequently altered by hemizygous dele

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Li, Xiao-Juan, Qing-Yu Ma, You-Ming Jiang, et al. "Xiaoyaosan Exerts Anxiolytic-like Effects by Down-regulating the TNF-α/JAK2-STAT3 Pathway in the Rat Hippocampus." In Insights into the Prevention and Treatment of Depression with Famous TCM Prescription Xiaoyaosan. B P International (a part of SCIENCEDOMAIN International), 2023. http://dx.doi.org/10.9734/bpi/mono/978-81-19315-94-9/ch13.

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Streszczenia konferencji na temat "Jak2-Stat3"

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Gritsina, Galina, Fang Xiao, Shane W. O'Brien, et al. "Abstract 1113: Targeting the JAK2/STAT3 pathway in ovarian cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1113.

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Overmoyer, BA, V. Almendro, S. Shu, et al. "Abstract P4-06-01: JAK2/STAT3 activity in inflammatory breast cancer supports the investigation of JAK2 therapeutic targeting." In Abstracts: Thirty-Fifth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 4‐8, 2012; San Antonio, TX. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/0008-5472.sabcs12-p4-06-01.

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Ballester, Beatriz, Javier Milara, Anselm Morell, et al. "Role of JAK2/STAT3 pathway in vascular function of pulmonary fibrosis patients." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4902.

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Chou, JC, PS Wang, SW Wang, and H. Lin. "PO-183 Prolactin activation of JAK2/STAT3 signalling pathway through GHR in NSCLC." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.704.

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Jhaveri, K., E. Teplinsky, R. Arzu, et al. "Abstract PD5-6: Sustained hyperactivated mTOR & JAK2/STAT3 pathways in inflammatory breast cancer (IBC): Evidence for mTOR plus JAK2 therapeutic targeting." In Abstracts: Thirty-Sixth Annual CTRC-AACR San Antonio Breast Cancer Symposium - Dec 10-14, 2013; San Antonio, TX. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/0008-5472.sabcs13-pd5-6.

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Harada, Daijiro, Daijiro Harada, Nagio Takigawa, et al. "Abstract 717: JAK2/STAT3 induces erlotinib-resistance in lung cancer cells harboring EGFR-activating mutations." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-717.

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Su, Wen-Pin, Ya-Chin Lo, Chien-Chung Lin, Helen H. W. Chen, Wu-Wei Lai, and Wu-Chou Su. "Abstract 1636: Anticancer drug-induced Jak2/Stat3 activation confers a survival advantage in lung cancer cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1636.

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Nam, Sangkil, Jun Xie, Angela Perkins, et al. "Abstract 864: Novel synthetic berbamine derivatives inhibit Jak2/Stat3 signaling and induce apoptosis of human melanoma cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-864.

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Jia, Zhenxian, Zhi Zhang, Ze Li, et al. "Abstract 4051: Anlotinib inhibits the progress of colorectal cancer cells by antagonizing glycolysis & JAK2-STAT3 signaling." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-4051.

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Nagathihalli, Nagaraj, Yugandhar Beesetty, Michelle Reyzer, Chanjuan Shi, Richard Caprioli, and Nipun Merchant. "Abstract B32: JAK2 inhibition blocks STAT3 signaling and enhances drug delivery and therapeutic response in pancreatic cancer." In Abstracts: AACR Special Conference on Pancreatic Cancer: Progress and Challenges; June 18-21, 2012; Lake Tahoe, NV. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.panca2012-b32.

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