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Journal articles on the topic "Sfp1"
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Bielaszewska, Martina, Rita Prager, Liz Vandivinit, Anne M�sken, Alexander Mellmann, Nicholas J. Holt, Phillip I. Tarr, Helge Karch, and Wenlan Zhang. "Detection and Characterization of the Fimbrial sfp Cluster in Enterohemorrhagic Escherichia coli O165:H25/NM Isolates from Humans and Cattle." Applied and Environmental Microbiology 75, no. 1 (October 31, 2008): 64–71. http://dx.doi.org/10.1128/aem.01815-08.
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ABSTRACT The sfp cluster, encoding Sfp fimbriae and located in the large plasmid of sorbitol-fermenting (SF) enterohemorrhagic Escherichia coli (EHEC) O157 (pSFO157), has been considered a unique characteristic of this organism. We discovered and then characterized the sfp cluster in EHEC O165:H25/NM (nonmotile) isolates of human and bovine origin. All seven strains investigated harbored a complete sfp cluster (carrying sfpA, sfpH, sfpC, sfpD, sfpJ, sfpF, and sfpG) of 6,838 bp with >99% nucleotide sequence homology to the sfp cluster of SF EHEC O157:NM. The sfp cluster in EHEC O165:H25/NM strains was located in an ∼80-kb (six strains) or ∼120-kb (one strain) plasmid which differed in structure, virulence genes, and sfp flanks from pSFO157. All O165:H25/NM strains belonged to the same multilocus sequence type (ST119) and were only distantly phylogenetically related to SF EHEC O157:NM (ST11). The highly conserved sfp cluster in different clonal backgrounds suggests that this segment was acquired independently by EHEC O165:H25 and SF EHEC O157:NM. Its presence in an additional EHEC serotype extends the diagnostic utility of PCR targeting sfpA as an easy and efficient approach to seek EHEC in patients' stools. The reasons for the convergence of pathogenic EHEC strains on a suite of virulence loci remain unknown.
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Xu, Zhiheng, and David Norris. "The SFP1 Gene Product of Saccharomyces cerevisiae Regulates G2/M Transitions During the Mitotic Cell Cycle and DNA-Damage Response." Genetics 150, no. 4 (December 1, 1998): 1419–28. http://dx.doi.org/10.1093/genetics/150.4.1419.
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Abstract In eukaryotic cells, checkpoint pathways arrest cell-cycle progression if a particular event has failed to complete appropriately or if an important intracellular structure is defective or damaged. Saccharomyces cerevisiae strains that lack the SFP1 gene fail to arrest at the G2 DNA-damage checkpoint in response to genomic injury, but maintain their ability to arrest at the replication and spindle-assembly checkpoints. sfp1Δ mutants are characterized by a premature entrance into mitosis during a normal (undamaged) cell cycle, while strains that overexpress Sfp1p exhibit delays in G2. Sfp1p therefore acts as a repressor of the G2/M transition, both in the normal cell cycle and in the G2 checkpoint pathway. Sfp1 is a nuclear protein with two Cys2His2 zinc-finger domains commonly found in transcription factors. We propose that Sfp1p regulates the expression of gene products involved in the G2/M transition during the mitotic cell cycle and the DNA-damage response. In support of this model, overexpression of Sfp1p induces the expression of the PDS1 gene, which is known to encode a protein that regulates the G2 checkpoint.
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Brunder, Werner, A. Salam Khan, Jörg Hacker, and Helge Karch. "Novel Type of Fimbriae Encoded by the Large Plasmid of Sorbitol-Fermenting Enterohemorrhagic Escherichia coli O157:H−." Infection and Immunity 69, no. 7 (July 1, 2001): 4447–57. http://dx.doi.org/10.1128/iai.69.7.4447-4457.2001.
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ABSTRACT Sorbitol-fermenting (SF) enterohemorrhagic Escherichia coli (EHEC) O157:H− have emerged as important causes of diarrheal diseases and the hemolytic-uremic syndrome in Germany. In this study, we characterized a 32-kb fragment of the plasmid of SF EHEC O157:H−, pSFO157, which differs markedly from plasmid pO157 of classical non-sorbitol-fermenting EHEC O157:H7. We found a cluster of six genes, termed sfpA,sfpH, sfpC, sfpD,sfpJ, and sfpG, which mediate mannose-resistant hemagglutination and the expression of fimbriae.sfp genes are similar to the pap genes, encoding P-fimbriae of uropathogenic E. coli, but thesfp cluster lacks homologues of genes encoding subunits of a tip fibrillum as well as regulatory genes. The major pilin, SfpA, despite its similarity to PapA, does not cluster together with known PapA alleles in a phylogenetic tree but is structurally related to the PmpA pilin of Proteus mirabilis. The putative adhesin gene sfpG, responsible for the hemagglutination phenotype, shows significant homology neither to papGnor to other known sequences. Sfp fimbriae are 3 to 5 nm in diameter, in contrast to P-fimbriae, which are 7 nm in diameter. PCR analyses showed that the sfp gene cluster is a characteristic of SF EHEC O157:H− strains and is not present in other EHEC isolates, diarrheagenic E. coli, or otherEnterobacteriaceae. The sfp gene cluster is flanked by two blocks of insertion sequences and an origin of plasmid replication, indicating that horizontal gene transfer may have contributed to the presence of Sfp fimbriae in SF EHEC O157:H−.
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Meng, Kun, Jiang Li, Yanan Cao, Pengjun Shi, Bo Wu, Xiaoyu Han, Yingguo Bai, Ningfeng Wu, and Bin Yao. "Gene cloning and heterologous expression of a serine protease fromStreptomyces fradiaevar.k11." Canadian Journal of Microbiology 53, no. 2 (February 2007): 186–95. http://dx.doi.org/10.1139/w06-122.
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The gene sfp1, which encodes a predicted serine proteinase designated SFP1, was isolated by the screening of a gene library of the feather-degrading strain Streptomyces fradiae var.k11. The open reading frame of sfp1 encodes a protein of 454 amino acids with a calculated molecular mass of 46.19 kDa. Sequence analysis reveals that SFP1 possesses a typical pre-pro-mature organization that consists of a signal sequence, an N-terminal propeptide region, and a mature proteinase domain. The pre-enzyme of SFP1 was expressed in Escherichia coli and consequently purified. The 25.6 kDa fraction with protease activity separated by gel filtration chromatography indicated that the mature enzyme of SFP1 was formed by autolysis of the propeptide after its expression. The purified SFP1 is active under a broad range of pH and temperature. SFP1 has pH and temperature optima of pH 8.5 and 65 °C for its caseinolytic activity and pH 9 and 62 °C for its keratinolytic activity. SFP1 was sharply inhibited by the serine proteinase inhibitor phenylmethyl sulfonyl fluoride and exhibited a good stability to solvents, detergents, and salts. Comparison of the protease activity of SFP1 with other commercial proteases indicates that SFP1 has a considerable caseinolytic and keratinolytic activity as does proteinase K.
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Fingerman, Ian, Vijayalakshmi Nagaraj, David Norris, and Andrew K. Vershon. "Sfp1 Plays a Key Role in Yeast Ribosome Biogenesis." Eukaryotic Cell 2, no. 5 (October 2003): 1061–68. http://dx.doi.org/10.1128/ec.2.5.1061-1068.2003.
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ABSTRACT Sfp1, an unusual zinc finger protein, was previously identified as a gene that, when overexpressed, imparted a nuclear localization defect. sfp1 cells have a reduced size and a slow growth phenotype. In this study we show that SFP1 plays a role in ribosome biogenesis. An sfp1 strain is hypersensitive to drugs that inhibit translational machinery. sfp1 strains also have defects in global translation as well as defects in rRNA processing and 60S ribosomal subunit export. Microarray analysis has previously shown that ectopically expressed SFP1 induces the transcription of a large subset of genes involved in ribosome biogenesis. Many of these induced genes contain conserved promoter elements (RRPE and PAC). Our results show that activation of transcription from a reporter construct containing two RRPE sites flanking a single PAC element is SFP1 dependent. However, we have been unable to detect direct binding of the protein to these elements. This suggests that regulation of genes containing RRPEs is dependent upon Sfp1 but that Sfp1 may not directly bind to these conserved promoter elements; rather, activation may occur through an indirect mechanism.
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Lopez, Antonio Diaz, Krisztina Tar, Undine Krügel, Thomas Dange, Ignacio Guerrero Ros, and Marion Schmidt*. "Proteasomal degradation of Sfp1 contributes to the repression of ribosome biogenesis during starvation and is mediated by the proteasome activator Blm10." Molecular Biology of the Cell 22, no. 5 (March 2011): 528–40. http://dx.doi.org/10.1091/mbc.e10-04-0352.
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The regulation of ribosomal protein (RP) gene transcription is tightly linked to the nutrient status of the cell and is under the control of metabolic signaling pathways. In Saccharomyces cerevisiae several transcriptional activators mediate efficient RP gene transcription during logarithmic growth and dissociate from RP gene promoters upon nutrient limitation. Repression of RP gene transcription appears to be regulated predominantly by posttranslational modification and cellular localization of transcriptional activators. We report here that one of these factors, Sfp1, is degraded by the proteasome and that the proteasome activator Blm10 is required for regulated Sfp1 degradation. Loss of Blm10 results in the stabilization and increased nuclear abundance of Sfp1 during nutrient limitation, increased transcription of RP genes, increased levels of RPs, and decreased rapamycin-induced repression of RP genes. Thus we conclude that proteasomal degradation of Sfp1 is mediated by Blm10 and contributes to the repression of ribosome biogenesis under nutrient depletion.
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Chang, Che-Kang, Min-Chi Yang, Hsueh-Fen Chen, Yi-Ling Liao, and Chung-Yu Lan. "The Role of Sfp1 in Candida albicans Cell Wall Maintenance." Journal of Fungi 8, no. 11 (November 13, 2022): 1196. http://dx.doi.org/10.3390/jof8111196.
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The cell wall is the first interface for Candida albicans interaction with the surrounding environment and the host cells. Therefore, maintenance of cell wall integrity (CWI) is crucial for C. albicans survival and host-pathogen interaction. In response to environmental stresses, C. albicans undergoes cell wall remodeling controlled by multiple signaling pathways and transcription regulators. Here, we explored the role of the transcription factor Sfp1 in CWI. A deletion of the SFP1 gene not only caused changes in cell wall properties, cell wall composition and structure but also modulated expression of cell wall biosynthesis and remodeling genes. In addition, Cas5 is a known transcription regulator for C. albicans CWI and cell wall stress response. Interestingly, our results indicated that Sfp1 negatively controls the CAS5 gene expression by binding to its promoter element. Together, this study provides new insights into the regulation of C. albicans CWI and stress response.
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Lee, Shao-Yu, Hsueh-Fen Chen, Ying-Chieh Yeh, Yao-Peng Xue, and Chung-Yu Lan. "The Transcription Factor Sfp1 Regulates the Oxidative Stress Response in Candida albicans." Microorganisms 7, no. 5 (May 14, 2019): 131. http://dx.doi.org/10.3390/microorganisms7050131.
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Candida albicans is a commensal that inhabits the skin and mucous membranes of humans. Because of the increasing immunocompromised population and the limited classes of antifungal drugs available, C. albicans has emerged as an important opportunistic pathogen with high mortality rates. During infection and therapy, C. albicans frequently encounters immune cells and antifungal drugs, many of which exert their antimicrobial activity by inducing the production of reactive oxygen species (ROS). Therefore, antioxidative capacity is important for the survival and pathogenesis of C. albicans. In this study, we characterized the roles of the zinc finger transcription factor Sfp1 in the oxidative stress response against C. albicans. A sfp1-deleted mutant was more resistant to oxidants and macrophage killing than wild-type C. albicans and processed an active oxidative stress response with the phosphorylation of the mitogen-activated protein kinase (MAPK) Hog1 and high CAP1 expression. Moreover, the sfp1-deleted mutant exhibited high expression levels of antioxidant genes in response to oxidative stress, resulting in a higher total antioxidant capacity, glutathione content, and glutathione peroxidase and superoxide dismutase enzyme activity than the wild-type C. albicans. Finally, the sfp1-deleted mutant was resistant to macrophage killing and ROS-generating antifungal drugs. Together, our findings provide a new understanding of the complex regulatory machinery in the C. albicans oxidative stress response.
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Hosiner, Dagmar, Harri Lempiäinen, Wolfgang Reiter, Joerg Urban, Robbie Loewith, Gustav Ammerer, Rudolf Schweyen, David Shore, and Christoph Schüller. "Arsenic Toxicity to Saccharomyces cerevisiae Is a Consequence of Inhibition of the TORC1 Kinase Combined with a Chronic Stress Response." Molecular Biology of the Cell 20, no. 3 (February 2009): 1048–57. http://dx.doi.org/10.1091/mbc.e08-04-0438.
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The conserved Target Of Rapamycin (TOR) growth control signaling pathway is a major regulator of genes required for protein synthesis. The ubiquitous toxic metalloid arsenic, as well as mercury and nickel, are shown here to efficiently inhibit the rapamycin-sensitive TORC1 (TOR complex 1) protein kinase. This rapid inhibition of the TORC1 kinase is demonstrated in vivo by the dephosphorylation and inactivation of its downstream effector, the yeast S6 kinase homolog Sch9. Arsenic, mercury, and nickel cause reduction of transcription of ribosome biogenesis genes, which are under the control of Sfp1, a TORC1-regulated transcriptional activator. We report that arsenic stress deactivates Sfp1 as it becomes dephosphorylated, dissociates from chromatin, and exits the nucleus. Curiously, whereas loss of SFP1 function leads to increased arsenic resistance, absence of TOR1 or SCH9 has the opposite effect suggesting that TORC1 has a role beyond down-regulation of Sfp1. Indeed, we show that arsenic activates the transcription factors Msn2 and Msn4 both of which are targets of TORC1 and protein kinase A (PKA). In contrast to TORC1, PKA activity is not repressed during acute arsenic stress. A normal level of PKA activity might serve to dampen the stress response since hyperactive Msn2 will decrease arsenic tolerance. Thus arsenic toxicity in yeast might be determined by the balance between chronic activation of general stress factors in combination with lowered TORC1 kinase activity.
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Hsu, Chun-Min, Yi-Ling Liao, Che-Kang Chang, and Chung-Yu Lan. "Candida albicans Sfp1 Is Involved in the Cell Wall and Endoplasmic Reticulum Stress Responses Induced by Human Antimicrobial Peptide LL-37." International Journal of Molecular Sciences 22, no. 19 (September 30, 2021): 10633. http://dx.doi.org/10.3390/ijms221910633.
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Candida albicans is a commensal fungus of humans but can cause infections, particularly in immunocompromised individuals, ranging from superficial to life-threatening systemic infections. The cell wall is the outermost layer of C. albicans that interacts with the host environment. Moreover, antimicrobial peptides (AMPs) are important components in innate immunity and play crucial roles in host defense. Our previous studies showed that the human AMP LL-37 binds to the cell wall of C. albicans, alters the cell wall integrity (CWI) and affects cell adhesion of this pathogen. In this study, we aimed to further investigate the molecular mechanisms underlying the C. albicans response to LL-37. We found that LL-37 causes cell wall stress, activates unfolded protein response (UPR) signaling related to the endoplasmic reticulum (ER), induces ER-derived reactive oxygen species and affects protein secretion. Interestingly, the deletion of the SFP1 gene encoding a transcription factor reduced C. albicans susceptibility to LL-37, which is cell wall-associated. Moreover, in the presence of LL-37, deletion of SFP1 attenuated the UPR pathway, upregulated oxidative stress responsive (OSR) genes and affected bovine serum albumin (BSA) degradation by secreted proteases. Therefore, these findings suggested that Sfp1 positively regulates cell wall integrity and ER homeostasis upon treatment with LL-37 and shed light on pathogen-host interactions.
Dissertations / Theses on the topic "Sfp1"
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VIGANO', MATTEO. "Yeast cell size control: an interplay among ribosome biogenesis, protein synthesis and MAPK routes." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2011. http://hdl.handle.net/10281/19945.
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Cell-size homeostasis requires that proliferating cells coordinate growth and cell cycle, such that each division is matched by a doubling of mass. Size homeostasis is a universal but poorly understood feature of the cell cycle control. In the unicellular budding yeast Saccharomyces cerevisiae, the coordination of division with growth occurs at Start, a short interval during late G1 phase, after which cells are committed to division. A prerequisite for the passage through Start is the attainment of a critical cell size, whose value is set by ploidy and growth conditions.
The critical-size threshold maintains uniform the cell size over many generations, and under minimal nutrient conditions forces cells to accumulate the energy stores required to complete the division cycle.
Nutrients modulate the critical cell-size threshold according to the proliferation rate. Generally, cells growing slowly on a poor medium pass Start at a smaller size than fast-growing cells on a rich medium.
In S. cerevisiae mutants that subvert the size control process have two phenotypes: small (whi) and large (lge). The former undergo Start a smaller cell size and the latter at a larger. Moreover, a systematic determination of cell-size distributions for all yeast deletion strains identified many new potential Start regulators. Many of the genes encoding potential Start repressors are implicated in ribosome biogenesis, suggesting the existence of a link between these two seemingly disparate processes. One of the smallest whi mutant is linket to SFP1 gene deletion. sfp1Δ cells display a disproportionate effect on size relative to the change in growth rate.
SFP1 gene encodes a zinc-finger protein that is a key transcriptional regulator of ribosome biogenesis whose function is required for normal yeast growth. Nuclear localization of Sfp1, requires active TORC1 and it is highly stress sensitive. In addition, Sfp1 interacts directly with and is phosphorylated by TORC1. In contrast to Sch9 kinase, a major downstream target of TORC1, TORC1 phosphorylation of Sfp1 is unaffected by either osmotic or nutritional stresses, suggesting a different mode of regulation. Significantly, Sfp1, through its transcriptional activation function, exerts a negative feedback control on TORC1 activity toward the Sch9 kinase. Sfp1 also interacts with Mrs6, a conserved Rab escort protein that in turn regulates Sfp1 nuclear localization. The Mrs6 interaction with Sfp1 and TORC1 is related to a still poorly understood connection between TOR signaling and vesicle transport.
The aim of this work has been to better characterized the relationship among Sfp1, the cell size control and some signalling pathways involved in the coordination of division with growth.
In order to better elucidate the role of Sfp1 as a negative regulator of Start, we analyzed the level of some of the key players of the G1 to S transition, the G1 cyclins (Cln1-3) and the Cki Sic1, in a sfp1 mutant. sfp1Δ cells are characterized by a whi phenotype, slow growth, decreased budding index elongation of G1 phase and reduction of G2/M transition. Accordingly with some aspects of this phenotype, the Cln1-2 level resulted decreased while Cln3 levels were unaffected in agreement with data reporting that the mechanism through which Sfp1 couples ribosome biogenesis to Start is independent of Cln3. Interestingly, the main effect of the SFP1 deletion is on Sic1 that resulted entirely nuclear, all linked to Clb5 and stabilized by phosphorylation on threonine 173 (Thr173). Phosphorylation that is well known to induce Sic1 accumulation by preventing its degradation. In the sfp1 mutant, Sic1 stabilization is required for both the elongation of the G1 phase and the reduction of the G2/M transition. A similar situation that involves Sic1 stabilization by phosphorylation on Thr173 but leading to a G1 arrest is observed after inhibition of TORC1 by rapamycin where Sic1 accumulates in the nucleus to avoid improper Clb5/6-Cdc28-driven DNA replication under conditions of poor nutrient availability. This parallelism is in line with the fact that Sfp1 associated with Tor1 kinase and that this binding is essential for a correct localization of TORC1 together with Sfp1 at the RP promoters.
A condition of poor nutrient availability can be considered as a stress condition for a cell. Similarly, the activation of the Hog1 MAP kinase after osmotic stress also induces a cellular response where the stabilization of Sic1, always via Thr173 phosphorylation is involved. Moreover, in this context, the cellular response to SFP1 inactivation appears more similar to the response to osmotic stress than that to rapamycin. In fact, the latter induces a G1 arrest linked to a Sic1 stabilization but subsequently a decrease of Cln3 accumulation takes place; such a decrease is essential for maintaining a prolonged G1 arrest. On the contrary, after the osmotic stress Sic1 is stabilized, Cln1 and Cln2 are low, Cln3 levels are unaffected as in the mutant. In addition, the stress response do not always provoke a cell cycle arrest, but is often a slowdown of cell cycle progression, necessary for cell adaptation to new conditions. Only if the stress is too intense, cells arrest growth. Yeast cells modulate stress response via the activation of mitogen-activated protein kinases (MAPKs) which respond to different conditions such as pheromone signals (mediated by the MAPK Fus3), osmolarity (mediated by the MAPK Hog1), nutrient deprivation (mediated by the MAPK Kss1) and cell wall stress (mediated by the MAPK Slt2). Since the first three MAPKs pathways use basically the same signaling machinery, when one of the three pathways is activated, the others are suppressed (cross-talk). The stress response linked to SFP1 inactivation involves a complex cross-talk between the Hog1 and Kiss1 pathways. Both pathways are activated but only Kiss1 is phosphorylated. Kss1 is the MAP kinase that primarily functions under conditions of nutrient deprivation such as the lack of nitrogen and/or glucose in the growth medium. Under these conditions the signal mucin Msb2 regulates the activation of the filamentous growth (FG) pathway that induces the phosphorylation of Kss1, necessary to guarantee cell survival. The lack of Sfp1 is sensed by the cell as a condition of nutrient scarcity. In fact, under optimal growth conditions, Sfp1 localizes to the nucleus, where it promotes the RP and RiBi genes expression. In response to changes in nutrient availability, Sfp1 is released from RP and RiBi gene promoters and exits from the nucleus; thus, the ribosome biogenesis is down-regulated. Moreover, since Msb2 is also required for activation of the Hog1 pathway a reciprocal inhibitory loop takes place between the Hog1 and Kss1 pathways allowing stable activation of the latter. We found that once activated Kiss1 is able to stabilized Sic1.
We hypothesize that the activation of the FG pathway following Sfp1 lost of function involves a glycosylation defective-like response. In fact, activation of FG pathway by inhibition of N-glycosylation combined with a specific O-glycosylation defect induces activation of both Hog1 and Kss1 pathways and only Kss1 is phosphorylated. We found that SFP1 inactivation induces some defects that are also observed following the inhibition of glycosylation such as alterations in cell wall permeability, activation of the cell wall integrity pathway and alteration in the secretory pathway.
All our data indicate that not only Sfp1 is regulated by stress and nutrients (both affecting its localization), but that Sfp1 can, in turn, regulate the stress response. The linker between Sfp1 and stress response pathway is the secretory pathway. We can hypothesize that a reduction of ribosome biogenesis may induce a defect in the secretory pathway leading to the activation of Msb2 and thus of the FG pathway. The exit from the nucleus of Sfp1, necessary for the reduction of ribosome biogenesis, allows the release of the Rab GTPase that is essential to switch off the defect in the secretory pathway. Consequently, the inactivation of SFP1 induces a complex activation of the MAPKs pathway that is responsible of the regulation of different aspects that characterized the mutant. The main of these is the regulation of the G1-S transitions by the stabilization of Sic1. Finally we showed that consequently to the SFP1 inactivation (probably due to the alteration in the secretory pathway), the mutant cells are characterized by an alteration of Cytoplasmic volume/ Protein content linked to an increase in the cytoplasmic volume. This let us to speculate that growth might be composed of two elements: the Size that is the growth in cell volume and the Mass that is the increase in the protein content. Consequently, alterations of cell growth in response to changes in the environmental conditions imply a coordinate regulation of Size and Mass with the aim of maintaining their ratio constant. One of the key elements necessary to maintain this balance is Sfp1.
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Martinez, Sanz Juan. "Analyse de l'interaction centrine - Sfi1." Paris 6, 2008. http://www.theses.fr/2008PA066480.
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Sfi1 est une protéine récemment découverte qui est impliquée dans le processus de division cellulaire. Concrètement, son rôle est intimement lié à la duplication des MTOCs (centres organisateurs de microtubules) chez les organismes eucaryotes, un rôle partagé avec la centrine. Les centrines sont des calciprotéines de la superfamille EF-hand très conservées chez les eucaryotes et impliquées dans des fonctions cellulaires diverses, comme la duplication des MTOCs, la réparation de l'ADN et l'exportation nucléaire de l'ARNm. La découverte de l'interaction entre la centrine et Sfi1 nous a conduit à nous intéresser à l'étude structurale et biochimique du complexe Sfi1-centrine. Sfi1 possède plusieurs motifs de liaison aux centrines (chacun d'entre eux pouvant lier une molécule de centrine) tout le long de sa structure. Ces séquences répétées présentent des résidus conservés qui correspondent au motif classique 1-4-8 de liaison aux centrines. Ce travail est centré sur la compréhension de la liaison des molécules de centrine de manière individuelle et collective à la protéine Sfi1. Pour cela, des études structurales par RMN de l'extrémité C-terminale de la centrine 2 humaine (HsCen2) en complexe avec un peptide de 20 résidus, correspondant à la séquence répétée n°17 de Sfi1 humaine (hSfi1), ont été réalisées. Celles-ci ont permis de comprendre les bases structurales de la liaison Sfi1-centrine. En outre, des études biochimiques ont été réalisées concernant le domaine de Sfi1 de levure (ScSfi1) contenant 6 séquences répétées avec la centrine de levure (Cdc31). Ce complexe, ainsi que divers variants de Sfi1 nous ont permis d'explorer les caractéristiques de l'interaction de la centrine avec un enchainement de séquences répétées de Sfi1Sfi1 is a recently discovered protein that is involved in cell division, with its specific role in the MTOC duplication in eukaryotes, a function also shared by centrins. Centrins are well conserved calciproteins in eukaryotes belonging to the EF-hand superfamily and they are involved in diverse cellular functions, like MTOC duplication, DNA repair and nuclear mRNA transport. The discovery of the interaction between centrins and Sfi1 led us to be interested in the structural and biochemical study of the complex Sfi1-centrin. Sfi1 has several centrin-linking motifs along its structure (each one able to link one centrin molecule). These repeated sequences have well conserved residues corresponding to the classical 1-4-8 centrin-link motif. This work is focussed on the understanding of individual and collective centrin linking to Sfi1. In order to achieve this, we have made NMR structural experiments with the C-terminus of HsCen2 complexed with a 20-residue peptide corresponding to repeat n°17 of hSfi1. These experiments have allowed us to understand the structural basis of the Sfi1-centrin binding. In parallel, biochemical studies have been made with a yeast Sfi1 (ScSfi1) domain that contains 6 repeats in a complex with yeast centrin (Cdc31). This complex, and some Sfi1 mutants made of it, have allowed us to explore the interaction characteristics of the centrin with several Sfi1 repeats
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Ugolini, Françoise. "SFRP1 et la voie WNT dans la cancérogenèse mammaire." Aix-Marseille 2, 2001. http://www.theses.fr/2000AIX22051.
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Bouhlel, Bougdhira Imen. "The centrin-binding protein Sfi1 : functions in fission yeast and human." Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS465/document.
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Le centrosome est le centre organisateur des microtubules dans les cellules animales, il nucléé les microtubules interphasiques ainsi que le fuseau mitotique. Les centrosomes sont produits par duplication, mécanisme rigoureusement régulé au cours du cycle cellulaire. En effet, un centrosome comporte deux centrioles qui se dupliquent une fois par cycle cellulaire. Des erreurs de duplication conduisant à plus de deux centrosomes induisent la formation de fuseaux multipolaires et provoquent des défauts de ségrégation des chromosomes. Chez la levure Schizosaccharomyces pombe, un organisme modèle pour l’étude de la division cellulaire, les homologues des centrosomes sont les SPBs (pour Spindle Pole Body). Une structure annexe spécifique liée aux SPBs est appelée demi-pont (quand les SPBs ne sont pas dupliqués) puis pont (quand elle relie les deux SPBs dupliqués). Les deux principaux composants du pont chez la levure S. pombe sont Cdc31 et Sfi1. Sfi1 est une protéine linéaire formée de répétitions en hélice α formant des sites de liaison pour la Centrine/Cdc31. Sfi1 s’assemble en réseau de molécules parallèles interagissant avec le SPB via leur domaine N-terminal. Lors de la première partie de ma thèse, j’ai démontré que Sfi1 est requis pour la duplication et la séparation des deux SPBs. Dans la première partie de ma thèse, je me suis intéressée aux fonctions de Sfi1 chez la levure. Cette étude a permis de démontrer que Sfi1 est un composant du demi-pont et qu’il est essentiel pour la duplication des SPBs et l’assemblage d’un fuseau bipolaire. De plus, nous avons déterminé que le pont est dupliqué en fin de mitose. Enfin, nous avons aussi montré que la déstabilisation du pont menant à sa rupture en mitose, dépend de la phosphorylation de Cdc31 par la kinase mitotique Cdk1. Lors de la seconde partie de ma thèse, je me suis intéressée au complexe Sfi1/Centrine dans les cellules humaines. J’ai confirmé que Sfi1 est localisée aux centrioles. De plus, j’ai montré que la déplétion de Sfi1 dans les cellules RPE1, conduit à une perte de localisation de la Centrine, suggérant soit un défaut de recrutement, soit une déstabilisation. De plus, en absence de Sfi1, les cellules RPE1 ne sont plus capables de former de cil primaire. Ce résultat suggère que Sfi1 et la Centrine sont requis pour la ciliogénèse. Enfin, j’ai aussi démontré que la déplétion deSfi1 induit un arrêt de cycle cellulaire dans les cellules non tumorales RPE1. Dans les cellules cancéreuses, HeLa, le cycle n’est pas arrêté mais j’ai pu observer une prolongation du temps de mitose. En conclusion mes travaux montrent que bien que la fonction de Sfi1/Centrin ne soit pas conservée, le complexe reste essentiel pour l’intégrité structurale et fonctionnelle du centrosomeThe centrosome is the main microtubule organizing center. It nucleates and organizes interphase microtubule and contributes to the assembly of the bipolar mitotic spindle. To do so, the centrosome, present in one copy at the beginning of the cell cycle, duplicates to produce a second copy. The duplication process is tightly controlled and regulated since centrosome over-duplication can lead to multipolar mitotic spindles and promote genome instability and tumorigenesis. The duplication of the yeast centrosome, the SPB (Spindle pole body), begins with the duplication of the half bridge. This appendage is composed of Sfi1/Cdc31 complex organized in a parallel array attached to the core SPB. SPB duplication relies on the assembly of a second array of Sfi1/Cdc31, anti-parallel to the first one, creating thereby an assembly site for the new SPB. Therefore Sfi1 is essential for SPB duplication and our work defined the timing of half-bridge duplication and some of the regulatory mechanisms that favor bridge splitting to release duplicated centrosomes and allow spindle assembly at mitotic onset. Sfi1 and Cdc31/Centrins are conserved in human cells where the centrosome is composed of two centrioles surrounded by the pericentriolar material. Centrins are concentrated in the distal end of centrioles. Sfi1 has also been localized to centrioles, but its function remained unknown. Thus, we started investigating Sfi1 function in human cells. We found that Sfi1 depletion leads to a decrease in Centrin recruitment to the centrioles. It also leads to a cell cycle arrest in G1 in RPE1 cells, an event previously observed in presence of defects in centriole biogenesis. In HeLa cells where the cell cycle is not affected, Sfi1 depletion leads to a mitotic delay. Moreover, Sfi1 depletion leads to cilium assembly. To conclude, these results altogether point towards a role of human Sfi1 in centriole biogenesis
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Fossen, Trond. "SFP - målinger og vurderinger for mekanisk ventilerte kontorbygg." Thesis, Norges teknisk-naturvitenskapelige universitet, Institutt for energi- og prosessteknikk, 2008. http://urn.kb.se/resolve?urn=urn:nbn:no:ntnu:diva-12870.
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Denne oppgaven tar for seg hvilke målinger som er nødvendig for å bestemme SFP-faktoren for et typisk nyere kontorbygg med mekanisk ventilasjon. Den tar for seg hvordan disse målingene kan utføres, hva slags måleutstyr som kan benyttes, og hvordan nøyaktigheten til målingene kan bestemmes.Oppgaven tar så for seg gjennomføring av målinger for å bestemme SFP-faktoren for to bygninger. Disse to bygningene er Høyskolen i Oslo (HiO) og PricewaterhouseCoopers-, eller PWC-bygget i Bjørvika i Oslo. Det gis en innføring i de to bygningenes ventilasjonsanlegg og oppbyggingen av disse samt en gjennomgang av styresystemene for ventilasjonsanleggene. Det måles på ett aggregat i hver bygning. For HiO velges aggregat 36.13 som betjener et auditorium med VAV-styring. For PWC-bygget velges aggregat 36.09 som betjener hovedsakelig cellekontorer og styres som CAV. Alle målinger blir utført ved hjelp av differansetrykkmåling over viftene. Aggregatet ved HiO klarer akkurat å komme seg ned på kravet i teknisk forskrift om 2,0 kW/m3/s ved bruk av gjennomsnittlig SFP over driftstiden, men ved personbelastning i lokalet er SFP-verdien 2,66 kW/m3/s. Aggregatet ved PWC-bygget ligger på 2,0 kW/m3/s ved full innregulert drift og klarer dermed fint forskriftskravet. Målingene viser likevel at det ville være mye energi å spare på VAV-styring av anlegget fremfor CAV.Forbedring av ventilasjonsdesign er også en del av oppgaven, og det beregnes hvordan strengere krav til maksimal lufthastighet og alternativ utforming av fordelingskammer kan redusere strømningsmotstanden i et anlegg. Dette viste seg å kunne redusere SFP-faktoren for aggregat 36.09 ved PWC-bygget til 1,52 kW/m3/s ved å ikke tillate hastigheter over 3 m/s samt å benytte en alternativ utforming av fordelingskammeret.Det presenteres forslag til forbedringer i rutiner og programvare for ventilasjonsdesign som kan redusere SFP-fakoren i fremtidige kontorbygninger, og det diskuteres hvorvidt de løsninger som fremkommer i denne oppgaven vil være økonomisk lønnsomme.Til slutt kommer anbefalinger for videre arbeid med problemstillingen.
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Jenson, Lacey Jo. "Induction and Inhibition of a Neuronal Phenotype in Spodoptera Frugiperda (Sf21) Insect Cells." Thesis, Virginia Tech, 2010. http://hdl.handle.net/10919/40929.
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Due to the increasing resistance demonstrated by insects to conventional insecticides, the need for compounds with novel modes of action is becoming more urgent. Also, the discovery and production of new insecticides is vital as regulations and restrictions on conventional insecticides become increasingly stringent (Casida and Quistad 1998). Research in this area requires screening of many candidate compounds which is costly and time-consuming. The goal of this research was to produce in vitro insect neurons from Sf21 insect ovarian cell lines, which could lead to new high throughput screening methods and a way to mass produce insect material for basic research. This study used a culture of Sf21 cells and a mixture of differentiation agents to produce viable neuron-like cells. In the presence of the molting hormone 20-hydroxyecdysone (20-HE), or insulin, in the growth medium, Sf21 cells began to express neuronal morphology, or the production of elongated, axon-like processes within 2-3 days. Maximal differentiation occurred when in the presence of 42 μM 20-HE or 10 μM insulin. Effects were maximal on day 2 for 20-E and day 3 for insulin. Insulin was more potent at day 2 for inducing differentiation (EC₅₀ = 247 nM) than 20-HE (EC₅₀ = 13 μM). In combination, 20-HE and insulin produced apparent synergistic effects on differentiation. Caffeine, a central nervous system (CNS) stimulant, inhibited induction of elongated processes by 20-HE and/or insulin. Caffeine was a potent inhibitor of 42 μM 20-HE, with an IC50 of 9 nM, and the inhibition was incomplete, resulting in about one quarter of the differentiated cells remaining, even at high concentrations (up to 1 mM). The ability to induce a neural phenotype simplifies studies with of insect cells, compared to either the use of primary nervous tissue or genetic engineering techniques. The presence of ion channels or receptors in the differentiated cells remains to be determined. If they are present, high throughput screening for new insecticides will be accelerated and made more economical by the utility of this method.Master of Science
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Matégot, Raphaël. "Contrôle de l’expression des gènes par les micro-ARN nucléaires : étude des mécanismes moléculaires." Thesis, Université Côte d'Azur (ComUE), 2018. http://www.theses.fr/2018AZUR4059/document.
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La découverte de l’ARN interférence et des micro-ARN a permis de définir un principe majeur de régulation de l’expression des gènes, et a produit de nouveaux outils pour la médecine. Chez les mammifères, l’étude des fonctions des micro-ARN a été restreinte au cytoplasme, bien qu’ils soient aussi présents dans le noyau.Cette thèse présente une série d’expériences visant à caractériser les facteurs moléculaires requis pour l’activité nucléaire des micro-ARN. Nous avons débuté ce projet en explorant les partenaires ARN-dépendant de la protéine AGO2 par immunoprécipitation et spectrométrie de masse quantitative. Parmi les interactants ARN-dépendants, nous nous sommes concentrés sur trois protéines nucléaires abondantes : SFPQ, PSPC1 et NONO qui forment la famille drosophila behavior and human splicing (DBHS). Nous avons démontré que le complexe RISC nucléoplasmique est associé aux protéines SFPQ, PSPC1 et NONO dans plusieurs lignées cellulaires murines et humaines, d’une manière qui dépend de SFPQ. Des expériences de type HITS-CLIP de la protéine AGO2 et/ou de la protéine SFPQ dans des cellules souches nous ont permis de montrer que SFPQ se lie préférentiellement aux 3’UTR longs en utilisant deux motifs spécifiques. En effet, SFPQ contrôle significativement environ 20% de l’activité de liaison de AGO2, ce qui est répercuté au niveau transcriptomique. Cependant, cette activité concerne uniquement les sites de liaison de SFPQ proches (<500 nucléotides) de AGO2. De plus, nous avons observé que cette régulation s’étend aux ARNm cytoplasmiques. Ce résultat suggère que la liaison et l’agrégation de la protéine SFPQ à l’ARN programme la structure du 3’UTR et donc les possibilités de ciblage par les miARN dans le noyau, et ceci d’une manière qui semble préservée dans le cytoplasme. Enfin, nous avons montré en particulier que l’expression de SFPQ contrôle le programme de ciblage par let-7a, et module la transition des cellules souches vers l’état différencié. Ces résultats contribuent à la diversité des mécanismes de régulation de l’activité des miARN. Dans la deuxième partie du projet, nous avons exploré les partenaires ARN-indépendant de la protéine nucléaire AGO2. Nous avons découvert que la protéine AGO2 interagit avec le complexe CCR4-NOT1 et l’exosome nucléaire d’une manière indépendante de l’ARN. Nous proposons une série d’expériences visant à confirmer ces résultats. Brièvement, l’hypothèse de travail qui semble la plus cohérente avec les données actuelles est la liaison directe de l’exosome au module CNOT2-CNOT3 du complexe CCR4-NOT1. Ce modèle permettrait d’expliquer le mécanisme d’extinction des gènes par les miARN nucléaires qui reposerait donc sur leur interaction avec les complexes CCR4-NOT1 et exosome. Son mode opératoire comprendrait des protéines de liaison à l’ARN et des micro-ARN pour sélectionner les ciblesThe discovery of RNA interference and micro-RNA has unravelled a fundamental principle of gene expression regulation, and has produced new tools for medicine. In mammals, the study of micro-RNA functions have been confined to the cytoplasm, although there is a growing body of evidence about their presence in the nucleus.This thesis present a set of experiments directed towards understanding the molecular factors required for nuclear miRNA activity.We started this project by exploring the RNA-dependent interactors of AGO2 by immunoprecipitation followed by quantitative mass spectrometry analysis. We focused on three partners: SFPQ, PSPC1 and NONO which are abundant nuclear proteins and belong to the DBHS family (drosophila behavior and human splicing). We demonstrated that the nucleoplasmic RISC complex associates with DBHS proteins in multiple murine and human cell lines in an SFPQ-dependent manner.HITS-CLIP experiments of AGO2 and SFPQ proteins in mouse embryonic stem cells showed that SFPQ preferentially binds long 3’UTR using two specific motifs. Using these motifs, SFPQ significantly controls about 20% of local AGO2 binding activity and target mRNA stability as we observe by transcriptomic analysis. SFPQ mode of action appears to be local and SFPQ motifs are functional only when proximal to AGO2 binding sites in a window of 500 nucleotides.Moreover, although SFPQ is only nuclear, we observe that SFPQ has an effect on cytoplasmic mRNAs, which suggests that SFPQ binding and aggregation to mRNA in the nucleus programs the 3’UTR for miRNA targeting, in a way that appears preserved in the cytoplasm.In particular, we found that SFPQ controls let-7 targeting program and modulates embryonic stem cell differentiation into neuron cells.These results contribute to expand the diversity of miRNA regulatory mechanisms.In the second part of the project, we explored the RNA-independent interactors of AGO2. We discovered that nuclear AGO2 interacts with CCR4-NOT1 complex and the RNA exosome in an RNA-independent manner.We propose a set of experiments to confirm these results, based on a new working model. Briefly, the most likely hypothesis to explain the current data is the direct binding of RNA exosome to the CNOT2-CNOT3 module of CCR4-NOT1 complex.This model would explain the silencing mechanism of genes by nuclear miRNAs, whose activity would depend on the RISC complex interaction with CCR4-NOT1 complex and RNA exosome.Hence, the RNA exosome would use both RNA binding proteins and miRNAs to select targets for degradation, based on CCR4-NOT1 mode of action
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Schmull, Sebastian [Verfasser], and Martin [Akademischer Betreuer] Fassnacht. "Charakterisierung der pathogenetisch-relevanten Rolle von SF1 beim Nebennierenrindenkarzinom = Characterisation of the pathogenetic-relevant role of SF1 in adrenocortical carcinoma / Sebastian Schmull. Betreuer: Martin Fassnacht." Würzburg : Universitätsbibliothek der Universität Würzburg, 2011. http://d-nb.info/1018163360/34.
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Hosono, Yuji. "Splicing factor proline/glutamine-rich is a novel autoantigen of dermatomyositis and associated with anti-melanoma differentiation-associated gene 5 antibody." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225498.
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PAN, YOUWEN. "Behavior of Listeria monocytogenes Biofilms in a Simulated Food Processing (SFP) Ecosystem." NCSU, 2005. http://www.lib.ncsu.edu/theses/available/etd-08252005-000030/.
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The purpose of the research has been to develop an experimental biofilm ecocystem for the characterization of Listeria monocytogenes biofilms in a simulated food processing (SFP) environment. Individual strains of L. monocytogenes were initially surveyed for their ability to attach to surfaces and form biofilms under a variety of conditions. Five strains of L. monocytogenes were then screened for optimal cell attachment and biofilm formation. Significant differences in surface attachment and biofilm formation were observed among the different strains of L. monocytogenes. The biofilms of the five-strain mixture of L. monocytogenes were formed on surfaces that are commonly used in food processing facilities, such as stainless steel and Teflon®. The biofilms were subjected to the SFP system in sequential 24-h daily cycles. Conditions of the SFP system included: starvation, washing, rinsing, and sanitation that routinely occur in a food processing plant. Cell survival in biofilms was determined during the time course of the experiment. The susceptibility of the cells in biofilms and detached cells to different sanitizers was measured. The morphology of the cells in biofilms and the planktonic cells detached from biofilms was observed. The study indicated that the progressive resistance developed by L. monocytogenes biofilms to a sanitizer could protect the cells in biofilms from this and other sanitizing agents. The progressive resistance and cross protection was observed in biofilms, but not in detached cells. These findings could provide a basis for further research on the mechanism of progressive resistance to stresses by L. monocytogenes in biofilms under food processing conditions. The data may help to establish effective sanitation programs for food processing and related industries.
Books on the topic "Sfp1"
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Dowlin, Kenneth E. SFPL 2000: The technology vision. San Francisco, CA: San Francisco Public Library, 1995.
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Hurley, Morgan J., Daniel Gottuk, John R. Hall, Kazunori Harada, Erica Kuligowski, Milosh Puchovsky, José Torero, John M. Watts, and Christopher Wieczorek, eds. SFPE Handbook of Fire Protection Engineering. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-2565-0.
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Guerrazzi, Austin. SFPE Guide to Fire Risk Assessment. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-17700-2.
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DiNenno, Philip J. SFPE handbook of fire protection engineering. 4th ed. Quincy, Mass: National Fire Protection Association, 2008.
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Association, National Fire Protection, and Society of Fire Protection Engineers., eds. SFPE handbook of fire protection engineering. Quincy, Mass: National Fire Protection Association, 1988.
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Society of Fire Protection Engineers. and International Code Council, eds. The SFPE code official's guide to performance-based design review. [Bethesda, MD: Society of Fire Protection Engineers and International Code Council], 2004.
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American Society of Civil Engineers., Society of Fire Protection Engineers., and Structural Engineering Institute, eds. Standard calculation methods for structural fire protection: ASCE/SEI/SFPE 29-05. Reston, Va: American Society of Civil Engineers, 2007.
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Dunlap, Mary C. Allegations of discriminatory law enforcement against SFPD officers: A need for further information. San Francisco: [Office of Civilian Complaints?], 1999.
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Francisco), California Grand Jury (San. San Francisco Police Department/Crime Laboratory (SFPD/CL) and San Francisco Medical Examiner/Toxicology Laboratory (SFME/TL). [San Francisco, Calif: Grand Jury, 1996.
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SFPE engineering standard on calculation methods to predict the thermal performance of structural and fire resistive assemblies. Bethesda, MD: Society of Fire Protection Engineers, 2015.
Find full textBook chapters on the topic "Sfp1"
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Yan, Shanshan. "SFP1 Layer." In The Right Periphery in L2 Chinese, 33–53. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003275428-3.
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Yan, Shanshan. "SFP3 Layer." In The Right Periphery in L2 Chinese, 77–97. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003275428-5.
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Yan, Shanshan. "SFP2 Layer." In The Right Periphery in L2 Chinese, 54–76. London: Routledge, 2022. http://dx.doi.org/10.4324/9781003275428-4.
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Wehrum, D., A. Hartmann, R. Stoehr, R. Gruetzmann, C. Pilarsky, and H. D. Saeger. "Einfluss von SFRP1 auf Pankreaszellen." In Chirurgisches Forum und DGAV Forum 2010, 53–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-12192-0_20.
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Zhang, Guo-Qiang. "A Representation of SFP." In Logic of Domains, 47–72. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4612-0445-9_3.
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Zhang, Guo-Qiang. "A Logic of SFP." In Logic of Domains, 73–102. Boston, MA: Birkhäuser Boston, 1991. http://dx.doi.org/10.1007/978-1-4612-0445-9_4.
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Kamimura, Tsutomu, and Adrian Tang. "Retracts of SFP objects." In Lecture Notes in Computer Science, 135–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/3-540-16816-8_29.
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Asa, Sylvia L. "Steroidogenic Factor 1 (SF1)." In Endocrine Pathology, 749–50. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-62345-6_5054.
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Asa, Sylvia L. "Steroidogenic Factor 1 (SF1)." In Encyclopedia of Pathology, 1–2. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-28845-1_5054-1.
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Alessi, F., P. Baldan, and F. Honsell. "Partializing stone spaces using SFP domains." In TAPSOFT '97: Theory and Practice of Software Development, 478–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/bfb0030620.
Full textConference papers on the topic "Sfp1"
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Song, Yong Mann, Jong Yeob Jung, and Sunil Nijhawan. "FUELPOOL: A Computer Program to Model CANDU Spent Fuel Pool Severe Accident Progression and Consequences." In 2020 International Conference on Nuclear Engineering collocated with the ASME 2020 Power Conference. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/icone2020-16634.
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Abstract CANDU PHWR spent fuel pools (SFPs), smaller than a tennis court, contain up to 38,000 or more (49,000 in Wolsong)fuel bundles in geometries not replicated in any other power reactor. Therefore, the phenomenological issues, accident progression pathways and effectiveness of mitigative actions are somewhat different. This requires a dedicated approach in progression and consequence assessments of potential accidents and development of mitigation measures. The SFPs house densely packed fuel bundles stacked in about a hundred vertical stainless steel tray towers, each containing 24 spent fuel bundles in each of the 16 or more (19 in Wolsong) horizontal fish basket style steel trays. Some of theupto 10 year worth of the on-line refuelled bundles in the SFP are at relatively high decay powers as fuel trays are prepped for the towers in near daily basis. In addition, there is a provision (see Figure 1) that a full core of bundles 20 days after being at full power can be transferred to the spent fuel bay at any time. About 4.5m of additional water layer on top of the tray towers provide radiation protection and a healthy margin to small rate of fluid loss.
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Xiang, Qiao, Chin Guok, Franck Le, John MacAuley, Harvey Newman, and Y. Richard Yang. "SFP." In SIGCOMM '18: ACM SIGCOMM 2018 Conference. New York, NY, USA: ACM, 2018. http://dx.doi.org/10.1145/3234200.3234207.
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Wang, Han, Longfei Luo, Liang Shi, Changlong Li, Chun Jason Xue, Qingfeng Zhuge, and Edwin H. M. Sha. "SFP." In GLSVLSI '21: Great Lakes Symposium on VLSI 2021. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3453688.3461492.
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Feldman, Michael B. "SF1." In the 2008 ACM annual international conference. New York, New York, USA: ACM Press, 2008. http://dx.doi.org/10.1145/1454474.1454476.
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Shiomi, T., B. Mercer, P. Bodine, and J. D'Armiento. "SFRP1 Regulates Tissue Injury and Repair." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1974.
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Yuan, Deng, Gao Yang, Wu Junhui, Cheng Tiehan, Wang Jun, and Tang Cheng. "Design and Electromagnetic Analysis of SFPM." In 2016 International Conference on Cybernetics, Robotics and Control (CRC). IEEE, 2016. http://dx.doi.org/10.1109/crc.2016.018.
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Zhang, Yu-Ming, Jun-Wei Hsieh, Chun-Chieh Lee, and Kuo-Chin Fan. "SFPN: Synthetic FPN for Object Detection." In 2022 IEEE International Conference on Image Processing (ICIP). IEEE, 2022. http://dx.doi.org/10.1109/icip46576.2022.9897517.
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Guo, Chao, Zhenzhen Ge, Feiye Liao, Peng Chen, and Dongyu He. "Assessment on Accident and Mitigation of Spent Fuel Pool in a Typical PWR." In 2022 29th International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/icone29-91550.
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Abstract In consideration of low power rate and large water inventory in spent fuel pool (SFP), the accident progression may be very slow and the fuel melt accident was considered to be very unlikely in SFP. However, the accident in Fukushima Dai-ichi Nuclear Power Plant implies the possibility of severe accident in SFP and highlights the importance of accident management of SFP. As the fuel building has no three-barriers containing radioactive products like the reactor building and SFP has significantly larger fuel inventory, the potential consequences of severe accident (radioactive materials release and hydrogen production) could be far beyond the capability of practical mitigation measures in design. Since Fukushima accident, lots of efforts related to SFP simulation are made by developers of several severe accident simulation codes. For ASTEC code, models about radiative heat transfer and Zircaloy oxidation are added in V2.1 which makes it possible to have a better prediction of severe accident in SFP. In this paper, representative scenarios (loss of coolant, loss of cooling) in SFP of a typical pressurized water reactor (PWR) design are simulated with ASTEC code. Accident progression and phenomena are presented. The influence of potential mitigation measures is studied. Suggestions to the design of SFP and accident mitigation strategies are provided according to the analysis results.
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Ko, Fu-Kuang, Thomas K. S. Liang, and Chung-Yu Yang. "Development of Thermal Analysis Capability of Dry Storage Cask for Spend Fuel Interim Storage." In 10th International Conference on Nuclear Engineering. ASMEDC, 2002. http://dx.doi.org/10.1115/icone10-22665.
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As most of the nuclear power plants, on-site spent fuel pools (SFP) of Taiwan’s plants were not originally designed with a storage capacity for all the spent fuel generated over the operating life by their reactors. For interim spent fuel storage, dry casks are one of the most reliable measures to on-site store over-filled assemblies from SFPs. The NUHOMS®-52B System consisting of a canister stored horizontally in a concrete module is selected for thermal evaluation in this paper. The performance of each cask in criticality, radioactive, material and thermal needs to be carefully addressed to ensure its enduring safety. Regarding the thermal features of dry storage casks, three different kinds of heat transfer mechanisms are involved, which include natural convection heat transfer outside and/or inside the canister, radiation heat transfer inside and outside the canister, and conduction heat transfer inside the canister. To analyze the thermal performance of dry storage casks, RELAP5-3D is adopted to calculate the natural air convection and radiation heat transfer outside the canister to the ambient environment, and ANSYS is applied to calculate the internal conduction and radiation heat transfer. During coupling iteration between codes, the heat energy across the canister wall needs to be conserved, and the inner wall temperature of the canister needs to be converged. By the coupling of RELAP5-3D and ANSYS, the temperature distribution within each fuel assembly inside canisters can be calculated and the peaking cladding temperature can be identified.
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Graham, Luke A., Jack L. Jewell, Kevin D. Maranowski, Max V. Crom, Stewart A. Feld, Joseph M. Smith, James G. Beltran, et al. "LW VCSELs for SFP+ applications." In Integrated Optoelectronic Devices 2008, edited by Chun Lei and James K. Guenter. SPIE, 2008. http://dx.doi.org/10.1117/12.771288.
Full textReports on the topic "Sfp1"
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Granot, David, and Richard Amasino. Regulation of Senescence by Sugar Metabolism. United States Department of Agriculture, January 2003. http://dx.doi.org/10.32747/2003.7585189.bard.
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Research objectives a. Analyze transgenic plants that undergo rapid senescence due to increased expression of hexokinase. b. Determine if hexokinase-induced senescence accelerates natural senescence using senescence specific promoters that drive expression of a reporter gene (GUS) and a cytokinin producing gene (IPT - isopentyl transferase). c. Isolate and analyze plant genes that suppress sugar-induced cell death (SICD) in yeast, genes that potentially are involved in programmed cell death and senescence in plants. Background to the topic Leaf senescence is a regulated process of programmed cell death (PCD) in which metabolites are recycled to other active parts of the plant. Senescence associated genes (SAGs) are expressed throughout leaf senescence. Sugar flux and metabolism is thought to playa fundamental regulatory role in senescence. We found that transgenic tomato plants with high hexokinase activity, the initial enzymatic step of sugar (hexose) metabolism, undergo rapid leaf senescence, directly correlated with hexokinase activity. These plants provide a unique opportunity to analyze the regulatory role of sugar metabolism in senescence, and its relation to cytokinin, a senescence-inhibiting hormone. In addition, we found that sugar induces programmed cells death of yeast cells in direct correlation to hexokinase activity. We proposed to use the sugar induced cell death (SICD) to isolate Arabidopsis genes that suppress SICD. Such genes could potentially be involved in senescence induced PCD in plants. Major conclusions The promoters of Arabidopsis senescence-associated genes, SAG12 and SAGI3, are expressed in senescing tomato leaves similar to their expression in Arabidopsis leaves, indicating that these promoters are good senescence markers for tomato plants. Increased hexokinase activity accelerated senescence and induced expression of pSAG12 and pSAG13 promoters in tomato plants, suggesting that sugar regulate natural senescence via hexokinase. Expression of IPT, a cytokinin producing gene, under pSAG12 and pSAG13 promoters, delayed senescence of tomato leaves. Yet, senescence accelerated by hexokinase was epistatic over cytokinin, indicating that sugar regulation of senescence is dominant over the senescence-inhibiting hormone. A gene designated SFP1, which is similar to the major super family monosaccharide transporters, is induced during leaf senescence in Arabidopsis and may be involved in sugar transport during senescence. Accordingly, adult leaves accumulate sugars that may accelerate hexokinase activity. Light status of the entire plant affects the senescence of individual leaves. When individual leaves are darkened, senescence is induced in the covered leaves. However, whole adult plant placed in darkness show delayed senescence. In a search for Arabidopsis genes that suppress SICD we isolated 8 cDNA clones which confer partial resistance to SICD. One of the clones encodes a vesicle associated membrane protein - VAMP. This is the first evidence that vesicle trafficking might be involved in cell death. Implications Increased hexokinase activity accelerates senescence. We hypothesized that, reduced hexokinase activity may delay senescence. Preliminary experiments using a hexokinase inhibitor support this possible implication. Currently we are analyzing various practical approaches to delay leaf senescence via hexokinase inhibition. .
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Almand, Kathleen H., Long T. Phan, Therese P. McAllister, Monica A. Starnes, and John L. Gross. NIST-SFPE workshop for development of a national R&D roadmap for structural fire safety design and retrofit of structures :. Gaithersburg, MD: National Institute of Standards and Technology, 2004. http://dx.doi.org/10.6028/nist.ir.7133.
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Report on the International Symposium on Quality of Care in China. Population Council, 2000. http://dx.doi.org/10.31899/rh2000.1041.
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In 1995, China’s State Family Planning Commission (SFPC), the governmental agency charged with developing and implementing China’s population policy, issued an official call for the reorientation of the family planning program from a focus on demographic targets to meeting clients’ needs. In support of this reorientation effort, the SFPC selected six rural counties and five urban districts with comparatively good socioeconomic conditions as pilot sites for a quality-of-care experiment. This report provides a summary of an international symposium on quality of care held in Beijing from November 17–19, 1999. The symposium was sponsored by SFPC with the support of the Ford Foundation as part of the international collaboration on China’s quality-of-care initiative. The purpose of the symposium was threefold: to review the experiences of China’s quality-of-care initiative in the pilot counties and districts to date; to discuss strategies for institutionalizing the quality-of-care approach in the pilot sites; and to discuss expansion and further development of the program throughout China, in keeping with the SFPC’s decision that the quality-of-care experiment should be expanded nationwide.