Relevant bibliographies by topics / C-Jun N-terminal kinase (JNK)

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'C-Jun N-terminal kinase (JNK)'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "C-Jun N-terminal kinase (JNK)"

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Liu, Jing, Yuzuru Minemoto, and 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, no. 24 (December 15, 2004): 10844–56. http://dx.doi.org/10.1128/mcb.24.24.10844-10856.2004.

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ABSTRACT Two ubiquitously expressed isoforms of c-Jun N-terminal protein kinase (JNK), JNK1 and JNK2, have shared functions and different functions. However, the molecular mechanism is unknown. Here we report that JNK1, but not JNK2, is essential for tumor necrosis factor alpha (TNF-α)-induced c-Jun kinase activation, c-Jun expression, and apoptosis. Using mouse fibroblasts deficient in either Jnk1 or Jnk2, we found that JNK1 was activated by TNF-α, whereas JNK2 activation was negligible. In addition, JNK2 interfered with JNK1 activation via its “futile” phosphorylation by upstream kinases. Co
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Ngoei, 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, and Marie A. Bogoyevitch. "Characterization of a novel JNK (c-Jun N-terminal kinase) inhibitory peptide." Biochemical Journal 434, no. 3 (February 24, 2011): 399–413. http://dx.doi.org/10.1042/bj20101244.

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An improved understanding of the roles of protein kinases in intracellular signalling and disease progression has driven significant advances in protein kinase inhibitor discovery. Peptide inhibitors that target the kinase protein substrate-binding site have continued to attract attention. In the present paper, we describe a novel JNK (c-Jun N-terminal kinase) inhibitory peptide PYC71N, which inhibits JNK activity in vitro towards a range of recombinant protein substrates including the transcription factors c-Jun, ATF2 (activating trancription factor 2) and Elk1, and the microtubule regulatory
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Messoussi, A., G. Chevé, K. Bougrin, and A. Yasri. "Insight into the selective inhibition of JNK family members through structure-based drug design." MedChemComm 7, no. 4 (2016): 686–92. http://dx.doi.org/10.1039/c5md00562k.

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The c-Jun N-terminal kinase (JNK) family, which comprises JNK1, JNK2 and JNK3, belongs to the mitogen-activated protein kinase (MAPK) superfamily, whose members regulate myriad biological processes, including those implicated in tumorigenesis and neurodegenerative disorders.
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Schepetkin, Igor A., Oleksander S. Karpenko, Anastasia R. Kovrizhina, Liliya N. Kirpotina, Andrei I. Khlebnikov, Stepan I. Chekal, Alevtyna V. Radudik, Maryna O. Shybinska, and Mark T. Quinn. "Novel Tryptanthrin Derivatives with Selectivity as c–Jun N–Terminal Kinase (JNK) 3 Inhibitors." Molecules 28, no. 12 (June 16, 2023): 4806. http://dx.doi.org/10.3390/molecules28124806.

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The c-Jun N-terminal kinase (JNK) family includes three proteins (JNK1-3) that regulate many physiological processes, including cell proliferation and differentiation, cell survival, and inflammation. Because of emerging data suggesting that JNK3 may play an important role in neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease, as well as cancer pathogenesis, we sought to identify JNK inhibitors with increased selectivity for JNK3. A panel of 26 novel tryptanthrin-6-oxime analogs was synthesized and evaluated for JNK1-3 binding (Kd) and inhibition of cellular i
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Sedmíková, M., J. Petr, A. Dörflerová, J. Nevoral, B. Novotná, T. Krejčová, E. Chmelíková, and L. Tůmová. "Inhibition of c-Jun N-terminal kinase (JNK) suppresses porcine oocyte ageing in vitro." Czech Journal of Animal Science 58, No. 12 (November 25, 2013): 535–45. http://dx.doi.org/10.17221/7088-cjas.

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Oocyte ageing is a complex of processes that occur when matured in vitro oocytes are, after reaching the metaphase II stage, exposed to further in vitro culture. Aged oocytes remaining at the metaphase II stage undergo spontaneous parthenogenetic activation, or cellular death, through apoptosis (fragmentation) or lysis. The key factor in apoptotic pathway regulation is c-Jun-N-terminal kinase (JNK), stress kinase from the mitogene-activated protein kinase (MAPK) family. To investigate the effect of JNK inhibition on porcine oocytes ageing, cleavage rate, and embryonic development after parthen
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Unger, Elizabeth K., Merisa L. Piper, Louise E. Olofsson, and Allison W. Xu. "Functional Role of c-Jun-N-Terminal Kinase in Feeding Regulation." Endocrinology 151, no. 2 (February 1, 2010): 671–82. http://dx.doi.org/10.1210/en.2009-0711.

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c-Jun-N-terminal kinase (JNK) is a signaling molecule that is activated by proinflammatory signals, endoplasmic reticulum (ER) stress, and other environmental stressors. Although JNK has diverse effects on immunological responses and insulin resistance in peripheral tissues, a functional role for JNK in feeding regulation has not been established. In this study, we show that central inhibition of JNK activity potentiates the stimulatory effects of glucocorticoids on food intake and that this effect is abolished in mice whose agouti-related peptide (AgRP) neurons are degenerated. JNK1-deficient
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Choi, Hong Seok, Ann M. Bode, Jung-Hyun Shim, Sung-Young Lee, and Zigang Dong. "c-Jun N-Terminal Kinase 1 Phosphorylates Myt1 To Prevent UVA-Induced Skin Cancer." Molecular and Cellular Biology 29, no. 8 (February 9, 2009): 2168–80. http://dx.doi.org/10.1128/mcb.01508-08.

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ABSTRACT The c-Jun N-terminal kinase (JNK) signaling pathway is known to mediate both survival and apoptosis of tumor cells. Although JNK1 and JNK2 have been shown to differentially regulate the development of skin cancer, the underlying mechanistic basis remains unclear. Here, we demonstrate that JNK1, but not JNK2, interacts with and phosphorylates Myt1 ex vivo and in vitro. UVA induces substantial apoptosis in JNK wild-type (JNK +/+) or JNK2-deficient (JNK2 −/−) mouse embryonic fibroblasts but has no effect on JNK1-deficient (JNK1 −/−) cells. In addition, UVA-induced caspase-3 cleavage and
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LoGrasso, Philip, and Theodore Kamenecka. "Inhibitors of c-jun-N-Terminal Kinase (JNK)." Mini-Reviews in Medicinal Chemistry 8, no. 8 (July 1, 2008): 755–66. http://dx.doi.org/10.2174/138955708784912120.

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Ma, 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.

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Depression is one of the most common emotional disorders. The cause of depression is still not clear. C-Jun N-terminal kinase (JNK) is one number of mitogen activated protein kinase (MAPK) family, which is closely related to the occurrence of many diseases. At present, it is believed that JNK plays an important role in the parthenogenesis of depression, but the specific mechanism is not clear. This review will focus on the possible mechanism of JNK protein and JNK signaling pathway affecting the parthenogenesis of depression.
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Ye, Zhiqiang, Yuxian Chen, Rongkai Zhang, Haitao Dai, Chun Zeng, Hua Zeng, Hui Feng, Gengheng Du, Hang Fang, and Daozhang Cai. "c-Jun N-terminal kinase – c-Jun pathway transactivates Bim to promote osteoarthritis." Canadian Journal of Physiology and Pharmacology 92, no. 2 (February 2014): 132–39. http://dx.doi.org/10.1139/cjpp-2013-0228.

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Osteoarthritis (OA) is a chronic degenerative joint disorder. Previous studies have shown abnormally increased apoptosis of chondrocytes in patients and animal models of OA. TNF-α and nitric oxide have been reported to induce chondrocyte ageing; however, the mechanism of chondrocyte apoptosis induced by IL-1β has remained unclear. The aim of this study is to identify the role of the c-Jun N-terminal kinase (JNK) – c-Jun pathway in regulating induction of Bim, and its implication in chondrocyte apoptosis. This study showed that Bim is upregulated in chondrocytes obtained from the articular cart
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Dissertations / Theses on the topic "C-Jun N-terminal kinase (JNK)"

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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.

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In spite of improvements in the care of the critically ill patient, both elective and emergency vascular surgical interventions are associated with significant morbidity and mortality. Successful reperfusion of the ischaemic limb often initiates a systemic inflammatory response syndrome (SIRS), which may be complicated by multiple organ failure, including Acute Lung Injury (All) and the Acute Respiratory Distress Syndrome (ARDS). An exaggerated inflammatory response has been shown to play an integral role in the development of ARDS following lower torso or limb ischaemia-reperfusion injury. JN
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Kyula, 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.

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Lanuza, 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.

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Es va generar un ratolí transgènic amb la capacitat d'activar JNK específicament al pàncrees. Tot i que aquests ratolins no tenen cap afectació morfoestructural en els seus illots pancreàtics ni diferències en el contingut total d'insulina però presenten intolerància a la glucosa i no secreten insulina en resposta a hiperglucèmia. A nivell molecular, les cèl•lules β pancreàtiques amb JNK activa, tenen un bloqueig a la via de senyalització d'insulina que fa que es redueixi la secreció d'insulina i l'expressió de gens diana de la insulina. El tractament amb rossiglitazona, un fàrmac del grup de
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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.

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La maladie d'Alzheimer (MA) se caractérise par l'accumulation de peptides d'amyloïde-β42 (Aß₄₂), de protéine tau hyperphosphorylée (ptau) et une perte neuronale. Les niveaux d'Aß₄₂ et de tau au niveau du liquide céphalo-rachidien (LCR) des patients sont utilisés comme biomarqueurs diagnostique. Les protéines PKR et JNK sont des kinases impliquées dans la production d'AE342, la phosphorylation de tau et la mort neuronale. L'accumulation de leur forme active a été mise en évidence dans le cerveau de patients MA. Il existe trois isoformes de JNK. JNK1 et JNK2 sont ubiquitaires et JNK3 est presque
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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.

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Polycystic kidney disease is an inherited degenerative disease in which the uriniferous tubules are replaced by expanding fluid-filled cysts that ultimately destroy organ function. Autosomal dominant polycystic kidney disease (ADPKD) is the most common form, afflicting approximately 1 in 1,000 people. It primarily is caused by mutations in the transmembrane proteins Polycystin-1 (PKD1) and Polycystin-2 (PKD2). The most proximal effects of polycystin mutations leading to cyst formation are not known, but pro-proliferative signaling must be involved for the tubule epithelial cells to increase in
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Santos, Fernando Reyes, Maggie K. Diamond-Stanic, Mujalin Prasannarong, and 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.

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Insulin resistance of the mammalian skeletal muscle glucose transport system, one cause of which is oxidative stress, leads to the development of type 2 diabetes. While the direct contributions to insulin resistance of certain stress-activated serine kinases have been described previously, the specific contribution of c-Jun N-terminal kinase (JNK) is not fully understood. Therefore, we assessed the role of JNK in insulin resistance caused by in vitro exposure to the oxidant hydrogen peroxide (H₂O₂). Soleus muscles from lean Zucker rats were incubated in low levels (~30 μM) of H₂O₂ in the absen
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Wang, 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.

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To explore the potential mechanisms of tendon degeneration, we investigated the role of c-Jun N-terminal Kinase (JNK) activation and the regulation of matrix metalloproteinase 1 (MMP1) in tendon matrix degradation under oxidative stress. JNK and MMP1 activity in samples from normal and ruptured human supraspinatus tendons were evaluated by immunohistochemistry. Real-time quantitative PCR was utilized to evaluate MMP1 mRNA expression and western blotting for MMP1 and JNK protein detection. JNK activation and increased MMP1 activity were found in the torn human supraspinatus tendon tissue, as we
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Yu, 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.

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Breast cancer is the second most common malignancy in the world, accounting for over 1.7 million new diagnoses and an estimated 500,000 deaths per year (1). Overexpression of the receptor tyrosine kinase ErbB2, also known as Her2 or Neu, occurs in over 30% of breast cancers and correlates with metastasis, poor prognosis, and decreased survival (1, 2). Although therapeutics targeting ErbB2 show clinical efficacy, many patients display no initial response or develop drug resistance over time (2). A deeper understanding of the molecular basis of ErbB2-driven tumorigenesis is thus required for the
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Joy, Jery 1992. "Chromosomal instability : interplay between proteotoxic and metabolic stress." Doctoral thesis, Universitat Pompeu Fabra, 2020. http://hdl.handle.net/10803/668516.

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Chromosomal Instability (CIN) and associated aneuploidy are salient features of the majority of human solid tumors. In the Drosophila epithelial model of CIN, the generation of highly aneuploid karyotypes drive cell delamination and c-Jun N-terminal Kinase (JNK) dependent cell death. Aneuploidy associated generation of Reactive Oxygen Species (ROS) plays a key role in the activation of JNK. When delaminating cells are maintained in the tissue by apoptosis inhibition, aberrant karyotypes promote a cell-autonomous malignant behavior. Here we have dissected the molecular mechanisms under
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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.

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JNK1 (c-Jun N-terminal kinase 1) has been studied in numerous biological phenomena, but its role in skin inflammation diseases has not been fully defined yet. We therefore evaluated the role of JNK1 in imiquimod-induced dermatitis, a classical model that shares many features with human psoriasis. We showed that JNK1 was necessary for the expression of inflammatory markers and for acanthosis induced by imiquimod. We demonstrated that the loss of JNK1 in dendritic cells or myeloid cells reduced inflammatory markers but did not affect acanthosis induced by imiquimod. In vitro experiments in bone
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Books on the topic "C-Jun N-terminal kinase (JNK)"

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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.

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Vallerie, Sara Nicole. Regulation of metabolism by c-Jun N-terminal kinase. 2010.

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Book chapters on the topic "C-Jun N-terminal kinase (JNK)"

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Kim, Byung-Jin, and Donald J. Zack. "The Role of c-Jun N-Terminal Kinase (JNK) in Retinal Degeneration and Vision Loss." In Retinal Degenerative Diseases, 351–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_43.

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Zhan, Xuanzhi, Vsevolod V. Gurevich, and Eugenia V. Gurevich. "Scaffolding c-Jun N-Terminal Kinase Cascades: Mechanistic Insights from the Reconstituted Arrestin-JNK Cascades." In 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.

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Sclip, Alessandra, Xanthi Antoniou, and Tiziana Borsello. "Cortical Neurons Culture to Study c-Jun N-Terminal Kinase Signaling Pathway." In Protein Kinase Technologies, 189–202. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-824-5_10.

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Chromik, A. M., A. M. Müller, J. Körner, O. Belyaev, M. Albrecht, F. Schmitz, T. Herdegen, W. Uhl, and U. Mittelkötter. "Die genetische Inaktivierung der c-Jun N-terminalen Kinase 1 und 2 (JNK1 und JNK2) verschlimmert die chronische DSS-Colitis der Maus." In Chirurgisches Forum 2006, 215–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-34668-6_73.

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Yatsushige, H., M. Yamaguchi-Okada, C. Zhou, J. W. Calvert, J. Cahill, A. R. T. Colohan, and John H. Zhang. "Inhibition of c-Jun N-terminal kinase pathway attenuates cerebral vasospasm after experimental subarachnoid hemorrhage through the suppression of apoptosis." In Acta Neurochirurgica Supplement, 27–31. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-75718-5_6.

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Chromik, Ansgar Michael, S. Kersting, A. M. Müller, M. Albrecht, C. Hilgert, L. Frick, T. Herdegen, U. Mittelkötter, and 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." In Chirurgisches Forum 2008, 217–19. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-78833-1_79.

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"C-Jun N-Terminal Kinase (JNK)." In Encyclopedia of Cancer, 873. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_1193.

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"c-Jun N-Terminal Kinase." In Encyclopedia of Cancer, 1085. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-46875-3_100558.

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"JNK (Jun amino terminal kinase)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1047. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_8890.

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Lam, KSL, X. Zhang, RLC Wong, and 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." In 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.

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Conference papers on the topic "C-Jun N-terminal kinase (JNK)"

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White, SR, MK Abe, BA Marroquin, D. Lascano, and R. Stern. "c-Jun N-Terminal Kinase (JNK) and c-Jun Mediate Early Migration after Injury in Differentiated Airway Epithelial Cells." In 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.

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Du, Lili, Tinghu Zhang, Tamer Kaoud, Nathanael Gray, Kevin Dalby, and Kenneth Y. Tsai. "Abstract 1941: Distinct roles of c-Jun N-terminal kinase (JNK) isoforms in skin cancer." In 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.

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Palmieri, C., B. Rudraraju, A. Giannoudis, D. Moore, J. Shaw, S. Chan, IO Ellis, et al. "Abstract P5-08-17: A study of c-Jun N-terminal kinase (JNK) and c-Jun as biomarkers in early breast cancer." In 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.

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Mohamed, MR, FJ Cubero, MM Woitok, RJ Davis, and C. Trautwein. "Hepatocytic c-Jun N-terminal kinases (JNK) protect against cystogenesis in NEMO-deficient mice." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677220.

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Silva, Patricia M. R., Ana Carolina Arantes, Tatiana P. T. Ferreira, Cristiane Garcia, Patricia R. M. Rocco, IM Fierro, RL Simoes, Vincent Lagente, and Marco A. Martins. "EFFECT OF C-JUN NH2-TERMINAL KINASE (JNK) INHIBITOR SP600125 ON EXPERIMENTAL SILICOSIS IN MICE." In 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.

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Ebelt, ND, and 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." 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-p6-04-17.

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Fanburg, Barry L., Lin Wei, and Yinglin Liu. "Interaction Of C-Jun N-terminal Kinase (JNK) And Other Serotonin Activated Signaling Pathways In Pulmonary Artery Smooth Muscle Cells." In 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.

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Chu, Feng-Min, Shuang-Shii Lian, and Yen-Jen Sung. "Particulate Joint Replacement Materials Induce Apoptosis of Rabbit Synoviocytes Cell Line HIG-82 through c-Jun N-Terminal Kinase (JNK) Pathway." In 2009 2nd International Conference on Biomedical Engineering and Informatics. IEEE, 2009. http://dx.doi.org/10.1109/bmei.2009.5305639.

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Wei, L., Y. Liu, and BL Fanburg. "C-Jun N-Terminal Kinase (JNK) Regulates Serotonin-Mediated Proliferation and Migration of Pulmonary Artery Smooth Muscle Cells through the Akt Pathway." In 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.

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McCoy, Francis G. P., Ian Paul, Jane L. Hurwitz, Barry O'Hagan, Krzysztofa Odrzywol, James T. Murray, George McKerr, and 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." In 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.

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Reports on the topic "C-Jun N-terminal kinase (JNK)"

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LoGrasso, Philip, and Serge Przedborski. c-jun-N-Terminal Kinase (JNK) for the Treatment of Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada596507.

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Chen, Yi-Rong. C-Jun N-terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1999. http://dx.doi.org/10.21236/ada374120.

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3

Chen, Yi-Rong. C-Jun N-terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 1998. http://dx.doi.org/10.21236/ada353790.

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4

Chen, Yi-Rong, and Tse-Hua Tan. C-Jun N-Terminal Kinase and Apoptosis in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2000. http://dx.doi.org/10.21236/ada392179.

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5

Ehrlich, Marcelo, John S. Parker, and 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, September 2013. http://dx.doi.org/10.32747/2013.7699840.bard.

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Abstract:
Project Title: "Development of a plasmid-based reverse genetics system for the Bluetongue and Epizootic Hemorrhagic Disease viruses to allow comparative characterization of the function of the NS3 viroporin in viral egress". Project details: No - IS-4192-09; Participants – Ehrlich M. (Tel Aviv University), Parker J.S. (Cornell University), DermodyT.S. (Vanderbilt University); Period - 2009-2013. Orbiviruses are insect-borne infectious agents of ruminants that cause diseases with considerable economical impact in Israel and the United States. The recent outbreaks of BTV in Europe and of Epizoot
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