Relevant bibliographies by topics / HMGCS2

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  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'HMGCS2'

Author: Grafiati
Published: 10 March 2023

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Journal articles on the topic "HMGCS2"

1

Wang, Yuan-Hsi, Fat-Moon Suk, and Yi-Jen Liao. "Loss of HMGCS2 Enhances Lipogenesis and Attenuates the Protective Effect of the Ketogenic Diet in Liver Cancer." Cancers 12, no. 7 (July 4, 2020): 1797. http://dx.doi.org/10.3390/cancers12071797.

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Hepatocellular carcinoma (HCC) is the most common primary malignant liver tumor with limited treatment. The ketogenic diet (KD) emerged as a metabolic therapy for cancer; however, the antitumor effect on HCC remains controversial. We previously reported that the ketogenesis rate-limiting enzyme, 3-hydroxymethylglutaryl-CoA synthase 2 (HMGCS2), was downregulated in most patients with HCC. The knockdown of HMGCS2 enhanced the proliferation and metastasis ability of HCC cells. However, the role of HMGCS2 in affecting KD-mediated metabolic effects remains unclear. Here, we report that KD feeding upregulates HMGCS2 expression and inhibits HCC tumor growth, while a reverse correlation between tumor size and HMGCS2 expression was observed. We found that HCC cells with HMGCS2 downregulation possess altered lipid metabolism that increases fatty acid, triglyceride, and cholesterol synthesis. Under KD feeding, a higher tumor growth rate was observed in HMGCS2 knockdown tumors, which had increased lipid synthesis-related marker expression and a positive correlation between lipid quantity and tumor weight. In conclusion, these results demonstrate that the downregulation of HMGCS2 attenuates the protective effect of the KD by shifting ketone production to enhance de novo lipogenesis in HCC. Our study elucidates a new molecular mechanism underlying the crosstalk between HMGCS2 expression and the KD in cancer treatment, which provides more information for precision medicine in developing personalized treatment strategies.
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Venable, Andrea H., Lauren E. Lee, Kyle Feola, John Santoyo, Tatyana Broomfield, and Sarah C. Huen. "Fasting-induced HMGCS2 expression in the kidney does not contribute to circulating ketones." American Journal of Physiology-Renal Physiology 322, no. 4 (April 1, 2022): F460—F467. http://dx.doi.org/10.1152/ajprenal.00447.2021.

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The mitochondrial enzyme hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) catalyzes the rate-limiting step of ketogenesis. Although the liver constitutively expresses HMGCS2 and is considered the main ketogenic organ, HMGCS2 is induced in the kidney during fasting, leading to the proposal that the kidney contributes to fasting ketosis. We showed kidney HMGCS2 does not contribute to circulating ketones during fasting and cannot compensate for hepatic ketogenic insufficiency.
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Zou, Kejian, Yan Hu, Musheng Li, Hongli Wang, Yuhua Zhang, Ling Huang, Yuanwen Xie, et al. "Potential Role of HMGCS2 in Tumor Angiogenesis in Colorectal Cancer and Its Potential Use as a Diagnostic Marker." Canadian Journal of Gastroenterology and Hepatology 2019 (July 1, 2019): 1–8. http://dx.doi.org/10.1155/2019/8348967.

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Objective. HMGCS2 is the rate-limiting enzyme of ketogenesis, which is vital for tumor initiation or metastasis. The aim of this study is to determine the relationship between HMGCS2 and tumor angiogenesis.Materials and Methods. The study consisted of 100 cases with colorectal cancer and healthy control, the expression of HMGCS2 and the microvessel density (MVD) (marker: CD31) were analyzed by immunohistochemistry and tube formation, and the centration ofβ-hydroxybutyrate in serum was assessed by biochemical analysis.Results. The results showed that HMGCS2 expression is significantly reduced in colorectal cancer compared with healthy control, which is inversely correlated with MVD in colorectal cancer by IHC analysis. What is more, knockdown HMGCS2 expression in HT-29 cells significantly contributed endothelial cell tube formation.Conclusion. These findings implying HMGCS2 may have a negative regulation of tumor angiogenesis and provide an approach to inhibit tumor angiogenesis.
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Kim, Ji Tae, Chang Li, Heidi L. Weiss, Yuning Zhou, Chunming Liu, Qingding Wang, and B. Mark Evers. "Regulation of Ketogenic Enzyme HMGCS2 by Wnt/β-catenin/PPARγ Pathway in Intestinal Cells." Cells 8, no. 9 (September 19, 2019): 1106. http://dx.doi.org/10.3390/cells8091106.

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The Wnt/β-catenin pathway plays a crucial role in development and renewal of the intestinal epithelium. Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), a rate-limiting ketogenic enzyme in the synthesis of ketone body β-hydroxybutyrate (βHB), contributes to the regulation of intestinal cell differentiation. Here, we have shown that HMGCS2 is a novel target of Wnt/β-catenin/PPARγ signaling in intestinal epithelial cancer cell lines and normal intestinal organoids. Inhibition of the Wnt/β-catenin pathway resulted in increased protein and mRNA expression of HMGCS2 and βHB production in human colon cancer cell lines LS174T and Caco2. In addition, Wnt inhibition increased expression of PPARγ and its target genes, FABP2 and PLIN2, in these cells. Conversely, activation of Wnt/β-catenin signaling decreased protein and mRNA levels of HMGCS2, βHB production, and expression of PPARγ and its target genes in LS174T and Caco2 cells and mouse intestinal organoids. Moreover, inhibition of PPARγ reduced HMGCS2 expression and βHB production, while activation of PPARγ increased HMGCS2 expression and βHB synthesis. Furthermore, PPARγ bound the promoter of HMGCS2 and this binding was enhanced by β-catenin knockdown. Finally, we showed that HMGCS2 inhibited, while Wnt/β-catenin stimulated, glycolysis, which contributed to regulation of intestinal cell differentiation. Our results identified HMGCS2 as a downstream target of Wnt/β-catenin/PPARγ signaling in intestinal epithelial cells. Moreover, our findings suggest that Wnt/β-catenin/PPARγ signaling regulates intestinal cell differentiation, at least in part, through regulation of ketogenesis.
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Wang, Yuan-Hsi, Chao-Lien Liu, Wan-Chun Chiu, Yuh-Ching Twu, and Yi-Jen Liao. "HMGCS2 Mediates Ketone Production and Regulates the Proliferation and Metastasis of Hepatocellular Carcinoma." Cancers 11, no. 12 (November 26, 2019): 1876. http://dx.doi.org/10.3390/cancers11121876.

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Hepatocellular carcinoma (HCC) is the most common primary malignant tumor worldwide; however, the traditional therapeutic approaches and survival rates are still limited. To improve current therapies, it is necessary to investigate the molecular mechanisms underlying liver cancer and to identify potential therapeutic targets. The aims of this study were to verify the mechanisms and therapeutic potential of the ketogenesis rate-limiting enzyme 3-Hydroxymethylglutaryl-CoA synthase 2 (HMGCS2) in HCC. Immunohistochemical staining of human liver disease tissue arrays showed that HMGCS2 is abundantly expressed in normal liver tissues but is downregulated in cirrhosis and HCC tissues. In HCC patients, lower HMGCS2 expression was correlated with higher pathological grades and clinical stages. In our investigation of the molecular mechanisms of HMGCS2 in HCC, we showed that knockdown of HMGCS2 decreased ketone production, which promoted cell proliferation, cell migration, and xenograft tumorigenesis by enhancing c-Myc/cyclinD1 and EMT signaling and by suppressing the caspase-dependent apoptosis pathway. Ketone body treatment reduced the proliferation- and migration-promoting effects of HMGCS2 knockdown in cells. In contrast, HMGCS2 overexpression increased the intracellular ketone level and inhibited cell proliferation, cell migration, and xenograft tumorigenesis. Finally, ketogenic diet administration significantly inhibited liver cancer cell growth in mice. Our studies highlight the potential therapeutic strategy of targeting HMGCS2-mediated ketogenesis in liver cancer.
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Suk, Fat-Moon, Chien-Ying Wu, Wan-Chun Chiu, Chia-Ying Chien, Tzu-Lang Chen, and Yi-Jen Liao. "HMGCS2 Mediation of Ketone Levels Affects Sorafenib Treatment Efficacy in Liver Cancer Cells." Molecules 27, no. 22 (November 18, 2022): 8015. http://dx.doi.org/10.3390/molecules27228015.

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Primary liver cancer is the fifth leading death of cancers in men, and hepatocellular carcinoma (HCC) accounts for approximately 90% of all primary liver cancer cases. Sorafenib is a first-line drug for advanced-stage HCC patients. Sorafenib is a multi-target kinase inhibitor that blocks tumor cell proliferation and angiogenesis. Despite sorafenib treatment extending survival, some patients experience side effects, and sorafenib resistance does occur. 3-Hydroxymethyl glutaryl-CoA synthase 2 (HMGCS2) is the rate-limiting enzyme for ketogenesis, which synthesizes the ketone bodies, β-hydroxybutyrate (β-HB) and acetoacetate (AcAc). β-HB is the most abundant ketone body which is present in a 4:1 ratio compared to AcAc. Recently, ketone body treatment was found to have therapeutic effects against many cancers by causing metabolic alternations and cancer cell apoptosis. Our previous publication showed that HMGCS2 downregulation-mediated ketone body reduction promoted HCC clinicopathological progression through regulating c-Myc/cyclin D1 and caspase-dependent signaling. However, whether HMGCS2-regulated ketone body production alters the sensitivity of human HCC to sorafenib treatment remains unclear. In this study, we showed that HMGCS2 downregulation enhanced the proliferative ability and attenuated the cytotoxic effects of sorafenib by activating expressions of phosphorylated (p)-extracellular signal-regulated kinase (ERK), p-P38, and p-AKT. In contrast, HMGCS2 overexpression decreased cell proliferation and enhanced the cytotoxic effects of sorafenib in HCC cells by inhibiting ERK activation. Furthermore, we showed that knockdown HMGCS2 exhibited the potential migratory ability, as well as decreasing zonula occludens protein (ZO)-1 and increasing c-Myc expression in both sorafenib-treated Huh7 and HepG2 cells. Although HMGCS2 overexpression did not alter the migratory effect, expressions of ZO-1, c-Myc, and N-cadherin decreased in sorafenib-treated HMGCS2-overexpressing HCC cells. Finally, we investigated whether ketone treatment influences sorafenib sensitivity. We showed that β-HB pretreatment decreased cell proliferation and enhanced antiproliferative effect of sorafenib in both Huh7 and HepG2 cells. In conclusion, this study defined the impacts of HMGCS2 expression and ketone body treatment on influencing the sorafenib sensitivity of liver cancer cells.
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Ding, Rongrong, Tianyou Chen, Yuan Zhang, Xiaorong Chen, Liping Zhuang, and Zongguo Yang. "HMGCS2 in metabolic pathways was associated with overall survival in hepatocellular carcinoma: A LASSO-derived study." Science Progress 104, no. 3 (July 2021): 003685042110317. http://dx.doi.org/10.1177/00368504211031749.

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This integrated bioinformatic study aimed to investigate potential prognostic candidates in hepatocellular carcinoma (HCC). In the GSE14520, GSE101685, and The Cancer Genome Atlas (TCGA) datasets, differentially expressed genes (DEGs) were identified and functional pathways of common DEGs were enriched. The least absolute shrinkage and selection operator (LASSO) model was used to screen the potential parameters associated with overall survival (OS) in HCC patients. Metabolic pathways were the most significantly enriched functional pathways of common DEGs in these three datasets. After LASSO model analysis, HMGCS2, UGP2, BCLC staging and TNM staging were screened as potential prognostic candidates for OS in HCC patients in GSE14520. HMGCS2 in the metabolic pathway was significantly downregulated in tumor tissues and peripheral blood mononuclear cells in HCC patients (all p < 0.05). Cox regression model indicated that HMGCS2 might be associate with OS in HCC patients in GSE14520 and in the TCGA ( p = 0.029 and p = 0.05, respectively). Kaplan–Meier analysis demonstrated that HMGCS2 downregulation in tumors contributed to an unfavorable OS in HCC patients, both in GSE14520 and in the TCGA ( p = 0.0001 and p = 0.0002, respectively). Additionally, HMGCS2 was significantly downregulated in HCC patients with high alpha-fetoprotein (AFP), main tumor size >5 cm, multinodular, advanced tumor staging including BCLC, TNM and CLIP (all p < 0.05). HMGCS2 was involved in metabolic pathways, and downregulated HMGCS2 in tumors was associated with unfavorable OS in HCC patients.
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Helenius, Terhi O., Julia O. Misiorek, Joel H. Nyström, Lina E. Fortelius, Aida Habtezion, Jian Liao, M. Nadeem Asghar, et al. "Keratin 8 absence down-regulates colonocyte HMGCS2 and modulates colonic ketogenesis and energy metabolism." Molecular Biology of the Cell 26, no. 12 (June 15, 2015): 2298–310. http://dx.doi.org/10.1091/mbc.e14-02-0736.

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Simple-type epithelial keratins are intermediate filament proteins important for mechanical stability and stress protection. Keratin mutations predispose to human liver disorders, whereas their roles in intestinal diseases are unclear. Absence of keratin 8 (K8) in mice leads to colitis, decreased Na/Cl uptake, protein mistargeting, and longer crypts, suggesting that keratins contribute to intestinal homeostasis. We describe the rate-limiting enzyme of the ketogenic energy metabolism pathway, mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase 2 (HMGCS2), as a major down-regulated protein in the K8-knockout (K8−/−) colon. K8 absence leads to decreased quantity and activity of HMGCS2, and the down-regulation is not dependent on the inflammatory state, since HMGCS2 is not decreased in dextran sulfate sodium-induced colitis. Peroxisome proliferator–activated receptor α, a transcriptional activator of HMGCS2, is similarly down-regulated. Ketogenic conditions—starvation or ketogenic diet—increase K8+/+ HMGCS2, whereas this response is blunted in the K8−/− colon. Microbiota-produced short-chain fatty acids (SCFAs), substrates in the colonic ketone body pathway, are increased in stool, which correlates with decreased levels of their main transporter, monocarboxylate transporter 1 (MCT1). Microbial populations, including the main SCFA-butyrate producers in the colon, were not altered in the K8−/−. In summary, the regulation of the SCFA-MCT1-HMGCS2 axis is disrupted in K8−/− colonocytes, suggesting a role for keratins in colonocyte energy metabolism and homeostasis.
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Yi, Weijie, Xiao Xie, Miying Du, Yongjun Bu, Nannan Wu, Hui Yang, Chong Tian, et al. "Green Tea Polyphenols Ameliorate the Early Renal Damage Induced by a High-Fat Diet via Ketogenesis/SIRT3 Pathway." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–14. http://dx.doi.org/10.1155/2017/9032792.

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Scope. Several reports in the literature have suggested the renoprotective effects of ketone bodies and green tea polyphenols (GTPs). Our previous study found that GTP consumption could elevate the renal expression of the ketogenic rate-limiting enzyme, which was decreased by a high-fat diet (HFD) in rats. Here, we investigated whether ketogenesis can mediate renoprotection by GTPs against an HFD. Methods and Results. Wistar rats were fed a standard or HFD with or without GTPs for 18 weeks. The renal oxidative stress level, kidney function, renal expression, and activity levels of mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase 2 (HMGCS2) and sirtuin 3(SIRT3) were detected. The increased renal oxidative stress and the loss of renal function induced by the HFD were ameliorated by GTPs. Renal ketogenesis and SIRT3 expression and activity levels, which were reduced by the HFD, were restored by GTPs. In vitro, HEK293 cells were transfected with the eukaryotic expression plasmid pcDNA HMGCS2. GTP treatment could upregulate HMGCS2 and SIRT3 expression. Although SIRT3 expression was not affected by HMGCS2 transfection, the 4-hydroxy-2-nonenal (4-HNE) level and the acetyl-MnSOD (K122)/MnSOD ratio were reduced in HMGCS2-transfected cells in the context of H2O2. Conclusion. The ketogenesis/SIRT3 pathway mediates the renoprotection of GTPs against the oxidative stress induced by an HFD.
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Geisler, Caroline E., Susma Ghimire, Randy L. Bogan, and Benjamin J. Renquist. "Role of ketone signaling in the hepatic response to fasting." American Journal of Physiology-Gastrointestinal and Liver Physiology 316, no. 5 (May 1, 2019): G623—G631. http://dx.doi.org/10.1152/ajpgi.00415.2017.

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Ketosis is a metabolic adaptation to fasting, nonalcoholic fatty liver disease (NAFLD), and prolonged exercise. β-OH butyrate acts as a transcriptional regulator and at G protein-coupled receptors to modulate cellular signaling pathways in a hormone-like manner. While physiological ketosis is often adaptive, chronic hyperketonemia may contribute to the metabolic dysfunction of NAFLD. To understand how β-OH butyrate signaling affects hepatic metabolism, we compared the hepatic fasting response in control and 3-hydroxy-3-methylglutaryl-CoA synthase II (HMGCS2) knockdown mice that are unable to elevate β-OH butyrate production. To establish that rescue of ketone metabolic/endocrine signaling would restore the normal hepatic fasting response, we gave intraperitoneal injections of β-OH butyrate (5.7 mmol/kg) to HMGCS2 knockdown and control mice every 2 h for the final 9 h of a 16-h fast. In hypoketonemic, HMGCS2 knockdown mice, fasting more robustly increased mRNA expression of uncoupling protein 2 (UCP2), a protein critical for supporting fatty acid oxidation and ketogenesis. In turn, exogenous β-OH butyrate administration to HMGCS2 knockdown mice decreased fasting UCP2 mRNA expression to that observed in control mice. Also supporting feedback at the transcriptional level, β-OH butyrate lowered the fasting-induced expression of HMGCS2 mRNA in control mice. β-OH butyrate also regulates the glycemic response to fasting. The fast-induced fall in serum glucose was absent in HMGCS2 knockdown mice but was restored by β-OH butyrate administration. These data propose that endogenous β-OH butyrate signaling transcriptionally regulates hepatic fatty acid oxidation and ketogenesis, while modulating glucose tolerance. NEW & NOTEWORTHY Ketogenesis regulates whole body glucose metabolism and β-OH butyrate produced by the liver feeds back to inhibit hepatic β-oxidation and ketogenesis during fasting.
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Dissertations / Theses on the topic "HMGCS2"

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De, Rosa Maria Caterina. "Studio dell’espressione di geni coinvolti in pathways metabolici regolati da nutrienti." Doctoral thesis, Universita degli studi di Salerno, 2015. http://hdl.handle.net/10556/1864.

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2014-2015
Il profilo sierico, con particolare riferimento ai livelli di biomarkers, rappresenta uno strumento efficace ed affidabile per la diagnosi di malattie metaboliche, come il diabete o le malattie cardiovascolari. La composizione del siero è influenzata sia dal metabolismo endogeno che dall’apporto nutrizionale. In effetti, lo stile alimentare, con particolare riferimento alla qualità e alla quantità dell’apporto nutrizionale, può fortemente influenzare il rischio e la progressione di malattia, poiché alcuni nutrienti agiscono come composti bioattivi. A questo proposito, la letteratura attuale indica un importante ruolo di specifiche molecole nutrizionali provenienti dalla dieta che interessano specifiche vie metaboliche. L'obiettivo del nostro progetto è quello di individuare pathways metabolici regolati da nutrienti, con lo scopo di identificare possibili taget terapeutici in stati patologici. [ a cura dell'autore]
XIII n.s.
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Saada-Bouzid, Esma. "Étude génomique et fonctionnelle de la dérégulation du gène HMGA2 dans les tumeurs adipocytaires." Thesis, Nice, 2015. http://www.theses.fr/2015NICE4000/document.

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Les tumeurs adipocytaires (TA) bénignes sont majoritairement constituées par les lipomes, alors que les TA malignes sont principalement des Tumeurs Lipomateuses Atypiques (TLA)/ liposarcome (LPS) bien différenciés (LBD) et les LPS dédifférenciés (LDD). Le gène HMGA2 (High Mobility Group A2) est remanié dans certains lipomes et amplifié dans les TLA/LBD et LDD. Ainsi, nous avons émis l’hypothèse que HMGA2 jouait un rôle fondamental dans la genèse des TA bénignes et malignes. En faveur de cette hypothèse, nous avons observé une surexpression constante de HMGA2 dans les TLA/LBD et LDD avec amplification de HMGA2 et les lipomes avec remaniement de HMGA2. Dans un cas de lipomatose, hypertrophie pathologique du tissu adipeux sans anomalie du gène HMGA2, une surexpression de HMGA2 était associée à une inhibition de l’expression de plusieurs microARN let-7. En revanche, nos travaux ne sont pas en faveur d’un rôle prépondérant des microARN let7 dans la surexpression de HMGA2 dans les TA. Nous nous sommes également intéressés aux gènes partenaires de fusion avec HMGA2 dans les lipomes et avons notamment identifié une nouvelle fusion impliquant PPAP2B (Phosphatidic Acid Phosphatase type 2B) localisé en 1p32. Nous avons aussi confirmé le rôle du gène NFIB (9p22) dans les lipomes. Enfin, nous avons établi des corrélations pronostiques dans une grande série de 116 TLA/LBD et LDD : l’amplification de HMGA2 était associée à l’histotype TLA/LBD et à une survie longue alors que les amplifications de CDK4 et JUN sont associées au type LDD et une survie courte. Ainsi, nos données confortent l’hypothèse d’un rôle précoce et majeur de HMGA2 dans la genèse des TA bien différenciées
Benign adipocytic tumors (AT) are mainly represented by lipomas whereas most malignant AT are Atypical Lipomatous Tumors/Well-differentiated liposarcomas (ALT/WDLPS) and dedifferentiated liposarcomas (DDLPS). HMGA2 gene (High Mobility Group A2) is rearranged in some lipomas and amplified in ALT/WDLPS and DDLPS. Thus, we hypothesized that HMGA2 played a fundamental role in benign and malignant AT genesis. In favor of this hypothesis, we observed a constant overexpression of HMGA2 in amplified ALT/WDLPS and DDLPS, and in rearranged lipomas. In a case of lipomatosis, that is a pathological proliferation of the adipocytic tissu without rearrrangement of HMGA2, the overexpression of HMGA2 was asssociated with an inhibition of the expression of several let-7 microRNAs. However, we did not find a leading role of let-7 microRNAs in the deregulation of HMGA2 expression in AT. We also studied partner fusion genes of HMGA2 in lipomas and have specifically identified a new fusion involving PPAP2B (Phosphatidic Acid Phosphatase type 2B) which is located in 1p32. We also confirmed the role of NFIB gene (9p22) in lipomas. Finally, we have established prognostic correlations in a series of 116 ALT/WDLPS and DDLPS: HMGA2 amplification was associated with ALT/WDLPS histotype and a longer survival whereas respective CDK4 and JUN amplification were associated with DDLPS and shorter survival. Thus, our data support the hypothesis of an early and major role of HMGA2 in the genesis well differentiated AT
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Alvarado, Cárdenas Marcelo. "Estatinas y autoimnunidad. métodos de detección e importancia de los anticuerpos anti-HMGCR." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/666849.

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Los inhibidores de la 3-hidroxi-3-metilglutaril coenzima A reductasa (HMGCR), conocidos como estatinas, son los fármacos más utilizados en el tratamiento de la hipercolesterolemia y en la prevención tanto primaria como secundaria de enfermedades cardiovasculares y asociadas a aterosclerosis. A pesar de que son bien tolerados por la mayoría de los pacientes y de tener un perfil muy seguro, algunos pacientes presentan ciertos efectos adversos entre los que destacan las alteraciones musculares. La descripción reciente de una forma de toxicidad muscular inmunomediada asociada a anticuerpos dirigidos contra la enzima 3-hidroxi-3-metilglutaril coenzima A reductasa (anti-HMGCR), sustrato frente al que actúan las estatinas, implica a estos fármacos como responsables en parte de fenómenos autoinmunes asociados a la administración del fármaco. Los objetivos de esta Tesis Doctoral, están encaminados a establecer la prevalencia de estos anticuerpos en la población general tratada con estatinas, pero también en enfermedades autoinmunes, entre las que las miopatías inflamatorias –por estar incluida la miopatía necrosante inmunomediada en el grupo- y las hepatitis autoinmunes –por explorar la reproducibilidad del modelo tóxico-inmunológico atribuido a la miopatía necrosante inmunomediada por estatinas- tienen una especial relevancia. En estos estudios se ha podido comprobar que la prevalencia en la población general es inferior al 1%, tal y como otros grupos han publicado, y que en los pacientes con enfermedades autoinmunes la prevalencia es también baja, con la salvedad de las miopatías inflamatorias, en las que aumenta a expensas de las formas relacionadas con las estatinas (miopatía necrosante inmunomediada). No se ha conseguido reproducir el modelo en los pacientes con hepatitis autoinmune. Otros grupos a estudio, como las dislipemias familiares graves o la prevención secundaria del ictus, que contemplan la administración de estatinas a dosis altas han mostrado también una muy baja prevalencia. La determinación de los anticuerpos anti-HMGCR es un punto relevante de estudio de estos pacientes, por lo que en esta Tesis se ha explorado la reproducibilidad y fiabilidad de dos técnicas de ELISA –una realizada en nuestro laboratorio (in-house) y otra comercial- observando una excelente concordancia entre ambas. Así mismo se ha descrito un nuevo patrón de inmunofluorescencia indirecta en triple tejido (HALIP), característico de estos autoanticuerpos, y que facilita su diagnóstico por su simplicidad y posibilidad de realización en la mayoría de laboratorios Finalmente, se ha establecido un algoritmo diagnóstico-terapéutico sobre la actitud a tomar ante pacientes que reciben terapia con estatinas y presentan alteraciones musculares.
Drugs that inhibit the enzyme, 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR), known as statins, are one of the most widely used medications. Statin use is associated with reductions in cardiovascular risk and mortality due to cardiovascular disease. Muscle toxicity is recognized as the main adverse effect of these drugs. Recently, an immune-mediated muscle toxicity associated with antibodies against HMGCR has been described. It means a possible statins-related autoimmune mechanism of toxicity. The aims of this Doctoral Thesis include the study of the prevalence of these anti-HMGCR antibodies in patients from the community treated with statins, but also the prevalence of anti-HMGCR antibodies in patients with different autoimmune diseases, especially in idiopathic inflammatory myopathies –given that immune-mediated necrotizing myopathy belongs to the group- and in autoimmune hepatitis –in order to examine the reproducibility of the well-known toxic-immunologic model of immune-mediated necrotizing myopathy. Data obtained from these studies shown that prevalence in patients from the community treated with statins was less than 1%, and similar data was obtained in patients with autoimmune diseases. Only patients with idiopathic inflammatory myopathies, because of the inclusion of patients with statin-associated immune-mediated necrotizing myopathy, showed a higher prevalence. On the other hand we failed to demonstrate that patients with autoimmune hepatitis were positive to these anti-HMGCR antibodies. We also studied other groups of patients, such as those with severe familiar dyslipidemia and those in secondary prevention after a cerebrovascular event, treated with high doses of statins, but the prevalence was again less than 1%. Method for anti-HMGCR detection is a relevant issue in the study of these patients. Thus, one of the points addressed in this Doctoral Thesis was to study de reproducibility and concordance of different test. Both ELISA test, in-house and commercial showed an excellent concordance. Moreover, a distinct and characteristic immunofluorescence pattern on triple rat tissue not previously described, that we called HALIP (HMGCR Associated Liver IFL Pattern) was found. This pattern would help to identify patients with statin-associated autoimmune myopathy in a standard laboratory setting. A practical approach to establish clinical recommendations regarding the muscle complaints related to statin use is reported as an algorithm at the end of the Doctoral Thesis.
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Crabbe, T. B. "Studies on the adenylate cyclase and HMGCoA reductase of the yeast Saccharomyces cerevisiae." Thesis, University of Liverpool, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233812.

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Wei, Linxuan, Xiaolin Liu, Wenjing Zhang, Yuyan Wei, Yingwei Li, Qing Zhang, Ruifen Dong, et al. "Overexpression and oncogenic function of HMGA2 in endometrial serous carcinogenesis." E-CENTURY PUBLISHING CORP, 2016. http://hdl.handle.net/10150/614759.

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The high-mobility group A protein 2 (HMGA2) is a non-histone chromatin factor highly expressed in fetal tissue and malignant tumors but rarely detected within normal adult tissues. The clinical implications and biological functions of HMGA2 in endometrial carcinoma are largely unknown. Here we report that HMGA2 expression was barely detected in benign endometrium samples (2 of 28 samples). However, HMGA2 expression increased significantly from precancerous lesion endometrial glandular dysplasia (7 of 17, 41.2%), to serous endometrial intraepithelial carcinoma (5 of 8, 62.5%) and to full blown endometrial serous carcinoma (39 of 59, 66.1%). Functional characterization of HMGA2 revealed that the gene has both tumor growth promotion and metastasis. In addition, HMGA2 induced epithelial-mesenchymal transition (EMT) through modulation vimentin and β-catenin. Furthermore, HMGA2 overexpression started from endometrial serous precancers, non-invasive cancers, as well as in full blown carcinomas in a p53 knockout mouse model we recently established in our laboratory. Our findings suggest that HMGA2 may serve as a useful diagnostic marker in the assessment of endometrial serous cancer and its precursor lesions.
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6

Hawsawi, Ohuod. "Role of High Mobility Group A2 (HMGA2) in Prostate Cancer." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2019. http://digitalcommons.auctr.edu/cauetds/184.

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High mobility group A2 (HMGA2) is a non-histone protein highly expressed during the development but is low or absent in most adult tissues. Epithelial-mesenchymal transition (EMT) plays a critical role in prostate cancer progression and metastasis. HMGA2 has been shown to promote EMT in separate studies. Interestingly, wild-type HMGA2 and truncated (lacking the 3’UTR) HMGA2 isoforms are overexpressed in many cancers. However, there are no studies on the role of each isoform in prostate cancer progression. We hypothesized that wild-type and truncated HMGA2 promotes prostate cancer progression by different mechanisms. We analyzed the expression of HMGA2 in the prostate panel by western blot analysis and the localization in prostate tissue microarray by immunohistochemistry. We stably overexpressed wild-type and truncated HMGA2 cDNA in LNCaP cells and measured the expression and the localization of HMGA2 as well as EMT markers. We also performed the migration and cell viability assays. We analyzed phospho-ERK in cells overexpressing HMGA2 as well as inhibition with U0126 (MAPK inhibitor). To explore the role of truncated HMGA2, we measured the reactive oxygen species (ROS) concentration by DCFDA dye, as well as analyzing Jun-D as a putative downstream effector of HMGA2. Additionally, we knocked down Jun-D and performed the migration and cell viability assays. We treated ARCaP-M mesenchymal cells with camalexin, a 3-thizol-2-yl-indole (a natural product, as a candidate to target HMGA2) in vitro and in vivo in nude mice. Our results showed an increase in nuclear HMGA2 expression with prostate cancer progression as compared to normal tissue. LNCaP cells overexpressing wild-type but not truncated HMGA2 displayed nuclear localization and induced EMT via the ERK1/2 pathway, and this effect could be reversed by treating the cells with U0126. Conversely, truncated HMGA2 displayed cytoplasmic expression and increased prostate cancer migration via increasing Jun-D expression and ROS; this could be antagonized by Jun-D knockdown. Finally, treating ARCaP-M aggressive prostate cancer cells with camalexin reduce its expression in vitro and in vivo. In conclusion, both wild-type and truncated HMGA2 induce prostate cancer progression by different mechanisms which may be targeted by camalexin.
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Aktürk, Onur Altuntaş İrfan. "Hiperkolesterolemi oluşturulan ratlarda, HMGCoA redüktaz inhibitörü ilaçlarla (Statinler) tedavinin hipokampal NMDA reseptörü subunitlerine etkisi /." Isparta : SDÜ Tıp Fakültesi, 2006. http://tez.sdu.edu.tr/Tezler/TT00294.pdf.

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Eisa-Beygi, Shahram. "HMGCR Pathway Mediates Cerebral-Vascular Stability and Angiogenesis in Developing Zebrafish." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/26112.

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Intracerebral hemorrhage (ICH) is a severe form of stroke, with a high mortality rate and often resulting in irreversible neurological deterioration. Although animal studies have provided insight into the etiology of the disease, many of the causative genes and mechanisms implicated in cerebral-vascular malformations are unknown. Treatment options remain ineffective. With the present models, the pathophysiological consequences of ICH can only be assessed in situ and after histological analysis. Furthermore, common deficiencies of the current models include the heterogeneity, low expression and low reproducibility of the desired phenotype. Hence, there is a requirement for novel approaches to model ICH pathogenesis. Zebrafish (Danio rerio) has gained recognition as a vertebrate model for stroke research. Through a combination of pharmacological blockers, metabolite rescue, genetic approaches, and confocal imaging analysis, I demonstrate a requirement for the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) pathway in regulating developmental cerebral-vascular stabilization. A transient loss in HMGCR function induces ICH, characterised by progressive dilation of blood vessels, vascular permeability and vessel rupture. These effects are likely due to reduced prenylation of Rho GTPases, evidenced by morpholino-mediated blocking of the prenylation pathway and in vivo assessment of endothelial-specific localization of cdc42, a Rho GTPase family protein. These results are in conformity with recent clinical and experimental evidence. I have further shown that this model consistently replicates common pathoghysiological processes associated with ICH. The hemorrhages are associated with the disruption of the blood-brain barrier, vessel disintegration, hematoma expansion and edema into the adjacent brain regions. Also, enhanced apoptosis, activation of inflammatory mediators in the periphery of the hematoma, enriched heme oxygenase 1 (HO-1) expression and localised thrombosis were observed in these embryos. I show that the patterning and distribution of catecholaminergic neurons, response to sensory stimulus and swimming speed were impaired as a consequence of ICH. These results suggest that HMGCR contributes to cerebral-vascular stabilisation through Rho GTPase mediated-signalling and that zebrafish can serve as a powerful paradigm for the systemic analysis of the etiological and pathophysiological underpinnings of ICH and can help establish the basis for future studies into screening for putative therapeutics and elucidating mechanisms aiding functional recovery.
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Villazon-Gonzales, Claudia. "Influência de variantes do receptor de LDL e da HMGCoA redutase na resposta à atorvastatina." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-10062009-152818/.

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A influencia dos polimorfismos genéticos de HMGCoA redutase (HMGCR) e LDL receptor (LDLR) na resposta a atorvastatina (10 mg/dia/4semanas) foi avaliada em individuos hipercolesterolemicos (HC). Amostras de sangue foram coletadas de 153 HC e 182 normolipidemicos (NL) para determinações de lipideos séricos e extração de DNA. Polimorfismos de troca única (SNP) HMGCR (A11898T e T24558G) e LDLR (C16730T, C20001T, G26857A) foram detectados. por PCR-RFLP. Os alelos HMGCR 11898T e 24558G foram associados com menores triglicérides e VLDL-C séricos nos grupos NL e HC (p<0,05). Além disso, o SNP HM0CR T24558G foi relacionado com HDL-C e apoAI séricos aumentados em resposta a atorvastatina no grupo HC. O alelo LDLR 20001 C foi associado com maior apoAI sérica basal no grupo NL (p=O,034) e com melhor resposta de apoAI a atorvastatina no grupo HC (p=O,045). Foi observada relação entre o haplótipo heterozigoto LDLR 20001 C/16730T e redução significativa de apoB e aumento de apoAI no soro após o tratamento com atorvastatina (pInfluence of the HMGCoA reductase (HMGCR) and LDL receptor (LDLR) gene polymorphisms on response to atorvastatin (10 mg/day/4weeks) was evaluated in hypercholesterolemic (HC) individuais. Blood samples were collected from 153 HC and 182 normolipidemic (NL) individuais for serum lipids determinations and DNA extratcion. Single nucleotide polymorphisms (SNP) HMGCR (A11898T e T24558G) and LDLR (C16730T, C20001T, G26857A) were detected by PCR-RFLP. HMGCR 11898T and 24558G alleles were associated with lower serum triglycerides and VLDL-C in NL and HC groups (p<0.05). Moreover, the SNP HMGCR T24558G was related to increased serum HDL-C and apoAI in response to atorvastatin in the HC group. The LDLR 20001 C allele was associated with higher basal serum apoAI in the NL group (p=0.034) and with better response of apoAI to atorvastatin in HC group (p=0.045). There was a relationship between heterozygote LDLR 20001 C/16730T haplotype and a significant reduction of apoB and increase in apoAI serum leveis after atorvastatin treatment (p<0.05). In conclusion, the HMGCR A11898T e T24558G SNPs influence serum triglycerides and VLDL-C independently of the lipemic status and LDLR 20001 C/16730T haplotype is associated with better serum apoB and Apol response to atorvastatin treatment.
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Annewanter, Franka Maria [Verfasser]. "Expression von TRAIL-Rezeptoren und HMGA2 im duktalen Pankreasadenokarzinom / Franka Maria Annewanter." Kiel : Universitätsbibliothek Kiel, 2014. http://d-nb.info/1064306101/34.

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Books on the topic "HMGCS2"

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Great Britain. Parliament. House of Commons. Defence Committee. Strategic export controls: HMG's annual report for 2003, licensing policy and parliamentary scrutiny : first joint report of session 2004-05. London: Stationery Office, 2005.

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Gelder, Wiebke. Identifizierung von mit HMGA2 interagierenden Proteinen. GRIN Verlag GmbH, 2011.

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Reports from the Defence, Foreign Affairs, International Development, and Trade and Industry Committees: Strategic Export Controls: HMG's Annual Report ... and Parliamentary Scrutiny, Session 2005-06. Stationery Office, 2006.

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Great Britain: Ministry of Defence. Reports from the Defence, Foreign Affairs, International Development, and Trade and Industry Committees : Session 2004-05, strategic export controls: HMG's annual report for 2003, licensing policy and Parliamentary scrutiny, response of the Secretaries of State for Defence, Foreign and Commonwealth Affairs, International Development, and Trade and Industry. Stationery Office, The, 2005.

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Great Britain: Ministry of Defence. Reports from the Business and Enterprise, Defence, Foreign Affairs and International Development Committees : Session 2007-08 : Strategic Export Controls : HMG's Annual Report for 2006, Quarterly Reports for 2007, Licensing Policy and Parliamentary Scrutiny: Response of the Secretaries of State for Defence, Foreign and Commonwealth Affairs, International Development and Business, Enterprise and Regulatory Reform. Stationery Office, The, 2008.

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Great Britain: Foreign and Commonwealth Office Staff. Reports from the Defence, Foreign Affairs, International Development and Trade and Industry Committees Session 2006-07: Strategic export controls, HMG's annual report for 2005, quarterly reports for 2006, licensing policy and Parliamentary scrutiny, response of the Secretaries of State for Defence, Foreign and Commonwealth Affairs, International Development and Business, Enterprise and Regulatory Reform. Stationery Office, The, 2007.

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Book chapters on the topic "HMGCS2"

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Betteridge, Zoe, and Neil J. McHugh. "Newly Described Myositis Autoantibodies: HMGCR, NT5C1A, SAE, PUF60." In Managing Myositis, 199–207. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-15820-0_22.

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Soma, M. R., E. Doneffi, V. Dimitri, A. Corsini, and R. Paoletti. "HMGCoA Reductase Enzyme Inhibitors Effects on Proliferation of Arterial Myocytes." In Cellular Metabolism of the Arterial Wall and Central Nervous System, 255–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-84949-7_19.

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Petrovič, Uroš, and Ana Plemenitaš. "Regulation of HMGCoA Reducíase Activity by Salt Stress in Hortaea werneckii." In Non-Conventional Yeasts in Genetics, Biochemistry and Biotechnology, 131–34. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-55758-3_20.

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"HMGA2." In Encyclopedia of Cancer, 1710–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_2773.

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Chauvet, Norbert, Evelyne Galibert, Anne-Cecile Meunier, Valerie Rigau, Guillaume Osterstock, Eric Baccino, Monica Fedele, et al. "Cadherin Changes in Human Pituitary Adenomas Can Be Reproduced in cKO-Men1 and HMGA2 Mouse Models." In TRANSLATIONAL - Pituitary Neoplasia, P1–423—P1–423. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p4.p1-423.

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Conference papers on the topic "HMGCS2"

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Yang, J., X. Pan, C. Liang, L. Liu, and G. Yu. "HMGCS2 Deficiency Mediated Alveolar Epithelial Cell Lipid Metabolic Re-Programing Promote Pulmonary Fibrosis Progression by Fibroblast Activation." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4422.

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Ashida, Shingo, Chiaki Kawada, and Keiji Inoue. "Abstract 79: Stromal regulation of prostate cancer cell proliferation by mevalonate pathway enzymes HMGCS1 and HMGCR." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-79.

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Chang, Jinseok, Minjae Kim, Dae Choi, and Yongseok Kang. "Performance & Fuel Efficiency Development of the New In-Line 6 Cylinders 3L Diesel Engine System for the Genesis' 1st SUV." In FISITA World Congress 2021. FISITA, 2021. http://dx.doi.org/10.46720/f2021-caf-028.

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"The new 3L diesel engine for passenger cars has been developed as the highly-performing and environment-friendly 3rd generation engine of Hyundai Motor Group. It is the newly-developed inline – 6 cylinders 3.0L diesel engine, and its performance for power, fuel efficiency, NVH, and responsiveness has been optimized for the first SUV of the GENESIS brand, GV80 - Project code: JX1. The future trend of powertrain is that although electrification and hybridization are continuously increasing, the internal combustion engine is still expected to play a role as a powertrain with sufficient production volume even in the future after 2030. This engine is equipped with an aluminum block, a common rail of pressure 2200 bar, a ball bearing turbocharger, a water-cooled intercooler, an LP(Low Pressure) & HP (High Pressure) EGR system, and has an LNT, a DPF , and an SCR as after-treatment devices. The combustion system of this engine was newly developed in common with HMG’s new diesel 2.0, 2.2, and 3.0L module engines. The combustion chamber has been improved in shape and spray compared to HMG’s previous V6 3L engine. And configuration of Injector nozzle, NTP, and valve timing have been optimized for the new combustion chamber. The turbo-charger has also been newly optimized for the power, fuel efficiency and responsiveness of the new engine. Accordingly, the responsiveness of the engine has been remarkably improved compared to the previous engine, and the power performance of the vehicle has also been improved very well. The performance of the intake manifold was also improved through several times with focus on air and EGR distribution, and also on cost, weight reduction, and robustness. The back pressure level of the exhaust system was developed in consideration of both power and NVH performance with focus on the GENESIS brand. In consideration of this, the engine's NVH showed better results than the engines of the previous HMG’s and competitors. Its maximum power advanced 7% more than the previous HMG’s engine, and it has also become a 3L diesel engine with the highest power, overtaking competitors. The engine's fuel efficiency is improved by about 6% over the previous HMG's engine. In addition, the results were 5-10% better than competitors' engines, and vehicle fuel efficiency was 13% superior to the previous HMG’s and 8-9% superior to competitors. Through this, it has secured the world's best fuel efficiency and power performance competitiveness. For the after-treatment devices, the EMS mapping development of the exhaust heating was efficiently progressed according to the state of the after-treatment devices, and the water-cooled intercooler and the complex EGR system were developed to operate properly including the extended RDE at low temperature. The SCR system showed a high NOx conversion efficiency of over 80% in regulatory modes such as WLTC and RDE STEP2. The new 3L diesel engine’s performance accords with the world-best-class fuel efficiency and high-performance for the world-premium brand GENESIS, satisfying with the latest environmental regulation EURO6d."
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"HMG's Unified Incident Reporting and Alert Scheme." In IEE Colloquium on Information Security - Is It Safe? IEE, 1996. http://dx.doi.org/10.1049/ic:19960885.

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Kaur, Harpreet, Marianne Hütt, Xing-gang Mao, Brent A. Orr, Charles G. Eberhart, and Eric H. Raabe. "Abstract 3031: HMGA2 promotes invasion and stemness in glioblastoma." 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.am2014-3031.

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Conlon, Tracey A., Patricia E. Fitzsimons, Abhidhamma Kaninde, Ingrid Borovickova, and Ellen Crushell. "P426 Profound metabolic acidosis and hypertriglyceridaemia in mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase- 2 deficiency (HMGCS2D)." In Faculty of Paediatrics of the Royal College of Physicians of Ireland, 9th Europaediatrics Congress, 13–15 June, Dublin, Ireland 2019. BMJ Publishing Group Ltd and Royal College of Paediatrics and Child Health, 2019. http://dx.doi.org/10.1136/archdischild-2019-epa.762.

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Dobersch, S., K. Rubio, and G. Barreto. "HMGA2 mediated histone deposition is required for TGFB1 induced transcription." In 60. Kongress der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e. V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678058.

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Kaur, Harpreet, Marianne Hütt-Cabezas, Isabella Taylor, Laura Asnaghi, Fausto Rodriguez, Brent A. Orr, Charles G. Eberhart, and Eric H. Raabe. "Abstract 4222: Targeting HMGA2 suppresses GBM stemness, invasion and tumorigenicity." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4222.

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Burnett, Riesa, Hitesh Appaiah, Poornima Bhat-Nakshatri, Jim Wikel, Peter Crooks, William Mathews, and Harikrishna Nakshatri. "Abstract 1344: HMGA2-targeted drug discovery for breast cancer brain metastasis." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1344.

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Piscuoglio, Salvatore, Pierlorenzo Pallante, Federico Cappuzzo, Inti Zlobec, Alessandro Lugli, Alfredo Fusco, and Luigi M. Terracciano. "Abstract 3195: HMGA1 and HMGA2 over-expression in human lung carcinoma." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-3195.

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Reports on the topic "HMGCS2"

1

Aly, Radi, James H. Westwood, and Carole L. Cramer. Novel Approach to Parasitic Weed Control Based on Inducible Expression of Cecropin in Transgenic Plants. United States Department of Agriculture, May 2003. http://dx.doi.org/10.32747/2003.7586467.bard.

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Our overall goal was to engineer crop plants with enhanced resistance to Orobanche (broomrape) based on the inducible expression of sarcotoxin-like peptide (SLP). A secondary objective was to localize small proteins such as SLP in the host-parasite union in order to begin characterizing the mechanism of SLP toxicity to Orobanche. We have successfully accomplished both of these objectives and have demonstrated that transgenic tobacco plants expressing SLP under control of the HMG2 promoter show enhanced resistance to O. aegyptiaca and O. ramosa . Furthermore, we have shown that proteins much larger than the SLP move into Orobanche tubercles from the host root via either symplastic or apoplastic routes. This project was initiated with the finding that enhanced resistance to Orobanche could be conferred on tobacco, potato, and tomato by expression of SLP (Sarcotoxin IA is a 40-residue peptide produced as an antibiotic by the flesh fly, Sarcophaga peregrina ) under the control of a low-level, root-specific promoter. To improve the level of resistance, we linked the SLP gene to the promoter from HMG2, which is strongly inducible by Orobanche as it parasitizes the host. The resulting transgenic plants express SLP and show increased resistance to Orobanche. Resistance in this case is manifested by increased growth and yield of the host in the presence of the parasite as compared to non-transgenic plants, and decreased parasite growth. The mechanism of resistance appears to operate post-attachment as the parasite tubercles attached to the transgenic root plants turned necrotic and failed to develop normally. Studies examining the movement of GFP (approximately 6X the size of SLP) produced in tobacco roots showed accumulation of green fluorescence in tubercles growing on transformed plants but not in those growing on wild-type plants. This accumulation occurs regardless of whether the GFP is targeted to the cytoplasm (translocated symplastically) or the apoplastic space (translocated in xylem). Plants expressing SLP appear normal as compared to non-transgenic plants in the absence of Orobanche, so there is no obvious unintended impact on the host plant from SLP expression. This project required the creation of several gene constructs and generation of many transformed plant lines in order to address the research questions. The specific objectives of the project were to: 1. Make gene constructs fusing Orobanche-inducible promoter sequences to either the sarcotoxin-like peptide (SLP) gene or the GFP reporter gene. 2. Create transgenic plants containing gene constructs. 3. Characterize patterns of transgene expression and host-to-parasite movement of gene products in tobacco ( Nicotiana tabacum L.) and Arabidopsis thaliana (L.). 4. Characterize response of transgenic potato ( Solanum tuberosum L.) and tomato ( Lycopersicon esculentum Mill .) to Orobanche in lab, greenhouse, and field. Objectives 1 and 2 were largely accomplished during the first year during Dr. Aly's sabbatical visit to Virginia Tech. Transforming and analyzing plants with all the constructs has taken longer than expected, so efforts have concentrated on the most important constructs. Work on objective 4 has been delayed pending the final results of analysis on tobacco and Arabidopsis transgenic plants. The implications of this work are profound, because the Orobanche spp. is an extremely destructive weed that is not controlled effectively by traditional cultural or herbicidal weed control strategies. This is the first example of engineering resistance to parasitic weeds and represents a unique mode of action for selective control of these weeds. This research highlights the possibility of using this technique for resistance to other parasitic species and demonstrates the feasibility of developing other novel strategies for engineering resistance to parasitic weeds.
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Ginzberg, Idit, Richard E. Veilleux, and James G. Tokuhisa. Identification and Allelic Variation of Genes Involved in the Potato Glycoalkaloid Biosynthetic Pathway. United States Department of Agriculture, August 2012. http://dx.doi.org/10.32747/2012.7593386.bard.

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Steroidal glycoalkaloids (SGAs) are secondary metabolites being part of the plant defense response. The two major SGAs in cultivated potato (Solanum tuberosum) are α-chaconine and α-solanine, which exhibit strong cellular lytic properties and inhibit acetylcholinesterase activity, and are poisonous at high concentrations for humans. As SGAs are not destroyed during cooking and frying commercial cultivars have been bred to contain low levels, and their content in tubers should not exceed 20 mg/100 g fresh weight. However, environmental factors can increase tuber SGA content above the safe level. The focus of the proposed research was to apply genomic approaches to identify candidate genes that control potato SGA content in order to develop tools for potato improvement by marker-assisted selection and/or transgenic approaches. To this end, the objectives of the proposal included identification of genes, metabolic intermediates and allelic variations in the potato SGAbiosynthetic pathway. The SGAs are biosynthesized by the sterol branch of the mevalonic acid/isoprenoid pathway. Transgenic potato plants that overexpress 3-hydroxy-3-methylglutaryl-CoA reductase 1 (HMG1) or squalene synthase 1 (SQS1), key enzymes of the mevalonic acid/isoprenoid pathway, exhibited elevated levels of solanine and chaconine as well as induced expression of genes downstream the pathway. These results suggest of coordinated regulation of isoprenoid (primary) metabolism and SGA secondary metabolism. The transgenic plants were further used to identify new SGA-related candidate genes by cDNA-AFLP approach and a novel glycosyltransferase was isolated. In addition, genes involved in phytosterol biosynthesis may have dual role and synthesize defense-related steroidal metabolites, such as SGAs, via lanosterol pathway. Potato lanosterol synthase sequence (LAS) was isolated and used to prepare transgenic plants with overexpressing and silencing constructs. Plants are currently being analyzed for SGA content. The dynamics of SGA accumulation in the various organs of a potato species with high SGA content gave insights into the general regulation of SGA abundance. Leaf SGA levels in S. chacoense were 10 to 20-fold greater than those of S. tuberosum. The leptines, SGAs with strong antifeedant properties against Colorado potato beetles, were present in all aerial tissues except for early and mid-developmental stages of above ground stolons, and accounted for the high SGA content of S. chacoense. These results indicate the presence of regulatory mechanisms in most tissues except in stolons that limit the levels of α-solanine and α-chaconine and confine leptine accumulation to the aerial tissues. The genomes of cultivated and wild potato contain a 4-member gene family coding for SQS. Three orthologs were cloned as cDNAs from S. chacoense and heterologously expressed in E. coli. Squalene accumulated in all E. coli lines transformed with each of the three gene constructs. Differential transcript abundance in various organs and amino acid sequence differences in the conserved domains of three isoenzymes indicate subfunctionalization of SQS activity and triterpene/sterol metabolism. Because S. chacoense and S. phureja differ so greatly for presence and accumulation of SGAs, we selected four candidate genes from different points along the biosynthetic pathway to determine if chcor phuspecific alleles were associated with SGA expression in a segregating interspecific diploid population. For two of the four genes (HMG2 and SGT2) F2 plants with chcalleles expressed significantly greater total SGAs compared with heterozygotes and those with phualleles. Although there are other determinants of SGA biosynthesis and composition in potato, the ability of allelic states at two genes to affect SGA levels confirms some of the above transgenic work where chcalleles at two other loci altered SGA expression in Desiree. Present results reveal new opportunities to manipulate triterpene/sterol biosynthesis in more targeted ways with the objective of altering SGA content for both human health concerns and natural pesticide content without disrupting the essential metabolism and function of the phytosterol component of the membranes and the growth regulating brassinosteroids.
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