Relevant bibliographies by topics / Stearoyl CoA desaturase

Academic literature on the topic 'Stearoyl CoA desaturase'

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Published: 4 June 2021
Last updated: 25 April 2022

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Journal articles on the topic "Stearoyl CoA desaturase"

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Oatman, Nicole, Julie Reisz, Angelo D’Alessandro, and Biplab Dasgupta. "TAMI-55. THE EVOLUTIONARY ENIGMA OF FATTY ACID DESATURATION IN GLIOBLASTOMA." Neuro-Oncology 22, Supplement_2 (November 2020): ii225. http://dx.doi.org/10.1093/neuonc/noaa215.942.

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Abstract Fatty acid desaturation is an enzymatic reaction in which a double bond is introduced into an acyl chain. Of the four functionally distinct desaturase subfamilies, the First Desaturase Family of enzymes introduce the first double bond into a saturated fatty acid, resulting in the synthesis of monounsaturated fatty acids (MUFA). MUFA are essential components of membrane and storage lipids and exert a profound influence on the fluidity of biological membranes. A disequilibrium in saturated to unsaturated fatty acid ratio alters cell growth, differentiation and response to external stimuli, and thus affects a range of pathologies including cancer. The most abundant and key First Desaturase Family enzyme is the delta 9 desaturate called Stearoyl Co-A Desaturase (SCD and SCD5 in humans, and SCD1-4 in mice). SCD desaturates Stearoyl-CoA (C18) and palmitoyl-CoA (C16) to oleoyl-CoA (C18:1) and palmitoyl-CoA (C16:1), respectively. Besides SCD, the only known First Desaturase in mammals with dual function is FADS2 which desaturates palmitate to Sapienate (C16:1, a positional isomer of palmitoleate) in skin cells. A recent study showed that some cancer cells can use FADS2 to bypass the SCD reaction. SCD and SCD5 are by far the most abundant desaturases expressed in the human brain. We made an unexpected discovery that SCD undergoes monoallelic codeletion with PTEN on chromosome 10, and is also highly methylated in glioblastoma (GBM). More surprisingly, all GBM cell lines with SCD codeletion/methylation (that expressed very little SCD protein) are completely resistant to SCD/SCD5 inhibition, yet their phospholipids contained abundant oleic acid. It is unknown if GBMs bypassed SCD, but retained the delta 9 desaturation reaction through a novel enzymatic activity. Our targeted and untargeted metabolomics studies revealed unexpected findings that cannot be explained by conventional wisdom, and may lead to identification of novel lipogenic targets in GBM.
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Oatman, Nicole, and Biplab Dasgupta. "DDRE-15. THE EVOLUTIONARY ENIGMA OF FATTY ACID DESATURATION IN GLIOBLASTOMA." Neuro-Oncology Advances 3, Supplement_1 (March 1, 2021): i9. http://dx.doi.org/10.1093/noajnl/vdab024.037.

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Abstract Fatty acid desaturation is an enzymatic reaction in which a double bond is introduced into an acyl chain. Of the four functionally distinct desaturase subfamilies, the First Desaturase Family of enzymes introduce the first double bond into a saturated fatty acid, resulting in the synthesis of monounsaturated fatty acids (MUFA). MUFA are essential components of membrane and storage lipids and exert a profound influence on the fluidity of biological membranes. A disequilibrium in saturated to unsaturated fatty acid ratio alters cell growth, differentiation and response to external stimuli, and thus affects a range of pathologies including cancer. The most abundant and key First Desaturase Family enzyme is the delta 9 desaturate called Stearoyl Co-A Desaturase (SCD and SCD5 in humans, and SCD1-4 in mice). SCD desaturates Stearoyl-CoA (C18) and palmitoyl-CoA (C16) to oleoyl-CoA (C18:1) and palmitoyl-CoA (C16:1), respectively. Besides SCD, the only known First Desaturase in mammals with dual function is FADS2 which desaturates palmitate to Sapienate (C16:1, a positional isomer of palmitoleate) in skin cells. A recent study showed that some cancer cells can use FADS2 to bypass the SCD reaction. SCD and SCD5 are by far the most abundant desaturases expressed in the human brain. We made an unexpected discovery that SCD undergoes monoallelic codeletion with PTEN on chromosome 10, and is also highly methylated in glioblastoma (GBM). More surprisingly, all GBM cell lines with SCD codeletion/methylation (that expressed very little SCD protein) are completely resistant to SCD/SCD5 inhibition, yet their phospholipids contained abundant oleic acid. It is unknown if GBMs bypassed SCD, but retained the delta 9 desaturation reaction through a novel enzymatic activity. Our targeted and untargeted metabolomics studies revealed unexpected findings that cannot be explained by conventional wisdom, and may lead to identification of novel lipogenic targets in GBM.
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Kawashima, Y., N. Uy-Yu, and H. Kozuka. "Sex-related differences in the enhancing effects of perfluoro-octanoic acid on stearoyl-CoA desaturase and its influence on the acyl composition of phospholipid in rat liver. Comparison with clofibric acid and tiadenol." Biochemical Journal 263, no. 3 (November 1, 1989): 897–904. http://dx.doi.org/10.1042/bj2630897.

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The effects of the peroxisome proliferators clofibric acid (p-chlorophenoxyisobutyric acid), tiadenol [2,2′-(decamethylenedithio)diethanol] and perfluoro-octanoic acid (PFOA) on hepatic stearoyl-CoA desaturation in male and female rats were compared. Treatment of male rats with the three peroxisome proliferators increased markedly the activity of stearoyl-CoA desaturase. Administration of clofibric acid or tiadenol to female rats increased greatly the hepatic activity of stearoyl-CoA desaturase, the extent of the increases being slightly less pronounced than those of male rats. In contrast with the other two peroxisome proliferators, however, PFOA did not change the activity of stearoyl-CoA desaturase in female rats. Hormonal manipulations revealed that this sex-related difference in the effect of PFOA on stearoyl-CoA desaturase activity is strongly dependent on testosterone. The increase in stearoyl-CoA desaturase activity by peroxisome proliferators was not accompanied by any notable increases in the microsomal content of cytochrome b5 or the activity of NADH: cytochrome b5 reductase. The administration of the peroxisome proliferators greatly altered the acyl composition of hepatic phosphatidylcholine and phosphatidylethanolamine (namely the proportions of C18:1 and C20:3,n-9 fatty acids increased in both phospholipids), and the alterations were partially associated with the increase in stearoyl-CoA desaturase activity.
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Kikuchi, Kohtaro, and Hidekazu Tsukamoto. "Stearoyl-CoA desaturase and tumorigenesis." Chemico-Biological Interactions 316 (January 2020): 108917. http://dx.doi.org/10.1016/j.cbi.2019.108917.

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Lu, He, Xin Qin, Jing Zhang, Shuang Zhang, Yu Zhu, and Wei Hua Wu. "Molecular target analysis of stearoyl-CoA desaturase genes of protozoan parasites." Acta Parasitologica 63, no. 1 (March 26, 2018): 48–54. http://dx.doi.org/10.1515/ap-2018-0006.

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AbstractProtozoan parasites can synthesize polyunsaturated fatty acids. They possess stearoyl-CoA desaturase to convert stearate into oleate and linoleate. Stearoyl-CoA desaturase are the key enzymes required for the synthesis of unsaturated fatty acids. It seems attractive to evaluate the possibility of using unsaturated fatty acid biosynthesis pathways as drug targets. In this study, the authors investigate codon usage bias, base composition variations and protein sequence in ten available complete stearoyl-CoA desaturase gene sequences fromToxoplasma gondii,Neospora caninumetc. The results show that fatty acid desaturase genes GC content high of parasitic protozoa genes, GC content up to 63.37%, while fatty acid desaturase genes of parasitic protozoa prefers to use codon ending with G/C. In addition, the expected curve was also drawn to reveal the relationship of ENC and GC3s when the codon usage was only subjected to the nucleotide composition constraint. The genes lied on the expected curve in ENC-plot, indicating nucleotide composition constraint played a role in the condon usage pattern. Protein analysis, we find that all proteins are stearoyl-CoA desaturase, have sites of iron-binding active centers and contain three conserved His-rich motifs. If stearoyl-CoA desaturase is unusual to these parasites, it provides basis as a promising target for the development of selective chemical intervention. Therefore, the Bioinformatics analysis of protein and codon can help improve the work of genetic engineering and drug screening.
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Hao, Pan, Xia Cui, Jing Liu, Muzi Li, Yong Fu, and Qun Liu. "Identification and characterization of stearoyl-CoA desaturase in Toxoplasma gondii." Acta Biochimica et Biophysica Sinica 51, no. 6 (May 29, 2019): 615–26. http://dx.doi.org/10.1093/abbs/gmz040.

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Abstract Few information of the function of stearoyl-coenzyme A (CoA) desaturase (SCD) in apicomplaxan parasite has been obtained. In this study, we retrieved a putative fatty acyl-CoA desaturase (TGGT1_238950) by a protein alignment with Plasmodium falciparum SCD in ToxoDB. A typical Δ9-desaturase domain was revealed in this protein. The putative desaturase was tagged with HA endogenously in Toxoplasma gondii, and the endoplasmic reticulum localization of the putative desaturase was revealed, which was consistent with the fatty acid desaturases in other organisms. Therefore, the TGGT1_238950 was designated T. gondii SCD. Based on CRISPR/Cas9 gene editing technology, SCD conditional knockout mutants in the T. gondii TATi strain were obtained. The growth in vitro and pathogenicity in mice of the mutants suggested that SCD might be dispensable for tachyzoite growth and proliferation. The SCD-overexpressing line was constructed to further explore SCD function. The portion of palmitoleic acid and oleic acid were increased in SCD-overexpressing parasites, compared with the RH parental strain, indicating that T. gondii indeed is competent for unsaturated fatty acid synthesis. The SCD-overexpressing tachyzoites propagated slower than the parental strain, with a decreased invasion capability and weaker pathogenicity in mice. The TgIF2α phosphorylation and the expression changes of several genes demonstrated that ER stress was triggered in the SCD-overexpressing parasites, which were more apt toward autophagy and apoptosis. The function of unsaturated fatty acid synthesis of TgSCD was consistent with our hypothesis. On the other hand, SCD might also be involved in tachyzoite autophagy and apoptosis.
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Ntambi, James M., Makoto Miyazaki, and Agnieszka Dobrzyn. "Regulation of stearoyl-CoA desaturase expression." Lipids 39, no. 11 (November 2004): 1061–65. http://dx.doi.org/10.1007/s11745-004-1331-2.

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Ntambi, James M., Youngjin Choi, Yeonhwa Park, Jeffrey M. Peters, and Michael W. Pariza. "Effects of Conjugated Linoleic Acid (CLA) on Immune Responses, Body Composition and Stearoyl-CoA Desaturase." Canadian Journal of Applied Physiology 27, no. 6 (December 1, 2002): 617–27. http://dx.doi.org/10.1139/h02-036.

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Conjugated linoleic acid (CLA) has shown a wide range of biologically beneficial effects; reduction of incidence and severity of animal carcinogenesis, reduction of the adverse effects of immune stimulation, reduction of severity of atherosclerosis, growth promotion in young rats, and modulation of stearoyl-CoA desaturase (SCD). One of the most interesting aspects of CLA is its ability to reduce body fat while enhancing lean body mass which is associated with the trans-10,cis-12 isomer of CLA. The effects of CLA are unique characteristics that have not been observed with other polyunsaturated fatty acids. In this review, we will focus on the effects of CLA on immune responses, body compositional changes and stearoyl-CoA desaturase. Key words:trans-10,cis-12 CLA
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Sæther, Thomas, Thien N. Tran, Helge Rootwelt, Bjørn O. Christophersen, and Trine B. Haugen. "Expression and Regulation of Δ5-Desaturase, Δ6-Desaturase, Stearoyl-Coenzyme A (CoA) Desaturase 1, and Stearoyl-CoA Desaturase 2 in Rat Testis." Biology of Reproduction 69, no. 1 (July 1, 2003): 117–24. http://dx.doi.org/10.1095/biolreprod.102.014035.

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Murphy, D. J., I. E. Woodrow, and K. D. Mukherjee. "Substrate specificities of the enzymes of the oleate desaturase system from photosynthetic tissue." Biochemical Journal 225, no. 1 (January 1, 1985): 267–70. http://dx.doi.org/10.1042/bj2250267.

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In the microsomal fraction from young pea (Pisum sativum L.) leaves, the oleoyl moieties from oleoyl-CoA are principally transferred to the sn-2 position of phosphatidylcholine by oleoyl-CoA:1-acyl-lysophosphatidylcholine acyltransferase. The major product of this acyl transfer is 1-palmitoyl(stearoyl)-2-oleoyl phosphatidylcholine. The 1-palmitoyl(stearoyl)-2-oleoyl phosphatidylcholine is subsequently converted into 1-palmitoyl(stearoyl)-2-linoleoyl phosphatidylcholine by the oleate desaturase complex without equilibrating with the bulk membrane phosphatidylcholine pool. Hence, both the acyl transfer to phosphatidylcholine and the subsequent desaturation of oleoyl moieties occur on the sn-2 position of phosphatidylcholine, and there is also a functional coupling of the acyltransferase and oleate desaturase.
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Dissertations / Theses on the topic "Stearoyl CoA desaturase"

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Al-Jeryan, Lulwa A. "Characterization of a human stearoyl CoA desaturase gene." Thesis, Glasgow Caledonian University, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.251231.

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Dempsey, Kate E. "Characterisation of a human stearoyl CoA desaturase gene (SCD2)." Thesis, Glasgow Caledonian University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.369995.

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MacDonald, Marcia Leigh. "Stearoyl-CoA desaturase : role in metabolic syndrome, atherosclerosis and inflammation." Thesis, University of British Columbia, 2009. http://hdl.handle.net/2429/24653.

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Combination of the risk factors obesity, insulin resistance, dyslipidemia, and hypertension, often described as the "metabolic syndrome," increases the risk of developing diabetes and cardiovascular disease. Stearoyl-coenzyme A desaturase (SCD) activity has been implicated in the metabolic syndrome; however, earlier studies on the beneficial metabolic effects of SCD1 deficiency have been confined to normolipidemic mice, and the role of SCD in the context of atherosclerosis has not been examined. The primary purpose of this thesis was to investigate the effect of decreased SCD activity on susceptibility to atherosclerosis in mice. Thus, the overarching hypothesis driving the work was that SCD activity is atherogenic. As well, we examined the effect of absence of SCD1 on features of the metabolic syndrome and chronic inflammation in a mouse model of familial hyperlipidemia. An additional objective was to determine the effect of SCD1 deficiency on dextran sulfate sodium (DSS)-induced acute colitis with DSS dosing adjusted to account for genotypic differences in fluid consumption. These studies help us understand SCD functions in lipid metabolism and evaluate its attractiveness as a therapeutic target for the metabolic syndrome or atherosclerosis. After the Scd1ab-J mutation was characterized, mice carrying this allele were crossed with the low density lipoprotein receptor (LDLR)-deficient mouse strain. Features of the metabolic syndrome and atherosclerotic lesion area were evaluated in mice challenged with a Western diet for twelve weeks. In studies of colonic inflammation, wild-type controls were treated with 3.5% DSS for 5 days to induce moderately severe colitis, while the concentration of DSS given to SCD1-deficient mice was lowered to 2.5% to control for increased fluid consumption. Despite an antiatherogenic metabolic profile, SCD1 deficiency increased atherosclerosis in hyperlipidemic LDLR-deficient mice. Absence of SCD1 also led to chronic inflammation of the skin and increased plasma inflammatory markers, but did not accelerate inflammation in DSS-induced acute colitis when DSS intake was controlled. These findings reinforce the crucial role of chronic inflammation in promoting atherosclerosis, even in the presence of antiatherogenic metabolic characteristics, and suggest that inflammation must be closely monitored in studies of SCD inhibitors for treatment of the metabolic syndrome in humans.
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lefrevre, pascal. "Regulation genetique de la stearoyl coa desaturase hepatique de poulet." Rennes, Agrocampus Ouest, 1998. http://www.theses.fr/1998NSARIA07.

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L'importance de la stearoyl coa desaturase hepatique (scd1) a ete mise en evidence dans les mecanismes conduisant a la formation du tissu adipeux abdominal du poulet et plusieurs resultats suggerent l'implication du gene lui-meme dans la variabilite du caractere. Dans le but de verifier si l'hypothese d'une regulation essentiellement transcriptionnelle du gene scd1 hepatique etait verifiee ou non chez le poulet, l'etude de la regulation de l'expression de scd1 par des effecteurs hormonaux a ete entreprise. Ensuite, nous avons cherche a identifier des zones genomiques qui pourraient rendre compte d'une difference d'activite de scd1 correlee avec le taux de tissu adipeux des animaux. Pour cela, des regions cis de reponse aux principaux effecteurs de la regulation de l'expression de scd1 ont ete recherchees sur la partie 5 amont du gene. Nous avons etabli que le modele d'hepatocytes en culture primaire issu de poulet en croissance, d'environ 6 semaines, est un modele adapte a l'etude des genes de la lipogenese. Il permet d'eviter l'inconvenient majeur de la culture d'hepatocytes embryonnaires dans lesquels certains genes impliques dans la transduction de signaux hormonaux ne s'expriment pas. Ainsi, les interrogations concernant la difference de role joue par l'insuline sur la regulation des genes de la lipogenese entre les rongeurs et l'oiseau, ont commence a etre levees. En effet, nous avons montre que la regulation positive de l'expression de scd1 par l'insuline est essentiellement transcriptionnelle, ce qui est comparable aux observations faites chez les rongeurs. L'effet du glucagon sur l'expression de scd1 hepatique est egalement transcriptionnel. De plus, nous suggerons un effet du glucagon distinct de celui de l'insuline dans les hepatocytes de poulet. Par des experiences de transfection transitoire, nous avons montre que l'acide arachidonique, l'etya et le clofibrate avaient un effet inhibiteur sur la transcription du gene scd1 de poulet. Il apparait que l'effet du clofibrate sur la transcription de scd1 est oppose entre les especes souris et poulet. L'effet de l'etya sur la transcription de scd1 est plus rapide et plus court que celui de l'acide arachidonique, ce qui suggere que ces deux acides gras de meme structure (20 : 4) agissent par deux voies de regulation differentes. Le fragment de la partie 5 flanquante du gene scd1 compris entre 375 et +125 nucleotides contient les sequences necessaires a l'activite basale du promoteur de ce gene. De plus, les elements cis de reponse a l'insuline, a l'acide arachidonique, a l'etya et au clofibrate sont localises dans cette region. Les 83 nucleotides en 5 de ce fragment sont indispensables a l'activite de ce promoteur. Ils contiennent deux boites caat putatives et sont hautement conserves entre le rat, la souris et le poulet. Ce travail rassemble les premiers resultats concernant la regulation genetique de scd1 hepatique de poulet. Il permet de proposer des orientations pour des investigations futures vers la caracterisation d'elements regulateurs du gene scd1.
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Williams, Catherine Ann. "The role of stearoyl-CoA desaturase in lipid and lipoprotein metabolism." Thesis, University of Nottingham, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537664.

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Pinnameneni, Srijan Kumar, and s3083722@student rmit edu au. "Role of stearoyl-CoA desaturase1 in fatty acid-induced insulin resistance." RMIT University. Medical Sciences, 2006. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20070119.162450.

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Recent investigations suggest that reducing stearoyl CoA desaturase (SCD) 1 expression confers protection against obesity and insulin resistance, whereas others show that increasing SCD1 expression protects cells from lipotoxicity. The overall aim of this thesis was to establish the role of SCD1 expression in fatty acid metabolism and insulin stimulated glucose disposal in skeletal muscle. In vitro and in vivo studies were conducted to investigate the relationship between fatty acid subtype, SCD1 expression and fuel metabolism. The role of fatty acid subtype on fatty acid metabolite accumulation and insulin resistance was initially examined in rats. Rats were provided with a low fat diet or a high fat diet consisting of predominantly saturated (SAT) or polyunsaturated fatty acids (PUFA). Rats fed a SAT diet were insulin resistant and had increased skeletal muscle diacylglycerol content whereas rats fed a PUFA diet retained insulin sensitivity and accumulated triacylglycerol rather than diacylglycerol. Interestingly, SCD1 mRNA and protein content were elevated in SAT rats compared with PUFA fed and control fed rats, indicating a possible involvement of SCD1 in the aetiology of insulin resistance. Subsequently, SCD1 expression was examined in the skeletal muscle of various rodent models of genetic and diet-induced obesity. SCD1 content was consistently upregulated in the skeletal muscle of obese rodents. To determine whether SCD1 contributes to or protects from fatty-acid induced insulin resistance, SCD1 levels were transiently altered in L6 skeletal muscle myotubes. Short interfering (si) RNA was used to decrease SCD1 content and a pcDNA3.1/HygromSCD1 vector was introduced to increase SCD1 content. Reducing SCD1 protein resulted in marked esterification of exogenous fatty acids into diacylglycerol and ceramide. Insulin-stimulated Akt (acute transforming retrovirus thymoma) phosphorylation and 2-deoxyglucose uptake were reduced with SCD1 siRNA. Exposure of L6 myotubes to palmitate abolished insulin-stimulated glucose uptake in both control and SCD1 siRNA myotubes. Transient overexpression of SCD1 resulted in triacylglycerol esterification but attenuated ceramide and diacylglycerol accumulation and protected myotubes from fatty acid-induced insulin resistance. Further, these changes were associated with reduced phosphorylation of c-Jun Amino-Terminal Kinase (JNK) and the inhibitor of IêB kinase (IKK), both of which impair insulin signalling. These studies indicated that SCD1 protects from cellular toxicity in L6 myotubes by preventing excessive accumulation of bioactive lipid metabolites. Collectively, these experiments indicate that increasing SCD1 expression may be a protective mechanism designed to prevent insulin resistance in obese phenotypes.
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Ferdous, Zannatul. "Functional and phenotypic characterization of the stearoyl CoA desaturase gene of Anopheles coluzzii." Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/50707.

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Malaria is an infectious disease caused by Plasmodium parasites that are transmitted by the bite of female Anopheles mosquitoes. Successful acquisition and transmission of malaria parasites requires a female mosquito obtaining a blood meal from human hosts. The blood meal, which is rich in protein, is required for egg development. Most of the ingested protein is converted to lipid and stored in the fat body where vitellogenesis takes place. In this process, saturated fatty acids are converted to unsaturated fatty acids by the stearoyl-CoA desaturase (SCD1). Unsaturated fatty acids are also essential for maintaining cell membrane fluidity and other housekeeping functions. The main aim of this thesis was to functionally and phenotypically characterize the function of SCD1 during blood meal metabolism in the African mosquito vector Anopheles coluzzii. RNA interference (RNAi) silencing of the SCD1 gene and administration of a small molecule inhibitor of SCD1 had a significant impact on the survival of female mosquitoes following a blood meal. SCD1 knockdown (KD) caused a 100% mortality within 48 h after a human blood meal, while addition of the SCD1 small molecule inhibitor sterculic acid (SA) in the blood meal caused a 50% mortality within 72 h of blood meal. Microscopic analysis showed that SCD1 KD mosquitoes failed to develop eggs in response to the blood meal, while their thorax was filled with blood at 24 h post blood meal. These findings were highly consistent with electron microscopy data that showed increased plasma membrane rigidity and depletion of lipid droplets in the midgut epithelial cells. Transcriptional profiling using A. coluzzii oligonucleotide DNA microarrays showed that genes involved in protein, lipid and carbohydrate metabolism, as well as a large number of immunity genes were the most affected in blood-fed SCD1 KD versus control mosquitoes. Metabolomics profiling highlighted the biochemical framework by which the SCD1 KD phenotype is manifested after a blood meal, revealing increased amounts of saturated fatty acids and TCA cycle (and other interlinked pathway) intermediates in SCD1 KD and SA-treated mosquitoes. The data reported in this thesis reveal that silencing of SCD1 in female A. coluzzii mosquitoes leads to a metabolic syndrome primarily associated with the increase of saturated fatty acids and TCA cycle intermediates, which affects important biological functions leading to premature mosquito death. The accumulation of saturated fatty acids is also the likely cause of a potent immune response observed in the absence of infection, which resembles an auto-inflammatory reaction. These data provide important leads for the development of novel interventions aiming to block transmission of mosquito-borne diseases.
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Oatman, Nicole. "Mechanisms regulating cancer cell sensitivity and acquired resistance to Stearoyl-CoA Desaturase inhibition." University of Cincinnati / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1573572568302598.

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Dance, Lyndsey Jane Elizabeth. "The genetic and molecular mechanism of CLA formation in cattle : the role of stearoyl-CoA desaturase." Thesis, University of Bristol, 2009. http://hdl.handle.net/1983/21aa24ed-b002-4155-a972-3daaabad56ac.

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Feng, Shulan. "Using milk somatic cells to study stearoyl-CoA desaturase enzyme activity in dairy cows." Thesis, University of Nottingham, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479368.

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Books on the topic "Stearoyl CoA desaturase"

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Ntambi, Ph.D., James M., ed. Stearoyl-CoA Desaturase Genes in Lipid Metabolism. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7.

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Ph.D. James M. Ntambi. Stearoyl-CoA Desaturase Genes in Lipid Metabolism. Springer, 2013.

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James M. Ntambi Ph.D. Stearoyl-CoA Desaturase Genes in Lipid Metabolism. Springer, 2013.

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Book chapters on the topic "Stearoyl CoA desaturase"

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Schomburg, Dietmar, and Dörte Stephan. "Stearoyl-CoA desaturase." In Enzyme Handbook, 759–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-57942-4_157.

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Popeijus, Herman E. "SCD (Stearoyl-CoA Desaturase)." In Encyclopedia of Signaling Molecules, 4847–53. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101551.

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Popeijus, Herman E. "SCD (Stearoyl-CoA Desaturase)." In Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101551-1.

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Parimoo, Satish, and Pappas Apostolos. "Skin Stearoyl-CoA Desaturase Genes." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 13–25. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_2.

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Bond, Laura M., and James M. Ntambi. "Stearoyl-CoA Desaturase Isoforms 3 and 4: Avenues for Tissue-Specific ∆9 Desaturase Activity." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 131–40. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_11.

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Smith, Stephen B. "Functional Development of Stearoyl-CoA Desaturase Gene Expression in Livestock Species." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 141–59. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_12.

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Bernlohr, David A., and M. Daniel Lane. "Early Studies on Role of Stearoyl-CoA Desaturase During Preadipocyte Differentiation." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 1–11. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_1.

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Cantley, Jennifer L., Lucas M. O’Neill, James M. Ntambi, and Michael P. Czech. "The Cellular Function of Stearoyl-CoA Desaturase-2 in Development and Differentiation." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 119–30. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_10.

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Bernard, L., C. Leroux, and Y. Chilliard. "Expression and Nutritional Regulation of Stearoyl-CoA Desaturase Genes in the Ruminant Mammary Gland: Relationship with Milk Fatty Acid Composition." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 161–93. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_13.

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Watts, Jennifer L. "Physiological Functions and Regulation of C. elegans Stearoyl-CoA Desaturases." In Stearoyl-CoA Desaturase Genes in Lipid Metabolism, 195–207. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7969-7_14.

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Conference papers on the topic "Stearoyl CoA desaturase"

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Copland, John Alton, Laura A. Marlow, Ilah Bok, James L. Miller, Matsuda Akiko, Yan W. Asmann, Vivekananda Sarangi, et al. "Abstract 192: Targeting stearoyl CoA desaturase 1 (SCD1) in hepatobilliary carcinoma." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-192.

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Luyimbazi, D., A. Akcakanat, L. Zhang, Y. Zheng, and F. Meric-Bernstam. "mTOR modulates cellular fat metabolism by regulating stearoyl-CoA desaturase 1 transcription." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6030.

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CORRÊA DA SILVA, FELIPE, Licio Augusto Velloso, ROBERTA HADDAD TÓVOLLI, JOSEANE MORARI, LUCAS F R NASCIMENTO, and DANIELA S RAZOLLI. "Characterization of Stearoyl-CoA Desaturase 2 (SCD2) in the Brain of Rodents." In XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-51647.

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Roemeling, Christina Anna Elizabeth Von, Thomas Caulfield, Yaqing Qie, Derek C. Radisky, Xiujie Liu, Yuanxin Chen, Joshua Knight, John Copland, and Betty Kim. "Abstract LB-189: Blockade of stearoyl CoA desaturase 1 promotes immunogenic clearance of tumors." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-lb-189.

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Gleba, Justyna J., Laura A. Marlow, Erin E. Miller, James L. Miller, Aylin Alasonyalilar-Demirer, Yi Guo, Kabir Mody, et al. "Abstract 1004: Defining stearoyl-CoA desaturase 1 as a molecular therapeutic target against cholangiocarcinoma." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-1004.

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Belkaid, Anissa, Rodney J. Ouellette, and Marc E. Surette. "Abstract 1706: Estrogen induces stearoyl-CoA desaturase expression in human MCF-7 breast carcinoma cells." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1706.

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Ma, Kin Fai, Eunice Yuen Ting Lau, Irene Oi Lin Ng, and Kin Wah Lee. "Abstract 4772: Stearoyl-CoA Desaturase (SCD1) regulates liver tumor initiating cells through modulating ER stress." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4772.

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Ma, Kin Fai, Jessica Lo, Eunice Yuen-Ting Lau, John A. Copland, Irene Oi-Lin Ng, and Terence Kin-Wah Lee. "Abstract 1003: Targeting liver-tumor initiating cells via hampering the lipogenesis pathways through stearoyl - CoA desaturase." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-1003.

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Sugaru, Eiji, Yudai Furuta, Yuichi Fukunaga, Hiroki Umehara, Tsuguteru Otsubo, Manabu Watanabe, Futoshi Hasegawa, Shingo Tojo, Miki Hashizume, and Hitoshi Ban. "Abstract 3069: DSP-0692, a novel and selective stearoyl-CoA desaturase (SCD) inhibitor targeting cancer stem cells." 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.am2018-3069.

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Holder, Ashley M., Ana M. Gonzalez-Angulo, Huiqin Chen, Argun Akcakanat, Kim Anh-Do, Fraser Symmans, Lajos Pusztai, Gabriel Hortobagyi, Gordon B. Mills, and Funda Meric-Bernstam. "Abstract 682: Increased stearoyl-CoA desaturase 1 expression is associated with shorter survival in breast cancer patients." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-682.

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