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Academic literature on the topic 'PKM1'

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Published: 7 September 2023
Last updated: 7 July 2024

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Journal articles on the topic "PKM1"

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Li, Lin, Siyuan Cheng, and Xiuping Yu. "The expression of PKM1 and PKM2 in benign and cancerous prostatic tissues." Journal of Clinical Oncology 41, no. 16_suppl (June 1, 2023): e17058-e17058. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e17058.

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e17058 Background: Prostate cancer (PCa) is the most diagnosed cancers in American men. After androgen deprivation therapy (ADT) fails, there is an increase in the aggressive neuroendocrine (NE) phenotype. Currently, there is no effective treatment for NE prostate cancer (NEPC). The metabolic reprogramming, one of the cancer hallmarks, regulates PCa progression and therapy resistance. However, the energy metabolism in NEPC has not been well studied yet. Pyruvate kinase (PK), catalyzing the final step of glycolysis, has PKM1, PKM2, PKL and PKR four isoforms. PKL and PKR are expressed in the liver and erythrocytes, respectively. Alternative splicing of PKM results in two isoforms, PKM1 and PKM2, which are expressed in most tissues. In prostate adenocarcinoma, loss of PKM1 promotes PCa progression whereas loss of PKM2 suppresses tumor growth. However, the expression pattern of PKM1 and PKM2 in NEPCa remains largely unknown. Methods: Immunofluorescence (IF), immunohistochemistry (IHC), Western blot and RT-qPCR were conducted to examine the expression of PKM1 and PKM2 in both murine and human prostatic tissues. The bioinformatics analysis was done using the publicly available RNA-Seq data obtained from the cBioportal, the Cancer Genome Atlas (TCGA), and the Cancer Cell Line Encyclopedia websites (CCLE). Results: TRAMP is a widely used PCa mouse model. TRAMP mice develop prostatic intraepithelial neoplasia (PIN) and the tumors progress into NEPC following castration. We found that PKM1 expression was detected in normal prostate but not in the PIN lesions. In the TRAMP NEPC tumors, PKM1 expression was detected in the NE areas but not in the adjacent PIN lesions. Compared with the adjacent PIN, NEPC cells displayed lower PKM2 expression. Further, we examined the expression of PKM1 and PKM2 in human prostatic tissues including benign prostatic hyperplasia (BPH), low-grade adenocarcinomas (AdPCa), high-grade AdPCa, and NEPC. We found that in BPH, basal epithelial cells express both PKM1 and PKM2. In PCa, PKM1 was robustly expressed in the stromal cells but its expression was absent in the cancer cells in majority of the specimens examined except a small number of samples where low level of PKM1 was detected in the cancer cells. However, PKM1 expression was detected in 9 out of 12 NEPC samples and colocalized with NE marker chromogranin A. This co-expression was also detected in the NE cells scattered on the prostate adenocarcinoma tissues. As for PKM2, its expression was detected in all the samples examined. However, different from previous report, PKM2 expression levels did not correlate with cancer grade in this cohort. Conclusions: PKM1 is expressed in the basal epithelial cells of benign prostates, a small subset of prostate adenocarcinomas, and 75% NEPC tumors. PKM2 is expressed throughout prostate development, in both benign and cancerous prostate. However, PKM2 expression does not correlate with tumor grade.
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Kim, Seong Ho, Ji Hun Wi, HyeRan Gwak, Eun Gyeong Yang, and So Yeon Kim. "Single-Cell FISH Analysis Reveals Distinct Shifts in PKM Isoform Populations during Drug Resistance Acquisition." Biomolecules 12, no. 8 (August 6, 2022): 1082. http://dx.doi.org/10.3390/biom12081082.

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The Warburg effect, i.e., the utilization of glycolysis under aerobic conditions, is recognized as a survival advantage of cancer cells. However, how the glycolytic activity is affected during drug resistance acquisition has not been explored at single-cell resolution. Because the relative ratio of the splicing isoform of pyruvate kinase M (PKM), PKM2/PKM1, can be used to estimate glycolytic activity, we utilized a single-molecule fluorescence in situ hybridization (SM-FISH) method to simultaneously quantify the mRNA levels of PKM1 and PKM2. Treatment of HCT116 cells with gefitinib (GE) resulted in two distinct populations of cells. However, as cells developed GE resistance, the GE-sensitive population with reduced PKM2 expression disappeared, and GE-resistant cells (Res) demonstrated enhanced PKM1 expression and a tightly regulated PKM2/PKM1 ratio. Our data suggest that maintaining an appropriate PKM2 level is important for cell survival upon GE treatment, whereas increased PKM1 expression becomes crucial in GE Res. This approach demonstrates the importance of single-cell-based analysis for our understanding of cancer cell metabolic responses to drugs, which could aid in the design of treatment strategies for drug-resistant cancers.
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Buneeva, Olga, Arthur Kopylov, Oksana Gnedenko, Marina Medvedeva, Alexander Veselovsky, Alexis Ivanov, Victor Zgoda, and Alexei Medvedev. "Proteomic Profiling of Mouse Brain Pyruvate Kinase Binding Proteins: A Hint for Moonlighting Functions of PKM1?" International Journal of Molecular Sciences 24, no. 8 (April 21, 2023): 7634. http://dx.doi.org/10.3390/ijms24087634.

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Affinity-based proteomic profiling is widely used for the identification of proteins involved in the formation of various interactomes. Since protein–protein interactions (PPIs) reflect the role of particular proteins in the cell, identification of interaction partners for a protein of interest can reveal its function. The latter is especially important for the characterization of multifunctional proteins, which can play different roles in the cell. Pyruvate kinase (PK), a classical glycolytic enzyme catalyzing the last step of glycolysis, exists in four isoforms: PKM1, PKM2, PKL, and PKR. The enzyme isoform expressed in actively dividing cells, PKM2, exhibits many moonlighting (noncanonical) functions. In contrast to PKM2, PKM1, predominantly expressed in adult differentiated tissues, lacks well-documented moonlighting functions. However, certain evidence exists that it can also perform some functions unrelated to glycolysis. In order to evaluate protein partners, bound to PKM1, in this study we have combined affinity-based separation of mouse brain proteins with mass spectrometry identification. The highly purified PKM1 and a 32-mer synthetic peptide (PK peptide), sharing high sequence homology with the interface contact region of all PK isoforms, were used as the affinity ligands. This proteomic profiling resulted in the identification of specific and common proteins bound to both affinity ligands. Quantitative affinity binding to the affinity ligands of selected identified proteins was validated using a surface plasmon resonance (SPR) biosensor. Bioinformatic analysis has shown that the identified proteins, bound to both full-length PKM1 and the PK peptide, form a protein network (interactome). Some of these interactions are relevant for the moonlighting functions of PKM1. The proteomic dataset is available via ProteomeXchange with the identifier PXD041321.
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Verbrugge, Sander A. J., Sebastian Gehlert, Lian E. M. Stadhouders, Daniel Jacko, Thorben Aussieker, Gerard M. J. de Wit, Ilse S. P. Vogel, et al. "PKM2 Determines Myofiber Hypertrophy In Vitro and Increases in Response to Resistance Exercise in Human Skeletal Muscle." International Journal of Molecular Sciences 21, no. 19 (September 25, 2020): 7062. http://dx.doi.org/10.3390/ijms21197062.

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Nearly 100 years ago, Otto Warburg investigated the metabolism of growing tissues and discovered that tumors reprogram their metabolism. It is poorly understood whether and how hypertrophying muscle, another growing tissue, reprograms its metabolism too. Here, we studied pyruvate kinase muscle (PKM), which can be spliced into two isoforms (PKM1, PKM2). This is of interest, because PKM2 redirects glycolytic flux towards biosynthetic pathways, which might contribute to muscle hypertrophy too. We first investigated whether resistance exercise changes PKM isoform expression in growing human skeletal muscle and found that PKM2 abundance increases after six weeks of resistance training, whereas PKM1 decreases. Second, we determined that Pkm2 expression is higher in fast compared to slow fiber types in rat skeletal muscle. Third, by inducing hypertrophy in differentiated C2C12 cells and by selectively silencing Pkm1 and/or Pkm2 with siRNA, we found that PKM2 limits myotube growth. We conclude that PKM2 contributes to hypertrophy in C2C12 myotubes and indicates a changed metabolic environment within hypertrophying human skeletal muscle fibers. PKM2 is preferentially expressed in fast muscle fibers and may partly contribute to the increased potential for hypertrophy in fast fibers.
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Kurihara-Shimomura, Miyako, Tomonori Sasahira, Chie Nakashima, Hiroki Kuniyasu, Hiroyuki Shimomura, and Tadaaki Kirita. "The Multifarious Functions of Pyruvate Kinase M2 in Oral Cancer Cells." International Journal of Molecular Sciences 19, no. 10 (September 25, 2018): 2907. http://dx.doi.org/10.3390/ijms19102907.

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Head and neck cancers, including oral squamous cell carcinoma (OSCC), are the sixth most common malignancies worldwide. OSCC frequently leads to oral dysfunction, which worsens a patient’s quality of life. Moreover, its prognosis remains poor. Unlike normal cells, tumor cells preferentially metabolize glucose by aerobic glycolysis. Pyruvate kinase (PK) catalyzes the final step in glycolysis, and the transition from PKM1 to PKM2 is observed in many cancer cells. However, little is known about PKM expression and function in OSCC. In this study, we investigated the expression of PKM in OSCC specimens and performed a functional analysis of human OSCC cells. We found that the PKM2/PKM1 ratio was higher in OSCC cells than in adjacent normal mucosal cells and in samples obtained from dysplasia patients. Furthermore, PKM2 expression was strongly correlated with OSCC tumor progression on immunohistochemistry. PKM2 expression was higher during cell growth, invasion, and apoptosis in HSC3 cells, which show a high energy flow and whose metabolism depends on aerobic glycolysis and oxidative phosphorylation. PKM2 expression was also associated with the production of reactive oxygen species (ROS) and integration of glutamine into lactate. Our results suggested that PKM2 has a variety of tumor progressive functions in OSCC cells.
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Li, Qinfeng, Chao Li, Abdallah Elnwasany, Gaurav Sharma, Yu A. An, Guangyu Zhang, Waleed M. Elhelaly, et al. "PKM1 Exerts Critical Roles in Cardiac Remodeling Under Pressure Overload in the Heart." Circulation 144, no. 9 (August 31, 2021): 712–27. http://dx.doi.org/10.1161/circulationaha.121.054885.

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Background: Metabolic remodeling precedes most alterations during cardiac hypertrophic growth under hemodynamic stress. The elevation of glucose utilization has been recognized as a hallmark of metabolic remodeling. However, its role in cardiac hypertrophic growth and heart failure in response to pressure overload remains to be fully illustrated. Here, we aimed to dissect the role of cardiac PKM1 (pyruvate kinase muscle isozyme 1) in glucose metabolic regulation and cardiac response under pressure overload. Methods: Cardiac-specific deletion of PKM1 was achieved by crossing the floxed PKM1 mouse model with the cardiomyocyte-specific Cre transgenic mouse. PKM1 transgenic mice were generated under the control of tetracycline response elements, and cardiac-specific overexpression of PKM1 was induced by doxycycline administration in adult mice. Pressure overload was triggered by transverse aortic constriction. Primary neonatal rat ventricular myocytes were used to dissect molecular mechanisms. Moreover, metabolomics and nuclear magnetic resonance spectroscopy analyses were conducted to determine cardiac metabolic flux in response to pressure overload. Results: We found that PKM1 expression is reduced in failing human and mouse hearts. It is important to note that cardiomyocyte-specific deletion of PKM1 exacerbates cardiac dysfunction and fibrosis in response to pressure overload. Inducible overexpression of PKM1 in cardiomyocytes protects the heart against transverse aortic constriction–induced cardiomyopathy and heart failure. At the mechanistic level, PKM1 is required for the augmentation of glycolytic flux, mitochondrial respiration, and ATP production under pressure overload. Furthermore, deficiency of PKM1 causes a defect in cardiomyocyte growth and a decrease in pyruvate dehydrogenase complex activity at both in vitro and in vivo levels. Conclusions: These findings suggest that PKM1 plays an essential role in maintaining a homeostatic response in the heart under hemodynamic stress.
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Kuranaga, Yuki, Nobuhiko Sugito, Haruka Shinohara, Takuya Tsujino, Kohei Taniguchi, Kazumasa Komura, Yuko Ito, Tomoyoshi Soga, and Yukihiro Akao. "SRSF3, a Splicer of the PKM Gene, Regulates Cell Growth and Maintenance of Cancer-Specific Energy Metabolism in Colon Cancer Cells." International Journal of Molecular Sciences 19, no. 10 (October 2, 2018): 3012. http://dx.doi.org/10.3390/ijms19103012.

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Serine and arginine rich splicing factor 3 (SRSF3), an SR-rich family protein, has an oncogenic function in various kinds of cancer. However, the detailed mechanism of the function had not been previously clarified. Here, we showed that the SRSF3 splicer regulated the expression profile of the pyruvate kinase, which is one of the rate-limiting enzymes in glycolysis. Most cancer cells express pyruvate kinase muscle 2 (PKM2) dominantly to maintain a glycolysis-dominant energy metabolism. Overexpression of SRSF3, as well as that of another splicer, polypyrimidine tract binding protein 1 (PTBP1) and heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1), in clinical cancer samples supported the notion that these proteins decreased the Pyruvate kinase muscle 1 (PKM1)/PKM2 ratio, which positively contributed to a glycolysis-dominant metabolism. The silencing of SRSF3 in human colon cancer cells induced a marked growth inhibition in both in vitro and in vivo experiments and caused an increase in the PKM1/PKM2 ratio, thus resulting in a metabolic shift from glycolysis to oxidative phosphorylation. At the same time, the silenced cells were induced to undergo autophagy. SRSF3 contributed to PKM mRNA splicing by co-operating with PTBP1 and hnRNPA1, which was validated by the results of RNP immunoprecipitation (RIP) and immunoprecipitation (IP) experiments. These findings altogether indicated that SRSF3 as a PKM splicer played a positive role in cancer-specific energy metabolism.
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Grant, Melissa M. "Pyruvate Kinase, Inflammation and Periodontal Disease." Pathogens 10, no. 7 (June 22, 2021): 784. http://dx.doi.org/10.3390/pathogens10070784.

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Pyruvate kinase (PK) is the final and rate-limiting enzyme in glycolysis. It has four isoforms PKM1, PKM2, PKL and PKR. PK can form homo tetramers, dimers or monomers. The tetrameric form has the most catalytic activity; however, the dimeric form has non-canonical functions that contribute to the inflammatory response, wound healing and cellular crosstalk. This brief review explores these functions and speculates on their role in periodontal disease.
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Williams, Allison Lesher, Vedbar Khadka, Mingxin Tang, Abigail Avelar, Kathryn J. Schunke, Mark Menor, and Ralph V. Shohet. "HIF1 mediates a switch in pyruvate kinase isoforms after myocardial infarction." Physiological Genomics 50, no. 7 (July 1, 2018): 479–94. http://dx.doi.org/10.1152/physiolgenomics.00130.2017.

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Alternative splicing of RNA is an underexplored area of transcriptional response. We expect that early changes in alternatively spliced genes may be important for responses to cardiac injury. Hypoxia inducible factor 1 (HIF1) is a key transcription factor that rapidly responds to loss of oxygen through alteration of metabolism and angiogenesis. The goal of this study was to investigate the transcriptional response after myocardial infarction (MI) and to identify novel, hypoxia-driven changes, including alternative splicing. After ligation of the left anterior descending artery in mice, we observed an abrupt loss of cardiac contractility and upregulation of hypoxic signaling. We then performed RNA sequencing on ischemic heart tissue 1 and 3 days after infarct to assess early transcriptional changes and identified 89 transcripts with altered splicing. Of particular interest was the switch in Pkm isoform expression (pyruvate kinase, muscle). The usually predominant Pkm1 isoform was less abundant in ischemic hearts, while Pkm2 and associated splicing factors (hnRNPA1, hnRNPA2B1, Ptbp1) rapidly increased. Despite increased Pkm2 expression, total pyruvate kinase activity remained reduced in ischemic myocardial tissue. We also demonstrated HIF1 binding to PKM by chromatin immunoprecipitation, indicating a direct role for HIF1 in mediating this isoform switch. Our study provides a new, detailed characterization of the early transcriptome after MI. From this analysis, we identified an HIF1-mediated alternative splicing event in the PKM gene. Pkm1 and Pkm2 play distinct roles in glycolytic metabolism and the upregulation of Pkm2 is likely to have important consequences for ATP synthesis in infarcted cardiac muscle.
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Lee, Yuumi, Yuko Ito, Kohei Taniguchi, Takashi Nuri, SangWoong Lee, and Koichi Ueda. "Experimental Study of Warburg Effect in Keloid Nodules: Implication for Downregulation of miR-133b." Plastic and Reconstructive Surgery - Global Open 11, no. 8 (August 2023): e5202. http://dx.doi.org/10.1097/gox.0000000000005202.

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Background: A keloid is composed of several nodules, which are divided into two zones: the central zone (CZ; a hypoxic region) and the marginal zone (MZ; a normoxic region). Keloid nodules play a key role in energy metabolic activity for continuous growth by increasing in number and total area. In this study, we aimed to investigate the roles of the zones in the execution of the Warburg effect and identify which microRNAs regulate this phenomenon in keloid tissue. Methods: Eleven keloids from patients were used. Using immunohistochemical analysis, 179 nodules were randomly chosen from these keloids to identify glycolytic enzymes, autophagic markers, pyruvate kinase M (PKM) 1/2, and polypyrimidine tract binding protein 1 (PTBP1). Western blot and qRT-PCR tests were also performed for PKM, PTBP1, and microRNAs (miR-133b and miR-200b, c). Results: Immunohistochemical analysis showed that the expression of the autophagic (LC3, p62) and glycolytic (GLUT1, HK2) were significantly higher in the CZ than in the MZ. PKM2 expression was significantly higher than PKM1 expression in keloid nodules. Furthermore, PKM2 expression was higher in the CZ than in the MZ. However, PKM1 and PTBP1 expression levels were higher in the MZ than in the CZ. The qRT-PCR analysis showed that miR-133b-3p was moderately downregulated in the keloids compared with its expression in the normal skin tissue. Conclusions: The Warburg effect occurred individually in nodules. The MZ presented PKM2-positive fibroblasts produced by activated PTBP1. In the CZ, PKM2-positive fibroblasts produced lactate. MiR-133b-3p was predicted to control the Warburg effect in keloids.
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Dissertations / Theses on the topic "PKM1"

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Hasan, Diya [Verfasser]. "Hypoxic regulation and selective silencing of pyruvate kinase isoforms PKM1 and PKM2 by siRNA / Diya Hasan." Gießen : Universitätsbibliothek, 2012. http://d-nb.info/1064024580/34.

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Delobelle, Quentin. "Simulations de dynamique moléculaire à haute résolution des isoformes 1 et 2 de la pyruvate kinase musculaire." Electronic Thesis or Diss., Sorbonne université, 2024. http://www.theses.fr/2024SORUS067.

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Le métabolisme glycolytique joue un rôle essentiel dans les processus physiologiques normaux et dans la croissance des cellules cancéreuses. Les isoformes 1 et 2 de la pyruvate kinase musculaire, appelées PKM1/2, sont des protéines cruciales qui régulent ce métabolisme. La caractérisation de la dynamique structurelle de ces biomolécules est donc importante pour développer de nouveaux médicaments dirigés contre les formes exprimées dans les cellules tumorales. Pour ce faire, nous avons réalisé des simulations de dynamique moléculaire (DM) de ces deux protéines à haute résolution, en nous appuyant sur des techniques d'échantillonnage adaptatif couplées au champ de forces polarisable AMOEBA afin de comprendre la flexibilité conformationnelle de l'enzyme dans ses différents états d'oligomérisation. Nous proposons une analyse structurale à haute résolution pour PKM2 et apportons de nouvelles données structurales pour PKM1. En effet, nous étudions le processus d'oligomérisation de l'enzyme PKM2 (du monomère au tétramère) et nous sommes notamment attachés à analyser la structuration de sites structuraux clés, notamment le site actif et la poche de fixation du Fructose Biphosphate (FBP), un inducteur conformationnel physiologique. Nous montrons également que la fixation du TEPP-46, un activateur pharmacologique de PKM2, induit des modifications structurales très proches de celles induites par la fixation du FBP, bien que les domaines d'interaction soient distincts. Enfin, nous décrivons la première simulation DM à haute résolution de la forme active de PKM1, qui présente de fortes similitudes structurelles avec la forme tétramérique de PKM2 liée au FBP. Ces résultats fournissent de nouvelles informations sur la dynamique structurelle et la structuration des sites clés pendant l'oligomérisation de PKM2, qui pourraient s'avérer cruciales pour la découverte de nouvelles molécules actives
In both normal physiological processes and cancer cell growth, glycolytic metabolism plays a pivotal role. The Pyruvate Kinase Muscle isoforms 1 and 2, denoted PKM1/2, are crucial proteins that regulate this metabolism. Characterizing the structural dynamics of these biomolecules is thus imperative in order to develop new drugs targeting PMK enzymes in tumor cells. To address this, we performed extensive molecular dynamics (MD) simulations of these two proteins at high-resolution. To do so, we employed adaptive sampling techniques coupled with the polarizable AMOEBA force field to understand the conformational flexibility of the enzyme. We propose a high-resolution structural analysis for PKM2 and introduce structural insights for PKM1. We are studying the oligomerization process of the PKM2 enzyme (from monomer to tetramer) while focusing on the structuring of key structural sites, in particular the active site and the binding pocket for Fructose Biphosphate (FBP), a physiological conformational inducer. We also provide data explaining the impact of TEPP-46, a pharmacological activator, on PKM2 structure and their similarity with PKM2 bound to FBP in conformity to biological results. Finally, we propose the first high-resolution MD simulation of the biological active PKM1 and reveal important structural information in link with strong structural similarities with PKM2 when linked to FBP. These findings provide new insights concerning the structural dynamics and key sites structuration during PKM2 oligomerization that could be critical in drug discovery
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Dayton, Talya Lucia. "Examining the roles of the pyruvate kinase isoforms, PKMI1 and PKM2, in systemic metabolism and tumor development." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/104176.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2016.
Cataloged from PDF version of thesis. Vita.
Includes bibliographical references.
Alternative splicing of the Pkm gene product generates the PKM1 and PKM2 isoforms of pyruvate kinase, and PKM2 expression is closely linked to embryogenesis, tissue regeneration, and cancer. PKM1 expression, on the other hand, is restricted mostly to skeletal muscle, heart, and brain. To interrogate the functional requirement for PKM1 or PKM2 during development and tissue homeostasis, we generated germline PKM1 (Pkm1-/-) or PKM2 null mice (Pkm2-/-). Unexpectedly, despite being the primary isoform expressed in most wild-type adult tissues, we found that Pkm2' mice are viable and fertile. Thus, PKM2 is not required for embryonic or postnatal development. Loss of PKM2 leads to compensatory expression of PKM1 in the tissues that normally express PKM2. We found that Pkm1-/- mice are also viable and fertile. Thus, neither PKM isoform is required for embryonic or postnatal development. In Pkm1-/- mice, loss of PKM1 leads to compensatory expression of PKM2 in the tissues that normally express PKM1. Aside from distinct changes in the plasma metabolite profiles of Pkm1-/- mice compared to wild-type (WT) mice, germline loss of PKMI appears to be of little phenotypic consequence. In contrast, PKM2 loss leads to a striking phenotype: spontaneous development of hepatocellular carcinoma (HCC) with high penetrance that is accompanied by progressive changes in systemic metabolism characterized by altered systemic glucose homeostasis, inflammation, and hepatic steatosis. Therefore, in addition to its role in cancer metabolism, PKM2 plays a role in controlling systemic metabolic homeostasis and inflammation, thereby preventing HCC by a non-cell-autonomous mechanism. To interrogate the cell-autonomous functional requirement for PKM2 during tumor initiation, we used a conditional Pkm2 allele (Pkm2f/) to abolish PKM2 expression in the context of two Kras driven mouse models - for lung adenocarcinoma and soft-tissue sarcoma (STS). In the sarcoma model, where the presumed tumor cell-of-origin expresses PKM1, deletion of PKM2 led to delayed tumor formation. In contrast, in the lung cancer model the presumed tumor cell-of-origin expresses PKM2 and deletion of PKM2 had no effect on tumor latency or tumor area. PKM2-null sarcomas expressed PKM1 and contained a high number of infiltrating PKM2+ stromal cells. Metabolite analysis of sarcoma cell lines generated from PKM2-null and wild-type tumors revealed metabolic changes in the PKM2-null tumors. These results argue that the consequences of PKM2 loss during tumor initiation depend on the tumor type and that the requirement for PKM2 expression can be overcome through metabolic adaptation. Taken together, the work presented in this thesis provides key insights into the pleiotropic roles played by PKM1 and PKM2 in the contexts of normal and malignant proliferation and in tumor and systemic metabolism. Our findings contribute to a more complete understanding of the distinct cell-intrinsic and cell-extrinsic roles of PKM isoform expression in the context of cancer, and may potentially inform strategies that target metabolism for the treatment of cancer.
by Talya Lucia Dayton.
Ph. D.
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Torbett, Neil Edward. "Cellular roles of PKN1." Thesis, University College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406323.

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Kuntz, Ashley L. "The Role of PKS1 in Root Phototropism." Miami University Honors Theses / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=muhonors1177531764.

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Kappe, Eva Christina. "Molekularbiologische Untersuchungen am PKD1-Gen der Katze." Giessen : VVB Laufersweiler, 2008. http://d-nb.info/990148246/04.

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Damasceno, Luis Eduardo Alves. "Envolvimento da enzima Piruvato Quinase M2 (PKM2) na diferenciação de linfócitos Th17 e patogênese da encefalomielite autoimune experimental." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17147/tde-23042018-150809/.

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Nos últimos anos, um importante destaque tem sido dado aos linfócitos Th17 para o desenvolvimento e manutenção da inflamação associada à autoimunidade. A esclerose múltipla é uma doença autoimune desmielinizante do SNC, cuja patogênese está associada à resposta do padrão Th17. Evidências têm demonstrado que estas células são submetidas a uma reprogramação metabólica após serem ativadas, sendo essa adequação essencial para sua completa diferenciação e aquisição de funções efetoras. A enzima Piruvato Quinase M2 (PKM2) participa da etapa final da glicólise convertendo fosfoenolpiruvato em piruvato. Estudos recentes demonstraram que a fosforilação de PKM2 a torna capaz de translocar para o núcleo, onde adquire um papel no controle da expressão gênica. Nesse sentido, o objetivo deste estudo foi avaliar o envolvimento da PKM2 na diferenciação de linfócitos Th17, bem como sua participação no desenvolvimento da encefalomielite autoimune experimental (EAE), um modelo animal de esclerose múltipla. Observou-se que durante o processo de diferenciação, os linfócitos Th17 aumentam a expressão gênica de PKM2 bem como a sua forma fosforilada (Y105). De forma interessante, tanto a inibição farmacológica como a deleção gênica da PKM2 especificamente em linfócitos T promoveram uma redução da diferenciação e expansão da subpopulação Th17, que foi associada com diminuição na expressão de moléculas efetoras e fatores de transcrição chave para o estabelecimento do fenótipo Th17. Em um contexto de resposta autoimune, notou-se que PKM2 é superexpressa nos órgãos linfóides periféricos e sistema nervoso central de animais com EAE, sendo correlacionada com o infiltrado de células inflamatórias. Corroborando com os dados in vitro, a deficiência de PKM2 em linfócitos T promoveu redução dos sinais clínicos da EAE, acompanhada de baixa frequência de linfócitos Th17 e menor expressão de moléculas inflamatórias do perfil Th17. Adicionalmente, o tratamento farmacológico com o inibidor da PKM2 atenuou a progressão e gravidade da EAE. Portanto, esses achados implicam um importante papel para PKM2 em doenças autoimunes por regular o desenvolvimento e função de linfócitos Th17.
Over the past few years, an important highlight has been given to Th17 lymphocytes for the development and maintenance of autoimmunity-associated inflammation. Multiple sclerosis is a CNS demyelinating autoimmune disease that is associated to Th17-mediated response. Some evidences have demonstrated that those cells undergo metabolic reprogramming after being activated, which is essential for their complete differentiation and acquisition of effector functions. The enzyme Pyruvate kinase M2 (PKM2) participates at the final step of glycolysis by converting phosphoenolpyruvate into pyruvate. Recent studies have demonstrated that PKM2 phosphorylation allows its translocation into the nucleus, where it plays a role in controlling gene expression. Thus, the aim of this study was to evaluate the involvement of PKM2 in Th17 lymphocytes differentiation, as well as its role in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. It was perceived that during differentiation process, Th17 lymphocytes increase PKM2 gene expression, and also its phosphorylated form (Y105). Interestingly, both pharmacological inhibition and T-lymphocyte-specific PKM2 gene deletion promoted a reduction in differentiation and expansion of Th17 subpopulation, being associated to diminished expression of effector molecules and key transcription factors for the establishment of Th17 phenotype. In the context of an autoimmune response, it was noticed that PKM2 is overexpressed in peripheral lymphoid organs and central nervous system of EAE-bearing mice, which was correlated with the inflammatory cell infiltration. Corroborating with in vitro data, the deficiency of PKM2 in T lymphocytes led to a reduction of EAE clinical score along with low Th17 frequency and diminished expression of Th17-related inflammatory molecules. Additionally, pharmacological treatment with the PKM2 inhibitor attenuated EAE progression and severity. Therefore, these findings imply an important role for PKM2 in autoimmune diseases by regulating the development and function of Th17 lymphocytes.
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Kunze, Markus. "Abbau von Chlorbenzol in Pseudomonas putida GJ31: das Plasmid pKW1." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=967443148.

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Hughes, Jim. "Comparative analysis of the PKD1 gene and protein, polycystin-1." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300891.

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Sneddon, Tam Paterson. "The characterisation of genes (HG) homologous to the PKD1 locus." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365319.

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Books on the topic "PKM1"

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Ceha, Rakhmat. Proceeding seminar hasil penelitian dan PKM 2010. Edited by Universitas Islam Bandung. [Bandung]: Pusat Penerbitan Universitas (P2U), LPPM Unisba, 2011.

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Adam, Ramlah. Dr. Burhanuddin Al-Helmy: Kajian mengenai kegiatannya dalam PKMM, 1946-1948. Kuala Lumpur: Akademi Pengajian Melayu, 1993.

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Salleh, Abdul Majid Mat. Memoir Abdul Majid Salleh dalam PKMM dan kesatuan buruh: Dengan puisi perjuangan. Bangi: Penerbit Universiti Kebangsaan Malaysia, 2004.

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Terasing, Indonesia Direktorat Bina Masyarakat. Laporan hasil pendataan proyek PKMT lokasi Kandis, Kecamatan Kandis, Kabupaten Bengkalis, Propinsi Riau. [Jakarta]: Direktorat Bina Masyarakat Terasing, Direktorat Jenderal Bina Kesejahteraan Sosial, Departemen Sosial RI, 1985.

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Indonesia. Direktorat Bina Masyarakat Terasing. Laporan hasil pendataan proyek PKMT lokasi Nagerawe, Kabupaten Ngada, Propinsi Nusa Tenggara Timur. [Jakarta]: Direktorat Bina Masyarakat Terasing, Direktorat Jenderal Bina Kesejahteraan Sosial, Departemen Sosial RI, 1989.

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Indonesia. Direktorat Bina Masyarakat Terasing., ed. Laporan hasil pendataan proyek PKMT lokasi Bonekancitala, Kecamatan Kabawo, Kabupaten Muna, Propinsi Sulawesi Tenggara. [Jakarta]: Direktorat Bina Masyarakat Terasing, Direktorat Jenderal Bina Kesejahteraan Sosial, Departemen Sosial RI, 1991.

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Indonesia. Direktorat Bina Masyarakat Terasing., ed. Laporan hasil pendataan proyek PKMT lokasi Tunang, Kecamatan Mempawah Hulu, Kabupaten Pontianak, Propinsi Kalimantan Barat. [Jakarta]: Direktorat Bina Masyarakat Terasing, Direktorat Jenderal Bina Kesejahteraan Sosial, Departemen Sosial RI, 1987.

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Indonesia. Direktorat Bina Masyarakat Terasing. Laporan hasil pendataan proyek PKMT lokasi Gunung Mesir, Kecamatan Talo, Kabupaten Bengkulu Selatan, Propinsi Bengkulu. [Jakarta]: Direktorat Bina Masyarakat Terasing, Direktorat Jenderal Bina Kesejahteraan Sosial, Departemen Sosial RI, 1989.

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Indonesia. Direktorat Bina Masyarakat Terasing. Laporan hasil pendataan proyek PKMT lokasi Teras, Kecamatan Tanjung Palas, Kabupaten Bulungan, Propinsi Kalimantan Timur. [Jakarta]: Direktorat Bina Masyarakat Terasing, Direktorat Jenderal Bina Kesejahteraan Sosial, Departemen Sosial RI, 1989.

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Laporan hasil pendataan proyek PKMT lokasi Sarausan, Kecamatan Siberut Selatan, Kabupaten Padang Pariaman, Propinsi Sumatera Barat. [Jakarta]: Direktorat Bina Masyarakat Terasing, Direktorat Jenderal Bina Kesejahteraan Sosial, Departemen Sosial RI, 1987.

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Book chapters on the topic "PKM1"

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "PKM (Hamster)." In Encyclopedia of Signaling Molecules, 1435. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101056.

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Harris, P. C. "The TSC2/PKD1 Contiguous Gene Syndrome." In Hereditary Kidney Diseases, 76–82. Basel: KARGER, 1997. http://dx.doi.org/10.1159/000059872.

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "PKD (isoforms: PKD1/PKCμ, PKD2, PKD3/PKCν)." In Encyclopedia of Signaling Molecules, 1434. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101053.

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Koren, Y. "Will PKM be Adopted by Industry?" In Parallel Kinematic Machines, 271–73. London: Springer London, 1999. http://dx.doi.org/10.1007/978-1-4471-0885-6_18.

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Heisel, U., J. O. Hestermann, H. Böhler, and N. Plischke. "Verfahren der Positionsmessung und Kalibrierung bei PKM." In FTK 2000, 368–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-59804-3_22.

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Freund, Kerstin, and Steffen Rupp. "PKMS – das Potential elektronischer Dokumentation zur Optimierung der Wertschöpfung nutzen." In Digitale Transformation von Dienstleistungen im Gesundheitswesen III, 287–305. Wiesbaden: Springer Fachmedien Wiesbaden, 2017. http://dx.doi.org/10.1007/978-3-658-13642-0_18.

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Nigatu, Hassen, and Yimesker Yihun. "Algebraic Insight on the Concomitant Motion of 3RPS and 3PRS PKMs." In Proceedings of the 2020 USCToMM Symposium on Mechanical Systems and Robotics, 242–52. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-43929-3_22.

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Bröker, Daniel, and Alexander Steinbüchel. "Megaplasmid pKB1 of the Rubber-Degrading Bacterium Gordonia westfalica Strain Kb1." In Microbial Megaplasmids, 297–309. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-85467-8_14.

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Yasuda, Hiroki, and Hideyuki Mukai. "Electrophysiological Technique for Analysis of Synaptic Function of PKN1 in Hippocampus." In Protein Kinase Technologies, 349–60. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-824-5_19.

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Shah, Ajit K. "Pharmacokinetic Modeling Program (PKMP): A Software for PK/PD Data Analysis." In Pharmacokinetics and Pharmacodynamics of Nanoparticulate Drug Delivery Systems, 101–39. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-83395-4_7.

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Conference papers on the topic "PKM1"

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"From Ignorance Map to Informing PKM4E Framework: Personal Knowledge Management for Empowerment." In InSITE 2018: Informing Science + IT Education Conferences: La Verne California. Informing Science Institute, 2018. http://dx.doi.org/10.28945/3984.

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Aim/Purpose: [This Proceedings paper was revised and published in the 2018 issue of the journal Issues in Informing Science and Information Technology, Volume 15] The proposed Personal Knowledge Management (PKM) for Empowerment (PKM4E) Framework expands on the notions of the Ignorance Map and Matrix for further supporting the educational concept of a PKM system-in-progress. Background: The accelerating information abundance is depleting the very attention our cognitive capabilities are able to master, one key cause of individual and collective opportunity divides. Support is urgently needed to benefit Knowledge Workers independent of space (developed/developing countries), time (study or career phase), discipline (natural or social science), or role (student, professional, leader). Methodology: The Design Science Research (DSR) project introducing the novel PKM System (PKMS) aims to support a scenario of a ‘Decentralizing KM Revolution’ giving more power and autonomy to individuals and self-organized groups. Contribution: The portrayal of potential better solutions cannot be accommodated by one-dimensional linear text alone but necessitates the utilization of visuals, charts, and blueprints for the concept as well as the use of colors, icons, and catchy acronyms to successfully inform a diverse portfolio of audiences and potential beneficiaries. Findings: see Recommendation for Researchers Recommendations for Practitioners: The PKM4E learning cycles and workflows apply ‘cumulative synthesis’, a concept which convincingly couples the activities of researchers and entrepreneurs, and assists users to advance their capability endowments via applied learning. Recommendation for Researchers: In substituting document-centric with meme-based knowledge bases, the PKMS approach merges distinctive voluntarily shared knowledge objects/assets of diverse disciplines into a single unified digital knowledge repository and provides the means for advancing current metrics and reputation systems. Impact on Society: The PKMS features provide the means to tackle the widening opportunity divides by affording knowledge workers with continuous life-long support from trainee, student, novice, or mentee towards professional, expert, mentor, or leader. Future Research: After completing the test phase of the PKMS prototype, its transformation into a viable PKM system and cloud-based server based on a rapid development platform and a noSQL-database is estimated to take 12 months.
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Schmitt, Ulrich. "Design Science Research Championing Personal Knowledge Management System Development." In InSITE 2016: Informing Science + IT Education Conferences: Lithuania. Informing Science Institute, 2016. http://dx.doi.org/10.28945/3410.

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Knowledge Management (KM) is governed by an ill-structured mishmash of complementing as well as conflicting interdisciplinary methodologies and based on physical and social technologies, which too often struggle to achieve their stakeholders’ objectives due to diverse scholarly contributions, repetitive polemic discourses, and misguided organizational KM system generations. A novel Personal Knowledge Management (PKM) Concept and Prototype System currently under development take a fresh look and aim to support individuals’ academic and professional growth as well as their roles as contributors and beneficiaries of institutional and societal performance. A PKM System (PKMS), hence, is meant to aid life-long-learning, resourcefulness, creativity, and teamwork of knowledge workers. Such a scope offers appealing and viable opportunities for stakeholders in the educational, professional, and developmental context. A recent article employed the systems thinking techniques of the transdiscipline of Informing Science (IS) to align and validate the more specific models and methodologies central to the PKMS concept. In line with the interdisciplinary nature of the concept, further conference papers and journal articles have been disseminated and received feedback from a wide range of disciplines. This follow-up article turns to the creative process at the heart of the concept and application introduced in the prior publications. Similar to the IS-benchmarking approach, the design thinking is validated against accepted general design science research guidelines. These guidelines are meant to supplement the reactive behavioral (natural) science paradigm with the proactive design science paradigm in order to support information technology (IT) researchers in creating innovative IT artefacts that extend human and social capabilities and meet desired outcomes. Rather than to justify the research paradigm of the PKMS project in an ad hoc and fragmented manner with each new paper, the objective is a dedicated article which presents the design science research perspectives comprehensively as evidence of their relevance, utility, rigor, and publishability in Information Systems research outlets. The URL links to all prior publications facilitate a kind of ‘Long Discussion Case’ to potentially assist IT researchers and entrepreneurs engaged in similar projects.
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Wiens, Gloria J. "Parameter Sensitivity in System Identification of Parallel Mechanisms." In ASME 2002 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2002. http://dx.doi.org/10.1115/detc2002/dac-34110.

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This paper presents a study on the sensitivity of the dynamics of parallel kinematic mechanisms (PKMs) and their effects on the system identification of inertial parameters. Comparing the sensitivity of the individual terms in the equations of motion, a delineation of areas prone to convergence errors in the presence of measurement noise and design parameter variations can be characterized. The design parameter variations evaluated were the strut masses, platform mass, joint location errors and friction. Comparative observations are made using sample trajectory based characterizations. Detailed results are presented for the University of Florida Special 6-6 PKM.
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Xi, Fengfeng, Marcel Verner, and Chris Mechefske. "Error Sensitivity Analysis for Optimal Calibration of Parallel Kinematic Machines." In ASME 2002 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2002. http://dx.doi.org/10.1115/detc2002/dac-34113.

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In this paper, error sensitivity analysis is discussed for the purpose of optimal calibration of parallel kinematic machines (PKMs). The idea is to find a less error sensitive area in the workspace for calibration. To do so, an error model is developed that takes into consideration all the geometric errors due to imprecision in manufacturing and assembly. Based on this error model, it is shown that the error mapping from the geometric errors to the pose error of the PKM depends on the Jacobian inverse. The Jacobian inverse would introduce spurious errors that would affect the calibration results, if used without proper care. Hence, it is suggested to select the areas in the workspace with smaller condition numbers for calibration. A case study is presented to illustrate the proposed method.
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Bi, Z. M., and Guoping Wang. "Real-Time Error Prediction for High-Precision Operation of Parallel Kinematic Machines." In ASME 2012 International Manufacturing Science and Engineering Conference collocated with the 40th North American Manufacturing Research Conference and in participation with the International Conference on Tribology Materials and Processing. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/msec2012-7201.

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Closed-loop parallel kinematic machines (PKMs) have been proposed to improve precision and operation speed over conventional machine tools and robots. However, an embarrassing dilemma is that most of the existing PKMs achieve very lower precision in contrast to equivalent serial machine tools or robots, which are competitive to same tasks. Limited works have been conducted to evaluate errors thus improve precision of machine in real-time control. It becomes necessary to explore the relation of the motion error with the dynamics of a PKM. In this paper, the new model of the error evaluation has been proposed; three major sources of error under consideration are the deformations of the components under dynamic loads, the deformations at joint contacts, and the clearances of passive joints. To illustrate the modeling procedure, the dynamic model of machine is developed to determine internal forces among components and locations of joint contacts. Errors caused by machine dynamics are evaluated analytically in real time; in particular, the errors happened at the contacts of passive joints are estimated based on Hertz theory. The developed error models can be applied to compensate the motion errors of tool tip in real-time. The Exechon parallel kinematic machine is used as a case study, the results from simulation has been compared with the test data.
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Danovaro, Emanuele, Tadas Remencius, Alberto Sillitti, and Giancarlo Succi. "PKM." In Companion of the 13th international conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1370175.1370196.

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Angel, L., A. Traslosheros, J. M. Sebastian, and L. Pari. "High-speed Visual Servoing of PKMs." In 2007 IEEE International Symposium on Industrial Electronics. IEEE, 2007. http://dx.doi.org/10.1109/isie.2007.4374924.

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Shamblin, Scott A., and Gloria J. Wiens. "Characterization of Dynamics in Special 6-6 PKMs." In ASME 2000 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/detc2000/mech-14165.

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Abstract This paper presents a study on the contributions of the dynamics on the performance of a special 6-6 parallel kinematic mechanisms, with application to machine tools. Using Kane’s method, the dynamics equations of motion are derived with inclusion of the strut masses. Comparative observations are made using both workspace and sample trajectory based characterizations.
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"Synthesizing Design and Informing Science Rationales for Driving a Decentralized Generative Knowledge Management Agenda." In InSITE 2019: Informing Science + IT Education Conferences: Jerusalem. Informing Science Institute, 2019. http://dx.doi.org/10.28945/4230.

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[This Proceedings paper was revised and published in the 2019 issue of Informing Science: The International Journal of an Emerging Transdiscipline, Volume 22.] Aim/Purpose: In a world of rapidly expanding complexity and exponentially increasing data availability, IT-based knowledge management tools will be needed to manage and curate available information. This paper looks at a particular tool architecture that has been previously proposed: The Personal Knowledge Management System (PKMS). The specific focus is on how the proposed architecture conforms to design science principles that relate to how it is likely to evolve. Background: We first introduce some recent informing science and design science research frameworks, then examine how the PKMS architecture would conform to these. Methodology: The approach taken is conceptual analysis. Contribution: The analysis provides a clearer understanding of how the proposed PKMS would serve the diverse-client ambiguous-target (DCAT) informing scenario and how it could be expected to evolve. Findings: We demonstrate how the PKMS informing architecture can be characterized as a “social machine” that appears to conform to a number of principles that would facilitate its long-term evolution. Future Research: The example provided by the paper could serve as a model future research seeking to integrate design science and informing science in the study of IT artefacts.
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Mu¨ller, Andreas. "On the Terminology for Redundant Parallel Manipulators." In ASME 2008 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/detc2008-49112.

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Different types of redundancy in parallel kinematics machines (PKM) can be used to improve their kinematic and dynamic properties. The meaning of redundancy of PKM is often differently understood in the literature. In this paper a terminology for redundant PKM is proposed. The basis for this classification is a general mathematical model. With the help of this model PKM are regarded as non-linear control systems. The different types of redundancy are clearly distinguished, and their potential applications are discussed. Redundancy is considered from a geometric point of view. Redundancy is a means to deal with singularities of PKM. The different types of singular configurations are considered in the paper, and the potential of redundancy to cope with such situations is discussed. Again singularities are considered from a geometric point of view.
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Reports on the topic "PKM1"

1

Henry, R. S. Parallel Kinematic Machines (PKM). Office of Scientific and Technical Information (OSTI), March 2000. http://dx.doi.org/10.2172/752338.

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Jaggi, Meena, and Subhash C. Chauhan. Modulation of Beta-catenin Activity With PKD1 Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada502884.

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Jaggi, Meena, and Subhash C. Chauhan. Modulation of Beta-catenin activity with PKD1 in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2010. http://dx.doi.org/10.21236/ada524563.

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Jaggi, Meena, and Subhash C. Chauhan. Modulation of Beta-catenin Activity with PKD1 in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, April 2012. http://dx.doi.org/10.21236/ada599991.

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Zorn, G. RADIUS Attributes for IEEE 802.16 Privacy Key Management Version 1 (PKMv1) Protocol Support. RFC Editor, June 2010. http://dx.doi.org/10.17487/rfc5904.

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Popov, Todor M., Gergana S. Stancheva, Silva G. Giragosyan, Orlin V. Stoyanov, Sylvia E. Valcheva, Emil I. Tsenev, Radka P. Kaneva, and Diana P. Popova. Correlations between PKM2, HIF‑1α, c‑Myc and p53 mRNA Expression Levels in Laryngeal Carcinoma. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, May 2018. http://dx.doi.org/10.7546/crabs.2018.05.14.

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