Relevant bibliographies by topics / Kinases mark

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

Academic literature on the topic 'Kinases mark'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Kinases mark"

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Jaleel, Mahaboobi, Fabrizio Villa, Maria Deak, et al. "The ubiquitin-associated domain of AMPK-related kinases regulates conformation and LKB1-mediated phosphorylation and activation." Biochemical Journal 394, no. 3 (2006): 545–55. http://dx.doi.org/10.1042/bj20051844.

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Recent work indicates that the LKB1 tumour suppressor protein kinase, which is mutated in Peutz–Jeghers cancer syndrome, phosphorylates and activates a group of protein kinases that are related to AMPK (AMP-activated protein kinase). Ten of the 14 AMPK-related protein kinases activated by LKB1, including SIK (salt-induced kinase), MARK (microtubule-affinity-regulating kinase) and BRSK (brain-specific kinase) isoforms, possess a ubiquitin-associated (UBA) domain immediately C-terminal to the kinase catalytic domain. These are the only protein kinases in the human genome known to possess a UBA d
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Saito, Taro, Toshiya Oba, Sawako Shimizu, Akiko Asada, Koichi M. Iijima, and Kanae Ando. "Cdk5 increases MARK4 activity and augments pathological tau accumulation and toxicity through tau phosphorylation at Ser262." Human Molecular Genetics 28, no. 18 (2019): 3062–71. http://dx.doi.org/10.1093/hmg/ddz120.

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Abstract Hyperphosphorylation of the microtubule-associated protein tau is associated with many neurodegenerative diseases, including Alzheimer’s disease. Microtubule affinity-regulating kinases (MARK) 1–4 and cyclin-dependent kinase 5 (Cdk5) are tau kinases under physiological and pathological conditions. However, their functional relationship remains elusive. Here, we report a novel mechanism by which Cdk5 activates MARK4 and augments tau phosphorylation, accumulation and toxicity. MARK4 is highly phosphorylated at multiple sites in the brain and in cultured neurons, and inhibition of Cdk5 a
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Matenia, Dorthe, Bettina Griesshaber, Xiao-yu Li, et al. "PAK5 Kinase Is an Inhibitor of MARK/Par-1, Which Leads to Stable Microtubules and Dynamic Actin." Molecular Biology of the Cell 16, no. 9 (2005): 4410–22. http://dx.doi.org/10.1091/mbc.e05-01-0081.

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MARK/Par-1 is a kinase involved in development of embryonic polarity. In neurons, MARK phosphorylates tau protein and causes its detachment from microtubules, the tracks of axonal transport. Because the target sites of MARK on tau occur at an early stage of Alzheimer neurodegeneration, we searched for interaction partners of MARK. Here we report that MARK2 is negatively regulated by PAK5, a neuronal member of the p21-activated kinase family. PAK5 suppresses the activity of MARK2 toward its target, tau protein. The inhibition requires the binding between the PAK5 and MARK2 catalytic domains, bu
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Biernat, Jacek, Yong-Zhong Wu, Thomas Timm, et al. "Protein Kinase MARK/PAR-1 Is Required for Neurite Outgrowth and Establishment of Neuronal Polarity." Molecular Biology of the Cell 13, no. 11 (2002): 4013–28. http://dx.doi.org/10.1091/mbc.02-03-0046.

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Protein kinases of the microtubule affinity-regulating kinase (MARK) family were originally discovered because of their ability to phosphorylate certain sites in tau protein (KXGS motifs in the repeat domain). This type of phosphorylation is enhanced in abnormal tau from Alzheimer brain tissue and causes the detachment of tau from microtubules. MARK-related kinases (PAR-1 and KIN1) occur in various organisms and are involved in establishing and maintaining cell polarity. Herein, we report the ability of MARK2 to affect the differentiation and outgrowth of cell processes from neuroblastoma and
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Emptage, Ryan P., Mark A. Lemmon, and Kathryn M. Ferguson. "Molecular determinants of KA1 domain-mediated autoinhibition and phospholipid activation of MARK1 kinase." Biochemical Journal 474, no. 3 (2017): 385–98. http://dx.doi.org/10.1042/bcj20160792.

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Protein kinases are frequently regulated by intramolecular autoinhibitory interactions between protein modules that are reversed when these modules bind other ‘activating’ protein or membrane-bound targets. One group of kinases, the MAP/microtubule affinity-regulating kinases (MARKs) contain a poorly understood regulatory module, the KA1 (kinase associated-1) domain, at their C-terminus. KA1 domains from MARK1 and several related kinases from yeast to humans have been shown to bind membranes containing anionic phospholipids, and peptide ligands have also been reported. Deleting or mutating the
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Weeks, Amy M. "Kinases leave their mark on caspase substrates." Biochemical Journal 478, no. 17 (2021): 3179–84. http://dx.doi.org/10.1042/bcj20210399.

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Apoptosis is a cell death program that is executed by the caspases, a family of cysteine proteases that typically cleave after aspartate residues during a proteolytic cascade that systematically dismantles the dying cell. Extensive signaling crosstalk occurs between caspase-mediated proteolysis and kinase-mediated phosphorylation, enabling integration of signals from multiple pathways into the decision to commit to apoptosis. A new study from Maluch et al. examines how phosphorylation within caspase cleavage sites impacts the efficiency of substrate cleavage. The results demonstrate that while
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Turab Naqvi, Ahmad Abu, Gulam Mustafa Hasan, and Md Imtaiyaz Hassan. "Targeting Tau Hyperphosphorylation via Kinase Inhibition: Strategy to Address Alzheimer's Disease." Current Topics in Medicinal Chemistry 20, no. 12 (2020): 1059–73. http://dx.doi.org/10.2174/1568026620666200106125910.

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Microtubule-associated protein tau is involved in the tubulin binding leading to microtubule stabilization in neuronal cells which is essential for stabilization of neuron cytoskeleton. The regulation of tau activity is accommodated by several kinases which phosphorylate tau protein on specific sites. In pathological conditions, abnormal activity of tau kinases such as glycogen synthase kinase-3 β (GSK3β), cyclin-dependent kinase 5 (CDK5), c-Jun N-terminal kinases (JNKs), extracellular signal-regulated kinase 1 and 2 (ERK1/2) and microtubule affinity regulating kinase (MARK)
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Brown, Fiona C., Eric Still, Paolo Cifani, et al. "Aberrant Phosphorylation of MEF2C Is Dispensable for Hematopoiesis, and Induces Chemotherapy Resistance and Susceptibility to MARK Kinase Inhibition Therapy in Acute Myeloid Leukemia." Blood 128, no. 22 (2016): 436. http://dx.doi.org/10.1182/blood.v128.22.436.436.

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Abstract For patients with acute myeloid leukemia (AML), failure to achieve complete remission after induction therapy or relapse after complete remission represents the major barrier to cure for both children and adults. Although genomics has revealed the mechanisms of pathogenesis of AML, the molecular mechanisms of chemotherapy resistance remain largely unknown. Using high-resolution mass spectrometry proteomics, we identified aberrant phosphorylation of MEF2C S222 in primary chemoresistant human AML specimens, and using capillary nanoimmunoassays, established its prevalence and prognostic
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Sun, Xianglan, Ling Gao, Hung-Yu Chien, Wan-Chun Li, and Jiajun Zhao. "The regulation and function of the NUAK family." Journal of Molecular Endocrinology 51, no. 2 (2013): R15—R22. http://dx.doi.org/10.1530/jme-13-0063.

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AMP-activated protein kinase (AMPK) is a critical regulator of cellular and whole-body energy homeostasis. Twelve AMPK-related kinases (ARKs; BRSK1, BRSK2, NUAK1, NUAK2, QIK, QSK, SIK, MARK1, MARK2, MARK3, MARK4, and MELK) have been identified recently. These kinases show a similar structural organization, including an N-terminal catalytic domain, followed by a ubiquitin-associated domain and a C-terminal spacer sequence, which in some cases also contains a kinase-associated domain 1. Eleven of the ARKs are phosphorylated and activated by the master upstream kinase liver kinase B1. However, mo
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Dequiedt, Franck, Maud Martin, Julia Von Blume, et al. "New Role for hPar-1 Kinases EMK and C-TAK1 in Regulating Localization and Activity of Class IIa Histone Deacetylases." Molecular and Cellular Biology 26, no. 19 (2006): 7086–102. http://dx.doi.org/10.1128/mcb.00231-06.

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ABSTRACT Class IIa histone deacetylases (HDACs) are found both in the cytoplasm and in the nucleus where they repress genes involved in several major developmental programs. In response to specific signals, the repressive activity of class IIa HDACs is neutralized through their phosphorylation on multiple N-terminal serine residues and 14-3-3-mediated nuclear exclusion. Here, we demonstrate that class IIa HDACs are subjected to signal-independent nuclear export that relies on their constitutive phosphorylation. We identify EMK and C-TAK1, two members of the microtubule affinity-regulating kina
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Dissertations / Theses on the topic "Kinases mark"

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La, Carbona Stéphanie. "Étude fonctionnelle de la protéine Kin1, une kinase de la famille KIN-1/PAR-1/MARK, chez "Schizosaccharomyces pombe"." Rennes 1, 2005. http://www.theses.fr/2005REN1S110.

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La protéine Kin1 de "Schizosaccharomyces pombe" appartient à la famille de kinases KIN-1/PAR-1/MARK. Nous avons montré que Kin1 est impliquée dans l'organisation de la nouvelle extrémité après la cytodiérèse, la séparation cellulaire, la polarisation complète du cytosquelette d'actine en interphase et le positionnement du site de division cellulaire. La protéine GFP-Kin1 surexprimée se localise au cortex cellulaire sur un ou deux pôles. Pour cela, le motif KA1 en C-terminal, la région médiane et l'activité kinase sont requis. La protéine Kin1-myc exprimée à un niveau endogène se localise aux p
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Kragelj, Jaka. "Structure and dynamics of intrinsically disordered regions of MAPK signalling proteins." Thesis, Grenoble, 2014. http://www.theses.fr/2014GRENV060/document.

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Les voies de transduction du signal cellulaire permettent aux cellules de répondre aux signaux de l'environnement et de les traiter. Les voies de transduction de kinases MAP (MAPK) sont bien conservées dans toutes les cellules eucaryotes et sont impliquées dans la régulation de nombreux processus cellulaires importants. Les régions intrinsèquement désordonnées (RID), présentes dans de nombreuses MAPK, n'étaient pas encore structurellement caractérisées. Les RID de MAPK sont particulièrement importantes car elles contiennent des motifs de liaison qui contrôlent les interactions entre les protéi
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Aoidi, Rifdat. "Étude du rôle de la voie ERK/MAPK dans le développement embryonnaire chez la souris." Doctoral thesis, Université Laval, 2017. http://hdl.handle.net/20.500.11794/27476.

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Tableau d'honneur de la Faculté des études supérieures et postdoctorales, 2016-2017<br>Les mammifères possèdent deux MAP kinases kinases (MEK1 et MEK2), impliquées dans l’activation de la voie ERK/MAPK essentielle pour la différenciation, la prolifération et la survie cellulaire. Le premier objectif de cette thèse était de déterminer si les fonctions des kinases MEK1 et MEK2 sont redondantes durant le développement embryonnaire. Les souris Mek1-/- meurent à mi-gestation d’une malformation du placenta. Les souris Mek2-/- ne présentent aucun phénotype majeur, suggérant que ces deux protéines ont
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Chen, Xi. "The role of PI3K and ERK/MAPK signal transduction cascades in long-term memory formation /." Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6248.

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Li, Xiaoyu. "Regulation of the kinase MARK from Rattus norvegicus (Berkenhout, 1769) activation by MARKK and inhibition by PAK5 /." [S.l.] : [s.n.], 2006. http://deposit.ddb.de/cgi-bin/dokserv?idn=980208378.

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Timm, Thomas. "Reinigung und Charakterisierung einer MARK-aktivierenden Kinase." [S.l. : s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=969477872.

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Pang, Wei Wei. "The role of mitochondria in regulating MAPK signalling pathways during oxidative stress." University of Western Australia. School of Biomedical, Biomolecular and Chemical Sciences, 2006. http://theses.library.uwa.edu.au/adt-WU2007.0026.

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[Truncated abstract] Reactive oxygen species (ROS) have been implicated to play a major role in many pathological conditions including heart attack and stroke. Their ability to modulate the extracellular signal-regulated protein kinase (ERK) and c-Jun Nterminal kinase (JNK) signalling pathways, thereby influencing cellular response has been well-documented. Recent studies implicate a central role for mitochondria in ERK and JNK activation by ROS although the mechanisms remained unresolved. Using Jurkat T-lymphocyte as a cell model, this study demonstrated increased mitochondrial ROS production
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Mahan, Kristin Lynn. "Circadian oscillation of MAPK activity and cAMP in the hippocampus : implications for memory persistence /." Thesis, Connect to this title online; UW restricted, 2008. http://hdl.handle.net/1773/6304.

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Borysov, Sergiy I. "B-Raf is an essential component of the mitotic machinery critical for activation of MAPK signaling during mitosis in Xenopus egg extracts." [Tampa, Fla] : University of South Florida, 2006. http://purl.fcla.edu/usf/dc/et/SFE0001759.

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McCarthy, Pierre C. "Regulation of MyD88 signalling by MAPK activated kinases." Thesis, University of Dundee, 2015. https://discovery.dundee.ac.uk/en/studentTheses/ba214a96-e0d3-460e-8230-5931096601a2.

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Books on the topic "Kinases mark"

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Midmer, Michael. Identification of NKIAMRE, the human homologue to the MAPK/CDK-related protein kinase NKIATRE, and its loss in leukemic blasts with 5q-syndrome. National Library of Canada, 1999.

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Hodgkiss, Andrew. Introduction to cancer biology. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0001.

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A brief introduction to cancer biology, aimed at psychiatrists, is offered. Selective DNA transcription, the cell cycle, receptor tyrosine kinases, and cell signalling pathways are introduced, using the EGFR/RAS/MAPK pathway as an exemplar. The molecular pathology of oncogenesis is summarized, including discussion of oncogenes, tumour suppressor genes, and examples of driver mutations. The exploitation of such mutations in stratified medicine, using molecularly targeted agents, is mentioned. Finally, Hanahan and Weinberg’s six hallmarks of cancer are listed, adding angiogenesis and metastasis
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Book chapters on the topic "Kinases mark"

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, et al. "Microtubule Affinity Regulating Kinases (MARK)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_161.

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Drewes, Gerard. "Microtubule Affinity Regulating Kinases (MARK)." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_161.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, et al. "Mitogen-Activated Protein Kinase (MAPK)/Extracellular Signal-Regulated Kinase (ERK) Kinases 1/2 (MEK1/2)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100810.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, et al. "MAPK Erk Kinase 3." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100755.

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Kumar, S., and S. M. Blake. "Pharmacological Potential of p38 MAPK Inhibitors." In Inhibitors of Protein Kinases and Protein Phosphates. Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/3-540-26670-4_4.

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Laufer L, Stefan, Simona Margutti, and Dowinik Hauser. "Medicinal Chemistry Approaches for the Inhibition of the p38 MAPK Pathway." In Protein Kinases as Drug Targets. Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527633470.ch9.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, et al. "MAPK (Mitogen Activating Protein Kinase)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100754.

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Gewies, Andreas, Jürgen Ruland, Alexey Kotlyarov, et al. "MAPK Kinase 1/2 (MAPKK1/2)." In Encyclopedia of Signaling Molecules. Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_100756.

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Zlobin, Andrei, Jeffrey C. Bloodworth, and Clodia Osipo. "Mitogen-Activated Protein Kinase (MAPK) Signaling." In Predictive Biomarkers in Oncology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95228-4_16.

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Page, Carine, and Anton F. Doubell. "Mitogen-activated protein kinase (MAPK) in cardiac tissues." In Biochemistry of Signal Transduction in Myocardium. Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1275-8_6.

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Conference papers on the topic "Kinases mark"

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Sheikh, Abdul Q., Andrei Kogan, and Daria A. Narmoneva. "Electromagnetic Field Mediates Capillary-Like Network Formation via MAPK/ERK Signaling Cascade." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206710.

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Abnormal angiogenesis (formation of capillaries) plays an important role in the impaired diabetic wound healing and has emerged as a new target area for therapeutic interventions. Pulsed magnetic field therapy, which was initially used for healing of bone fractures, has been recently introduced as a potential therapy to treat diabetic and chronic wounds [1], although the mechanisms responsible for improved healing are still unclear. Electromagnetic fields (EMF) have been shown to act as a directional cues in cellular responses such as migration and activations of several signal transduction ca
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Shoni, Melina, Jinyan Du, Junzheng Yang, et al. "Abstract 1271: Aberrant activation of Spleen Tyrosine Kinase in ovarian cancer identified through a global phosphorylation profiling of protein tyrosine kinases." 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.am2012-1271.

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Chen, Jing, Taro Hitosugi, Jun Fan, Sumin Kang, Ting-Lei Gu, and Titus Boggon. "Abstract 997: Oncogenic tyrosine kinases are localized to mitochondria and regulate cancer metabolism by phosphorylating key components of pyruvate dehydrogenase kinase complex." 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.am2012-997.

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Kashyap, Meghana, Kristen T. Carter, Brent C. Sauer та Christopher T. Chen. "NF-κB Mediates Cartilage Degradation Induced by Trauma Injury and Interleukin-1". У ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14513.

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Chondrocyte death, induced by impact injury (necrosis) and/or apoptotic inducers such as cytokines, and high level of nitric oxide, is important for the development of post-traumatic arthritis (PTA) [1–3]. The upregulation of pro-inflammatory cytokines, such as interleukin −1 (IL-1) and Tumor necrosis factor (TNF) α, is known to mediate cartilage degradation in inflammatory diseases and after trauma injury [1,2, 6–9]. IL-1 induces the degradation of proteoglycan (PG) in cartilage through NF-κB and Mitogen-activated protein kinases (MAPK: p38, ERK and JNK) pathways [1,2,6]. IL-1 is highly upreg
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Weidert, Eric, Payal Khanna, Francisco Vital-Lopez, and Cheng Dong. "Model Simulations Reveal VCAM-1 Augment PAK Activation Rates to Amplify p38 MAPK and VE-Cadherin Phosphorylation." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80364.

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Metastasis is a complex process mediated by both adhesion molecules and chemokine secretion [1]. One important event during cancer metastasis is tumor cell extravasation through the endothelium [1]. In melanoma cancer, tumor cell extravasation is mediated by very late antigen (VLA)-4 molecule adhesion to vascular cell adhesion molecules (VCAM)-1 on endothelial cells [2]. High expression levels of VLA-4 integrin are associated with a marked increase in melanoma extravasation through endothelial layers [2]. The binding of VLA-4 to VCAM -1 induces the activation of downstream mitogen activated pr
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Kemmis, Carly M., and Diane R. Wagner. "FAK, SMAD and MAPK Pathways Diverge During Osteogenic and Chondrogenic Differentiation of Adipose-Derived Mesenchymal Cells." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206474.

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Adipose-derived mesenchymal cells (AMCs) are a promising cell source for orthopaedic tissue engineering applications due to their accessibility and multi-lineage potential [1]. However, future use in bone and cartilage regeneration requires a comprehensive understanding of the pathways driving AMCs to osteogenic and chondrogenic lineages. We have previously demonstrated the dual function of a single medium containing bone morphogenetic protein-6 (BMP-6) on differentiation of AMCs; in the presence of BMP-6, monolayer culture induces osteogenic differentiation while pellet culture stimulates cho
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Muralidhara, Chaitanya, Abhijit Ramachandran, and Vinay K. Jain. "Abstract 3683: Crenolanib, a novel Type I, mutant-specific inhibitor of Class III receptor tyrosine kinases, preferentially binds to phosphorylated kinases." 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.am2012-3683.

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Ou, Wenbin, Yisheng Jiao, Fanguo Meng, Haimeng Zhou, and Aiyuan Wang. "Abstract 1092: Targeting multiple receptor tyrosine kinases in ovarian cancers." 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.am2012-1092.

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Moncayo, Gerald E., Michal Grzmil, Yuhua Wang, Stephan Frank, Adrian Merlo, and Hemmings A. Brian. "Abstract 1240: The role of hematopoietic protein kinases in GBM." 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.am2012-1240.

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Vermeer, Paola D., Megan Bell, Kimberly Lee, et al. "Abstract LB-143: ErbB2, EphrinB1, Src kinase and PTPN13 signaling complex regulates MAP kinase signaling in human cancers." 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-lb-143.

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