Relevant bibliographies by topics / SCD1

Academic literature on the topic 'SCD1'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 April 2023

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Journal articles on the topic "SCD1"

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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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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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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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Hirota, Kouji, Kayoko Tanaka, Kunihiro Ohta, and Masayuki Yamamoto. "Gef1p and Scd1p, the Two GDP-GTP Exchange Factors for Cdc42p, Form a Ring Structure that Shrinks during Cytokinesis inSchizosaccharomyces pombe." Molecular Biology of the Cell 14, no. 9 (September 2003): 3617–27. http://dx.doi.org/10.1091/mbc.e02-10-0665.

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Fission yeast Cdc42p, a small GTPase of the Rho family, is essential for cell proliferation and maintenance of the rod-like cell morphology. Scd1/Ral1p is a GDP-GTP exchange factor (GEF) for Cdc42p. This study and a parallel study by others establish that Gef1p is another GEF for Cdc42p. Deletions of gef1 and scd1 are synthetically lethal, generating round dead cells, and hence mimic the phenotype of cdc42 deletion. Gef1p is localized mainly to the cell division site. Scd1p is also there, but it is also detectable in other parts of the cell, including the nucleus, growing ends, and the tips of conjugation tubes. Gef1p and Scd1p form a ring structure at the cell division site, which shrinks during cytokinesis following the contraction of the actomyosin ring. Formation of the Gef1p/Scd1p ring apparently depends on the integrity of the actomyosin ring. In turn, recruitment of Cdc42p to the cell division site follows the shrinking Gef1p/Scd1p ring; the Cdc42p accumulates like a closing iris. These observations suggest that Gef1p and Scd1p may have a role in mediating between contraction of the actomyosin ring and formation of the septum, by recruiting active Cdc42p to the septation site.
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Dissertations / Theses on the topic "SCD1"

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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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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
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→G, c.762T→C and c.878C→T SNPs in exon 5 in both breeds and c.435G→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→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.
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
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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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.

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.

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.

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Cassafières, Cécile Dalhoumi Salah Fèvre Véronique Jove Camille Lefebvre Pascale Loiselet Martine Elaïdi Claudine. "Formation et évaluation en SCD." [S.l.] : [s.n.], 2005. http://www.enssib.fr/bibliotheque/documents/dcb/M-2005-RECH-02-vol1.pdf.

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Medeiros, Ana Carla. "Caracterização parcial do complexo SCF1 contendo a proteína FBXO25 fosforilada." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/17/17131/tde-09092015-110529/.

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A FBXO25 é parte de uma E3 ligase do tipo RING, (Really Interesting New Gene), oligomérica do tipo SCF, responsável pelo reconhecimento específico do substrato a ser degradado via Sistema Ubiquitina-Proteassoma (SUP). O SUP é o principal mecanismo proteolítico intracelular, responsável pela degradação de 80-90% das proteínas citosólicas e nucleares. A FBXO25 é capaz de formar um complexo SCF1 ativo (formado pela interação das proteínas Skp1, Cul1, Roc1 e uma proteína do tipo F-box), capaz de ubiquitinar seus substratos. Essa proteína se acumula no núcleo celular formando uma nova estrutura subnuclear denominada FANDs (FBXO25 Associated Nuclear Domains) que estão envolvidos na ubiquitinação nuclear. Nesse trabalho, purificamos complexos SCF1 (WT ou sem o domínio de interação com Skp1 (F)), tratados ou não com PMA, pela técnica de imunoprecipitação. Identificamos por espectrometria de massas um sítio de fosforilação essencial para FBXO25, quando células transfectadas são tratadas com o mitógeno PMA. Buscamos também por substratos diferencialmente ubiquitinados por esses complexos, por meio de ensaios em ProtoArrays®, identificando substratos envolvidos na via de sinalização ERK1/2.
The FBXO25 is an E3 ligase RING type (Really Interesting New Gene), SCF oligomeric type, responsible for the specific recognition of the substrate to be degraded via the ubiquitin-proteasome system (SUP). SUP is the main intracellular proteolytic mechanism responsible for 80-90% degradation of cytosolic and nuclear proteins. The FBXO25 is capable of forming a complex SCF1 (formed by the interaction of proteins Skp1, Cul1, Roc1 protein and a type F-box), resulting in an active SCF complex which is able to ubiquitinate their substrates. This protein accumulates in the nucleus forming a subnuclear structure called FANDs (FBXO25 Associated Nuclear Domains) that are involved in nuclear ubiquitination. In this work, we purify complex SCF1 (WT or F- box, which is not able to interact with Skp1), treated or not with PMA, by immunoprecipitation technique. We identified by mass spectrometry, an essential phosphorylation site for FBXO25, when it is phosphorylated under the action of the mitogenic reagent PMA. We also search for differentially ubiquitinated substrates for these complexes, by testing in ProtoArrays® identifying substrates involved in the signaling pathway ERK1 / 2.
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Books on the topic "SCD1"

1

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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Miner-Williams, Warren. Assessment and reporting of Sc1 at KS2. Cambridge: Pearson Publishing, 1994.

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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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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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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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Kaneko, T., and T. Kanomata. "4.1.3.1 (Sc1–xTi x )Fe2." In Magnetic Properties of d-Elements, Alloys and Compounds Under Pressure, 106–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-41834-1_47.

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Fernández, José Luis, Stephen Johnston, and Jaime Gosálvez. "Sperm Chromatin Dispersion (SCD) Assay." In A Clinician's Guide to Sperm DNA and Chromatin Damage, 137–52. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-71815-6_8.

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Klipstein, P. C., Y. Benny, Y. Cohen, R. Dobromislin, S. Elkind, R. Fraenkel, S. Gliksman, et al. "Advanced Infrared Photodetectors at SCD." In Springer Proceedings in Physics, 31–35. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-15-9259-1_8.

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Flint, R. Warren. "Case Study Examples of SCD." In Practice of Sustainable Community Development, 405–19. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5100-6_15.

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Conference papers on the topic "SCD1"

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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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Loh, Jia-Jian, Tin-Lok Wong, Shixun Lu, Helen HN Yan, Hoi-Cheong Siu, Dessy Chan, Max JF Kam, et al. "IDDF2022-ABS-0084 Adar1-mediated RNA editing of scd1 links lipid metabolism to drug resistance and self-renewal in gastric cancer." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 2–4 September 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-iddf.47.

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Souza, Milene, Marcio Balthazar, and Mônica Yassuda. "CAN COMPUTERIZED NEUROPSYCHOLOGICAL TESTS BETTER DISCRIMINATE SUBJECTIVE COGNITIVE DECLINE IN ELDERLY?" In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda097.

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Background: Subjects with subjective cognitive decline (SCD) are at higher risk of developing mild cognitive impairment (MCI) and Alzheimer’s dementia (AD). By definition, they perform normally on conventional neuropsychological tests. However, it is unclear whether computerized tests can detect subtle changes in this population. Objective: To compare cognitive performance in conventional and computerized tests of the CANTAB battery in people over 55 years old, divided into three subgroups: Controls, SCD and MCI, according to the NIA-AA 2018 criteria. Methods: We included 64 volunteers: 19 controls, 15 SCD, 30 MCI. Principal Component Analysis (PCA) model was used in both tests and naive bayes classifier were used to distinguish SCD from controls. Results: In conventional tests, variability of 57,17%, differentiating only the MCI. The CANTAB showed a subtle difference in dispersion between SCD and controls, with a variability of 30,12%. Cognitive functions with greater differentiation: episodic visual memory and new learning with variability of 72,65%, visual perception and immediate visual memory 51,95% variability, with similar results between the SCD and MCI groups. Attention and psychomotor speed 23,89%. Sustained attention and psychomotor speed with 71,3%. Adjusted for demographic variables, 52,63% of the SCD were classified as MCI in the computerized test, while the conventional one did not change. Conclusion: Computerized tests seem to be more sensitive in differentiating SCDs from controls, resembling the MCI group.
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Kassa, Debessay Fesehaye, and Klara Nahrstedt. "SCDA." In HPDC'13: The 22nd International Symposium on High-Performance Parallel and Distributed Computing. New York, NY, USA: ACM, 2013. http://dx.doi.org/10.1145/2462902.2462928.

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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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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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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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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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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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