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Статті в журналах з теми "Jak2-Stat3"
Hofmann, Hans-Dieter, and Matthias Kirsch. "JAK2-STAT3 signaling." JAK-STAT 1, no. 3 (July 2012): 191–93. http://dx.doi.org/10.4161/jkst.20446.
Повний текст джерелаZhou, 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.
Повний текст джерелаJin, 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.
Повний текст джерелаKim, Hyunkyung, Dongha Kim, Seon Ah Choi, Chang Rok Kim, Se Kyu Oh, Ki Eun Pyo, Joomyung Kim, 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 (October 30, 2018): 11766–71. http://dx.doi.org/10.1073/pnas.1805662115.
Повний текст джерелаBouaouiche, Sarra, Silvia Ghione, Randa Sghaier, Olivier Burgy, Cindy Racoeur, Valentin Derangère, Ali Bettaieb, and Stéphanie Plenchette. "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 (August 6, 2021): 8449. http://dx.doi.org/10.3390/ijms22168449.
Повний текст джерелаBarber, Ruth, Jenny Zobel, Daniel Beck, Sian Evans, Richard Elliott, Christopher J. Lord, Alan Ashworth, Andrew G. C. Porter, and Simon D. Wagner. "JAK2 Is a Direct BCL6 Target Gene: Implications for Therapy in Diffuse Large B-Cell Lymphoma." Blood 124, no. 21 (December 6, 2014): 3112. http://dx.doi.org/10.1182/blood.v124.21.3112.3112.
Повний текст джерелаLi, Yun-Qing. "Down-Regulation of Insulin Signaling Is Involved in Painful Diabetic Neuropathy in Type 2 Diabetes." Pain Physician 2;16, no. 2;3 (March 14, 2013): E71—E83. http://dx.doi.org/10.36076/ppj.2013/16/e71.
Повний текст джерелаLei, Bo, Ju Bai, Wanggang Zhang, Aili He, Yinxia Chen, Pengyu Zhang, Lu Qian, and Fuling Zhou. "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 (December 3, 2015): 1393. http://dx.doi.org/10.1182/blood.v126.23.1393.1393.
Повний текст джерелаZhang, Xuekang, Jun Zhou, Qian Hu, Zhengren Liu, Qiuhong Chen, Wenxiang Wang, Huaigen Zhang, Qin Zhang, and Yuanlu Huang. "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 (May 1, 2020): 3295–302. http://dx.doi.org/10.1166/jnn.2020.16416.
Повний текст джерелаLiu, Fa-Yu, Jawad Safdar, Zhen-Ning Li, Qi-Gen Fang, Xu Zhang, Zhong-Fei Xu, and Chang-Fu Sun. "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.
Повний текст джерелаДисертації з теми "Jak2-Stat3"
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.
Повний текст джерелаStudd, James. "The role of JAK2, STAT3 and ERBB2 in ovarian cancer." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24443.
Повний текст джерелаPoulot, 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.
Повний текст джерелаAlzheimer's disease (AD) is a neurodegenerative disease and the leading cause of dementia worldwide. During AD, astrocytes develop a reactive phenotype and exhibit molecular, morphological, and functional changes, which can induce deleterious and/or beneficial effects on neuronal function. Recently, single-cell/nucleus RNA sequencing (RNAseq) data have revealed the existence of distinct subpopulations of astrocytes in the brains of AD patients and in mouse models. However, the signaling cascades controlling these subpopulations, their functional characteristics, and their impacts on the functioning of the prefrontal cortex (PFC) remain unknown. The JAK2-STAT3 and NF-kB signaling pathways are known to be activated during AD and control the reactive state of astrocytes. Our team has developed astrocyte-specific lentivirus reporters for these two signaling pathways, in which the expression of CFP or GFP is controlled by NF-κB- and STAT3-dependent promoter sequences, respectively. These reporters allowed us to identify three astrocytic subpopulations based on their activated cascades, NF-kB+, STAT3+, and NF-kB+/STAT3+, in the PFC of AD model mice, APP/PS1dE9 mice, as well as APPNL-F/NL-F mice. First, we observed that the subpopulations are not topographically determined by their proximity to amyloid plaques. These observations subsequently led us to note that these subpopulations are also present in WT mice, suggesting that the subpopulations are probably innate. We then observed that the 2D territory area of NF-kB+ astrocytes is larger than that of STAT3+ and STAT3+/NF-kB+ astrocytes. After RNAseq analysis of the three subpopulations, we identified differentially expressed genes between the three subpopulations associated with specific functions of interest in the context of AD (proteostasis, synaptic regulation, lipid metabolism). We confirmed that STAT3+ and NF-κB+ subpopulations exhibit significantly different proteasome and lysosome activities in the PFC of APP/PS1dE9 mice. Observing higher expression of Cx30 and 43 transcripts in STAT3+ astrocytes, we also studied astrocytic coupling via gap junctions and hemichannel activity. We demonstrated through fluorescence recovery after photobleaching (FRAP) that the subpopulations are equivalently coupled via gap junctions, but the STAT3+ population shows increased hemichannel activity compared to the other two. Finally, using new lentiviral vectors, we specifically inhibited the STAT3+ or NF-kB+ subpopulations by inhibiting the corresponding signaling pathways in APP/PS1dE9 mice. We observed that these populations impact anxiety and social preference and memory in APP/PS1dE9 mice. Other characteristics of AD (amyloid plaques, dystrophic neurites, inflammation) are under study. This project has highlighted that astrocytic heterogeneity is controlled by different signaling pathways, and that these subpopulations exhibit different morphological, molecular, and functional profiles, potentially with differential impacts during AD that remain to be characterized
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.
Повний текст джерела[ES] La fibrosis pulmonar idiopática (FPI) es la enfermedad pulmonar con mayor incidencia y peor pronóstico. Estudios recientes sugieren que la familia de las cucurbitaceae, inhibidores selectivos de la ruta JAK2/STAT3, pueden mejorar la patogénesis de la enfermedad, al haberse confirmado sus propiedades antinflamatorias y antioxidantes en otras enfermedades. Sin embargo se desconoce su papel en FPI. En el presente trabajo se estudiaron dos modelos farmacológicos. En el modelo preventivo las ratas Wistar fueron instiladas con una dosis única de bleomicina intratraqueal (BLM)(3.75 U/kg; n=12) para inducir las lesión pulmonar. Durante 21 días se administró CuI (20mg/kg/día; n=6) o vehículo de CuI (control y grupo FPI) por vía intraperitoneal. El modelo curativo se diferencia del preventivo en el comienzo de la administración farmacológica a los 7 días de inducir la enfermedad. El seguimiento de la evolución animal y el ratio de ventilación-perfusión se realizó mediante las técnicas de imagen TC/SPECT. Se realizó el recuento y caracterización de las células totales extravasadas en lavado broncoalveolar (LBA) así como el contenido de proteína total y la concentración de IL- 6 e IL-13 en LBA y tejido pulmonar. Las tinciones de hematoxilina-eosina y masson tricrómico permitieron el estudio de la histología del tejido pulmonar. Se determinó la expresión génica y proteica de TGF-ß1, CTGF, COL1A y ET-1 mediante las técnicas de real time PCR y WB como marcadores de remodelado vascular. Las proteínas P-STAT3, P-SMAD3 y P-JAK2, fueron determinadas mediante cuantificación proteica e inmunohistoquimia. Por último se estudió la expresión y distribución de JAK2 y STAT3 en tejido de pacientes con fibrosis pulmonar e hipertensión pulmonar. La cuantificación de las imágenes TC/SPECT mostraron una reducción de las áreas fibróticas en el grupo tratado con CuI. El tratamiento farmacológico permitió el restablecimiento del espacio aéreo pulmonar hasta valores control en ambos modelos estudiados. El grupo con tratamiento farmacológico restauró el ratio de ventilación/perfusión tras administrar CuI durante 14 días. Las tinciones de hematoxilina eosina revelaron como el grupo animal tratado farmacológicamente presenta una mejora de la histología pulmonar, revirtiendo el remodelado vascular y la hipertrofia del ventrículo derecho. La tinción de masson tricrómico mostró una disminución de los depósitos de colágeno. Se determinó el valor de Ashcroft, evaluador del grado de fibrosis pulmonar, que descendió significativamente en el grupo tratado con CuI. Los resultados presentan una sobrexpresión génica y proteica de TGF-ß1, CTGF, COL1A y ET-1 en los grupos de bleomicina frente a las ratas control. Dicha condición fue revertida mediante el tratamiento con CuI que restableció los valores a niveles control. Los análisis proteicos e inmunohistoquíimicos de JAK2, STAT3 y SMAD3 revelaron una sobreexpresión en las ratas con bleomicina mientras que la expresión proteica fue inhibida en el grupo tratado con CuI. En consonancia con los resultados obtenidos, el análisis inmunohistoquímico del parénquima pulmonar de pacientes con FPI e HP asociada muestran una sobreeexpresión de las formas fosforiladas de JAK2 y STAT3 frente a la ausencia de expresión en tejido pulmonar sano. La administración curativa y preventiva de un inhibidor de la ruta JAK2/STAT3 puede ser un potencial tratamiento para la fibrosis pulmonar, ya que mejora parámetros indicativos de la patología.
[CAT] La fibrosi pulmonar idiopàtica (FPI) és la enfermetat pulmonar amb major incidència i pitjor pronostic. Estudis recents suggereixen que la família de les cucurbitàcies, Inhibidors selectius de la ruta JAK2 / STAT3, poden millorar la patogènesi de la malaltia, en haver-se confirmat les seues propietats antiinflamatòries i antioxidants En altres patologies. No obstant això es desconeix el seu paper en FPI. En el present treball es van estudiar 2 models farmacològics. En el model preventiu les rates Wistar foren instilades amb una dosi única de bleomicina intratraqueal (BLM) (3,75 U / kg; n = 12) per a induir les lesions pulmonars. Durant 21 dies es va administrar CuI (20 mg / kg / dia, n = 6) o Vehicle de CuI (control i grup FPI) per vía intraperitoneal. El model curatiu es diferència del preventiu en el començament de l'administració farmacológica als 7 dies d'induir l'enfermetat. El seguiment de l'evoluciò dels animals i el ratio de Ventilació-perfusió es va realitzar mitjançant tècniques d'imatge TC/SPECT. Es realitzà el recompte i caracterització de les cèl·lules totals extravasades en el llavat broncoalveolar (LBA). Així com el contingut de proteina total i la concentració d'IL-6 i IL-13 en LBA i teixit pulmonar. Les tincions d'hematoxilina-eosina i tricròmic de Masson van permetre l'estudi de la histologia del teixit pulmonar. Es va determinar l'expressió gènica i proteica de TGF-ß1, CTGF, COL1A i Et-1 mitjançant tècniques de PCR en temps real i WB com marcadors de remodelat vascular. Les proteïnes P-STAT3, P-SMAD3 i P-JAK2, varen ser determinades mitjançant quantificació proteica i inmunohistoquimia. Per últim se estudià l'expressió i distribució de JAK2 i STAT3 en teixit de pacients amb fibrosi pulmonar e hipertensió pulmonar. La quantificació de les imatges TC/SPECT mostraren una reducció de les àrees fibrótiques en el grup tractat amb CuI. El tractament farmacològic permet el restabliment de l'espai aeri pulmonar fins valors de control en els dos models estudiats. El grup amb tractament farmacològic va restaurar el ratio de ventilació/perfusió tras administrar Cul durant 14 dies. Les tincions d'hematoxilina eosina van revelar com el grup animal tractat farmacològicament presenta una Millora de la histologia pulmonar, revertint el remodelat vascular i la hipertròfia del ventricle dret. La tinció de tricròmic de Masson va mostrar una disminució dels dipòsits de col·lagen. Es va determinar el valor d'Ashcroft, avaluador del grau de fibrosi pulmonar, que va baixar significativament a el grup tractat amb CuI. Els resultats presenten una sobreexpressió gènica i proteica de TGF-ß1, CTGF, COL1A i Et-1 en els grups de bleomicina en comparacióa les rates control. Aquesta condició va ser revertida mitjançant el tractament amb CuI que va restablir els valors fins a nivel dels control. A nivell immunohistoquímic els resultats mostren una disminució dels dipòsits de COL1A en el grup tractat comparativament al grup sense tractament. Els anàlisi proteics i inmunohistoquíimics de JAK2, STAT3 i SMAD3 van revelar una sobreexpressió en les rates amb bleomicina mentre que l'expressió proteica va ser inhibida en el grup tractat amb CuI. D'acord amb els resultats obtinguts, l'anàlisi immunohistoquímic del parènquima pulmonar de pacients amb FPI i HP associada mostren sobreeexpresió de les formes fosforilades de JAK2 i STAT3 davant l'absència d'expressió en teixit pulmonar sa. La administració curativa i preventiva d'un inhibidor de la ruta JAK2 / STAT3 pot ser un potencial tractament per la fibrosi pulmonar, ja que millora paràmetres indicatius de la patologia.
Hernández Ribes, G. (2016). ESTUDIO DE LA RUTA CELULAR JAK2/STAT3 COMO POTENCIAL INHIBIDOR EN EL MODELO DE FIBROSIS PULMONAR [Tesis doctoral no publicada]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/64087
TESIS
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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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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 dos inibidores de JAK no tratamento dessa doença. O objetivo do presente estudo foi avaliar a expressão de JAK2-STAT3 em linfomas difusos de grandes células B e o impacto do uso de inibidores de JAK2 como AZD1480 e CYT387 no crescimento in vitro dessa linhagem tumoral. Foi realizada técnica de imuno-histoquímica com os anticorpos anti-STAT3 e anti-STAT3 fosforilado (p-STAT3) em linfonodos acometidos por linfoma difuso de grandes células B e comparado à linfonodos normais e reativos. Para avaliação do efeito terapêutico dos inibidores de JAK2 (AZD1480 e CYT387) foi realizado ensaio de viabilidade celular pelo método de azul de tripan utilizando linhagens celulares de linfoma difuso de grandes células B (CLBL-1) e análise de apoptose por citometria de fluxo utilizando o sistema Annexin V. Houve aumento significativo na expressão de STAT3 e p-STAT3 em linfomas difusos de grandes células B em comparação com linfonodos normais. Ambos os fármacos inibiram o crescimento celular em proporções dependentes da dose administrada e houve um aumento significativo nas taxas de apoptose das células tratadas com inibidores de JAK-2 em comparação ao grupo controle tratado com DMSO. Este é o primeiro estudo a avaliar a via JAK2/STAT3 em linfomas difusos de grandes céluslas B canino e esses dados permitem compreender e explorar o potencial terapêutico dos inibidores de JAK permitindo estudos futuros da eficácia clínica desses fármacos na oncologia veterinária
The Janus Kinase (JAK) and signal transducer and activator of transcription (STAT) pathway play important roles in the pathogenesis of hematologic malignancies. Activated JAK2-STAT3 signaling pathway promotes the growth and survival of a variety of lymphomas in human. There is a great demand for understanding JAK-STAT pathway in canine diffuse large B cell lymphoma (DLBCLs) and evaluating the therapeutic potential of JAK inhibitors. Our study aims to evaluate the expression of JAK2-STAT3 pathway in canine DLBCLs and to assess the impact of AZD1480 and CYT387, two novel JAK inhibitors, on canine DLBCL cell growth. Immunohistochemistry was performed in canine DLBCLs, normal and reactive lymph nodes with primary antibodies against STAT3 and phosphorylated STAT3 (p-STAT3). To evaluate the therapeutic effect of novel JAK inhibitors, canine DLBCL cell line CLBL-1 was treated with either AZD1480 or CYT387 and trypan blue viability assay was performed post treatment. There was a significant increase in expression of STAT3 and pSTAT3 in canine DLBCLs compared with the normal lymph node. Both AZD1480 and CYT387 inhibited canine DLBCL cells in a dose dependent manner. This is the first study to evaluate the JAK2/STAT3 pathway in canine DLBCLs. The knowledge of JAK2-STAT3 activity in canine DLBCLs enables us to understand and explore the therapeutic potential of JAK inhibitors. The dose dependent cell growth inhibition by novel JAK inhibitors in this study will lead into the future studies of the underlying mechanism
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.
Повний текст джерелаBanca: Felipe Augusto Ruiz Sueiro
Banca: Lucas Campos de Sá Rodrigues
Banca: Andrigo Barboza De Nardi
Banca: Letícia Abrahão Anai
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 dos inibidores de JAK no tratamento dessa doença. O objetivo do presente estudo foi avaliar a expressão de JAK2-STAT3 em linfomas difusos de grandes células B e o impacto do uso de inibidores de JAK2 como AZD1480 e CYT387 no crescimento in vitro dessa linhagem tumoral. Foi realizada técnica de imuno-histoquímica com os anticorpos anti-STAT3 e anti-STAT3 fosforilado (p-STAT3) em linfonodos acometidos por linfoma difuso de grandes células B e comparado à linfonodos normais e reativos. Para avaliação do efeito terapêutico dos inibidores de JAK2 (AZD1480 e CYT387) foi realizado ensaio de viabilidade celular pelo método de azul de tripan utilizando linhagens celulares de linfoma difuso de grandes células B (CLBL-1) e análise de apoptose por citometria de fluxo utilizando o sistema Annexin V. Houve aumento significativo na expressão de STAT3 e p-STAT3 em linfomas difusos de grandes células B em comparação com linfonodos normais. Ambos os fármacos inibiram o crescimento celular em proporções dependentes da dose administrada e houve um aumento significativo nas taxas de apopto... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: The Janus Kinase (JAK) and signal transducer and activator of transcription (STAT) pathway play important roles in the pathogenesis of hematologic malignancies. Activated JAK2-STAT3 signaling pathway promotes the growth and survival of a variety of lymphomas in human. There is a great demand for understanding JAK-STAT pathway in canine diffuse large B cell lymphoma (DLBCLs) and evaluating the therapeutic potential of JAK inhibitors. Our study aims to evaluate the expression of JAK2-STAT3 pathway in canine DLBCLs and to assess the impact of AZD1480 and CYT387, two novel JAK inhibitors, on canine DLBCL cell growth. Immunohistochemistry was performed in canine DLBCLs, normal and reactive lymph nodes with primary antibodies against STAT3 and phosphorylated STAT3 (p-STAT3). To evaluate the therapeutic effect of novel JAK inhibitors, canine DLBCL cell line CLBL-1 was treated with either AZD1480 or CYT387 and trypan blue viability assay was performed post treatment. There was a significant increase in expression of STAT3 and pSTAT3 in canine DLBCLs compared with the normal lymph node. Both AZD1480 and CYT387 inhibited canine DLBCL cells in a dose dependent manner. This is the first study to evaluate the JAK2/STAT3 pathway in canine DLBCLs. The knowledge of JAK2-STAT3 activity in canine DLBCLs enables us to understand and explore the therapeutic potential of JAK inhibitors. The dose dependent cell growth inhibition by novel JAK inhibitors in this study will lead into the future studies of the underlying mechanism
Doutor
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.
Повний текст джерелаAstrocyte reactivity is a hallmark of pathological conditions in the CNS including neurodegenerative diseases (ND) such as Alzheimer’s (AD) and Huntington’s (HD) diseases. Reactive astrocytes (RA) are identified by morphological changes but their functional features and influence on neurons are poorly understood, especially in ND. Therefore, we aimed at 1) identifying the signaling cascades involved in astrocyte reactivity in ND, 2) evaluating RA contribution to disease phenotype in ND models and 3) deciphering RA functional features. The JAK2/STAT3 pathway is a known trigger of astrocyte reactivity in CNS injuries. Here, we show that this pathway is a common inducer of astrocyte reactivity in AD and HD models. We developed new viral vectors to target this cascade in astrocytes and manipulate astrocyte reactivity in vivo. We used these vectors to determine the contribution of RA to neuronal dysfunction in HD mouse models. We found that RA do not primarily influence disease phenotype in HD. Last, we targeted the JAK2/STAT3 pathway in WT mice to characterize RA functional features in vivo. We show RA undergo transcriptional changes of numerous genes involved in metabolism, protein degradation pathways and immune response. Moreover, we show that astrocyte reactivity alters synaptic plasticity in the mouse hippocampus. Our results identify the JAK2/STAT3 pathway as a central cascade for astrocyte reactivity. The viral vectors developed in this project represent powerful tools to decipher the roles of RA in various ND models and to characterize RA functional features in vivo. Better understanding RA functions may lead to the identification of new therapeutic targets for ND
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.
Повний текст джерелаCeyzériat, 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.
Повний текст джерелаAstrocytes are emerging as key players in brain physiology. In Alzheimer’s disease (AD), astrocytes become reactive. Astrocyte reactivity (AR) is essentially characterized by morphological changes. But how the normal supportive functions of astrocytes are changed by their reactive state is unclear. Moreover, signaling cascades leading to AR are not yet determined. In this study, we aim to: 1/ demonstrate the JAK2-STAT3 pathway (Janus Kinase 2 - Signal Transducer and Activator of Transcription 3) is responsible for AR in neurodegenerative diseases ; 2/ understand the contribution of reactive astrocytes to molecular, cellular and functional alterations in AD. We already reported that the JAK2- STAT3 pathway is a central cascade for AR (Ben Haim et al., 2015). Here, we demonstrate, with new molecular tools based on viral vectors, that this pathway is necessary and sufficient to AR. Our results also show that the modulation of AR in two AD mouse models (APP/PS1dE9 and 3xTg-AD mice) influence several pathological hallmarks, but in a context-dependent manner. Overall, this work has generated new original tools to study reactive astrocytes in situ and it underlines the importance and complexity of their functions in neurodegenerative diseases
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.
Повний текст джерелаЧастини книг з теми "Jak2-Stat3"
Wu, Ruifan, and Xinxia Wang. "SOCS3/JAK2/STAT3 pathway in iPSCs." In Molecular Players in iPSC Technology, 303–17. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-90059-1.00009-9.
Повний текст джерелаDemir 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.
Повний текст джерелаNawwaf 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.
Повний текст джерелаCentonze, Giorgia, Jennifer Chapelle, Costanza Angelini, Dora Natalini, Davide Cangelosi, Vincenzo Salemme, Alessandro Morellato, Emilia Turco, and Paola Defilippi. "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.
Повний текст джерелаLi, Xiao-Juan, Qing-Yu Ma, You-Ming Jiang, Xiao-Hui Bai, Zhi-Yi Yan, Qun Liu, Qiu-Xia Pan, Yue-Yun Liu, and Jiaxu Chen. "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, 295–320. B P International (a part of SCIENCEDOMAIN International), 2023. http://dx.doi.org/10.9734/bpi/mono/978-81-19315-94-9/ch13.
Повний текст джерелаТези доповідей конференцій з теми "Jak2-Stat3"
Gritsina, Galina, Fang Xiao, Shane W. O'Brien, Marisa A. Maglaty, Ren-Huan Xu, Luis J. Sigal, Samuel Litwin, and Denise C. Connolly. "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.
Повний текст джерелаOvermoyer, BA, V. Almendro, S. Shu, G. Peluffo, SY Park, F. Nakhlis, JR Bellon, 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.
Повний текст джерелаBallester, Beatriz, Javier Milara, Anselm Morell, Sonia Contreras, Adela Serrano, Sonia González, and Julio Cortijo. "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.
Повний текст джерелаChou, 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.
Повний текст джерелаJhaveri, K., E. Teplinsky, R. Arzu, S. Giashuddin, Y. Sarfraz, M. Alexander, F. Darvishian, 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.
Повний текст джерелаHarada, Daijiro, Daijiro Harada, Nagio Takigawa, Kadoaki Ohashi, Eiki Ichihara, Toshio Kubo, Hiromasa Takeda, 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.
Повний текст джерелаSu, 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.
Повний текст джерелаNam, Sangkil, Jun Xie, Angela Perkins, Yuelong Ma, Fan Yang, Jun Wu, Yan Wang, 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.
Повний текст джерелаJia, Zhenxian, Zhi Zhang, Ze Li, Ang Li, Yuning Xie, Hongjiao Wu, Zhenbang Yang, Hongmei Zhang, and Xuemei Zhang. "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.
Повний текст джерелаNagathihalli, 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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