Relevant bibliographies by topics / SMC3

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Academic literature on the topic 'SMC3'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "SMC3"

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Morikawa, Hirofumi, Takashi Morishita, Shiho Kawane, Hiroshi Iwasaki, Antony M. Carr, and Hideo Shinagawa. "Rad62 Protein Functionally and Physically Associates with the Smc5/Smc6 Protein Complex and Is Required for Chromosome Integrity and Recombination Repair in Fission Yeast." Molecular and Cellular Biology 24, no. 21 (November 1, 2004): 9401–13. http://dx.doi.org/10.1128/mcb.24.21.9401-9413.2004.

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ABSTRACT Smc5 and Smc6 proteins form a heterodimeric SMC (structural maintenance of chromosome) protein complex like SMC1-SMC3 cohesin and SMC2-SMC4 condensin, and they associate with non-SMC proteins Nse1 and Nse2 stably and Rad60 transiently. This multiprotein complex plays an essential role in maintaining chromosome integrity and repairing DNA double strand breaks (DSBs). This study characterizes a Schizosaccharomyces pombe mutant rad62-1, which is hypersensitive to methyl methanesulfonate (MMS) and synthetically lethal with rad2 (a feature of recombination mutants). rad62-1 is hypersensitive to UV and gamma rays, epistatic with rhp51, and defective in repair of DSBs. rad62 is essential for viability and genetically interacts with rad60, smc6, and brc1. Rad62 protein physically associates with the Smc5-6 complex. rad62-1 is synthetically lethal with mutations in the genes promoting recovery from stalled replication, such as rqh1, srs2, and mus81, and those involved in nucleotide excision repair like rad13 and rad16. These results suggest that Rad62, like Rad60, in conjunction with the Smc5-6 complex, plays an essential role in maintaining chromosome integrity and recovery from stalled replication by recombination.
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Guacci, Vincent, and Douglas Koshland. "Cohesin-independent segregation of sister chromatids in budding yeast." Molecular Biology of the Cell 23, no. 4 (February 15, 2012): 729–39. http://dx.doi.org/10.1091/mbc.e11-08-0696.

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Cohesin generates cohesion between sister chromatids, which enables chromosomes to form bipolar attachments to the mitotic spindle and segregate. Cohesin also functions in chromosome condensation, transcriptional regulation, and DNA damage repair. Here we analyze the role of acetylation in modulating cohesin functions and how it affects budding yeast viability. Previous studies show that cohesion establishment requires Eco1p-mediated acetylation of the cohesin subunit Smc3p at residue K113. Smc3p acetylation was proposed to promote establishment by merely relieving Wpl1p inhibition because deletion of WPL1 bypasses the lethality of an ECO1 deletion (eco1Δ wpl1Δ). We find that little, if any, cohesion is established in eco1Δ wpl1Δ cells, indicating that Eco1p performs a function beyond antagonizing Wpl1p. Cohesion also fails to be established when SMC3 acetyl-mimics (K113Q or K112R,K113Q) are the sole functional SMC3s in cells. These results suggest that Smc3p acetylation levels affect establishment. It is remarkable that, despite their severe cohesion defect, eco1Δ wpl1Δ and smc3-K112R,K113Q strains are viable because a cohesin-independent mechanism enables bipolar attachment and segregation. This alternative mechanism is insufficient for smc3-K113Q strain viability. Smc3-K113Q is defective for condensation, whereas eco1Δ wpl1Δ and smc3-K112R,K113Q strains are competent for condensation. We suggest that Smc3p acetylation and Wpl1p antagonistically regulate cohesin's essential role in condensation.
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Eijpe, M., C. Heyting, B. Gross, and R. Jessberger. "Association of mammalian SMC1 and SMC3 proteins with meiotic chromosomes and synaptonemal complexes." Journal of Cell Science 113, no. 4 (February 15, 2000): 673–82. http://dx.doi.org/10.1242/jcs.113.4.673.

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In somatic cells, the heterodimeric Structural Maintenance of Chromosomes (SMC) proteins are involved in chromosome condensation and gene dosage compensation (SMC2 and 4), and sister chromatid cohesion and DNA recombination (SMC1 and 3). We report here evidence for an involvement of mammalian SMC1 and SMC3 proteins in meiosis. Immunofluorescence analysis of testis sections showed intense chromatin association in meiotic prophase cells, weaker staining in round spermatids and absence of the SMC proteins in elongated spermatids. In spermatocyte nuclei spreads, the SMC1 and SMC3 proteins localize in a beaded structure along the axial elements of synaptonemal complexes of pachytene and diplotene chromosomes. Both SMC proteins are present in rat spermatocytes and enriched in preparations of synaptonemal complexes. Several independent experimental approaches revealed interactions of the SMC proteins with synaptonemal complex-specific proteins SCP2 and SCP3. These results suggest a model for the arrangement of SMC proteins in mammalian meiotic chromatin.
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Eng, Thomas, Vincent Guacci, and Douglas Koshland. "Interallelic complementation provides functional evidence for cohesin–cohesin interactions on DNA." Molecular Biology of the Cell 26, no. 23 (November 15, 2015): 4224–35. http://dx.doi.org/10.1091/mbc.e15-06-0331.

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The cohesin complex (Mcd1p, Smc1p, Smc3p, and Scc3p) has multiple roles in chromosome architecture, such as promoting sister chromatid cohesion, chromosome condensation, DNA repair, and transcriptional regulation. The prevailing embrace model for sister chromatid cohesion posits that a single cohesin complex entraps both sister chromatids. We report interallelic complementation between pairs of nonfunctional mcd1 alleles (mcd1-1 and mcd1-Q266) or smc3 alleles (smc3-42 and smc3-K113R). Cells bearing individual mcd1 or smc3 mutant alleles are inviable and defective for both sister chromatid cohesion and condensation. However, cells coexpressing two defective mcd1 or two defective smc3 alleles are viable and have cohesion and condensation. Because cohesin contains only a single copy of Smc3p or Mcd1p, these examples of interallelic complementation must result from interplay or communication between the two defective cohesin complexes, each harboring one of the mutant allele products. Neither mcd1-1p nor smc3-42p is bound to chromosomes when expressed individually at its restrictive temperature. However, their chromosome binding is restored when they are coexpressed with their chromosome-bound interallelic complementing partner. Our results support a mechanism by which multiple cohesin complexes interact on DNA to mediate cohesion and condensation.
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Mito, Yoshiko, Asako Sugimoto, and Masayuki Yamamoto. "Distinct Developmental Function of Two Caenorhabditis elegans Homologs of the Cohesin Subunit Scc1/Rad21." Molecular Biology of the Cell 14, no. 6 (June 2003): 2399–409. http://dx.doi.org/10.1091/mbc.e02-09-0603.

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Cohesin, which mediates sister chromatid cohesion, is composed of four subunits, named Scc1/Rad21, Scc3, Smc1, and Smc3 in yeast. Caenorhabditis elegans has a single homolog for each of Scc3, Smc1, and Smc3, but as many as four for Scc1/Rad21 (COH-1, SCC-1/COH-2, COH-3, and REC-8). Except for REC-8 required for meiosis, function of these C. elegans proteins remains largely unknown. Herein, we examined their possible involvement in mitosis and development. Embryos depleted of the homolog of either Scc3, or Smc1, or Smc3 by RNA interference revealed a defect in mitotic chromosome segregation but not in chromosome condensation and cytokinesis. Depletion of SCC-1/COH-2 caused similar phenotypes. SCC-1/COH-2 was present in cells destined to divide. It localized to chromosomes in a cell cycle-dependent manner. Worms depleted of COH-1 arrested at either the late embryonic or the larval stage, with no indication of mitotic dysfunction. COH-1 associated chromosomes throughout the cell cycle in all somatic cells undergoing late embryogenesis or larval development. Thus, SCC-1/COH-2 and the homologs of Scc3, Smc1, and Smc3 facilitate mitotic chromosome segregation during the development, presumably by forming a cohesin complex, whereas COH-1 seems to play a role important for development but unrelated to mitosis.
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Viny, Aaron D., Christopher J. Ott, Barbara Spitzer, Martin A. Rivas, Cem Meydan, Efthymia Papalexi, Dana Yelin, et al. "Dose-Dependent Role of the Cohesin Complex in Normal and Malignant Hematopoiesis." Blood 126, no. 23 (December 3, 2015): 435. http://dx.doi.org/10.1182/blood.v126.23.435.435.

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Abstract Cohesin complex members have recently been identified as putative tumor suppressors in hematologic and epithelial malignancies. The cohesin complex guides chromosome segregation, however cohesin-mutant leukemias do not show genomic instability suggesting an alternate role in malignant transformation. We hypothesized reduced cohesin function alters chromatin structure and disrupts cis-regulatory architecture of hematopoietic stem/progenitor cells. We therefore investigated the impact of both complete loss and haploinsufficiency of Smc3, an obligate member of the cohesin complex, in normal hematopoiesis and in myeloid transformation by developing a conditional Smc3 knockout allele. Somatic loss of Smc3 in hematopoietic cells induced lethal bone marrow aplasia (median survival 11 days; p<0.001), with premature sister chromatid separation and abnormal nucleolar organization. Competitive transplant assays showed that Smc3 loss completely abrogated stem cell self-renewal in vivo. These data are consistent with an absolute requirement for the cohesin complex in hematopoietic stem/progenitor cells. By contrast, Smc3 haploinsufficiency increased self-renewal in vitro and in vivo, with increased serial replating, expanded hematopoietic stem/progenitor cells, and a self-renewal/engraftment advantage in competitive transplantation assays in vivo (Figure a). Smc3 haploinsufficiency altered coordinated transcriptional output, including reduced expression of master regulatory transcription factors governing lineage commitment. Consistent with these data, Smc3 loss resulted in expanded Cd150+ Cd48+ ST-HSC (p=0.008), reduction in Cd150+ Cd48- LT-HSC (p=0.001), and altered chromatin architecture with dysregulated expression of genes with specific chromatin architecture footprints. Smc3 haploinsufficiency cooperated with Flt3ITD to induce acute leukemia in vivo (Figure b), with dysregulated expression of hematopoietic master regulators and altered nucleolar topology similar to that observed in germline cohesinopathy syndromes and in AML patients with cohesin mutations (Figure c). To further explore the mechanism by which Smc3 loss cooperates with Flt3ITD to induce leukemia, we investigated chromatin cis-regulatory architecture with transposase hypersensitivity assays (ATAC-seq). We hypothesized that increased accessibility at cis-regulatory elements and the alterations in gene expression seen in cells with combined Smc3 haploinsufficiency and Flt3ITD may be in a large part driven by potentiated Stat signaling at chromatin. We analyzed 146 transcription factor recognition motifs within the THS differentially observed in Smc3Δ/+Flt3ITD and wild-type cells. Chromatin accessibility gained in Smc3Δ/+Flt3ITD cells are enriched in Stat family transcription factor binding sites, including Stat5. We also observed enrichment of the Stat5 gene expression signature in the Smc3Δ/+Flt3ITD cells compared to Smc3Δ/+, Flt3ITD and wild-type cells, suggesting the divergent mutations cooperate to potentiate oncogenic Stat5 signaling in HSPCs. Our results demonstrate a key dose-dependent role for the cohesin complex in hematopoiesis, and show that reduced cohesin functions to alter enhancer-mediated transcription and contribute to aberrant self-renewal and myeloid transformation. Figure 1. Figure 1. Disclosures Levine: Loxo Oncology: Membership on an entity's Board of Directors or advisory committees; CTI BioPharma: Membership on an entity's Board of Directors or advisory committees; Foundation Medicine: Consultancy.
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Kuan, Lídia, Frederico Pratas, Leonel Sousa, and Pedro Tomás. "MrBayes sMC3." International Journal of High Performance Computing Applications 32, no. 2 (June 30, 2016): 246–65. http://dx.doi.org/10.1177/1094342016652461.

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MrBayes is a popular software package for Bayesian phylogenetic inference, which uses an iterative approach to derive an evolutionary tree for a collection of species whose DNA sequences are known. Computationally, MrBayes is characterized by a large number of iterations, each composed of a set of tasks that isolated are not very time-consuming, but are globally computationally demanding. To accelerate the latest MrBayes 3.2, this paper presents MrBayes sMC3, which relies on the computational power of an heterogeneous CPU+GPU platform. For this, MrBayes sMC3 exploits both task and data-level parallelism while minimizing the overheads associated with kernel launches and CPU-GPU data transfers. Experimental results indicate that the proposed parallel approach, together with the proposed set of optimizations, allow for an application acceleration of up to 10× regarding the original MrBayes, and up to 3× regarding the Beagle Library. Furthermore, by analyzing the convergence rate of MrBayes sMC3 with that of the state-of-the-art approaches, a significant reduction in execution time is observed.
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Lu, Zhanping, Anna L. F. V. Assumpção, Aaron D. Viny, Ross L. Levine, and Xuan Pan. "YY1 Controls Hematopoietic Stem Cell Quiescence By Repressing Cohesin Expression." Blood 132, Supplement 1 (November 29, 2018): 3831. http://dx.doi.org/10.1182/blood-2018-99-118679.

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Abstract Hematopoietic stem cells (HSCs) are undifferentiated, self-renewing, pluripotent cells that have the capacity to differentiate into all mature lineage-specific cells in adult blood. Adult HSCs can remain in a quiescent state for a prolonged time, and quiescence is a fundamental characteristic of HSCs in adult bone marrow. Thus, the cell cycle must be precisely regulated. Yin Yang 1 (YY1) is a multifunctional transcription factor and Polycomb Group Protein (PcG) that is important for embryonic development, adult hematopoiesis, cell proliferation and maintaining higher-order chromosomal structure. We have generated YY1 conditional knockout mice (Yy1f/f Mx1-Cre) and showed that Yy1 deficient HSCs fail to self-renewal and had disrupted HSCs quiescence. Stem cell factor (SCF)/c-Kit signaling, a critical regulatory pathway in HSC development, is significantly downregulated in Yy1-/- HSCs. Interestingly, YY1 regulation of HSCs self-renewal and quiescence is independent on its PcG domain/function. Instead, YY1 occupied at Smc3 promoter area and repressed Smc3 expression. In Yy1-/-HSCs, Smc3 expression was upregulated. SMC3 is a core component of cohesin protein complex and plays critical roles in HSC self-renewal, myeloid differentiation and leukemogenesis. To further dissect the underlying mechanisms by which YY1 regulates SMC3 expression in HSCs, we have generated conditional knockout mice with YY1 homozygous deletion and SMC3 heterozygous deletion (Yy1f/f Smc3f/+Mx1-Cre). In Yy1-/- Smc3+/- bone marrow cells, SMC3 expression was normalized to the wild-type level. In adult bone marrow cells, YY1 physically interacted with cohesin complex proteins through its zinc finger domain. By analyzing the YY1, SMC1A and SMC3 ChIP-Seq database, our study showed that YY1 and cohesin co-occupied at promoter areas of genes that are critical for cell metabolism. Evidence from previous study showed that impaired metabolism, including increased reactive oxygen species (ROS) and decreased mitochondrial function, can cause defect in stem cell self-renewal and quiescence. In Yy1-/- Smc3+/-HSCs, cell quiescence was restored although HSC self-renewal was still impaired, indicates that YY1 and SMC3 may control HSC cell quiescence via regulating genes critical for cell metabolism. Our study identified YY1 as the first transcription factor that regulates expression of cohesin complex component SMC3. We are currently further dissecting underlying mechanisms and functional significances of metabolic pathways regulated by YY1-SMC3 axis in HSCs. Disclosures Levine: Imago: Equity Ownership; Isoplexis: Equity Ownership; Janssen: Consultancy, Honoraria; Gilead: Honoraria; Epizyme: Patents & Royalties; Loxo: Consultancy, Equity Ownership; C4 Therapeutics: Equity Ownership; Roche: Consultancy, Research Funding; Prelude: Research Funding; Qiagen: Equity Ownership, Membership on an entity's Board of Directors or advisory committees; Celgene: Consultancy, Research Funding; Novartis: Consultancy.
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Wang, Tianjiao, and John S. Welch. "Smc3 Haploinsufficiency and Smc3 Deletion Alter Hematopoiesis In Vivo." Blood 128, no. 22 (December 2, 2016): 2903. http://dx.doi.org/10.1182/blood.v128.22.2903.2903.

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Abstract Recurrent mutations in SMC3, encoding a cohesin subunit, have been identified in acute myeloid leukemia (AML) and other myeloid malignancies by our group and others. SMC3 mutations are heterozygous in AML patients. Missense, nonsense, and splice site mutations have been observed across all domains of SMC3. Given the breath of mutations, it is important to determine whether these represent recurrent loss-of-function mechanisms, or if some might have dominant negative effects. To determine the impact of Smc3 deletion on hematopoiesis, we studied both Smc3 haploinsufficient and Smc3 deficient mice as models of loss-of function and dominant negative phenotypes respectively. The Smc3 haploinsufficient mouse model has a lacZneo gene trap inserted in intron 3-4 of Smc3, which leads to a premature transcription stop and therefore produces a truncated and dysfunctional protein. The homozygous Smc3trap allele is embryonic lethal. The Smc3trap/+mice have an early growth defect, although their body weight catches up to wild type mice after 6 weeks of age. We found no difference in spleen weights, peripheral blood counts, and bone marrow (BM) compositions between Smc3trap/+ and wild type mice. The Smc3trap/+ BM cells formed similar number of colonies as wild type cells when plated in methylcellulose in vitro and lost self-renewal capabilities after replating for two weeks. Competitive repopulation assay in vivo showed neither advantage nor disadvantage for the Smc3trap/+BM cells (n=10). Thus, Smc3trap/+BM cells have normal colony forming capacity in vitro and normal homeostatic feedback in vivo. Further, we generated Smc3 conditionally deficient mice by removing the gene-trap cassette, which retains the loxP sites flanking exon 4 (Smc3fl), and crossing these mice with either Vav1-Cre+/- or ERT2-Cre+/- to delete the allele (Smc3fl/+/Vav1-Cre+/- is constitutively haploinsufficient in hematopoietic cells, whereas Smc3fl/+/ERT2-Cre+/-is only haploinsufficient when induced with tamoxifen). We characterized both models by serial replating assays, flow cytometry assays for hematopoietic stem/progenitor cells (HSPCs), and BM lineage in vitro and found no difference in these mice compared to the Smc3fl/+control. In contrast to the Smc3fl/+/Mx1-Cre+/- mice (Viny et al. JEM 212 (11): 1819-1832), we observed a significant competitive disadvantage for the Smc3fl/+/ERT2-Cre+/-BM cells (p<0.0001, n=10), most pronounced in Gr1+ myeloid cells in vivo (p<0.0001), implying Smc3 haploinsufficiency alters hematopoiesis in those mice in vivo. We characterized the effects of homozygous Smc3 loss on hematopoiesis in the inducible Smc3fl/fl/ERT2-Cre+/- mice by treating mice with tamoxifen at 6 weeks of age (Smc3fl/fl/Vav1-Cre+/- is embryonic lethal). Deletion of Smc3 led to rapid bone marrow failure and 100% lethality with a median survival of 8 days (n=4, 2 independent experiments). At the time of death, we observed severe reduction in the sizes of spleen (Sp) and thymus (Thy), in total number of BM, Sp, and Thy cells, and in white blood counts, lymphocytes, monocytes, and platelets. The Smc3 deficient BM cells had decreased levels of Smc3 by Western blot. The impact of Smc3 deletion on HSPC functions in vivo was assessed by a competitive repopulation assay of Smc3fl/fl/ERT2-Cre+/-BM cells (p<0.0001, n=10). Recipient mice were treated with tamoxifen after 6-week engraftment. After tamoxifen-mediated deletion, Smc3 deficient cells were rapidly outcompeted in vivo, indicating complete loss of HSPC functions. Collectively, these results suggest that Smc3 is necessary for normal hematopoiesis and for HSPC functions. The AML-associated SMC3 mutations are therefore unlikely to be dominant negative because the complete loss of Smc3 is incompatible with hematopoiesis. Disclosures No relevant conflicts of interest to declare.
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Laugsch, Magdalena, Jochen Seebach, Hans Schnittler, and Rolf Jessberger. "Imbalance of SMC1 and SMC3 Cohesins Causes Specific and Distinct Effects." PLoS ONE 8, no. 6 (June 12, 2013): e65149. http://dx.doi.org/10.1371/journal.pone.0065149.

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Dissertations / Theses on the topic "SMC3"

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Lam, Wing See. "THE ISOLATION AND CHARACTERIZATION OF ARABIDOPSIS AtSMC1 AND AtSMC3." Miami University / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=miami1092170063.

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Laugsch, Magdalena, Jochen Seebach, Hans Schnittler, and Rolf Jessberger. "Imbalance of SMC1 and SMC3 Cohesins Causes Specific and Distinct Effects." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-127228.

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SMC1 and SMC3 form a high-affinity heterodimer, which provides an open backbone of the cohesin ring, to be closed by a kleisin protein. RNAi mediated knock-down of either one heterodimer partner, SMC1 or SMC3, is expected to cause very similar if not identical phenotypes. However, we observed highly distinct, protein-specific phenotypes. Upon knock-down of human SMC1, much of SMC3 remains stable, accumulates in the cytoplasm and does not associate with other cohesin proteins. Most of the excess nuclear SMC3 is highly mobile and not or only weakly chromosome-associated. In contrast, human SMC3 knock-down rendered SMC1 instable without cytoplasmic accumulation. As observed by differential protein extraction and in FRAP experiments the remaining SMC1 or SMC3 proteins in the respective SMC1 or SMC3 knock-down experiments constituted a cohesin pool, which is associated with chromatin with highest affinity, likely the least expendable. Expression of bovine EGFP-SMC1 or mouse EGFP-SMC3 in human cells under conditions of human SMC1 or SMC3 knock-down rescued the respective phenotypes, but in untreated cells over-expressed exogenous SMC proteins mis-localized. Paucity of either one of the SMC proteins causes RAD21 degradation. These results argue for great caution in interpreting SMC1 and SMC3 RNAi or over-expression experiments. Under challenged conditions these two proteins unexpectedly behave differently, which may have biological consequences for regulation of cohesin-associated functions and for human cohesin pathologies.
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Laugsch, Magdalena, Jochen Seebach, Hans Schnittler, and Rolf Jessberger. "Imbalance of SMC1 and SMC3 Cohesins Causes Specific and Distinct Effects." Public Library of Science, 2013. https://tud.qucosa.de/id/qucosa%3A27288.

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SMC1 and SMC3 form a high-affinity heterodimer, which provides an open backbone of the cohesin ring, to be closed by a kleisin protein. RNAi mediated knock-down of either one heterodimer partner, SMC1 or SMC3, is expected to cause very similar if not identical phenotypes. However, we observed highly distinct, protein-specific phenotypes. Upon knock-down of human SMC1, much of SMC3 remains stable, accumulates in the cytoplasm and does not associate with other cohesin proteins. Most of the excess nuclear SMC3 is highly mobile and not or only weakly chromosome-associated. In contrast, human SMC3 knock-down rendered SMC1 instable without cytoplasmic accumulation. As observed by differential protein extraction and in FRAP experiments the remaining SMC1 or SMC3 proteins in the respective SMC1 or SMC3 knock-down experiments constituted a cohesin pool, which is associated with chromatin with highest affinity, likely the least expendable. Expression of bovine EGFP-SMC1 or mouse EGFP-SMC3 in human cells under conditions of human SMC1 or SMC3 knock-down rescued the respective phenotypes, but in untreated cells over-expressed exogenous SMC proteins mis-localized. Paucity of either one of the SMC proteins causes RAD21 degradation. These results argue for great caution in interpreting SMC1 and SMC3 RNAi or over-expression experiments. Under challenged conditions these two proteins unexpectedly behave differently, which may have biological consequences for regulation of cohesin-associated functions and for human cohesin pathologies.
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James, Rosalina Dee. "Cohesin proteins SMC1 and SMC3 : roles in aneuploidy and in meiotic chromosome dynamics /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/6333.

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Bessat, Mohamed Said Nooh. "Functional characterisation of cohesin subunit SMC3 and separase and their roles in the segregation of large and minichromosomes in Trypanosoma brucei." Thesis, University of Hull, 2009. http://hydra.hull.ac.uk/resources/hull:2179.

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The genome of the African trypanosome, Trypanosoma brucei, presents an unusual karyotype in which two main classes of chromosomes, large and small minichromosomes, need to be faithfully replicated and segregated during the cell cycle. Although the large and minichromosomes are colocalised and segregated by association with the mitotic spindle, minichromosomes exhibit segregation patterns that differ from those observed for large chromosomes. To address whether this difference is reflected at a molecular level, two different proteins that have highly conserved functions in eukaryotic chromosomes segregation were characterised in this study. The first protein, SMC3, is a component of the chromosome cohesion apparatus that holds sister chromatids together after their replication until segregation at anaphase. The second protein, separase, is a cysteine protease that resolves sister chromatid cohesion at the onset of anaphase and has, in other organisms, additional functions during mitosis. The T. brucei cohesin subunit, TbSMC3, localised to the nucleus as a chromatin-bound protein from G1 phase until metaphase and dissociated from chromatin during anaphase until the completion of cell division. On the other hand, cytoplasmic localisation of separase with nuclear exclusion was prevalent until the onset of metaphase when the protein re-localised to the nucleus, thus providing a potential control mechanism to prevent premature cohesin cleavage. Interference with the normal expression of SMC3 and separase by RNA interference resulted in defects in growth rate, cell cycle progression and chromosomes segregation. TbSMC3 depletion produced a lethal phenotype and inhibition of cell cycle progression. Similarly, lethality with severe inhibition of cell cycle progression was the main feature of separase depletion. Using fluorescence in situ hybridisation (FISH), it was shown that SMC3 depletion had no visible effect on the symmetric segregation of the minichromosome population, but interferes with the faithful mitotic segregation of large chromosomes. In contrast, separase depletion blocks the segregation of both large and minichromosomes. In separase-depleted mitotic cells, cohesins remained bound to chromatin, which is in contrast to rapid dissociation of cohesins from chromatin in wild-type mitotic cells. The severity of segregation phenotypes after separase depletion was additionally explained by defects in the mitotic spindle assembly. In both SMC3 and separase depleted cells, cytokinesis in the absence of mitosis/karyokinesis was not inhibited in procyclic cells, resulting in the generation of anucleate 'zoid' cells. The lethality imposed on trypanosome cells after depletion of both SMC3 and separase proteins indicate that they can serve as potential drug targets for anti-parasite chemotherapy.
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Parenti, I. "CORNELIA DE LANGE SYNDROME AND RELATED DISORDERS: NEW INSIGHTS INTO GLOBAL TRANSCRIPTIONAL DISTURBANCES DUE TO MUTATIONS IN CHROMATIN-ASSOCIATED FACTORS." Doctoral thesis, Università degli Studi di Milano, 2016. http://hdl.handle.net/2434/352028.

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Cornelia de Lange syndrome (CdLS) is a rare disorder characterized by an extensive clinical heterogeneity. The main features of the syndrome are characteristic facial dysmorphisms and a variable level of intellectual disability, growth retardation and developmental delay. Though, the number and severity of the clinical signs vary among patients. An extensive genetic heterogeneity partially accounts for the reported clinical variability. Mutations in different cohesin-associated proteins are in fact responsible for the onset of the syndrome. The known CdLS-genes include NIPBL, SMC1A, SMC3, RAD21 and HDAC8. Alterations in the cohesin loader NIPBL are found in more than half of CdLS cases and are associated with a classical phenotype and with a high frequency of limb malformations. In addition, mosaicism has been proven to play an important role in association with NIPBL. Mutations in the structural elements SMC1A, SMC3 and RAD21 and in the regulator HDAC8 account for about 10-15% of CdLS cases. The phenotype of those patients who harbor mutations in these genes is usually milder or atypical. The five genes all together, also taking into account the role of mosaicism, can explain about 70% of CdLS cases. In an internationally assembled cohort of patients we were able to identify 109 mutations in NIPBL, 8 mutations in SMC1A, 15 mutations in SMC3 and 11 mutations in HDAC8, thus increasing the total number of mutations so far described for CdLS. In addition, by the use of next generation sequencing techniques we were able to identify mutations in five genes different from cohesin in six unrelated patients with a clinical diagnosis of CdLS. The five genes include those encoding for different subunits of the chromatin remodeling complex named SWI/SNF and for the transcriptional repressor ANKRD11. Mutations in these genes have been so far associated to Coffin-Siris syndrome and KBG syndrome, respectively. Protein-protein interaction experiments also showed a direct interaction of the SWI/SNF subunit SMARCB1 with the cohesin-related proteins NIPBL and SMC3. These direct link between cohesin and SWI/SNF subunits indicate that mutations affecting the two protein complexes might determine the deregulation of overlapping sets of genes. Our newly identified variants contribute to a better understanding of the correlation between genotype and phenotype in the presence of mutations in the known-CdLS genes. Notwithstanding, different pehotypes have been observed in patients carrying the same DNA alteration, hence suggesting that environmental factors may play an important role in the delineation of the observed clinical features. Additionally, the identification of mutations in chromatin-associated factors responsible for syndromes different from CdLS indicate the existence of a broad pleiotropy that should be taken into account while assessing the clinical and molecular diagnosis. Furthermore, we investigated the molecular mechanisms underlying the syndrome in the presence of missense substitutions or small in-frame deletions in SMC1A, a X-linked gene that localizes in a region of the X-chromosome that partially escapes X-inactivation in humans. Our expression analysis revealed that the transcript is expressed at higher levels in females as compared to males, and that there are no differences in the expression of the SMC1A protein between healthy and affected females. In addition, pyrosequencing analysis showed that CdLS female patients harboring mutations in SMC1A tend to express the wild type allele at higher levels as compared to the mutant allele. All together, these data suggests that the pathogenesis of the syndrome in the presence of mutations affecting SMC1A which do not disrupt the reading frame might be linked to a dominant negative effect exerted by the mutant protein on the wild type.
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BOATENG, KINGSLEY A. "STUDIES ON ARABIDOPSIS PROTEINS REQUIRED FOR THE ESTABLISHMENT AND RELEASE OF SISTER CHROMATID COHESION." Miami University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=miami1185209243.

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Tingström, Victor. "Sequential parameter and state learning in continuous time stochastic volatility models using the SMC² algorithm." Thesis, KTH, Matematisk statistik, 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-177104.

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In this Master’s thesis, joint sequential inference of both parameters and states of stochastic volatility models is carried out using the SMC2 algorithm found in SMC2: an efficient algorithm for sequential analysis of state-space models, Nicolas Chopin, Pierre E. Jacob, Omiros Papaspiliopoulos. The models under study are the continuous time s.v. models (i) Heston, (ii) Bates, and (iii) SVCJ, where inference is based on options prices. It is found that the SMC2 performs well for the simpler models (i) and (ii), wheras filtering in (iii) performs worse. Furthermore, it is found that the FFT option price evaluation is the most computationally demanding step, and it is suggested to explore other avenues of computation, such as GPGPU-based computing.
I denna Masteruppsats estimeras sekventiellt parametrar och tillstånd i stokastiska volatilitetsmodeller nyttjandes SMC2 -algoritmen som återfinns i [1]. Modellerna som studeras är de kontinuerliga s.v.-modellerna (i) Heston, (ii) Bates och (iii) SVCJ, där inferens baseras på optionspriser. Vi finner att SMC2 presterar bra resultat för de enklare modellerna (i) och (ii) emedan filtrering för (iii) presterar sämre. Vi finner ytterligare att det beräkningsmässigt tyngsta steget är optionsprissättning nyttjandes FFT, därför föreslås det att undersöka andra beräkningssätt, såsom GPGPU-beräkning
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Ullal, Pranav. "Functional study of the Smc5/Smc6 complex through analysis of novel interactors." Thesis, Imperial College London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511891.

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Esteras, Bejar Miguel. "Development of methods for the study of the role of the Smc5-Smc6 complex in DNA stability." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11072.

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The Structural Maintenance of Chromosomes (SMC) proteins play a number of crucial roles in the metabolism of chromosomes. The Smc5-Smc6 complex is the least well understood of the complexes formed by SMC proteins. Hitherto, the Smc5-Smc6 complex has been linked to protein post-translational modification by sumoylation and restart of collapsed replication forks by homologous recombination between sister chromatids (SCR). However, a detailed characterization of the roles of the Smc5-Smc6 complex is missing. The objective of this study is to characterize the function of the Smc5-Smc6 complex in DNA repair by SCR, and to identify sumoylation substrates of MMS21, a E3-sumoligase subunit of the Smc5-Smc6 complex. Recent studies suggest that DNA single-strand nicks are transformed to doublestrand breaks in a replication-dependent manner, and this triggers SCR. I developed an assay for the activation of SCR based on the expression of a site-specific nickase. Unfortunately, a stable site-specific nick was observed in only 30% of the population. This percentage was insufficient for the study of the molecular role of the Smc5-Smc6 complex during SCR. However, this assay could be used to confirm and further characterize the activation of SCR upon replication-induced DNA damage. To study the role of sumoylation within the Smc5-Smc6 activity, I have developed a proteome-wide approach for the in vivo identification of sumoylation-sites by mass spectrometry. This technique can be used for the identification of MMS21 substrates and for the mapping of their sumo-acceptor lysines. The mapping of sumo-acceptor sites allows the generation of sumo-specific mutant proteins that can be used to study the function of sumoylation. More than 360 sumo-acceptor lysines, belonging to 245 different proteins, were identified. In vivo sumoylation at these lysines was verified by MS-independent methods. In addition, I developed a SILAC-based mass spectrometry assay for the quantitative study of site-specific sumoylation.
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Books on the topic "SMC3"

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Badrinarayanan, Anjana, ed. SMC Complexes. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9520-2.

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São Paulo (Brazil). Secretaria Municipal de Cultura., ed. Guia cultural da SMC. [São Paulo, Brazil]: SMC, 1992.

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Integrated Rural Development Project, Serenje-Mpika-Chinsali (Zambia), ed. The IRDP (SMC) cost, benefit simulation game. Mpika, Zambia: Republic of Zambia, Integrated Rural Development Project, Serenje-Mpika-Chinsali, 1985.

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O'Donohue, Daniel J. First-term retention of enlisted Selected Marine Corps (SMCR) Reservists. Monterey, California: Naval Postgraduate School, 1988.

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A, Levine, and United States. National Aeronautics and Space Administration., eds. Discovery of orbital decay in SMC X-1. [Washington, DC: National Aeronautics and Space Administration, 1992.

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Programme, United Nations Development. Mainstreaming SMC issues into MDG-based national development planning. Phnom Penh]: UNDP, 2008.

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(Firm), Sun Microsystems. Installing Solaris 1.1 SMCC Version A: (SunOS 4.1.3 and OpenWindows Version 3). Mountain View, CA: Sun Microsystems, 1992.

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The national action plan on sound management of chemicals (SMC) in Uganda. Kampala, Uganda: NEMA, 2010.

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J, Mooney Peter. New directions in reinforced thermoset plastics: SMC, BMC, pultrusion, filament winding, SRIM, RTM. Norwalk, CT: Business Communications Co., 1992.

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Poor man [sic] hydrogen generator on demand: A step-by-step building guide : SMCS HHO stephens multi cell systems hydrogen generator on demand. [Place of publication not identified]: Authorhouse, 2011.

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Book chapters on the topic "SMC3"

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Posypaiko, V. I., and E. A. Alekseeva. "SmCl3." In Phase Equilibria in Binary Halides, 389. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-9024-4_151.

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Posypaiko, V. I., and E. A. Alekseeva. "SmF3." In Phase Equilibria in Binary Halides, 390. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-9024-4_152.

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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. "SMCD." In Encyclopedia of Molecular Mechanisms of Disease, 1946. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7878.

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Gooch, Jan W. "SMC." In Encyclopedic Dictionary of Polymers, 672. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_10787.

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Chopin, Nicolas, and Omiros Papaspiliopoulos. "SMC Samplers." In Springer Series in Statistics, 329–55. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-47845-2_17.

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Utkin, Vadim, Alex Poznyak, Yury V. Orlov, and Andrey Polyakov. "Adaptive SMC." In SpringerBriefs in Mathematics, 99–108. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-41709-3_9.

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Agarwal, Pratyush, Krishnendu Chatterjee, Shreya Pathak, Andreas Pavlogiannis, and Viktor Toman. "Stateless Model Checking Under a Reads-Value-From Equivalence." In Computer Aided Verification, 341–66. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-81685-8_16.

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AbstractStateless model checking (SMC) is one of the standard approaches to the verification of concurrent programs. As scheduling non-determinism creates exponentially large spaces of thread interleavings, SMC attempts to partition this space into equivalence classes and explore only a few representatives from each class. The efficiency of this approach depends on two factors: (a) the coarseness of the partitioning, and (b) the time to generate representatives in each class. For this reason, the search for coarse partitionings that are efficiently explorable is an active research challenge.In this work we present $${\text {RVF-SMC}}$$ RVF-SMC , a new SMC algorithm that uses a novel reads-value-from (RVF) partitioning. Intuitively, two interleavings are deemed equivalent if they agree on the value obtained in each read event, and read events induce consistent causal orderings between them. The RVF partitioning is provably coarser than recent approaches based on Mazurkiewicz and “reads-from” partitionings. Our experimental evaluation reveals that RVF is quite often a very effective equivalence, as the underlying partitioning is exponentially coarser than other approaches. Moreover, $${\text {RVF-SMC}}$$ RVF-SMC generates representatives very efficiently, as the reduction in the partitioning is often met with significant speed-ups in the model checking task.
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Lundén, Daniel, Johannes Borgström, and David Broman. "Correctness of Sequential Monte Carlo Inference for Probabilistic Programming Languages." In Programming Languages and Systems, 404–31. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-72019-3_15.

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AbstractProbabilistic programming is an approach to reasoning under uncertainty by encoding inference problems as programs. In order to solve these inference problems, probabilistic programming languages (PPLs) employ different inference algorithms, such as sequential Monte Carlo (SMC), Markov chain Monte Carlo (MCMC), or variational methods. Existing research on such algorithms mainly concerns their implementation and efficiency, rather than the correctness of the algorithms themselves when applied in the context of expressive PPLs. To remedy this, we give a correctness proof for SMC methods in the context of an expressive PPL calculus, representative of popular PPLs such as WebPPL, Anglican, and Birch. Previous work have studied correctness of MCMC using an operational semantics, and correctness of SMC and MCMC in a denotational setting without term recursion. However, for SMC inference—one of the most commonly used algorithms in PPLs as of today—no formal correctness proof exists in an operational setting. In particular, an open question is if the resample locations in a probabilistic program affects the correctness of SMC. We solve this fundamental problem, and make four novel contributions: (i) we extend an untyped PPL lambda calculus and operational semantics to include explicit resample terms, expressing synchronization points in SMC inference; (ii) we prove, for the first time, that subject to mild restrictions, any placement of the explicit resample terms is valid for a generic form of SMC inference; (iii) as a result of (ii), our calculus benefits from classic results from the SMC literature: a law of large numbers and an unbiased estimate of the model evidence; and (iv) we formalize the bootstrap particle filter for the calculus and discuss how our results can be further extended to other SMC algorithms.
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Holze, Rudolf. "Ionic conductance of SmCl3." In Electrochemistry, 1636. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49251-2_1458.

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Holze, Rudolf. "Ionic conductance of SmI3." In Electrochemistry, 1638. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-49251-2_1460.

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Conference papers on the topic "SMC3"

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Filipovic, Ela, Nikolina Catlak, and Natasa Zenic. "Sport participation should not be observed as protective against smoking and drinking in adolescence; cross-sectional cluster-based analysis in Croatian southern regions." In 12th International Conference on Kinanthropology. Brno: Masaryk University Press, 2020. http://dx.doi.org/10.5817/cz.muni.p210-9631-2020-26.

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Purpose: Sport participation in adolescence is frequently observed as being protective against consumption of psychoactive substances (e.g. cigarettes and alcohol), but limited number of studies directly examined this problem while simultaneously observing consump-tion of cigarettes and alcohol. The aim of this study was to evidence the possible associations which may exist between different factors explaining participation in sports, and consumption of cigarettes and alcohol in adolescents from Croatia. Methods: The sample comprised 436 adolescents from coastal regions in Croatia (202 fe-males) aged 15–17 years who were tested by previously validated closed structured ques-tionnaire on sport factors (experience in sports [four point scale from “never participated” to “ > 5 years”], sport competitive achievement [four point scale ranging from “never competed” to “national/international competitive achievement”], number of sport training sessions per week [four point scale ranging from “didn’t participate” to “sometimes even twice a day”]), cigarette smoking (four point scale ranging from “never smoked” to “more than 10 cigarettes per day”), and alcohol consumption (measured by Alcohol Use Disorders Identification Test – AUDIT). Cluster analysis calculated on the basis of cigarette smoking and AUDIT results was used to form homogenous groups (substance misuse clusters – SMC). The Kruskall Wallis analysis of variance (KWA) was calculated to identify the differences between SMC in studied sport factors. Results: Four SMC were formed indicating: (i) high alcohol + high cigarettes (SMC1: n=42), (ii) high alcohol + low cigarettes (SMC2: n=115), (iii) low alcohol + low cigarettes (SMC3: n=226), and (iv) low alcohol + high cigarettes consumption (SMC4: n=53). When calculat-ed for total sample of participants, the KWA revealed significant differences among SMC, with significant post-hoc differences between SMC1 and SMC3 in all sport-factors (H test: 9.5-to-17.5, p 80% of all SMC1 members). Gender-specific KWA did not reveal significant differences among SMC in studied sport factors. Conclusion: Study results do not support the theory of protective effects of sport participation against substance misuse in adolescence. Even more, there are some indices that sport par-ticipation may be observed risk factor for consumption of cigarettes and alcohol in this age group. Social acceptance of smoking and drinking in sport-society in the region is probable reason for relatively high rates of substance misuse in adolescents who are actively involved in sports.
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Pascazio, Vito, and Giancarlo Ferraiuolo. "On the Use of Gaussian Markov Random Fields in Microwave Tomography: the Quadratic Case." In Signal Recovery and Synthesis. Washington, D.C.: OSA, 2001. http://dx.doi.org/10.1364/srs.2001.smc3.

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Matson, Charles L., and David W. Tyler. "Artifacts, Bias, and Super-Resolution." In Signal Recovery and Synthesis. Washington, D.C.: OSA, 2005. http://dx.doi.org/10.1364/srs.2005.smc3.

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Guizar-Sicairos, Manuel, Samuel T. Thurman, and James R. Fienup. "Efficient Image Registration Algorithms for Computation of Invariant Error Metrics." In Signal Recovery and Synthesis. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/srs.2007.smc3.

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Jurling, Alden S., and James R. Fienup. "A Fast Approximation Method for Broadband Phase Retrieval." In Signal Recovery and Synthesis. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/srs.2011.smc3.

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Chin, Sanghoon, and Luc Thévenaz. "Large multi Gbit/s delays generated in an all-optical tunable delay line preserving wavelength and signal bandwidth." In Slow and Fast Light. Washington, D.C.: OSA, 2008. http://dx.doi.org/10.1364/sl.2008.smc3.

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Lloyd, Seth W., Michel J. F. Digonnet, and Shanhui Fan. "Tactical-grade interferometric fiber optic gyroscope driven with a narrow-linewidth laser." In Optical Sensors. Washington, D.C.: OSA, 2011. http://dx.doi.org/10.1364/sensors.2011.smc3.

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Schneider, Thomas, Andrzej Wiatrek, and Ronny Henker. "Zero-Broadening, Zero-Distortion SBS-based Slow Light – an Overview." In Slow and Fast Light. Washington, D.C.: OSA, 2009. http://dx.doi.org/10.1364/sl.2009.smc3.

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Guo, C. Z., S. L. Chen, P. Dowd, and Y. H. Zhang. "Theoretical investigation of strained InGaAs/GaPAsSb type-II quantum wells on GaAs for long wavelength (1.3 µm) optoelectronic devices." In Spatial Light Modulators and Integrated Optoelectronic Arrays. Washington, D.C.: OSA, 1999. http://dx.doi.org/10.1364/slm.1999.smc3.

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Kurtz, Sarah. "High Efficiency Solar Cells for Large-Scale Electricity Generation." In Frontiers in Optics. Washington, D.C.: OSA, 2007. http://dx.doi.org/10.1364/fio.2007.smc3.

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Reports on the topic "SMC3"

1

Balkwill, David L. The DOE Subsurface Microbial Culture Collection (SMCC). Office of Scientific and Technical Information (OSTI), May 2006. http://dx.doi.org/10.2172/882497.

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Andreescu, R., and M. J. O'Shea. Hard Magnetic Properties of Multilayered SmCo/Co Permanent Magnets. Fort Belvoir, VA: Defense Technical Information Center, January 2001. http://dx.doi.org/10.21236/ada398436.

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Fox, M., C. Kassimis, and J. Stevens. IBM's Shared Memory Communications over RDMA (SMC-R) Protocol. RFC Editor, August 2015. http://dx.doi.org/10.17487/rfc7609.

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Harris, Vincent. Chemical Synthesis of Next Generation High Energy Product Hybrid SmCo Permanent Magnets for High Temperature Applications. Fort Belvoir, VA: Defense Technical Information Center, August 2010. http://dx.doi.org/10.21236/ada525642.

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AIR FORCE SPACE COMMAND SPACE MISSILE SYS CTR. Space and Missile Systems Center Tailoring: Tailoring of Risk Management Requirements in SMC-S-001 (2013). Fort Belvoir, VA: Defense Technical Information Center, January 2014. http://dx.doi.org/10.21236/ada619441.

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Chervak, Michelle, Tyson Grier, Ryan Steelman, Morgan Anderson, and Bruce Jones. Evaluation of Student Injuries at the Sergeants Major Course (SMC), Fort Bliss, Texas, August 2013-May 2014. Fort Belvoir, VA: Defense Technical Information Center, June 2016. http://dx.doi.org/10.21236/ad1012898.

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Hurst, Jestin. Lagoon Seepage Testing Plan for the Specific Manufacturing Capability (SMC) Complex Sewage Lagoons at Idaho National Laboratory, Butte County, Idaho. Office of Scientific and Technical Information (OSTI), June 2018. http://dx.doi.org/10.2172/1484699.

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Theodore, George. Investigation of the Role of Sialomucin Complex (SMC)/Muc4, a Unique Intramembranous HER-2/ErbB-2 Ligand as a Suppressor of Apoptosis. Fort Belvoir, VA: Defense Technical Information Center, April 2004. http://dx.doi.org/10.21236/ada426336.

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Zaraisky, E. I. Comparative study of tests for simultaneous diagnosis of AFP and beta-HCG oncoantigens by ICHA methods using nanozolot and IPMS-ELISA using isotopes Eu3+ and Sm3+. Sputnik+, 2018. http://dx.doi.org/10.18411/1684-2626n9_18.

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Zaraisky, E. I., A. A. Stepanov, and A. M. Poltavtsev. Express test for the simultaneous diagnosis of encountering PAMG-1 and PAMG - 2 using technique of immune chromatography using nanogold and IPMS-ELISA using isotopes Еi3+ and Sm3+. Editors of the Eurasian Scientific Journal, 2018. http://dx.doi.org/10.18411/esj_n12_2018-141-144.

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