Relevant bibliographies by topics / ERKs

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  2. Dissertations / Theses
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Academic literature on the topic 'ERKs'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "ERKs"

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Robbins, D. J., E. Zhen, M. Cheng, S. Xu, C. A. Vanderbilt, D. Ebert, C. Garcia, A. Dang, and M. H. Cobb. "Regulation and properties of extracellular signal-regulated protein kinases 1, 2, and 3." Journal of the American Society of Nephrology 4, no. 5 (November 1993): 1104–10. http://dx.doi.org/10.1681/asn.v451104.

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The extracellular signal-regulated kinases ERK1 and ERK2 are 43- and 41-kd enzymes activated by many extracellular cues. They lie within a protein kinase cascade that is used to achieve many cellular responses. In addition to the wide variety of regulatory contexts in which they are activated, they phosphorylate important regulatory proteins, including receptors, transcription factors, cytoskeletal proteins, and other protein kinases. Thus, the stimulation of this kinase cascade is thought to have a pleiotropic action. ERK1 and ERK2 are controlled by phosphorylation on threonine and tyrosine. To understand the regulatory mechanisms, wild-type and mutant ERKs were expressed in bacteria and phosphorylated with MEK, the enzyme that is upstream of ERKs. Wild-type proteins could be activated 500- to 1,000-fold in vitro by MEK. ERK3, an enzyme of 62 kd and only 50% identical to ERK1 and ERK2 in the catalytic core, was also phosphorylated by MEK in vitro. This suggests that all three of these enzymes are targets of common signaling pathways.
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Hochholdinger, Franz, Gottfried Baier, Anto Nogalo, Birgit Bauer, Hans H. Grunicke, and Florian Überall. "Novel Membrane-Targeted ERK1 and ERK2 Chimeras Which Act as Dominant Negative, Isotype-Specific Mitogen-Activated Protein Kinase Inhibitors of Ras-Raf-Mediated Transcriptional Activation of c-fos in NIH 3T3 Cells." Molecular and Cellular Biology 19, no. 12 (December 1, 1999): 8052–65. http://dx.doi.org/10.1128/mcb.19.12.8052.

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ABSTRACT Expression of constructs encoding fusion proteins of ERK1 and ERK2 containing a C-terminal farnesylation motif (CAAX) is predominantly localized at the cell membrane and was activated by coexpression of constitutively active Ha-RasL61 and epidermal growth factor. Both fusion proteins significantly inhibit the transcriptional activation of a c-fos–chloramphenicol acetyltransferase reporter induced by RasL61, constitutively active MEK1, or constitutively active RafBXB. The corresponding SAAX chimeras or overexpression of the wild-type ERKs did not interfere with the transcriptional activation of c-fos. The inhibition of the Ras-mediated c-fosinduction by ERK2-CAAX can in part be rescued by coexpression of a wild-type ERK2 but not by wild-type ERK1. We find that ERK1-CAAX acts in the same fashion, indicating that mitogen-activated protein kinase (MAPK)–CAAX chimeras interact in an isotype-specific manner. It is demonstrated that both ERK1-CAAX and ERK2-CAAX associate with the corresponding endogenous ERKs, which explains the isotype-specific inhibitory effects of the ERK-CAAX chimeras. Evidence is presented that expression of ERK-CAAX fusion proteins inhibits the nuclear translocation of the corresponding endogenous ERKs. Disruption of MAPK translocation by membrane targeting provides additional, independent proof that nuclear translocation of ERKs is essential for the transcriptional activation of c-fos.
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Smorodinsky-Atias, Karina, Tal Goshen-Lago, Anat Goldberg-Carp, Dganit Melamed, Alexei Shir, Navit Mooshayef, Jonah Beenstock, et al. "Intrinsically active variants of Erk oncogenically transform cells and disclose unexpected autophosphorylation capability that is independent of TEY phosphorylation." Molecular Biology of the Cell 27, no. 6 (March 15, 2016): 1026–39. http://dx.doi.org/10.1091/mbc.e15-07-0521.

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The receptor-tyrosine kinase (RTK)/Ras/Raf pathway is an essential cascade for mediating growth factor signaling. It is abnormally overactive in almost all human cancers. The downstream targets of the pathway are members of the extracellular regulated kinases (Erk1/2) family, suggesting that this family is a mediator of the oncogenic capability of the cascade. Although all oncogenic mutations in the pathway result in strong activation of Erks, activating mutations in Erks themselves were not reported in cancers. Here we used spontaneously active Erk variants to check whether Erk’s activity per se is sufficient for oncogenic transformation. We show that Erk1(R84S) is an oncoprotein, as NIH3T3 cells that express it form foci in tissue culture plates, colonies in soft agar, and tumors in nude mice. We further show that Erk1(R84S) and Erk2(R65S) are intrinsically active due to an unusual autophosphorylation activity they acquire. They autophosphorylate the activatory TEY motif and also other residues, including the critical residue Thr-207 (in Erk1)/Thr-188 (in Erk2). Strikingly, Erk2(R65S) efficiently autophosphorylates its Thr-188 even when dually mutated in the TEY motif. Thus this study shows that Erk1 can be considered a proto-oncogene and that Erk molecules possess unusual autoregulatory properties, some of them independent of TEY phosphorylation.
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Zakrzewska, Malgorzata, Lukasz Opalinski, Ellen M. Haugsten, Jacek Otlewski, and Antoni Wiedlocha. "Crosstalk between p38 and Erk 1/2 in Downregulation of FGF1-Induced Signaling." International Journal of Molecular Sciences 20, no. 8 (April 12, 2019): 1826. http://dx.doi.org/10.3390/ijms20081826.

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Mitogen-activated protein kinases (MAPK): Erk1 and Erk2 are key players in negative-feedback regulation of fibroblast growth factor (FGF) signaling. Upon activation, Erk1 and Erk2 directly phosphorylate FGF receptor 1 (FGFR1) at a specific serine residue in the C-terminal part of the receptor, substantially reducing the tyrosine phosphorylation in the receptor kinase domain and its signaling. Similarly, active Erks can also phosphorylate multiple threonine residues in the docking protein FGF receptor substrate 2 (FRS2), a major mediator of FGFR signaling. Here, we demonstrate that in NIH3T3 mouse fibroblasts and human osteosarcoma U2OS cells stably expressing FGFR1, in addition to Erk1 and Erk2, p38 kinase is able to phosphorylate FRS2. Simultaneous inhibition of Erk1/2 and p38 kinase led to a significant change in the phosphorylation pattern of FRS2 that in turn resulted in prolonged tyrosine phosphorylation of FGFR1 and FRS2 and in sustained signaling, as compared to the selective inhibition of Erks. Furthermore, excessive activation of p38 with anisomycin partially compensated the lack of Erks activity. These experiments reveal a novel crosstalk between p38 and Erk1/2 in downregulation of FGF-induced signaling.
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Robbins, D. J., and M. H. Cobb. "Extracellular signal-regulated kinases 2 autophosphorylates on a subset of peptides phosphorylated in intact cells in response to insulin and nerve growth factor: analysis by peptide mapping." Molecular Biology of the Cell 3, no. 3 (March 1992): 299–308. http://dx.doi.org/10.1091/mbc.3.3.299.

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The phosphorylation of extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2) in response to insulin in Rat 1 HIRc B cells and in response to nerve growth factor (NGF) in PC12 cells has been examined. ERK1 and ERK2 are phosphorylated on serine in the absence of the stimuli and additionally on tyrosine and threonine residues after exposure to NGF and insulin. NGF stimulates tyrosine phosphorylation of ERK1 more rapidly than threonine phosphorylation. Two-dimensional phosphopeptide maps of both ERK1 and ERK2 phosphorylated in intact cells treated with NGF or with insulin display the same three predominant phosphopeptides that comigrate when digests of ERK1 and ERK2 are mixed. As many as five additional phosphopeptides are detected under certain conditions. Autophosphorylated recombinant ERK2 also contains the three tryptic phosphopeptides found in ERKs labeled in intact cells. These experiments demonstrate that ERK1 and ERK2 are phosphorylated on related sites in response to two distinct extracellular signals. The data also support the possibility that autophosphorylation may be involved in the activation of the ERKs.
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Zhang, Yuanya, Xiahe Huang, Jinlong Wang, Xiaorong Wang, Xiaofei Liu, Yuhang Chen, Wu Xu, and Yingchun Wang. "Nitration-induced ubiquitination and degradation control quality of ERK1." Biochemical Journal 476, no. 13 (July 2, 2019): 1911–26. http://dx.doi.org/10.1042/bcj20190240.

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Abstract The mitogen-activated protein kinase ERK1/2 (ERKs, extracellular-regulated protein kinases) plays important roles in a wide spectrum of cellular processes and have been implicated in many disease states. The spatiotemporal regulation of ERK activity has been extensively studied. However, scarce information has been available regarding the quality control of the kinases to scavenge malfunctioning ERKs. Using site-specific mutagenesis and mass spectrometry, we found that the disruption of the conserved H-bond between Y210 and E237 of ERK1 through point mutation at or naturally occurring nitration on Y210 initiates a quality control program dependent on chaperon systems and CHIP (C-terminal of Hsp70-interacting protein)-mediated ubiquitination and degradation. The H-bond is also important for the quality control of ERK2, but through a distinct mechanism. These findings clearly demonstrate how malfunctioning ERKs are eliminated when cells are in certain stress conditions or unhealthy states, and could represent a general mechanism for scavenging malfunctioning kinases in stress conditions.
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Boulton, T. G., and M. H. Cobb. "Identification of multiple extracellular signal-regulated kinases (ERKs) with antipeptide antibodies." Cell Regulation 2, no. 5 (May 1991): 357–71. http://dx.doi.org/10.1091/mbc.2.5.357.

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A protein kinase characterized by its ability to phosphorylate microtubule-associated protein-2 (MAP2) and myelin basic protein (MBP) is thought to play a pivotal role in the transduction of signals from many receptors in response to their ligands. A kinase with such activity, named extracellular signal-regulated kinase 1 (ERK1), is activated rapidly by numerous extracellular signals, requires phosphorylation on tyrosine to be fully active, and in vitro can activate a kinase (a ribosomal S6 protein kinase) that is downstream in phosphorylation cascades. From the protein sequence predicted by the rat ERK1 cDNA, peptides were synthesized and used to elicit antibodies. The antibodies recognize both ERK1; a closely related kinase, ERK2; and a third novel ERK-related protein. Using these antibodies we have determined that ERK1 and ERK2 are ubiquitously distributed in rat tissues. Both enzymes are expressed most highly in brain and spinal cord as are their mRNAs. The third ERK protein was found in spinal cord and in testes. The antibodies detect ERKs in cell lines from multiple species, including human, mouse, dog, chicken, and frog, in addition to rat, indicating that the kinases are conserved across species. ERK1 and ERK2 have been separated by chromatography on Mono Q. Stimulation by insulin increases the phosphorylation of both kinases on tyrosine residues, as assessed by immunoblotting with phosphotyrosine antibodies, and retards their elution from Mono Q. Each of these ERKs appears to account for a distinct peak of MBP kinase activity. The activity in each peak is diminished by incubation with either phosphatase 2a or CD45. Therefore, both enzymes have similar modes of regulation and appear to contribute to the growth factor-stimulated MAP2/MBP kinase activity measured in cell extracts.
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Minden, A., A. Lin, T. Smeal, B. Dérijard, M. Cobb, R. Davis, and M. Karin. "c-Jun N-terminal phosphorylation correlates with activation of the JNK subgroup but not the ERK subgroup of mitogen-activated protein kinases." Molecular and Cellular Biology 14, no. 10 (October 1994): 6683–88. http://dx.doi.org/10.1128/mcb.14.10.6683.

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c-Jun transcriptional activity is stimulated by phosphorylation at two N-terminal sites: Ser-63 and -73. Phosphorylation of these sites is enhanced in response to a variety of extracellular stimuli, including growth factors, cytokines, and UV irradiation. New members of the mitogen-activated protein (MAP) kinase group of signal-transducing enzymes, termed JNKs, bind to the activation domain of c-Jun and specifically phosphorylate these sites. However, the N-terminal sites of c-Jun were also suggested to be phosphorylated by two other MAP kinases, ERK1 and ERK2. Despite these reports, we find that unlike the JNKs, ERK1 and ERK2 do not phosphorylate the N-terminal sites of c-Jun in vitro; instead they phosphorylate an inhibitory C-terminal site. Furthermore, the phosphorylation of c-Jun in vivo at the N-terminal sites correlates with activation of the JNKs but not the ERKs. The ERKs are probably involved in the induction of c-fos expression and thereby contribute to the stimulation of AP-1 activity. Our study suggests that two different branches of the MAP kinase group are involved in the stimulation of AP-1 activity through two different mechanisms.
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Minden, A., A. Lin, T. Smeal, B. Dérijard, M. Cobb, R. Davis, and M. Karin. "c-Jun N-terminal phosphorylation correlates with activation of the JNK subgroup but not the ERK subgroup of mitogen-activated protein kinases." Molecular and Cellular Biology 14, no. 10 (October 1994): 6683–88. http://dx.doi.org/10.1128/mcb.14.10.6683-6688.1994.

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c-Jun transcriptional activity is stimulated by phosphorylation at two N-terminal sites: Ser-63 and -73. Phosphorylation of these sites is enhanced in response to a variety of extracellular stimuli, including growth factors, cytokines, and UV irradiation. New members of the mitogen-activated protein (MAP) kinase group of signal-transducing enzymes, termed JNKs, bind to the activation domain of c-Jun and specifically phosphorylate these sites. However, the N-terminal sites of c-Jun were also suggested to be phosphorylated by two other MAP kinases, ERK1 and ERK2. Despite these reports, we find that unlike the JNKs, ERK1 and ERK2 do not phosphorylate the N-terminal sites of c-Jun in vitro; instead they phosphorylate an inhibitory C-terminal site. Furthermore, the phosphorylation of c-Jun in vivo at the N-terminal sites correlates with activation of the JNKs but not the ERKs. The ERKs are probably involved in the induction of c-fos expression and thereby contribute to the stimulation of AP-1 activity. Our study suggests that two different branches of the MAP kinase group are involved in the stimulation of AP-1 activity through two different mechanisms.
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Lu, Nathan, and Charles J. Malemud. "Extracellular Signal-Regulated Kinase: A Regulator of Cell Growth, Inflammation, Chondrocyte and Bone Cell Receptor-Mediated Gene Expression." International Journal of Molecular Sciences 20, no. 15 (August 3, 2019): 3792. http://dx.doi.org/10.3390/ijms20153792.

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Extracellular signal-regulated kinase (ERK) is a member of the mitogen-activated protein kinase family of signaling molecules. ERK is predominantly found in two forms, ERK1 (p44) and ERK2 (p42), respectively. There are also several atypical forms of ERK, including ERK3, ERK4, ERK5 and ERK7. The ERK1/2 signaling pathway has been implicated in many and diverse cellular events, including proliferation, growth, differentiation, cell migration, cell survival, metabolism and transcription. ERK1/2 is activated (i.e., phosphorylated) in the cytosol and subsequently translocated to the nucleus, where it activates transcription factors including, but not limited to, ETS, c-Jun, and Fos. It is not surprising that the ERK1/2 signaling cascade has been implicated in many pathological conditions, namely, cancer, arthritis, chronic inflammation, and osteoporosis. This narrative review examines many of the cellular events in which the ERK1/2 signaling cascade plays a critical role. It is anticipated that agents designed to inhibit ERK1/2 activation or p-ERK1/2 activity will be developed for the treatment of those diseases characterized by dysregulated gene expression through ERK1/2 activation.
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Dissertations / Theses on the topic "ERKs"

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Houdiard, Soizic. "Rôle des ERKs dans la régulation de l'hématopoièse murine : étude de l'isoforme ERK1." Paris 7, 2010. http://www.theses.fr/2010PA077089.

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L'hématopoïèse est un processus hautement régulé, initié au niveau des cellules souches hématopoïétiques (CSHs) et dont la régulation est assurée à travers une hiérarchie cellulaire. Ceci implique un mécanisme de régulation dynamique des fonctions des CSHs et de leur descendance. Les ERKS sont des acteurs clés de la régulation de la prolifération et de la différenciation dans de nombreux types cellulaires, suggérant un rôle important dans l'hématopoïèse qui n'a pas encore été étudié in vivo. L'étude des souris ERK1 ̄/ ̄ a mis en évidence une splénomégalie, caractérisée par une accumulation de progéniteurs érythroïdes et une augmentation du nombre d'érythroblastes immatures. L'activation de la voie de signalisation BMP4 permet la mise en place d'une érythropoïèse splénique et le développement de BFU-Es de stress. Dans les souris ERK1 ̄/ ̄ nous avons observé une forte augmentation du nombre de BFU-E de stress et de l'ARNm codant pour BMP4. Notre étude nous a donc permis de démontrer que ERK1 régule l'érythropoïèse splénique par son action sur l'expression de BMP4. De plus, l'étude de l'hématopoïèse médullaire a montré une augmentation du nombre de CSHs ainsi qu'un défaut de différenciation granulo-macrophagique dans les souris ERK1 ̄/ ̄. Des radiographies ont permis d'observer une augmentation de la densité osseuse dans des souris ERK1 ̄/ ̄, suggérant une ostéopétrose. Les mécanismes mis en jeu seront caractérisés par des expériences de transplantation de CSHs, par l'analyse de la différenciation monocytaire et mégacaryocytaire et par l'étude de l'ostéogénèse
Hematopoiesis is a highly regulated process, initiated by hematopoietic stem cells (HSCs), which implies a dynamic regulation of the functions of HSC and its descent. The ERKs kinases are keys regulators of proliferation and differentiation of different cells types. Their role could be important in hematopoiesis and have not been studied in vivo yet. We have examined the role of ERK1 in adult hematopoiesis in ERK1 ̄/ ̄ mice. Loss of ERK1 resulted in an enhanced splenic erythropoiesis, characterized by an accumulation of erythroid progenitors and an enhanced number of immature erythroblasts in the spleen. Splenic stress erythropoiesis response has been shown to require BMP4-dependent signalling in vivo and to rely on the expansion of stress BFU-Es. A great expansion of stress BFU-Es and an increased level of BMP4 mRNA were found in ERK1 ̄/ ̄ spleens, suggesting that ERK1 controls a BMP4-dependent step, regulating thé steady state of splenic erythropoiesis. Study of medullar hematopoiesis had also show an enhanced numbers of HSCs and a defect in granulo-macrophagic differentiation in ERK1 ̄/ ̄ mice. X-Rays analysis of wild-type and ERK1 ̄/ ̄ mice allowed us to observe an enhanced bone density in ERK1 KO mice. So, loss of ERK1 induces osteopetrosis. Mechanisms involved will be caracterised by HSCs transplantation experiments, analysis of monocyte and megacaryocyte differentiation and by study of osteogenesis
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Pucilowska, Joanna. "Inactivation of ERK1 and ERK2 Disrupts Cortical Progenitor Proliferation Leading to Abnormal Cytoarchitecture, Circuitry and Behavior, Modeling Human NCFC and Related Syndromes." Case Western Reserve University School of Graduate Studies / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=case1339100674.

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Silva, Heitor Fontes da. "Participação de quinases reguladas por sinais extracelulares na interação entre células-tronco mesenquimais e titânio durante a diferenciação osteoblástica e adipocítica." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/58/58136/tde-22112016-114429/.

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A osseointegração de implantes de titânio (Ti) é dependente da interação entre a superfície de Ti e células, a qual é modulada por diversas vias de sinalização intracelular. Sabe-se que as quinases reguladas por sinais extracelulares (ERKs), membros da família das proteínas quinases ativadas por mitógenos (MAPKs), atuam tanto na osteogênese, quanto na adipogênese e, portanto, podem estar envolvidas no processo de osseointegração de Ti. Nesse contexto, o objetivo do presente estudo foi avaliar se a interação entre células-tronco mesenquimais (CTMs) e superfícies de Ti usinada e com nanotopografia é modulada, ao menos em parte, por ERK1/2 e o consequente efeito da inibição dessas ERKs na diferenciação osteoblástica e adipocítica. Para isso, CTMs derivadas de medula óssea de ratos foram cultivadas sobre discos de Ti usinados e com nanotopografia em condições osteogênicas e adipogênicas, na presença ou não do inibidor de ERK1/2, PD98059, em concentração previamente determinada (25 μM) e foram avaliados parâmetros relacionados à diferenciação osteoblástica e adipocítica. Os resultados mostraram que a expressão gênica dos marcadores osteoblásticos RUNX2, osterix (OSX), fosfatase alcalina (ALP) e osteocalcina (OC) foi aumentada pela inibição da via de sinalização de ERK1/2 nas células crescidas sobre Ti usinado e apenas ALP e OC, naquelas crescidas sobre Ti com nanotopografia. A expressão proteica de RUNX2 foi discretamente maior nas células crescidas sobre Ti usinado, mas não sobre Ti com nanotopografia, quando ERK1/2 foram inibidas e essa inibição não afetou a formação de matriz extracelular mineralizada, independentemente da superfície de Ti avaliada. Com relação à diferenciação adipocítica, a inibição da via de sinalização de ERK1/2 aumentou a expressão gênica dos marcadores adipocíticos PPARγ, adiponectina (ADIPOQ) e proteína ligadora de ácido graxo do adipócito ( AP2) nas células crescidas sobre ambas as superfícies de Ti, com efeito mais acentuado na superfície usinada, sem afetar a formação de acúmulo lípidico. Em conclusão, os resultados mostraram que a inibição de ERK1/2 favoreceu a diferenciação osteoblástica de CTMs crescidas sobre a superfície de Ti usinada, mas não sobre Ti com nanotopografia. Além disso, a inibição de ERK1/2 favoreceu a diferenciação adipocítica de CTMs crescidas sobre as superfícies de Ti com nanotopografia e usinada, sendo o efeito mais acentuado na usinada. Considerando aplicações terapêuticas, esses resultados são relevantes para direcionar o desenvolvimento de superfícies de biomateriais que atuem em vias de sinalização que sabidamente modulam o processo de osteogênese.
Osseointegration of titanium (Ti) implants depends on interaction between Ti surface and cells, which is modulated by several intracellular signaling pathways. Extracellular signal-regulated kinases (ERKs) are members of mitogen-activated protein kinases (MAPKs) family and act on both osteogenesis and adipogenesis and, therefore, may be involved in the process of Ti osseointegration. In this context, the aim of this study was to evaluate if the interaction between mesenchymal stem cells (MSCs) and Ti surfaces, either machined or with nanotopography, is modulated, at least in part, by ERK1/2 and the effect of ERK1/2 inhibition on osteoblast and adipocyte differentiation. Rat bone marrow MSCs were cultured on Ti discs either machined or with nanotopography under osteogenic and adipogenic conditions, in presence or not of the ERK1/2 inhibitor, PD98059, at a concentration previously determined (25 μM) and it was evaluated parameters related to osteoblast and adipocyte differentiation. The results showed that gene expression of the bone markers RUNX2, osterix (OSX), alkaline phosphatase (ALP) and osteocalcin (OC) was increased by ERK1/2 signaling inhibition in cells grown on machined Ti and only ALP and OC in cells grown on Ti with nanotopography. RUNX2 protein expression was slightly higher in cells grown on machined Ti, but not on Ti with nanotopography, when ERK1/2 signaling was inhibited and such inhibition did not affect extracellular matrix mineralization, irrespective of the evaluated Ti surface. Regarding adipocyte differentiation, ERK1/2 signaling inhibition increased gene expression of the adipose tissue markers PPARγ, adiponectin (ADIPOQ) and adipocyte fatty acid-binding protein (AP2) in cells grown on both Ti surfaces, with more prominet effect on machined one, without affecting lipid accumulation. In conclusion, our results showed that ERK1/2 signaling inhibition favored osteoblast differentiation of MSCs grown on machined Ti, but not on Ti with nanotopography. In addition, ERK1/2 signaling inhibition favored adipocyte differentiation of MSCs grown on both Ti surfaces, being more noticeable on machined one. Considering therapeutical applications, these results are relevant to drive the development of biomaterial surfaces to act on signaling pathways that regulate the process of osteogenesis.
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Ellin, Dan. "The many behind the few : the lives and emotions of Erks and WAAFs of RAF Bomber Command 1939-1945." Thesis, University of Warwick, 2015. http://wrap.warwick.ac.uk/73976/.

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This thesis examines the lives and emotions of male and female ground personnel who served in Bomber Command during the Second World War. Histories of Bomber Command usually focus on the flyers, or on the strategy of the bombing campaign. The experiences of four fifths of the service, the ground personnel, are often neglected. They are frequently reduced to two dimensional stereotypes, as the ‘Erk’ who serviced the aircraft, or the WAAF ‘chop girl’ whose sexual promiscuity presaged death. The RAF assigned personnel to different trades ranging from the most technical to the most mundane. The central theme of this thesis is the gendered hierarchy of trades within Bomber Command. It was constructed in part by widespread beliefs about fear, heroism and stoicism, the interconnected discourses of class and gender, and specific quirks of RAF culture. These included its trade selection process, dialect, pay scale, and trades’ perceived importance to the raison d’être of Bomber Command. The hierarchy is important in explaining the experiences of ground personnel, as some personnel were overstretched while others felt that they were not ‘doing their bit.’ Bomber Command servicemen and women were part of a community that experienced high rates of air crew loss. This thesis also discusses their emotional responses to service life and the treatment by the RAF medical services of those who suffered breakdowns. In examining non-combatant military personnel who served on operational stations but were also part of the home front, my thesis will inform and bring together different areas of study. It gives a voice to an important but previously underrepresented group and in doing so, contributes to the histories of the RAF, emotions, military medicine and psychiatry, as well as understandings of the wartime experience, work and citizenship.
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Pinto, Rui Miguel Correia de Almeida. "Activação das vias de sinalização intracelular das ERKs 1 e 2 e da p38 em carcinomas de células de transição da bexiga." Dissertação, Faculdade de Medicina da Universidade do Porto, 2008. http://hdl.handle.net/10216/22310.

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Pinto, Rui Miguel Correia de Almeida. "Activação das vias de sinalização intracelular das ERKs 1 e 2 e da p38 em carcinomas de células de transição da bexiga." Master's thesis, Faculdade de Medicina da Universidade do Porto, 2008. http://hdl.handle.net/10216/22310.

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Atkinson, Peter Geoffrey Peel. "Studies on the mitogen-activated protein kinases ERK1 and ERK2." Thesis, University of Southampton, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307155.

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Fischer, April M. "The role of ERK1 and ERK2 in T cell development /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3166398.

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Richard-Legendre, Florence. "Régulation des voies de signalisation des JAK/STATs et des MAPK/ERKs par l'IL-6/sIL-6R chez les chondrocytes articulaires : implication dans la régulation des gènes matriciels." Caen, 2002. http://www.theses.fr/2002CAEN2021.

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L'interleukine-6 (IL-6) est une cytokine ayant un rôle majeur dans le système immunitaire et dans l'inflammation. Son rôle dans le métabolisme du cartilage est mal connu. Toutefois, il semblerait qu'elle puisse être impliquée à la fois dans les maladies inflammatoires et dégénératives du cartilage (arthrite et arthrose). L'objectif de notre travail a été d'étudier, chez les chondrocytes, les voies de signalisation mises en jeu par l'IL-6 et leur rôle dans ses effets biologiques. Nos résultats montrent que l'IL-6 en présence de son récepteur soluble sIL-6R, active à la fois les voies de signalisation des JAKs/STATs et des MAPK/ERKs. De plus, l'IL-6/sIL-6R inhibe la prolifération des chondrocytes, diminue l'expression de constituants matriciels (collagène de type II, axe protéique de liaison de l'agrécane) et augmente celle de métalloprotéases (collagénase de type 1, agrécanasess de type 1 et 2). Grâce à l'utilisation de parthénolide, qui inhibe l'activation des STATs, nous avons montré que l'IL-6/sIL-6R inhibe la transcription des constituants matriciels par l'intermédiaire de la voie JAK/STAT [etc]
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Volmat, Véronique. "Etude du contrôle spatio-temporel des MAP kinases, ERK1 et ERK2." Paris 11, 2003. http://www.theses.fr/2003PA112321.

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Les MAPKs p42/p44 (ERK) conduisent les signaux extracellulaires de la surface des cellules vers le noyau. Le transfert nucléaire de ERI est requis pour la conduction mitogénique. Nous avons montré que la navette nucléo-cytoplasmique de ERK est continuelle, même dans les cellules quiescentes. L'accumulation dans un compartiment sub-cellulaire dépend de protéines d'ancrage dont l'abondance, l'affinité et la localisation varient pendant la stimulation. Dans les cellules quiescentes, ERK est ancrée dans le cytoplasme par son activateur MEK. ERK s'accumule dans le noyau sous forme inactive au cours des stimulations prolongées. Ceci a été démontré avec des anticorps phospho-spécifiques, en corrélation avec l'état de phosphorylation d'une cible nucléaire de ERK. Les phosphatases responsables de l'inactivation nucléaire de ERK sont néo-synthétisées, spécifiques des tyrosines phosphorylées ou ont une double spécificité. Ces phosphatases se lient très spécifiquement à ERK puisque la micro-injection nucléaire de peptides possédant les sites d'appontage d'interacteurs de ERK, bloque la déphosphorylation nucléaire de ERK. Les phosphatases MKP1/2 sont candidats car induites par l'activation de la voie ERK et leur demie-vie est augmentée par phosphorylation via ERK. Afin de démontrer si MKP1/2 participent à l'ancrage nucléaire de ERK, plusieurs techniques ont été mises en œuvre pour diminuer l'expression des MKPs dans les cellules en culture. Méthodiquement nous avons participé à l'application au laboratoire de la nouvelle technique d'interférence ARN afin de diminue efficacement l'expression de protéines cibles telles que les isoformes de HIF-Proline-Hydroxylases et les MKPs
P42/p44 MAPKs (ERK) conduct extracellular signals from the cell surface to the nucleus to induce biological responses at the gene level. The nuclear transfer of ERKs is essential for mitogenic progression, since their forced cytoplasmic retention blocks the S-phase. Although the nucleo-cytoplasmic shuttling of ERK is permanent, the increased presence of ERK in a sub-cellular compartment is provided mainly anchoring proteins whose abundance, affinity and localization change during stimulation. Thus in quiescent cells, ERK is anchored in the cytoplasm by its activator MEK. The identity of ERK nuclear anchors of remains to be unveiled, however we showed that ERK accumulates in the nucleus in an inactive state during long-term stimulations. Phosphatases responsible for the nuclear inactivation of ERK neo-are synthesized, show a specificity towards phospho-tyrosine or double specificity and interact with specific docking sites. The probable candidates are the MKP1/2 phosphatases. These phosphatases are induced by activation of the ERK pathway and their half-life is increased upon ERK phosphorylation. In order to demonstrate if MKP1/2 participate in ERK nuclear anchoring, several techniques were tested to decrease MKP expression in cell cultures. With the new ARN interference technology, applied very effectively to decrease HIF1 alpha expression, the answer to this important question was to be provided
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Books on the topic "ERKs"

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Terrera, Guillermo Alfredo. El valle de los espíritus: Las luces cósmicas y la ciudad de Erks. Buenos Aires: Escuela Hermética Primordial de las Antípodas, 1987.

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van Tongeren, Paul, Paul Sars, Chris Bremmers, and Koen Boey, eds. Eros and Eris. Dordrecht: Springer Netherlands, 1992. http://dx.doi.org/10.1007/978-94-017-1464-8.

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Kuhan purtrihʹhā-yi tārīkh-i ʻakkāsī-i Īrān. Mashhad: Dānish Mūsavī, 2009.

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Beutin, Wolfgang. Eros, Eris: Beiträge zur Literaturpsychologie, zur Sprach- und Ideologiekritik. Stuttgart: H.-D. Heinz, 1994.

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Rectenwald, Michael. The eros of the baby boom eras and other poems. Bethesda, MD: Apogee Books, 1991.

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Eros et Eris: Mariages divins et mythe de succession chez Hésiode. Lyon: Presses universitaires de Lyon, 1985.

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Eros, anti-eros. San Francisco: City Lights Books, 1990.

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Elytēs, Odysseas. Eros, eros, eros: Selected and last poems. Port Townsend, Wash: Copper Canyon Press, 1998.

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Refik, Ahmet. Erku komite, erku ochir. Erevan: HH Gitutʻyunneri Azgayin Akademia, 1997.

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Khachʻatur, Gevorg. Eres aṛ eres: Banasteghtsutʻyunner. Erevan: Amaras, 1997.

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Book chapters on the topic "ERKs"

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Proske, Uwe, David L. Morgan, Tamara Hew-Butler, Kevin G. Keenan, Roger M. Enoka, Sebastian Sixt, Josef Niebauer, et al. "Extracellular Signal-Regulated Kinases (ERKs)." In Encyclopedia of Exercise Medicine in Health and Disease, 330. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_4217.

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Pinto, Adán, and Piero Crespo. "Analysis of ERKs’ Dimerization by Electrophoresis." In MAP Kinase Signaling Protocols, 335–42. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-795-2_20.

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Werz, Oliver, Eva Bürkert, Lutz Fischer, Dagmar Szellas, David Dishart, Bengt Samuelsson, Olof Rådmark, and Dieter Steinhilber. "5-Lipoxygenase Activation by Mapkapk-2 and Erks." In Advances in Experimental Medicine and Biology, 129–32. Boston, MA: Springer US, 2003. http://dx.doi.org/10.1007/978-1-4419-9194-2_26.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "ERK1/ERK2." In Encyclopedia of Signaling Molecules, 586–93. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_470.

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Robbins, David J., Erzhen Zhen, Mangeng Cheng, Colleen A. Vanderbilt, Douglas Ebert, Clark Garcia, Alphonsus Dang, and Melanie H. Cobb. "Extracellular Signal-Regulated Protein Kinases (ERKS) 1, 2, and 3." In The Cell Cycle, 61–66. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2421-2_7.

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Miki, Toru, Randa Hilal-Dandan, Laurence L. Brunton, Jean Sévigny, Kwok-On Lai, Nancy Y. Ip, Renping Zhou, et al. "Erk3 and Erk4." In Encyclopedia of Signaling Molecules, 593–96. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_542.

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Buscà, Roser, Jacques Pouysségur, and Philippe Lenormand. "ERK1 and ERK2." In Encyclopedia of Signaling Molecules, 1624–32. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_470.

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Mathien, Simon, Mathilde Soulez, Sonia Klinger, and Sylvain Meloche. "Erk3 and Erk4." In Encyclopedia of Signaling Molecules, 1632–38. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_542.

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Buscà, Roser, Jacques Pouysségur, and Philippe Lenormand. "ERK1 and ERK2." In Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_470-1.

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Mathien, Simon, Mathilde Soulez, Sonia Klinger, and Sylvain Meloche. "Erk3 and Erk4." In Encyclopedia of Signaling Molecules, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_542-1.

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Conference papers on the topic "ERKs"

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Cho, Yong Yeon. "Abstract 3127: Roles of ERKs-RSK2 signaling in human cancers." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-3127.

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Lee, Cheol-Jung, Hye Suk Lee, Hyung Won Ryu, Mee-Hyun Lee, Ji-Young Lee, Hyoung-Kyu Lee, Sei-Ryang Oh, and Yong-Yeon Cho. "Abstract A24: Targeting of ERKs with magnolin inhibits EGF-induced anchorage-independent cell transformation." In Abstracts: Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; Oct 27-30, 2013; National Harbor, MD. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1940-6215.prev-13-a24.

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Newton, Robert, Elizabeth M. King, Wei Gong, Christopher F. Rider, and Neil S. Holden. "Induction Of Mitogen-Activated Protein Kinase Phosphatase (MKP) 1 By Glucocorticoids Inhibits Extracellular-Regulated Kinases (ERKs) To Suppress GM-CSF Synthesis." 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.a4948.

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Mohamed, Islam, Ahmed Moahmed, Mennatallah Abdelkader, Alaaeldin Saleh, and Ala-Eddin Al-Moustafa. "Elaeagnus Angustifolia: a Promising Medicinal Plant for Cancer Theraby." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0124.

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Introduction: Elaeagnus angustifolia (EA) is a medicinal plant that has been used for centuries in treating many human diseases, in the Middle East, including fever, amoebic dysentery, gastrointestinal problems. However, the effect of EA plant extract on human cancer progression especially oral malignancy has not been investigated yet. Thus, first we examined the effect of EA flower extract on angiogenesis in ovo, and on selected parameters in human oral cancer cells. Materials and methods: Chorioallantoic membranes (CAMs) of chicken embryos at 3-7 days of incubation were used to assess the effect EAflower plant extract on angiogenesis. Meanwhile, cell proliferation, soft agar, cell cycle, cell invasion and cell wounding assays were performed to explore the outcome of EA plant extract on FaDu and SCC25 oral cancer cell lines. On the other hand, western blot analysis was carried out to evaluate E-cadherin and Erk1/Erk2 expression and activation, respectively, in FaDu and SCC25 under the effect of EA extract. Results: Our data show that EA extract inhibits cell proliferation and colony formation, in addition to the initiation of Scell cycle arrest and reductionof G1/G2 phases. In parallel, EA extract provokes differentiation to an epithelial phenotype “mesenchymal-epithelial transition: MET” which is the opposite of “epithelial-mesenchymal transition, EMT”: an important event in cell invasion and metastasis. Thus, EA extract causes a dramatic decrease in cell motility and invasion abilities of FaDu and SCC25 cancer cells in comparison with their controls. These changes are accompanied by an up-regulation of E-cadherin expression. The molecular pathway analysis of the EA flower extract reveals that it can inhibit the phosphorylation of Erk1/Erk2, which could be behind the inhibition of angiogenesis, the initiation of MET event and the overexpression of E-cadherin. Conclusions: Our findings indicate that EA plant extract can downgrade human oral cancer progression by the inhibition of angiogenesis and cell invasion via Erk1/Erk2 signaling pathways.
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Zavorotinskaya, Tatiana, Upasana Mehra, Yumin Dai, Michel Faure, Ken Crawford, Karen Yu, Jan Marie Cheng, et al. "Abstract LB-121: Dissecting MAPK pathway in BRAFmutmelanoma: Intricacies of ERK1 and ERK2." 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-lb-121.

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Monlish, Darlene A., and Jane E. Cavanaugh. "Abstract B94: The roles of ERK1/2 and ERK5 in age‐related breast cancer proliferation." 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-b94.

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Fisch, Avi, Jason Nikitczuk, Brian Weinberg, Juan Melli-Huber, Constantinos Mavroidis, and Charles Wampler. "Development of an Electro-Rheological Fluidic Actuator and Haptic Systems for Vehicular Instrument Control." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43514.

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Force-feedback methanisms have been designed to simplify and enahance the human-vehicle interface. The increase in secondary controls within vehicle cockpits has created a desire for a simpler, more efficient human-vehicle interface. Haptic system, or systems that interact with the operator’s sense of touch, can be used to consolidate various controls into fever, haptic feedback control devices, so that information can be transmitted to the operator and the operator can change control settings without requiring the driver’s visual attention. In this paper an Electro-Rheological Fluid (ERF) based actuator and mechanisms are presented that provide haptic feedback. ERSs are fluids that change their viscosity in response to an electric field. Using the electrically controlled rheological properties of ERFs, haptic devices have been developed that can resist human operator forces in a controlled and tunable fashion. The design of an ERF-based actuator and its application to a haptic knob and haptic joystick is presented. The analytical model is given, analyses are performed, and experimental systems and data are presented for the actuator. Conceptual methods for the application to the haptic devices are presented.
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Bartholomeusz, Chandra, Hitomi Saso, Ali Dadbin, Hiroko Masuda, Takahiro Kogawa, Steven Van Laere, François Bertucci, Gabriel N. Hortobagyi, and Naoto T. Ueno. "Abstract 858: ERK2 rather than ERK1 contributes to EMT and metastatic potential in triple-negative breast cancer." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-858.

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Bhatt, Akshita, Thomas Wright, Van Barnes, Suravi Chakrabarty, Patrick Flaherty, Matthew Burow, and Jane Cavanaugh. "Abstract 5042: Targeting the ERK5 and ERK1/2 pathways simultaneously induces mesenchymal to epithelial transition in TNBC." 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.am2020-5042.

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Shapiro, Jonathan S., Jonathan M. Smith, and David J. Farber. "EROS." In the seventeenth ACM symposium. New York, New York, USA: ACM Press, 1999. http://dx.doi.org/10.1145/319151.319163.

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Reports on the topic "ERKs"

1

Turner, M. S. The meaning of EROS/MACHO. Office of Scientific and Technical Information (OSTI), November 1993. http://dx.doi.org/10.2172/10104598.

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Shapiro, Jonathan S. Eros-based Confined Capability Client. Fort Belvoir, VA: Defense Technical Information Center, June 2006. http://dx.doi.org/10.21236/ada454977.

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Jolicoeur, J. Emergency Response Data System (ERDS) implementation. Office of Scientific and Technical Information (OSTI), April 1990. http://dx.doi.org/10.2172/7175236.

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Gondrom, T., R. Brandner, and U. Pordesch. Evidence Record Syntax (ERS). RFC Editor, August 2007. http://dx.doi.org/10.17487/rfc4998.

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Anderson, Richard M., Andrea E. Copping, and Frances B. Van Cleve. Environmental Risk Evaluation System (ERES) for Offshore Wind - Mock-Up of ERES, Fiscal Year 2010 Progress Report. Office of Scientific and Technical Information (OSTI), November 2010. http://dx.doi.org/10.2172/1009754.

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Symons, G. A. ERS, C-farm electrical distribution. Office of Scientific and Technical Information (OSTI), September 1996. http://dx.doi.org/10.2172/325640.

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Symons, G. A. ERS, AY-farm electrical distribution. Office of Scientific and Technical Information (OSTI), September 1996. http://dx.doi.org/10.2172/325641.

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Bellomy, J. R. ERS, C-Farm electrical distribution. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/434902.

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Muelaner, Jody Emlyn. Unsettled Issues in Electrical Demand for Automotive Electrification Pathways. SAE International, January 2021. http://dx.doi.org/10.4271/epr2021004.

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With the current state of automotive electrification, predicting which electrification pathway is likely to be the most economical over a 10- to 30-year outlook is wrought with uncertainty. The development of a range of technologies should continue, including statically charged battery electric vehicles (BEVs), fuel cell electric vehicles (FCEVs), plug-in hybrid electric vehicles (PHEVs), and EVs designed for a combination of plug-in and electric road system (ERS) supply. The most significant uncertainties are for the costs related to hydrogen supply, electrical supply, and battery life. This greatly is dependent on electrolyzers, fuel-cell costs, life spans and efficiencies, distribution and storage, and the price of renewable electricity. Green hydrogen will also be required as an industrial feedstock for difficult-to-decarbonize areas such as aviation and steel production, and for seasonal energy buffering in the grid. For ERSs, it is critical to understand how battery life will be affected by frequent cycling and the extent to which battery technology from hybrid vehicles can be applied. Unsettled Issues in Electrical Demand for Automotive Electrification Pathways dives into the most critical issues the mobility industry is facing.
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Gleckler, B. P. Environmental release summary (ERS) database CY 1997. Office of Scientific and Technical Information (OSTI), July 1998. http://dx.doi.org/10.2172/10148863.

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