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Artykuły w czasopismach na temat "C-Jun N-terminal kinase (JNK)"
Liu, Jing, Yuzuru Minemoto i Anning Lin. "c-Jun N-Terminal Protein Kinase 1 (JNK1), but Not JNK2, Is Essential for Tumor Necrosis Factor Alpha-Induced c-Jun Kinase Activation and Apoptosis". Molecular and Cellular Biology 24, nr 24 (15.12.2004): 10844–56. http://dx.doi.org/10.1128/mcb.24.24.10844-10856.2004.
Pełny tekst źródłaNgoei, Kevin R. W., Bruno Catimel, Nicole Church, Daisy S. Lio, Con Dogovski, Matthew A. Perugini, Paul M. Watt, Heung-Chin Cheng, Dominic C. H. Ng i Marie A. Bogoyevitch. "Characterization of a novel JNK (c-Jun N-terminal kinase) inhibitory peptide". Biochemical Journal 434, nr 3 (24.02.2011): 399–413. http://dx.doi.org/10.1042/bj20101244.
Pełny tekst źródłaMessoussi, A., G. Chevé, K. Bougrin i A. Yasri. "Insight into the selective inhibition of JNK family members through structure-based drug design". MedChemComm 7, nr 4 (2016): 686–92. http://dx.doi.org/10.1039/c5md00562k.
Pełny tekst źródłaSchepetkin, Igor A., Oleksander S. Karpenko, Anastasia R. Kovrizhina, Liliya N. Kirpotina, Andrei I. Khlebnikov, Stepan I. Chekal, Alevtyna V. Radudik, Maryna O. Shybinska i Mark T. Quinn. "Novel Tryptanthrin Derivatives with Selectivity as c–Jun N–Terminal Kinase (JNK) 3 Inhibitors". Molecules 28, nr 12 (16.06.2023): 4806. http://dx.doi.org/10.3390/molecules28124806.
Pełny tekst źródłaSedmíková, M., J. Petr, A. Dörflerová, J. Nevoral, B. Novotná, T. Krejčová, E. Chmelíková i L. Tůmová. "Inhibition of c-Jun N-terminal kinase (JNK) suppresses porcine oocyte ageing in vitro". Czech Journal of Animal Science 58, No. 12 (25.11.2013): 535–45. http://dx.doi.org/10.17221/7088-cjas.
Pełny tekst źródłaUnger, Elizabeth K., Merisa L. Piper, Louise E. Olofsson i Allison W. Xu. "Functional Role of c-Jun-N-Terminal Kinase in Feeding Regulation". Endocrinology 151, nr 2 (1.02.2010): 671–82. http://dx.doi.org/10.1210/en.2009-0711.
Pełny tekst źródłaChoi, Hong Seok, Ann M. Bode, Jung-Hyun Shim, Sung-Young Lee i Zigang Dong. "c-Jun N-Terminal Kinase 1 Phosphorylates Myt1 To Prevent UVA-Induced Skin Cancer". Molecular and Cellular Biology 29, nr 8 (9.02.2009): 2168–80. http://dx.doi.org/10.1128/mcb.01508-08.
Pełny tekst źródłaLoGrasso, Philip, i Theodore Kamenecka. "Inhibitors of c-jun-N-Terminal Kinase (JNK)". Mini-Reviews in Medicinal Chemistry 8, nr 8 (1.07.2008): 755–66. http://dx.doi.org/10.2174/138955708784912120.
Pełny tekst źródłaMa, Hongpeng. "Relationship Between c-Jun N-terminal Kinase and Depression". E3S Web of Conferences 185 (2020): 03029. http://dx.doi.org/10.1051/e3sconf/202018503029.
Pełny tekst źródłaYe, Zhiqiang, Yuxian Chen, Rongkai Zhang, Haitao Dai, Chun Zeng, Hua Zeng, Hui Feng, Gengheng Du, Hang Fang i Daozhang Cai. "c-Jun N-terminal kinase – c-Jun pathway transactivates Bim to promote osteoarthritis". Canadian Journal of Physiology and Pharmacology 92, nr 2 (luty 2014): 132–39. http://dx.doi.org/10.1139/cjpp-2013-0228.
Pełny tekst źródłaRozprawy doktorskie na temat "C-Jun N-terminal kinase (JNK)"
Arnold, Richard Graham. "The role of c-Jun-N-Terminal Kinase (JNK) in hindlimb ischaemia-reperfusion injury". Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.579569.
Pełny tekst źródłaKyula, Joan Nduku. "HSV-1 induced activation of C-JUN-N-Terminal Kinase (JNK) and P38 MAPK". Thesis, Glasgow Caledonian University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413914.
Pełny tekst źródłaLanuza, Masdeu Jordi. "Regulation and actions mediated by C-jun N-terminal kinase pathaway". Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/110348.
Pełny tekst źródłaAs a part of the research-line that deals with physiological and pharmacological (anti-inflammatory and/or anti-diabetic) actions conducted by some nuclear receptor (NR) ligands through negative interference with the c-Jun N-terminal kinase (JNK) signaling pathway, this project is focused on studying the effects of the activation of JNK in a mouse model and evaluating the capacity of those ligands to recover the homeostasis. In parallel, there is a second project about the characterization of the crosstalk between the JNK pathway and NF-κB, another major pathway in inflammation. The relevance of the activation of JNK in a wide range of pathologies with an inflammatory component, lead the group to the generation of a transgenic mouse carrying a a constitutively active form of the MAP2K of JNK, MKK7, with a conditional expression upon the regulation of the Cre recombinase. Despite these mice have no morphostructural affectation of the pancreatic islets or differences in the total insulin content, they have defective glucose homeostasis showing glucose intolerance and decreased insulin secretion in response to hyperglycemia. This reduction in glucoseinduced insulin release is β cell autonomous, as it is reproduced in isolated islets, and JNK activity dependent, as it is reverted by the specific inhibitor of JNK, TAT-JIPi. At molecular level, β-cells with activated JNK have a blockage in the insulin-signaling pathway that reduces the secretion of insulin and the expression of insulin target genes. The treatment with rosiglitazone, an insulin-sensitizing drug of the thiazolidinedione family that inhibits JNK activation, restored insulin secretion in response to glucose in isolated islets and in vivo. All these data indicate that the activation of JNK is sufficient to promote central insulin resistance but is not sufficient to induce islet hyperplasia or β-cell death. Moreover, these mice are protected from basal plasma hiperinsulinemia caused by aging or high fat diet challenge. Regarding the second project, the interaction between NF-κB.and JNK pathways, both signaling pathways are essential for the regulation of the immune and inflammatory response as well as other fundamental processes such as cell proliferation and survival. It was published that JNK was activating NF-κB. pathway by inducing the mRNA stabilization of the E3 ubiquitin ligase βTrcP. We have further reported that JNK is targeting the miRNA183/CRD-BP system to stabilize βTrCP mRNA. At a protein level we have shown that SPK1-βTrCP complex formation is required for JNKdependent SKP1 and βTrCP protein stabilization. Not only this but the βTrCP substrate β‐catenin is down regulated by the JNK-dependent increase of βTrCP and the protein levels of SKP2 and its substrate p27 are oppositely regulated by JNK
Gourmaud, Sarah. "Expression de c-Jun N-terminal kinase (JNK) dans la maladie d'Alzheimer : intérêts diagnostiques et thérapeutiques". Paris 7, 2014. http://www.theses.fr/2014PA077106.
Pełny tekst źródłaAlzheimer's disease (AD) is characterized by the accumulation of amyloid-β42 peptide (Aß₄₂), hyperphosphorylated tau (ptau) proteins and neuronal loss. Cerebrospinal fluid (CSF) Aß₄₂and tau levels in patients are used as diagnostic biomarkers. PKR and JNK are kinases involved in the production of Ar342, tau phosphorylation and neuronal death. The accumulation of their active form was demonstrated in AD brains. There are three isoforms of JNK. JNK1 and JNK2 are ubiquitous and JNK3 is almost exclusively expressed in brain. No studies have examined changes in JNK3 in AD. The aim of our study was to analyze in vitro the relationship between PKR and JNK and then to measure the expression of JNK isoforms in AD patients. Our results showed that PKR is involved in both JNK activation and deactivation, according to stress conditions. We also showed a decrease of neuronal apoptosis due to Aß₄₂ with a JNK inhibitor peptide. We measured an increase of the total form of JNK3 in AD frontal cortex and CSF. JNK3 signal colocalizes with Aß₄₂ in senile plaques. Thanks to the clinical monitoring of patients we have shown that the CSF level of JNK3 correlates with the cognitive decline. JNK3 could become a new diagnostic and prognostic biomarker for AD. These results, together with those of the literature, make JNK3 and PKR interesting therapeutic targets
Smith, Abigail O. "Defining the Role of c-Jun N-terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease". eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1141.
Pełny tekst źródłaSantos, Fernando Reyes, Maggie K. Diamond-Stanic, Mujalin Prasannarong i Erik J. Henriksen. "The Serine Kinase C-Jun N-Terminal Kinase (JNK) Contributes to Oxidant-Induced Insulin Resistance in Isolated Rat Skeletal Muscle". Thesis, The University of Arizona, 2012. http://hdl.handle.net/10150/244754.
Pełny tekst źródłaWang, Fang St George Clinical school UNSW. "Oxidative stress induced C-Jun N-terminal Kinase (JNK) activation in tendon cells upregulates MMP1 mRNA and protein expression". Awarded by:University of New South Wales. St George Clinical school, 2006. http://handle.unsw.edu.au/1959.4/28815.
Pełny tekst źródłaYu, Lola. "Investigating the role of the c-Jun NH2-terminal kinase pathway in ErbB2-driven breast cancer and macrophage polarization". eScholarship@UMMS, 2020. https://escholarship.umassmed.edu/gsbs_diss/1094.
Pełny tekst źródłaJoy, Jery 1992. "Chromosomal instability : interplay between proteotoxic and metabolic stress". Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/668516.
Pełny tekst źródłaLa inestabilidad cromosómica y la aneuploidía son características destacadas de la mayoría de los tumores sólidos en humanos. En el modelo epitelial de Drosophila, la generación de cariotipos altamente aneuploides promueve la delaminación y la muerte celular dependiente de c-Jun N-terminal Kinase (JNK). La producción de especies reactivas de oxígeno (ROS) juega un papel clave en la activación de JNK bajo dichas condiciones. Cuando las células delaminadas se mantienen en el tejido gracias a la inhibición de la apoptosis, los cariotipos aberrantes promueven un comportamiento maligno tumoral. En esta tesis hemos analizado los mecanismos moleculares subyacentes a la producción de ROS como consecuencia de la aneuploidía. Hemos demostrado que bajo una situación de inestablidad cromosómica se genera un estrés proteotóxico, detectado por la célula que activa los principales mecanismos de control de calidad de las proteínas. Además, dicho estrés, promueve la disfuncionalidad de las mitocondrias, favoreciendo la generación de ROS, que a su vez contribuye a la activación de JNK y a la delaminación celular al afectar el citoesqueleto de actina-miosina en los tejidos CIN.
Le, Aurore. "Deciphering the role of c-Jun N-Terminal Kinase (JNK1) in an in vivo model of skin inflammation". Doctoral thesis, Universite Libre de Bruxelles, 2020. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/314810.
Pełny tekst źródłaDoctorat en Sciences médicales (Médecine)
info:eu-repo/semantics/nonPublished
Książki na temat "C-Jun N-terminal kinase (JNK)"
Carbone, Ryan. Characterization of the role of c-Jun N-terminal kinase in L-glutamine starvation-induced apoptosis in Sp2/0-Ag14 hybridoma cells. Sudbury, Ont: Laurentian University, 2005.
Znajdź pełny tekst źródłaVallerie, Sara Nicole. Regulation of metabolism by c-Jun N-terminal kinase. 2010.
Znajdź pełny tekst źródłaCzęści książek na temat "C-Jun N-terminal kinase (JNK)"
Kim, Byung-Jin, i Donald J. Zack. "The Role of c-Jun N-Terminal Kinase (JNK) in Retinal Degeneration and Vision Loss". W Retinal Degenerative Diseases, 351–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_43.
Pełny tekst źródłaZhan, Xuanzhi, Vsevolod V. Gurevich i Eugenia V. Gurevich. "Scaffolding c-Jun N-Terminal Kinase Cascades: Mechanistic Insights from the Reconstituted Arrestin-JNK Cascades". W The Structural Basis of Arrestin Functions, 187–98. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-57553-7_14.
Pełny tekst źródłaSclip, Alessandra, Xanthi Antoniou i Tiziana Borsello. "Cortical Neurons Culture to Study c-Jun N-Terminal Kinase Signaling Pathway". W Protein Kinase Technologies, 189–202. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-824-5_10.
Pełny tekst źródłaChromik, A. M., A. M. Müller, J. Körner, O. Belyaev, M. Albrecht, F. Schmitz, T. Herdegen, W. Uhl i U. Mittelkötter. "Die genetische Inaktivierung der c-Jun N-terminalen Kinase 1 und 2 (JNK1 und JNK2) verschlimmert die chronische DSS-Colitis der Maus". W Chirurgisches Forum 2006, 215–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-34668-6_73.
Pełny tekst źródłaYatsushige, H., M. Yamaguchi-Okada, C. Zhou, J. W. Calvert, J. Cahill, A. R. T. Colohan i John H. Zhang. "Inhibition of c-Jun N-terminal kinase pathway attenuates cerebral vasospasm after experimental subarachnoid hemorrhage through the suppression of apoptosis". W Acta Neurochirurgica Supplement, 27–31. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-75718-5_6.
Pełny tekst źródłaChromik, Ansgar Michael, S. Kersting, A. M. Müller, M. Albrecht, C. Hilgert, L. Frick, T. Herdegen, U. Mittelkötter i W. Uhl. "Knock out der c-Jun N-terminalen Kinase 2 (JNK2) aggraviert die Entwicklung der chronischen DSS Colitis unabhängig von der intestinalen Zytokin-Expression". W Chirurgisches Forum 2008, 217–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-78833-1_79.
Pełny tekst źródła"C-Jun N-Terminal Kinase (JNK)". W Encyclopedia of Cancer, 873. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1193.
Pełny tekst źródła"c-Jun N-Terminal Kinase". W Encyclopedia of Cancer, 1085. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_100558.
Pełny tekst źródła"JNK (Jun amino terminal kinase)". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1047. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_8890.
Pełny tekst źródłaLam, KSL, X. Zhang, RLC Wong i A. Xu. "Selective Inactivation of c-Jun NH2 Terminal Kinase (JNK) in the Adipose Tissue Is Sufficient To Protect Against Diet-Induced-Obesity and Its Associated Metabolic Disorders in Mice." W The Endocrine Society's 92nd Annual Meeting, June 19–22, 2010 - San Diego, P1–414—P1–414. Endocrine Society, 2010. http://dx.doi.org/10.1210/endo-meetings.2010.part1.p9.p1-414.
Pełny tekst źródłaStreszczenia konferencji na temat "C-Jun N-terminal kinase (JNK)"
White, SR, MK Abe, BA Marroquin, D. Lascano i R. Stern. "c-Jun N-Terminal Kinase (JNK) and c-Jun Mediate Early Migration after Injury in Differentiated Airway Epithelial Cells." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2391.
Pełny tekst źródłaDu, Lili, Tinghu Zhang, Tamer Kaoud, Nathanael Gray, Kevin Dalby i Kenneth Y. Tsai. "Abstract 1941: Distinct roles of c-Jun N-terminal kinase (JNK) isoforms in skin cancer". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1941.
Pełny tekst źródłaPalmieri, C., B. Rudraraju, A. Giannoudis, D. Moore, J. Shaw, S. Chan, IO Ellis i in. "Abstract P5-08-17: A study of c-Jun N-terminal kinase (JNK) and c-Jun as biomarkers in early breast cancer". W Abstracts: Thirty-Eighth Annual CTRC-AACR San Antonio Breast Cancer Symposium; December 8-12, 2015; San Antonio, TX. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.sabcs15-p5-08-17.
Pełny tekst źródłaMohamed, MR, FJ Cubero, MM Woitok, RJ Davis i C. Trautwein. "Hepatocytic c-Jun N-terminal kinases (JNK) protect against cystogenesis in NEMO-deficient mice". W 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677220.
Pełny tekst źródłaSilva, Patricia M. R., Ana Carolina Arantes, Tatiana P. T. Ferreira, Cristiane Garcia, Patricia R. M. Rocco, IM Fierro, RL Simoes, Vincent Lagente i Marco A. Martins. "EFFECT OF C-JUN NH2-TERMINAL KINASE (JNK) INHIBITOR SP600125 ON EXPERIMENTAL SILICOSIS IN MICE". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1057.
Pełny tekst źródłaEbelt, ND, i CL Van Den Berg. "Abstract P6-04-17: The irreversible c-Jun N-terminal kinase (JNK) inhibitor, JNK-IN-8, sensitizes basal-like breast cancer cells to lapatinib". W 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-p6-04-17.
Pełny tekst źródłaFanburg, Barry L., Lin Wei i Yinglin Liu. "Interaction Of C-Jun N-terminal Kinase (JNK) And Other Serotonin Activated Signaling Pathways In Pulmonary Artery Smooth Muscle Cells". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1173.
Pełny tekst źródłaChu, Feng-Min, Shuang-Shii Lian i Yen-Jen Sung. "Particulate Joint Replacement Materials Induce Apoptosis of Rabbit Synoviocytes Cell Line HIG-82 through c-Jun N-Terminal Kinase (JNK) Pathway". W 2009 2nd International Conference on Biomedical Engineering and Informatics. IEEE, 2009. http://dx.doi.org/10.1109/bmei.2009.5305639.
Pełny tekst źródłaWei, L., Y. Liu i BL Fanburg. "C-Jun N-Terminal Kinase (JNK) Regulates Serotonin-Mediated Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells through the Akt Pathway." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1860.
Pełny tekst źródłaMcCoy, Francis G. P., Ian Paul, Jane L. Hurwitz, Barry O'Hagan, Krzysztofa Odrzywol, James T. Murray, George McKerr i Dean A. Fennell. "Abstract B30: Phosphorylation of c‐jun N terminal kinase (JNK) regulates induction of mitochondrial apoptosis by pro‐suvival BCL‐2 antagoinist obatoclax". W Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 15-19, 2009; Boston, MA. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/1535-7163.targ-09-b30.
Pełny tekst źródłaRaporty organizacyjne na temat "C-Jun N-terminal kinase (JNK)"
LoGrasso, Philip, i Serge Przedborski. c-jun-N-Terminal Kinase (JNK) for the Treatment of Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, październik 2013. http://dx.doi.org/10.21236/ada596507.
Pełny tekst źródłaChen, Yi-Rong. C-Jun N-terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 1999. http://dx.doi.org/10.21236/ada374120.
Pełny tekst źródłaChen, Yi-Rong. C-Jun N-terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 1998. http://dx.doi.org/10.21236/ada353790.
Pełny tekst źródłaChen, Yi-Rong, i Tse-Hua Tan. C-Jun N-Terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2000. http://dx.doi.org/10.21236/ada392179.
Pełny tekst źródłaEhrlich, Marcelo, John S. Parker i Terence S. Dermody. Development of a Plasmid-Based Reverse Genetics System for the Bluetongue and Epizootic Hemorrhagic Disease Viruses to Allow a Comparative Characterization of the Function of the NS3 Viroporin in Viral Egress. United States Department of Agriculture, wrzesień 2013. http://dx.doi.org/10.32747/2013.7699840.bard.
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