Relevant bibliographies by topics / SCD1

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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 'SCD1'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 June 2025

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Journal articles on the topic "SCD1"

1

Levitsky, A., A. Gozhenko, V. Velichko, and I. Selivanskaya. "The effect of dietary fat supplements on the activity of palmitic and stearic acid desaturases based on the results of a study of the fatty acid composition of neutral lipids in blood serum and liver of rats receiving a fat-free diet." Journal of Education, Health and Sport 12, no. 1 (January 18, 2022): 197–206. http://dx.doi.org/10.12775/jehs.2022.12.01.016.

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Background. Desaturase enzymes are involved in the formation of monoenoic acids from saturated fatty acids. One such enzyme is stearyl-CoA-desaturase (SCD1), which converts stearic acid to oleic acid. The aim of this work was to determine the effect of edible fats with different fatty acid compositions on SCD1 activity.
 Methods. High linoleic sunflower oil (HLSO), high oleic sunflower oil (HOSO) and palm oil (PO) were used. The rats were fed for 30 days with a semi-synthetic diet that did not contain any fats (FFD) and fat diets containing 5 % of each of the above oils. In animals, lipids were extracted from serum and liver and divided into 3 fractions: neutral lipids (NL), phospholipids (PL), and free fatty acids (FFA).
 The fatty acid composition of each fraction was determined by gas chromatography. The SCD18 activity was determined by the C18:1 n-9/C18:0 ‒ ratio, and the SCD16 activity was determined by the C16:1 n-7/C16:0 ratio.
 Results. A higher activity of SCD16 and SCD18 was found in the NL fraction, and the activity of SCD18 significantly exceeds that of SCD16. A decrease in the content of C16:0, C16:1 and C18:0 in the NL fraction of the liver and blood serum was shown. The activity of SCD16 in blood serum and liver decreases in rats fed fat diets­, while the activity of SCD18 does not decrease, and even increases with the consumption of HOSO.­
 Conclusions. To determine the SCD1 activity, it is advisable to use the C18:1/C18:0 ratio in terms of the level of fatty acids in the NL fraction. Fatty diet inhibits SCD16 activity, and consumption of HOSO increases SCD18 activity.
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2

Li, Ying-chun, Chang-rung Chen, and Eric C. Chang. "Fission Yeast Ras1 Effector Scd1 Interacts With the Spindle and Affects Its Proper Formation." Genetics 156, no. 3 (November 1, 2000): 995–1004. http://dx.doi.org/10.1093/genetics/156.3.995.

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Abstract Ras1 GTPase is the Schizosaccharomyces pombe homolog of the mammalian Ha-Ras proto-oncoprotein. Ras1 interacts with Scd1 (aka Ral1), a presumptive guanine nucleotide exchange factor for Cdc42sp, to control organization of the cytoskeleton. In this study, we demonstrated that the scd1 deletion (scd1Δ) induced hypersensitivity to microtubule destabilizing drugs and instability of the minichromosome. Overexpression of scd1 induced formation of abnormal spindles and chromosome missegregation. The scd1 deletion worsened the defects of spindle formation in tubulin mutants; by contrast, it did not induce lethality in mutants defective in the spindle pole bodies. These genetic data suggest that Scd1 can interact with tubulin with substantial specificity to affect proper spindle formation and chromosome segregation. Subcellular localization data further illustrated that a GFP-Scd1 fusion protein can associate with the spindle. Finally, we showed that unlike ras1Δ and scd1Δ, byr2Δ (affecting the Ras1 effector for mating) is not synthetically lethal with the tubulin mutations. These data collectively suggest that the Ras1 pathway can impinge upon microtubules through Scd1, but not Byr2, to affect proper spindle formation and chromosome segregation.
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Li, Yingchun, and Eric C. Chang. "Schizosaccharomyces pombeRas1 Effector, Scd1, Interacts With Klp5 and Klp6 Kinesins to Mediate Cytokinesis." Genetics 165, no. 2 (October 1, 2003): 477–88. http://dx.doi.org/10.1093/genetics/165.2.477.

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AbstractFission yeast Scd1 is an exchange factor for Cdc42 and an effector of Ras1. In a screen for scd1 interacting genes, we isolated klp5 and klp6, which encode presumptive kinesins. Klp5 and Klp6 form a complex to control the same processes, which so far include microtubule dynamics and chromosome segregation. We showed that klp5 or klp6 inactivation in combination with the scd1 deletion (scd1Δ) created a synthetic temperature-dependent growth defect. Further genetic analysis demonstrated that Klp5 and Klp6 interacted specifically with the Ras1-Scd1 pathway, but not with the Ras1-Byr2 pathway. In addition, Klp5 and Klp6 can stably associate with Scd1 and Cdc42. A deletion in the Scd1 C terminus, which contains the PB1 domain, prevented Scd1 binding to Klp5/6 and caused a growth defect in Klp5/6 mutant cells that is indistinguishable from that induced by scd1Δ. Analysis of the double-mutant phenotype indicated that at the nonpermissive temperature, cells failed to undergo cytokinesis efficiently. These cells contained abnormal contractile rings in which F-actin and Mid1, a key regulator of F-actin ring formation and positioning, are mispositioned and fragmented. These data suggest that Klp5/6 cooperate with the Ras1-Scd1 pathway to influence proper formation of the contractile ring for cytokinesis.
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Mnatsakanyan, Hayk, Caline Pechdimaljian, Roshani Jha, Alessandro Sammarco, Baolong Su, Kevin J. Williams, Steven J. Bensinger, and Christian E. Badr. "CSIG-17. SCD5 PROTECTS GLIOBLASTOMA STEM CELLS FROM DEATH AND DIFFERENTIATION BY MODULATING INTRACELLULAR LIPID COMPOSITION." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii42. http://dx.doi.org/10.1093/neuonc/noac209.166.

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Abstract Glioblastoma (GBM) is the most common malignant brain cancer in adults, enriched in a small subpopulation of glioma stem cells (GSC), which can drive tumor recurrence and therapeutic resistance. Considerable evidence suggests that the endogenous levels of unsaturated fatty acids (FA) are crucial regulators of GSCs survival and self-renewal. Stearoyl-CoA desaturase-1 (SCD-1) is the most abundant desaturase in humans. We have previously shown that SCD1 activity is required for GSCs self-renewal and brain tumor initiation. However, SCD1 orthologous isoform, SCD5, has been poorly characterized and its potential role in GBM has not been previously reported. We have observed that SCD5 is highly enriched in GSC both at the mRNA and protein levels. Genetic downregulation of SCD5 in GSCs led to a remarkable decrease in stem cell markers, impaired cell viability and the ability to form neurospheres. Further, the downregulation of SCD5 in GSCs orthotopically implanted in mice resulted in delayed tumor growth and extended overall survival. Shotgun lipidomics in GSCs after either SCD1 or SCD5 knock-down revealed a largely distinctive lipidome profile, highlighting the divergent role of these two isoforms in GBM lipid metabolism. Surprisingly, lipidomics analysis showed that both SCD1 and SCD5 are required to synthesize a variety of lipid species involved in receptor tyrosine kinase (RTKs) and GPCRs signal transduction, directly linking FA synthesis with the oncogenic signaling. We confirmed these results by immunoblot analysis. Using specific tagging and immunofluorescence analysis, we observed that, despite a spatial overlap in SCD1 and SCD5 expression, SCD5 is uniquely present in some subcellular locations. This suggests that different functions of these isoforms could be related to different subcellular localization. Altogether, our results underscore a novel function of SCD isoforms in GSCs metabolism and highlight SCD5 as a potential therapeutic target for GBM.
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Chu, Kiki, Makoto Miyazaki, Weng Chi Man, and James M. Ntambi. "Stearoyl-Coenzyme A Desaturase 1 Deficiency Protects against Hypertriglyceridemia and Increases Plasma High-Density Lipoprotein Cholesterol Induced by Liver X Receptor Activation." Molecular and Cellular Biology 26, no. 18 (September 15, 2006): 6786–98. http://dx.doi.org/10.1128/mcb.00077-06.

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ABSTRACT Stearoyl-coenzyme A desaturase (SCD) is the rate-limiting enzyme necessary for the biosynthesis of monounsaturated fatty acids. In this study, we investigated the regulation of mouse SCD1 by liver X receptor (LXR) and its role in plasma lipoprotein metabolism upon LXR activation. In vivo, the SCD1 gene remained induced upon LXR activation in the absence of sterol regulatory element-binding protein 1c (SREBP-1c), a known transcriptional regulator of SCD1. Serial deletion and point mutation analyses in reporter gene assays, as well as a gel mobility shift assay, identified an LXR response element in the mouse SCD1 promoter. In addition, SCD1 deficiency prevented the hypertriglyceridemic effect and reduced hepatic triglyceride accumulation associated with LXR activation despite induced hepatic expression of SREBP-1c protein and several SREBP1c and LXR target genes involved in lipoprotein metabolism. Unlike wild-type mice, SCD1-deficient mice failed to elevate the hepatic triglyceride monounsaturated acid (MUFA)/saturated fatty acid (SFA) ratio despite induction of the SCD2 gene. Together, these findings suggest that SCD1 plays a pivotal role in the regulation of hepatic and plasma triglyceride accumulation, possibly by modulating the MUFA-to-SFA ratio. In addition, SCD1 deficiency also increased plasma high-density lipoprotein cholesterol levels induced by LXR activation.
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Wei, Bin, Brian S. Hercyk, Nicholas Mattson, Ahmad Mohammadi, Julie Rich, Erica DeBruyne, Mikayla M. Clark, and Maitreyi Das. "Unique spatiotemporal activation pattern of Cdc42 by Gef1 and Scd1 promotes different events during cytokinesis." Molecular Biology of the Cell 27, no. 8 (April 15, 2016): 1235–45. http://dx.doi.org/10.1091/mbc.e15-10-0700.

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The Rho-family GTPase Cdc42 regulates cell polarity and localizes to the cell division site. Cdc42 is activated by guanine nucleotide exchange factors (GEFs). We report that Cdc42 promotes cytokinesis via a unique spatiotemporal activation pattern due to the distinct action of its GEFs, Gef1 and Scd1, in fission yeast. Before cytokinetic ring constriction, Cdc42 activation, is Gef1 dependent, and after ring constriction, it is Scd1 dependent. Gef1 localizes to the actomyosin ring immediately after ring assembly and promotes timely onset of ring constriction. Gef1 is required for proper actin organization during cytokinesis, distribution of type V myosin Myo52 to the division site, and timely recruitment of septum protein Bgs1. In contrast, Scd1 localizes to the broader region of ingressing membrane during cytokinetic furrowing. Scd1 promotes normal septum formation, and scd1Δ cells display aberrant septa with reduced Bgs1 localization. Thus we define unique roles of the GEFs Gef1 and Scd1 in the regulation of distinct events during cytokinesis. Gef1 localizes first to the cytokinetic ring and promotes timely constriction, whereas Scd1 localizes later to the ingressing membrane and promotes septum formation. Our findings are consistent with reports that complexity in GTPase signaling patterns enables exquisite precision over the control of cellular processes.
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Lamas, Iker, Nathalie Weber, and Sophie G. Martin. "Activation of Cdc42 GTPase upon CRY2-Induced Cortical Recruitment Is Antagonized by GAPs in Fission Yeast." Cells 9, no. 9 (September 12, 2020): 2089. http://dx.doi.org/10.3390/cells9092089.

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The small GTPase Cdc42 is critical for cell polarization in eukaryotic cells. In rod-shaped fission yeast Schizosaccharomyces pombe cells, active GTP-bound Cdc42 promotes polarized growth at cell poles, while inactive Cdc42-GDP localizes ubiquitously also along cell sides. Zones of Cdc42 activity are maintained by positive feedback amplification involving the formation of a complex between Cdc42-GTP, the scaffold Scd2, and the guanine nucleotide exchange factor (GEF) Scd1, which promotes the activation of more Cdc42. Here, we use the CRY2-CIB1 optogenetic system to recruit and cluster a cytosolic Cdc42 variant at the plasma membrane and show that this leads to its moderate activation also on cell sides. Surprisingly, Scd2, which binds Cdc42-GTP, is still recruited to CRY2-Cdc42 clusters at cell sides in individual deletion of the GEFs Scd1 or Gef1. We show that activated Cdc42 clusters at cell sides are able to recruit Scd1, dependent on the scaffold Scd2. However, Cdc42 activity is not amplified by positive feedback and does not lead to morphogenetic changes, due to antagonistic activity of the GTPase activating protein Rga4. Thus, the cell architecture is robust to moderate activation of Cdc42 at cell sides.
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Mnatsakanyan, Hayk, Elie Roumieh, Caline Pechdimaljian, Joelle El Hokayem, Alessandro Sammarco, and Christian Badr. "DNAR-12. STEAROYL-COA DESATURASE REGULATES DNA DAMAGE REPAIR IN GBM BY MODULATING PARP1 ACTIVITY." Neuro-Oncology 26, Supplement_8 (November 1, 2024): viii119—viii120. http://dx.doi.org/10.1093/neuonc/noae165.0463.

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Abstract Glioblastoma (GBM) is the most prevalent malignant brain cancer in adults, notorious for its aggressiveness and resistance to therapy. GBM patients commonly receive radiation therapy combined with temozolomide (TMZ), which engages tumor cells to promote lethal DNA damage and subsequent cytotoxicity. Active DNA repair mechanisms, particularly in a subset population of GBM stem-like cells (GSCs), drive therapeutic resistance, thus largely contributing to the bleak prognosis of GBM. Poly (ADP-ribose) polymerases (PARPs) are essential in various cellular processes, including DNA repair. We have previously reported that fatty acid desaturation mediated by Stearoyl-CoA desaturase 1 (SCD1) plays a cytoprotective role in GSCs. Inhibiting SCD prevents tumor initiation and inhibits DNA damage repair, hence sensitizing to radiation and TMZ. Yet, the mechanistic role of SCD in DNA damage regulation remained unknown. Here, we found that the expression of both human isoforms of SCD, SCD1, and SCD5, directly correlates with PARP protein levels and subcellular localization. Downregulating SCD1/5 in GSCs resulted in significantly lower levels of PARP1, coupled with increased DNA damage, as well as reduced DNA damage repair and chromosome assembly. Conversely, cells overexpressing SCD1/5 exhibited higher PARP1 expression and lower levels of basal DNA damage compared to control GSCs. Notably, SCD1/5 overexpression also led to increased resistance to TMZ. We show that SCD1/5 regulates PARP activity by controlling PARP1 subcellular localization. In addition to decreased total levels of PARP following SCD1/5 downregulation, we also found increased PARP1 self-PARylation. Using confocal microscopy, we show that when SCD1/5 is repressed, PARylated PARP translocates from the nucleus to the cytosol, rendering it unable to bind DNA and recruit DNA-repairing machinery. In conclusion, our study provides a direct link between fatty acid metabolism and PARP1-mediated DNA damage repair.
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Kelly, Felice D., and Paul Nurse. "Spatial control of Cdc42 activation determines cell width in fission yeast." Molecular Biology of the Cell 22, no. 20 (October 15, 2011): 3801–11. http://dx.doi.org/10.1091/mbc.e11-01-0057.

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The fission yeast Schizosaccharomyces pombe is a rod-shaped cell that grows by linear extension at the cell tips, with a nearly constant width throughout the cell cycle. This simple geometry makes it an ideal system for studying the control of cellular dimensions. In this study, we carried out a near-genome-wide screen for mutants wider than wild-type cells. We found 11 deletion mutants that were wider; seven of the deleted genes are implicated in the control of the small GTPase Cdc42, including the Cdc42 guanine nucleotide exchange factor (GEF) Scd1 and the Cdc42 GTPase-activating protein (GAP) Rga4. Deletions of rga4 and scd1 had additive effects on cell width, and the proteins localized independently of one another, with Rga4 located at the cell sides and Scd1 at the cell tips. Activated Cdc42 localization is altered in rga4Δ, scd1Δ, and scd2Δ mutants. Delocalization and ectopic retargeting experiments showed that the localizations of Rga4 and Scd1 are crucial for their roles in determining cell width. We propose that the GAP Rga4 and the GEF Scd1 establish a gradient of activated Cdc42 within the cellular tip plasma membrane, and it is this gradient that determines cell growth-zone size and normal cell width.
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Papadaki, Piyi, Véronique Pizon, Brian Onken, and Eric C. Chang. "Two Ras Pathways in Fission Yeast Are Differentially Regulated by Two Ras Guanine Nucleotide Exchange Factors." Molecular and Cellular Biology 22, no. 13 (July 1, 2002): 4598–606. http://dx.doi.org/10.1128/mcb.22.13.4598-4606.2002.

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ABSTRACT How a given Ras prreotein coordinates multiple signaling inputs and outputs is a fundamental issue of signaling specificity. Schizosaccharomyces pombe contains one Ras, Ras1, that has two distinct outputs. Ras1 activates Scd1, a presumptive guanine nucleotide exchange factor (GEF) for Cdc42, to control morphogenesis and chromosome segregation, and Byr2, a component of a mitogen-activated protein kinase cascade, to control mating. So far there is only one established Ras1 GEF, Ste6. Paradoxically, ste6 null (ste6Δ) mutants are sterile but normal in cell morphology. This suggests that Ste6 specifically activates the Ras1-Byr2 pathway and that there is another GEF capable of activating the Scd1 pathway. We thereby characterized a potential GEF, Efc25. Genetic data place Efc25 upstream of the Ras1-Scd1, but not the Ras1-Byr2, pathway. Like ras1Δ and scd1Δ, efc25Δ is synthetically lethal with a deletion in tea1, a critical element for cell polarity control. Using truncated proteins, we showed that the C-terminal GEF domain of Efc25 is essential for function and regulated by the N terminus. We conclude that Efc25 acts as a Ras1 GEF specific for the Scd1 pathway. While ste6 expression is induced during mating, efc25 expression is constitutive. Moreover, Efc25 overexpression renders cells hyperelongated and sterile; the latter can be rescued by activated Ras1. This suggests that Efc25 can recruit Ras1 to selectively activate Scd1 at the expense of Byr2. Reciprocally, Ste6 overexpression can block Scd1 activation. We propose that external signals can partly segregate two Ras1 pathways by modulating GEF expression and that GEFs can influence how Ras is coupled to specific effectors.
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Dissertations / Theses on the topic "SCD1"

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CAPUTO, MANUEL. "DEPDC1A, a novel SREBP1 cofactor, regulates fatty acid metabolism in breast cancer." Doctoral thesis, Università degli Studi di Trieste, 2018. http://hdl.handle.net/11368/2924764.

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Breast cancer (BC) figures as the most frequently diagnosed and the leading cause of cancer-related deaths among women worldwide. Despite considerable progress has been made in cancer detection and therapy assignment, several BCs become resistant to therapy and, moreover, a considerable proportion of patients develops metastasis during therapy or experiences relapse. Growing body of evidence indicates that alterations in tumour metabolism are linked to therapeutic resistance, tumour relapse and dissemination. These altered metabolic traits are caused by genetic alterations and environmental factors. The most frequently mutated gene in BC is the tumor suppressor TP53, a well-characterized transcription factor, which plays a central role in cellular homeostasis and prevention of tumour growth. In BC missense mutations occur very often in its DNA binding domain, providing neomorphic mutant p53 proteins that lose the wildtype onco-suppressive functions and acquire instead new oncogenic properties (Gain-of-Function). Indeed, mutant p53 proteins establish aberrant interactions with different transcription factors, thus inducing oncogenic transcriptional programs and metabolic reprogramming. Our previous work outlined a mutant p53 driven signature that promotes aggressiveness in BC in which DEP domain containing 1A (DEPDC1A) emerged as an important mediator of migration and invasiveness (Girardini et al., 2011). DEPDC1A expression is almost undetectable in normal cells, but it is overexpressed in different cancers and its overexpression is associated with poor prognosis. DEPDC1A is a transcriptional cofactor that exists in two different splice variants V1 and V2, but its role in oncogenesis, as well as in a physiological context, remains elusive. Here we show, through a high-throughput transcriptional analysis, that DEPDC1A is able to impinge on lipid metabolism. In particular we observed that mRNAs belonging to the fatty acids biosynthesis pathway genes ATP-Citrate Lyase (ACLY), Stearoyl-CoA Desaturase 1 (SCD1) and Elongation Of Very Long Chain Fatty Acids 6 (ELOVL6) were consistently downregulated upon DEPDC1A silencing suggesting a key role for this factor in controlling fatty acid metabolism in cancer cells. Indeed, ablation of DEDPC1A caused a significant decrease of lipid droplets content and fatty acid desaturation in MDA-MB-231 cell line. ACLY, SCD1 and ELOVL6, as a part of fatty acids biosynthesis pathway, are specific targets of Sterol Regulatory Element Binding Protein (SREBP) transcription factors, master regulators of lipid metabolism. Interestingly, protein co-immunoprecipitation and Chromatin Immunoprecipitation assays demonstrated that DEPDC1A physically interacts with SREBP1 and that it is required for an efficient transcriptional activation of this particular subset of genes, thus acting as transcriptional cofactor of SREBP1. Finally, we showed that DEPDC1A, through SCD1 upregulation, is able to promote aggressive phenotypes, such as migration, and that DEPDC1A overexpression in normal cells is sufficient to induce sensitization toward SCD1 inhibition. This study unveils a novel oncogenic transcriptional program induced by the aberrant interaction between DEPDC1A and SREBP1 transcription factor that is able to induce fatty acid biosynthesis and desaturation in cancer cells and to establish a metabolic addiction that can be potentially exploited in cancer therapy.
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MacDonald, Marcia L. E., Eck Miranda van, Reeni B. Hildebrand, Brian W. C. Wong, Nagat Bissada, Piers Ruddle, Anatol Kontush, et al. "Despite antiatherogenic metabolic characteristics, SCD1-deficient mice have increased inflammation and atherosclerosis." American Heart Association, 2008. http://hdl.handle.net/2429/9434.

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OBJECTIVE—Absence of stearoyl-CoA desaturase-1 (SCD1) in mice reduces plasma triglycerides and provides protection from obesity and insulin resistance, which would be predicted to be associated with reduced susceptibility to atherosclerosis. The aim of this study was to determine the effect of SCD1 deficiency on atherosclerosis. Methods and RESULTS—Despite an antiatherogenic metabolic profile, SCD1 deficiency increases atherosclerosis in hyperlipidemic low density lipoprotein receptor (LDLR)-deficient mice challenged with a western diet. Lesion area at the aortic root is significantly increased in males and females in two models of SCD1 deficiency. Inflammatory changes are evident in the skin of these mice, including increased intercellular adhesion molecule (ICAM)-1 and ulcerative dermatitis. Increases in ICAM-1 and interleukin-6 are also evident in plasma of SCD1-deficient mice. HDL particles demonstrate changes associated with inflammation, including, decreased plasma apoA-II and apoA-I and paraoxonase-1 and increased plasma serum amyloid A. Lipopolysaccharide-induced inflammatory response and cholesterol efflux are not altered in SCD1-deficient macrophages. In addition, when SCD1 deficiency is limited to bone-marrow derived cells, lesion size is not altered in LDLR-deficient mice. CONCLUSIONS—These studies reinforce the crucial role of chronic inflammation in promoting atherosclerosis, even in the presence of antiatherogenic biochemical and metabolic characteristics. [The original version of this article, along with updated information and services is located on the World Wide Web at: http://atvb.ahajournals.org/cgi/content/full/29/3/341] [UBC users: please click on the UBC eLink icon at the bottom of this record]
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Wehbi, Mariam. "Le récepteur du froid TRPM8 orchestre le métabolisme et la sécrétion des lipides par la régulation du SCD1 : implication de la physiologie de la prostate au syndrome métabolique et à l'insuffisance cardiaque." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10325.

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Le syndrome métabolique (MetS) représente une constellation d'anomalies interconnectées, dont l'obésité, la résistance à l'insuline, la dyslipidémie athérogène et l'hypertension. Tous ces facteurs augmentent le risque de maladies cardiovasculaires et de diabète de type 2. La dysrégulation du métabolisme lipidique et la perte de flexibilité métabolique jouent un rôle central dans la pathogenèse du MetS et de l'insuffisance cardiaque à fraction d'éjection préservée (HFpEF). La stéaroyl CoA désaturase 1 (SCD1), l'enzyme goulot d'étranglement qui convertit les acides gras saturés (AGS) en formes monoinsaturées (AGMI), a été proposée pour jouer un rôle clé dans le développement du MetS. Cette enzyme a été largement étudiée dans le cadre d'études métaboliques portant sur la physiopathologie cardiovasculaire. Nos résultats in vitro ont révélé que le récepteur du froid TRPM8 régule l'expression du SCD1 dans les cellules épithéliales de la prostate. Le récepteur transitoire de la mélastatine 8 (TRPM8), le récepteur du froid et du menthol, est essentiel à la thermosensation, bien que son rôle dans les organes du corps ne soit pas encore clair. En plus de TRPM8, nous avons précédemment cloné plusieurs isoformes, comme 4TM-TRPM8, qui peut être exprimé avec ou sans TRPM8. Dans nos travaux récents, nous avons caractérisé TRPM8(85) humaine dans les membranes du réticulum endoplasmique (RE) près de l'appareil de Golgi (AG) et dans les mitochondries des cellules épithéliales de la prostate. L'inhibition de TRPM8(85) induit une accumulation de gouttelettes lipidiques, une expansion et une fragmentation de l'AG, qui sont associées à une diminution du trafic vésiculaire vers le plasmalemme. En outre, l'analyse lipidomique révèle une forte augmentation des acides gras insaturés (AGI), induite par l'inactivation de TRPM8(85) et, dans une moindre mesure, par l'inactivation de TRPM8. L'augmentation des AGI est due à l'induction du gène ∆9 de la stéaroyl désaturase (Scd1). L'inhibition de SCD1 ou l'incubation avec du palmitate empêche l'expansion de l'AG dans les cellules silencieuses TRPM8(85). Enfin, nous avons démontré que TRPM8 régule SCD1 via le récepteur des androgènes. Comme SCD1 est un acteur majeur de la lipogenèse qui, lorsqu'il est dérégulé, entraîne des perturbations métaboliques, nous sommes passés à des études in vivo axées sur le phénotype métabolique de souris présentant une délétion globale de TRPM8. Nous avons observé des changements dans le profil lipidique de la prostate, du foie et du cœur chez les souris TRPM8 KO au niveau des AGMI, des AGS et d'autres espèces lipidiques. Dans le contexte du MetS développé chez ces souris KO à la suite d'un régime riche en graisses et en saccharose (HFHSD), nos résultats ont montré que les souris TRPM8 KO soumises au HFHSD présentaient un meilleur métabolisme du glucose et une sensibilité accrue à l'insuline. Dans le groupe TRPM8 KO sous HFHSD, le foie présentait une accumulation accrue de lipides par rapport aux souris WT. L'analyse échocardiographique a confirmé un développement précoce de l'insuffisance cardiaque avec fraction d'éjection préservée (HFpEF) chez les souris WT (augmentation de E/E'), alors que les souris KO étaient protégées. L'analyse transcriptomique a principalement révélé des profils de métabolisme lipidique distincts entre les différents groupes de souris. En conclusion, nos résultats démontrent que la dysrégulation de TRPM8 entraîne des modifications du profil lipidique dans des modèles in vitro et in vivo. Cela fait de TRPM8 une nouvelle cible potentielle pour le maintien de l'homéostasie du métabolisme lipidique, en particulier dans le cadre du MetS et du développement éventuel de l'HFpEF<br>Metabolic syndrome (MetS) represents a constellation of interconnected abnormalities, including obesity, insulin resistance, atherogenic dyslipidemia and hypertension. All of these factors increase the risk of cardiovascular diseases and type 2 diabetes. Dysregulation of lipid metabolism and the loss of metabolic flexibility play a central role in the pathogenesis of MetS and heart failure with preserved ejection fraction (HFpEF). Stearoyl CoA desaturase 1 (SCD1), the bottleneck enzyme that converts saturated fatty acids (SFA) into monounsaturated forms (MUFA), has been proposed to play a key role in the development of MetS. This enzyme has been extensively studied in metabolic studies concerning cardiovascular pathophysiology. Our in vitro results have revealed that the cold receptor TRPM8 regulates SCD1 expression in prostate epithelial cells. Transient receptor potential melastatin 8 (TRPM8), the cold and menthol receptor, is essential to thermosensation, although its roles in organs within the body are still unclear. In addition to TRPM8, we have previously cloned several isoforms, such as 4TM-TRPM8, which can be expressed with or without TRPM8. In our recent work, we characterized human TRPM8(85) in endoplasmic reticulum (ER) membranes near the Golgi apparatus (GA) and mitochondria in prostate epithelial cells. Silencing of TRPM8(85) induces lipid droplet accumulation, GA expansion and fragmentation, which are associated with a decrease in the vesicular trafficking to plasmalemma. Furthermore, lipidomic analysis reveals a strong shift in unsaturated fatty acids (UFAs), induced by TRPM8(85) silencing and to a lesser extent silencing of TRPM8. The increase in UFAs is caused by the induction of ∆9 stearoyl desaturase (Scd1) gene. Silencing SCD1 or incubating with palmitate prevents GA expansion in TRPM8(85)-silenced cells. Finally, we demonstrated that TRPM8 regulates SCD1 via the androgen receptor. As SCD1 is a major lipogenic player that, when dysregulated, leads to metabolic disruptions, we transitioned to in vivo studies focusing on the metabolic phenotyping of mice with a global deletion of TRPM8. We observed changes in the lipid profile of the prostate, liver and heart in the TRPM8 KO mice at the level of MUFA, SFA and other lipid species. In the context of MetS developed in these KO mice as a result of High Fat High Sucrose Diet (HFHSD), our results showed that TRPM8 KO mice on HFHSD exhibited improved glucose metabolism and increased insulin sensitivity. In the TRPM8 KO group on HFHSD, the liver showed increased lipid accumulation compared to the WT mice. Echocardiography analysis confirmed an early development of heart failure with preserved ejection fraction (HFpEF) in WT mice (increased E/E'), whereas KO mice were protected. Transcriptomics analysis primarily revealed distinct lipid metabolism profiles between the different mice groups. In conclusion, our results demonstrate that TRPM8 dysregulation leads to changes in the lipid profile in both in vitro and in vivo models. This positions TRPM8 as a potential new target for maintaining lipid metabolism homeostasis especially in the course of MetS and the eventual development of HFpEF
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Mattox, Cassie. "Examination of auxin transport and root development in the scd1-1 mutant in Arabidopsis thaliana." Winston-Salem, NC : Wake Forest University, 2009. http://dspace.zsr.wfu.edu/jspui/handle/10339/42592.

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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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Al, Darwich Abdulrahman. "Métabolisme lipidique et cryorésistance des embryons dans l’espèce bovine." Thesis, Tours, 2009. http://www.theses.fr/2009TOUR4031/document.

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Les embryons bovins produits in vitro sont plus sensibles à la cryoconservation que ceux produits in vivo, en partie à cause de leur contenu lipidique, triglycérides et phospholipides. L’objectif de ce travail visait à comprendre les mécanismes moléculaires responsables de cette différence. Le profil transcriptomique de gènes impliqués dans le métabolisme lipidique a été établi. Le niveau d'expression génique de l’adipophiline obtenu indique qu’il peut être un marqueur spécifique de l'accumulation des triglycérides et de la cryorésistance des embryons. Ainsi, l’accumulation des triglycérides pourrait être liée à une absence de dégradation des lipides et non à une synthèse de novo uniquement. L’ajout d’acides gras polyinsaturés, C18:2, C18:3 ou DHA dans le milieu de développement, a régulé l'expression génique de SCD1 et de FADS2, deux enzymes qui désaturent les lipides, et ce, probablement via la régulation de SREBP1, ce qui pourrait être en lien direct avec les modifications de la balance acides gras saturés / insaturés et jouer sur la fluidité membranaire et la cryorésistance<br>In vitro produced embryos are more sensitive to cryopreservation than those in vivo derived, partly because of their fat content, triglycerides and phospholipids. The objective of this work was to understand the molecular mechanisms responsible for this difference. mRNA expression of genes involved in lipid metabolism has been established. Results of adipophilin mRNA level indicates that it maybe a specific marker for triglycerides accumulation and embryo cryorésistance. Thus, triglyceride accumulation could be related to a lack of lipids degradation rather than new lipids synthesis only. Polyunsaturated fatty acids supplementation, C18: 2 C18: 3 or DHA in culture media regulated mRNA expression of SCD1 and FADS2, two enzymes involved in lipids desaturation, probably through SREBP1 regulation, which could be directly linked to changes in the balance of saturated / unsaturated fatty acids and could contribute to change membrane fluidity and embryo cryoresistance
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Hussain, Ghulam. "Rôle de la stéaroyl-CoA désaturase-1 dans le maintien de l'activité musculaire : étude d'un modèle lésionel pour la compréhension des altérations métaboliques caractéristiques de la sclérose latérale amyotrophique." Phd thesis, Université de Strasbourg, 2013. http://tel.archives-ouvertes.fr/tel-00921430.

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Les patients SLA et les souris modèles présentent un dysfonctionnement métabolique qui coïncide avec le changement de concentration de différentes espèces lipidiques. Notre hypothèse est qu'un tel dysfonctionnement métabolique au niveau musculaire conduirait aux premiers changements observés dans la SLA. Nous avons montré que l'expression de la stéaroyl-coenzyme A désaturase 1 (SCD1), une enzyme clé de la synthèse des acides gras mono-insaturés à partir des acides gras saturés, est diminuée dans le muscle avant les premiers symptômes moteurs observés chez les souris modèles de SLA. Dans ce modèle murin, les altérations en acides gras au niveau circulant et hépatique, traduisant les changements de SCD1,apparaissent lors des premiers symptômes de la pathologie. De plus, l'inhibition pharmacologique de l'activité de SCD1 mime le phénotype métabolique des souris modèles de SLA. Notre étude a ainsi montré que la diminution de la SCD1 joue un rôle important pour l'activité neuromusculaire. Elle module les besoins énergétiques, maintien l'activité musculaire par augmentation du métabolisme oxydatif et agit sur l'expression de gènes impliqués dans le développement et le fonctionnement de la jonction neuromusculaire. De plus, l'ablation du gène SCD1 stimule la récupération fonctionnelle musculaire après lésion du nerf. L'inhibition pharmacologique de SCD1 apporte également une protection au muscle. Nous avons pu conclure de cette étude qu'une modification de l'expression de SCD1 ainsi que du profil d'acides gras peut apporter une protection au muscle pour lutter contre la pathologie. En outre, des inhibiteurs de l'activité enzymatique de la SCD1 pourraient être développés comme traitement thérapeutique dans la SLA.
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Kgwatalala, Patrick M. 1973. "Genetic polymorphisms in the stearoyl-CoA desaturase1 (SCD1) gene and their influence on the conjugated linoleic acid (CLA) and monounsaturated fatty acids (MUFA) content of milk fat of Canadian Holstein and Jersey cows." Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=115690.

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Stearoyl-CoA desaturase1 (SCD1) catalyzes the synthesis of conjugated linoleic acid (CLA) and mono-unsaturated fatty acids (MUFA) in the mammary gland of ruminant animals. We hypothesized that single nucleotide polymorphisms (SNPs) in the coding region, 5' and 3' untranslted regions (UTRs) of the SCD1 gene would influence the activity of SCD1 enzyme and consequently account for some within-breed variations in milk CLA and MUFA. Sequence analysis of the coding region of the SCD1 gene of Jerseys and Holsteins revealed c.702A&rarr;G, c.762T&rarr;C and c.878C&rarr;T SNPs in exon 5 in both breeds and c.435G&rarr;A in exon 3 in Holsteins. The SNPs resulted in: A (G435A702T 762C878), A1 (A435A702T 762C878), B (G435G702C 762T878) and B1 (A435G702C 762T878) coding variants in Holsteins and only variants A and B in Jerseys. Only SNP 878C&rarr;T resulted in a non-synonymous codon change resulting in p.293Ala and p.293Val protein variants or alleles at the SCD1 locus. Subsequent association studies found significantly higher C10 index, C12 index and C14 index and consequently higher concentrations of C10:1 and C12:1 in p.293AA cows compared to the p.293VV cows in both breeds. The SCD1 genotype had no influence on concentrations of C141, C16:1, C18:1 and CLA in both breeds.<br>Sequence analysis of the 5' and 3' UTRs revealed no SNPs in the 5'UTR and a total of 14 SNPs in the 3'UTR of both breeds. The SNPs were in complete linkage disequilibrium resulting in 3 haplotypes or regulatory variants: H1 (G1571G1644C1763C2053A2584 A3007C3107G3208 T3290G 3497G3682A4399C4533G4881), H2 (G1571G1644A1763C2053A 2584G3007 C3107G3208T3290G3497G 3682A4399C4533G4881) and H3 (T 1571C1644A1763 T2053G2584G3007T 3107A3208C3290A3497A3682T 4399T4533A4881) in Holsteins and only H1 and H3 variants in Jerseys. A subsequent association study involving 862 Holstein cows, found the H1 regulatory variant to be associated with higher C10 and C12 desaturase indices and consequently with higher concentrations of C10:1 and C12:1 compared with the H3 variant. The effects of the H2 variant were intermediate to those of H1 and H3. 3'UTR genotype had no influence on the concentrations of C14:1, C16:1, C18:1 and CLA. The concentrations of C10:1 and C12:1 in milk fat could therefore be due to effects of SNPs in the open reading frame and the 3'UTR regions of the SCD1 gene. These results indicate that SNPs in the coding and 3'UTR regions of the SCD1 gene could be used as markers for genetic selection for increased C10:1 and C12:1 contents of milk.
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Schmitt, Florent. "Rôle de la stéaroyl-coenzyme A désaturase 1, une enzyme de synthèse des acides gras mono-insaturés, dans un modèle transgénique d’étude de la Sclérose Latérale Amyotrophique." Thesis, Strasbourg, 2013. http://www.theses.fr/2013STRAJ085/document.

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La sclérose latérale amyotrophique est une maladie neurodégénérative associée à un dysfonctionnement métabolique. Des altérations du métabolisme des lipides, décrites chez les patients SLA et les animaux modèles, pourraient participer à la mise en place des premières étapes de la maladie. L’objectif de cette thèse était d’étudier le rôle de la stéaroyl-coenzyme A désaturase 1 (SCD1), une enzyme clé du métabolisme des lipides, dans la SLA. En étudiant le profil d’acides gras périphériques dans un modèle de souris SLA, les souris SOD1m, nous avons vu une diminution de l’activité de la SCD1 dès les stades précoces (subcliniques) de la maladie. Cette diminution pourrait expliquer, à elle seule, les altérations du métabolisme des lipides caractéristiques de la SLA. La répercussion de la perte de l’activité de la SCD1 sur l’axe moteur a été étudiée. Une délétion du gène ou une inhibition pharmacologique de la SCD1 améliore la récupération fonctionnelle après lésion du nerf sciatique chez la souris sauvage. Nous avons cherché à voir si la perte d’activité de la SCD1 trouvée chez les souris SOD1m est un mécanisme de protection mis en place pour lutter contre l’évolution de la SLA. Nous avons traité des souris SOD1m avec un inhibiteur de l’activité de la SCD1. Le traitement a conduit à une augmentation du métabolisme oxydatif, une préservation de l’intégrité neuromusculaire ainsi qu’une amélioration de la survie des motoneurones. Nousconcluons que l’inhibition de la SCD1 représente une cible thérapeutique prometteuse dans la SLA<br>Amyotrophic lateral sclerosis is a neurodegenerative disease, associated with metabolic dysfunction. Alteration of lipid metabolism has been documented in ALS patients and animal models, and could participate to the first pathological steps of the disease. The objective of this thesis was to study the role of stearoyl-CoA desaturase 1 (SCD1), a key enzyme of lipid metabolism, in ALS. By studying the profile of peripheral fatty acids in an animal model of ALS, the SOD1 mice, we found that SCD1 activity was strongly reduced at early (sub-clinical) disease stage, and that this reduction could explain in itself the alteration of lipid metabolism characteristic of ALS. The impact of loss of SCD1 activity for the motor axis was then studied. Genetic deletion or pharmacological inhibition of SCD1 enhanced functional recovery after sciatic nerve injury in mice. Wefurther explored if the loss of SCD1 activity found in SOD1 mice is a protective mechanism elicited in response to ALS. We treated SOD1 mice with an inhibitor of SCD1 activity. The treatment resulted in exacerbated muscular oxidative metabolism,preservation of neuromuscular integrity and enhanced motor neuron survival. We conclude that inhibition of SCD1 represents a promising therapeutic target for ALS
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Warensjö, Eva. "Fatty Acid Desaturase Activities in Metabolic Syndrome and Cardiovascular Disease : Special Reference to Stearoyl-CoA-Desaturase and Biomarkers of Dietary Fat." Doctoral thesis, Uppsala University, Clinical Nutrition and Metabolism, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8312.

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<p>The development of the metabolic syndrome (MetS) and cardiovascular diseases have been suggested to be influenced more by the quality than the amount of dietary fat. The FA composition of serum lipids may be used as biomarkers of dietary fat quality. FAs can, however, also be endogenously synthesized by lipogenic enzymes such as elongases and desaturases. Three desaturases are important in humans: Stearoyl-CoA-desaturase (SCD), ∆6-desaturase (D6D) and ∆5-desaturase (D5D) and surrogate measures of desaturase activities can be estimated as product-to-precursor FA ratios.</p><p>In this thesis, we demonstrated that high SCD, D6D and low D5D estimated activities predicted MetS 20 years later, as well as cardiovascular and total mortality during a maximum of 33.7 years. The relation between D5D and MetS was independent of lifestyle and BMI, while the relation between SCD, D6D and MetS was confounded by BMI. Serum proportions of palmitic (16:0), palmitoleic (16:1) and dihomo-γ-linoleic acids were higher and the serum proportion of linoleic acid (LA) lower at baseline in those individuals who developed MetS. Further, LA was inversely related to mortality, while palmitic, palmitoleic and dihomo-γ-linoleic acids were directly associated with mortality. We also demonstrated that a diet rich in saturated fat “induced” a similar serum FA pattern (including estimated desaturase activities) that was associated with MetS, cardiovascular disease and mortality. We also propose that the SCD ratio [16:1/16:0] might be a novel and useful marker of dietary saturated fat, at least in Western high-fat diets. Finally, genetic variations in the human SCD1 gene were linked to obesity and insulin sensitivity, results that agree with data in SCD1 deficient mice.</p><p>This thesis suggests that dietary fat quality and endogenous desaturation may play a role in the development of metabolic and cardiovascular diseases and the results support current dietary guidelines.</p>
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Books on the topic "SCD1"

1

(Firm), SCDA Architects. SCDA interiors. Mulgrave, Vic: The Images Publishing Group Pty Ltd, 2016.

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Robert, Powell. The architecture of Soo Chan. Mulgrave, Vic: Images Publishing Group, 2004.

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National Writing Project (School Curriculum Development Committee), ed. The SCDC National Writing Project. [London]: [School Curriculum Development Committee], 1986.

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Semiconductors, Philips. Power diodes: Data handbook SC11. Eindhoven: Philips Semiconductors, 1999.

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Aaron, Betsky, and SCDA Architects (Firm), eds. SCDA architects: Selected and current works. Mulgrave, Vic: Images Publishing Group, 2004.

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AQA, ed. Sociology AS Level Unit 1 SCY1 January. London: AQA, 2001.

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Committee, School Curriculum Development. The National Curriculum, 5-16: Response from SCDC. London: School Curriculum Development Committee, 1987.

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Project, National Writing, ed. About writing: The SCDC National Writing Project newsletter. (London) ((45 Notting Hill Gate, W11 3JB)): School Curriculum Development Committee, 1985.

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Mick, Revell, and Northamptonshire (England). Education and Libraries Department. Inspection and Advisory Service. Science Team., eds. The Sc1 book: Investigations 5 - 16. [Northampton?]: Northamptonshire County Council Education and Libraries, 1993.

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First Year at School: Policy and Practice (Seminar) (1987 Newcombe House, London). Four-year-olds in school: AnNFER/SCDC Seminar report. (U.K.): National Foundation for Educational Research, 1987.

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Book chapters on the topic "SCD1"

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Liu, Gang. "Chapter 9. Stearoyl-CoA Desaturase 1 (SCD1) Inhibitors: Bench to Bedside Must Only Go Through Liver." In Drug Discovery, 249–69. Cambridge: Royal Society of Chemistry, 2012. http://dx.doi.org/10.1039/9781849735322-00249.

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Leung, Alexander K. C., Cham Pion Kao, Andrew L. Wong, Alexander K. C. Leung, Thomas Kolter, Ute Schepers, Konrad Sandhoff, et al. "SCD." In Encyclopedia of Molecular Mechanisms of Disease, 1895. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7389.

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Montgomery, Scott L. "Scientific translation." In Handbook of Translation Studies, 299–305. Amsterdam: John Benjamins Publishing Company, 2010. http://dx.doi.org/10.1075/hts.1.sci1.

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Orr, Harry T., and Huda Y. Zoghbi. "Pathophysiology of SCA1." In Molecular Mechanisms of Neurodegenerative Diseases, 271–83. Totowa, NJ: Humana Press, 2001. https://doi.org/10.1007/978-1-59259-006-3_11.

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Hofmann, Erik, Patrick Beck, and Erik Füger. "SCD Guide Preparation." In The Supply Chain Differentiation Guide, 35–45. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-31936-5_2.

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Blatt, Julie, April M. Evans, and Jessica Benjamin-Eze. "Stroke in SCD." In Manual for Night-Time Emergencies for Pediatric Hematology-Oncology Fellows, 78–80. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003473701-24.

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Blatt, Julie, April M. Evans, and Jessica Benjamin-Eze. "Priapism in SCD." In Manual for Night-Time Emergencies for Pediatric Hematology-Oncology Fellows, 72–74. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003473701-22.

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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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Blatt, Julie, April M. Evans, and Jessica Benjamin-Eze. "Aplastic Crisis in SCD." In Manual for Night-Time Emergencies for Pediatric Hematology-Oncology Fellows, 66–67. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003473701-19.

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Conference papers on the topic "SCD1"

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Yunfei, Shao, Fan Shuai, Wang Xiang, Jia Kunqi, Huang Yixuan, and He Guangyu. "Incentive Mechanism for SCDL-Based Demand Response." In 2024 IEEE Sustainable Power and Energy Conference (iSPEC), 404–9. IEEE, 2024. https://doi.org/10.1109/ispec59716.2024.10892475.

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Hussain, Adil, Kashif Naseer Qureshi, Faizan Zaman, Ayesha Aslam, and Tariq. "Minor Surface Cracks Detection using SCD11 Convolutional Neural Network." In 2024 4th International Conference on Emerging Smart Technologies and Applications (eSmarTA), 1–7. IEEE, 2024. http://dx.doi.org/10.1109/esmarta62850.2024.10638912.

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"DEGRADAÇÃO EM ÓRBITA DOS PAINÉIS SOLARES DOS SATÉLITES BRASILEIROS SCD1 E SCD2." In Anais Congresso Brasileiro de Energia Solar 2012. Associação Brasileira de Energia Solar, 2012. http://dx.doi.org/10.59627/cbens.2012.1835.

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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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Gruenewald, Sylvia, Carolyn Sperl, Patrick Steigemann, Alexander Walter, Sylvia Zacharias, Uwe Eberspaecher, Roland Neuhaus, et al. "Abstract 4989: 3D spheroid screen yields SCD1 pathway inhibitors for the treatment of cancer." 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.am2017-4989.

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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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Machmueller, AC, J. Ecker, and KP Janssen. "PO-229 The fatty acid desaturase SCD1 as crucial factor for tumour progression in colon cancer." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.263.

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Xuan, Yang, Mingo MH Yung, Arvin FS Chen, Hextan YS Ngan, and David W. Chan. "Abstract 5039: SCD1/FADS2 and ferroptosis signalings orchestrate ovarian cancer cell metabolism and metastatic progression in peritoneal metastases." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-5039.

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Noto, Alessia, Maria Elena Pisanu, Claudia De Vitis, Giovanni Sorrentino, Giannino Del Sal, Alfredo Budillon, Gennaro Ciliberto, and Rita Mancini. "Abstract 1052: Stearoyl-CoA-Desaturase (SCD1) regulates lung cancer stemness via stabilization and nuclear localization of YAP/TAZ." 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.am2016-1052.

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Jadhav, P., S. Ashokkumar, and N. Nagwekar. "Microbial load reduction using modified Solar Conduction Dryer with composite filters." In 21st International Drying Symposium. Valencia: Universitat Politècnica València, 2018. http://dx.doi.org/10.4995/ids2018.2018.7728.

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The present work studies the microbial load reduction in sapota and beet root by three different drying methods i.e. Open Sun Drying (OSD), Solar Conduction Drying (SCD) and a modified SCD with filters (SCDF). Parameters analyzed were water activity, moisture content, drying kinetics, Total Viable Counts, Total Fungal Counts and ash content. It was found that the samples dried in SCDF showed least microbial counts, faster drying times and lower ash content as comparison to OSD. This study shows that SCD and its modification provide a better alternative for low cost drying of fruits and vegetables for quality retention. Keywords: Microbial reduction; SCD Filters; Sapota; Beetroot
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Reports on the topic "SCD1"

1

Crawford, R. K. SCD1-general-purpose single-crystal diffractometer-reference instrument WBS 1.7.5. Office of Scientific and Technical Information (OSTI), January 1999. http://dx.doi.org/10.2172/12077.

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Douglas, Melissa. FY22 SCDS L2: Special Materials. Office of Scientific and Technical Information (OSTI), February 2021. http://dx.doi.org/10.2172/1764187.

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Duarte, Javier, Sergo Jindariani, Ben Kreis, Rivera Rivera, Nhan Tran, Jennifer Ngadiuba, Maurizio Pierini, et al. FERMILAB-SLIDES-19-706-SCD-V. Office of Scientific and Technical Information (OSTI), November 2019. http://dx.doi.org/10.2172/1630707.

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Zhou, Ruhua, Jingjing Xu, Jiaochen Luan, Weiyun Wang, Xinzhi Tang, Yanling Huang, Ziwen Su, Lei Yang, and Zejuan Gu. The Predictive Role of C-Reactive Protein on Sudden Death: A meta-analysis of prospective studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2021. http://dx.doi.org/10.37766/inplasy2021.11.0074.

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This study was a diagnostic research, so the content was decomposed according to PIRO : P: Patients diagnosed with sudden death; I: C-reactive protein; R: There is no gold standard for sudden death, and the definition of sudden death varies from literature to literature. The World Health Organization defines sudden death: "Patients who are normally healthy or seemingly healthy die suddenly due to natural diseases in an unexpectedly short period of time." In our study, sudden death is determined by the history, symptoms, physical examination and electrocardiogram results assesed by doctor. If death events were collected from the patients’ medical records, deaths coded using the International Classification of Diseases-9th Revision, codes 410 to 414 for non-SCD and 798.1 for SCD; or the International Classification of Diseases-10th Revision, codes I20 to I25 for non-SCD and I46 for SCD. All deaths registered as sudden deaths were confirmed in interviews with the patient’s physician or family members again. O: sudden death.
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Doyle, R. E. Cooling water for SSC experiments: Supplemental Conceptual Design Report (SCDR). Office of Scientific and Technical Information (OSTI), October 1989. http://dx.doi.org/10.2172/5168820.

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Ditrapani, Anthony R. A Dual-Ship Approach to the 21 st Century Surface Combatant (SC21) Program. Fort Belvoir, VA: Defense Technical Information Center, July 1995. http://dx.doi.org/10.21236/ada362411.

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7

Araujo, María Caridad, Romina Tomé, and Marta Rubio-Codina. Los primeros años de vida de los niños peruanos: Una fotografía sobre el bienestar y el desarrollo de los niños del Programa Nacional Cuna Más. Inter-American Development Bank, September 2016. http://dx.doi.org/10.18235/0010119.

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El Programa Nacional Cuna Más (PNCM) atiende a niños menores de 36 meses en zonas de pobreza y pobreza extrema con el objetivo de mejorar su nivel de desarrollo. El PNCM brinda dos servicios: el Servicio de Acompañamiento a Familias (SAF) en zonas rurales y el Servicio de Cuidado Diurno (SCD) en zonas urbanas. A partir de los datos de las líneas de base de las evaluaciones de impacto de ambos servicios, este documento describe y compara las características de los niños y niñas potencialmente beneficiarios y sus familias. Por lo general, los hogares de la muestra del SCD presentan mejores indicadores relacionados con el bienestar que los hogares del SAF: tipo de vivienda, nivel de riqueza, acceso a servicios, y mayor cantidad y variedad de materiales y actividades de juego. A pesar de ello, los niveles de desarrollo infantil son muy similares entre los niños en las dos muestras. Asimismo, seobservan brechas socioeconómicas en el desarrollo infantil más marcadas en los niños de la muestra del SAF que en los de la muestra del SCD. Si bien las muestras de análisis no tienen representatividad nacional, constituyen una inestimable fuente de información sobre el desarrollo infantil, la calidad del entorno familiar y las condiciones de vida de los niños y niñas menores de 2 años en hogares vulnerables en el Perú rural y urbano.
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8

Guttmann, G. Biological soft x-ray contact microscopy: Imaging living CHO-SC1 cells and other biological materials. Office of Scientific and Technical Information (OSTI), August 1989. http://dx.doi.org/10.2172/7001378.

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ADAMS, DAVID P., LAURENCE E. BROWN, RONALD S. GOEKE, JUAN A. ROMERO, and ANDREW D. SILVA. Evolution of Stress in ScD{sub 2}/Cr Thin Films Fabricated by Evaporation and High Temperature Reaction. Office of Scientific and Technical Information (OSTI), June 2001. http://dx.doi.org/10.2172/783088.

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ACOUSTICAL SOCIETY OF AMERICA NEW YORK. Minutes: Accredited Standards Committee on Noise, S12, U.S. Tag for ISO/ TC43/SC1 Noise and ISO/TC94/SC12 Hearing Protection. Fort Belvoir, VA: Defense Technical Information Center, May 1991. http://dx.doi.org/10.21236/ada239721.

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