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Автор: Grafiati
Опубліковано: 7 липня 2024
Оновлено: 7 липня 2024

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Статті в журналах з теми "Rfc1":

1

Amin, Neelam S., K. Michelle Tuffo, and Connie Holm. "Dominant Mutations in Three Different Subunits of Replication Factor C Suppress Replication Defects in Yeast PCNA Mutants." Genetics 153, no. 4 (December 1, 1999): 1617–28. http://dx.doi.org/10.1093/genetics/153.4.1617.

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Abstract To identify proteins that interact with the yeast proliferating cell nuclear antigen (PCNA), we used a genetic approach to isolate mutations that compensate for the defects in cold-sensitive (Cs−) mutants of yeast PCNA (POL30). Because the cocrystal structure of human PCNA and a p21WAF1/CIP1 peptide shows that the interdomain region of PCNA is a site of p21 interaction, we specifically looked for new mutations that suppress mutations in the equivalent region of yeast PCNA. In independent screens using three different Cs− mutants, we identified spontaneously arising dominant suppressor mutations in the RFC3 gene. In addition, dominant suppressor mutations were identified in the RFC1 and RFC2 genes using a single pol30 mutant. An intimate association between PCNA and RFC1p, RFC2p, and RFC3p is suggested by the allele-restricted suppression of 10 different pol30 alleles by the RFC suppressors. RFC1, RFC2, and RFC3 encode three of the five subunits of the replication factor C complex, which is required to load PCNA onto DNA in reconstituted DNA replication reactions. Genomic sequencing reveals a common region in RFC1p, RFC2p, and RFC3p that is important for the functional interaction with PCNA. Biochemical analysis of the wild type and mutant PCNA and RFC3 proteins shows that mutant RFC3p enhances the production of long DNA products in pol δ-dependent DNA synthesis, which is consistent with an increase in processivity.
2

Cullmann, G., K. Fien, R. Kobayashi, and B. Stillman. "Characterization of the five replication factor C genes of Saccharomyces cerevisiae." Molecular and Cellular Biology 15, no. 9 (September 1995): 4661–71. http://dx.doi.org/10.1128/mcb.15.9.4661.

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Replication factor C (RFC) is a five-subunit DNA polymerase accessory protein that functions as a structure-specific, DNA-dependent ATPase. The ATPase function of RFC is activated by proliferating cell nuclear antigen. RFC was originally purified from human cells on the basis of its requirement for simian virus 40 DNA replication in vitro. A functionally homologous protein complex from Saccharomyces cerevisiae, called ScRFC, has been identified. Here we report the cloning, by either peptide sequencing or by sequence similarity to the human cDNAs, of the S. cerevisiae genes RFC1, RFC2, RFC3, RFC4, and RFC5. The amino acid sequences are highly similar to the sequences of the homologous human RFC 140-, 37-, 36-, 40-, and 38-kDa subunits, respectively, and also show amino acid sequence similarity to functionally homologous proteins from Escherichia coli and the phage T4 replication apparatus. All five subunits show conserved regions characteristic of ATP/GTP-binding proteins and also have a significant degree of similarity among each other. We have identified eight segments of conserved amino acid sequences that define a family of related proteins. Despite their high degree of sequence similarity, all five RFC genes are essential for cell proliferation in S. cerevisiae. RFC1 is identical to CDC44, a gene identified as a cell division cycle gene encoding a protein involved in DNA metabolism. CDC44/RFC1 is known to interact genetically with the gene encoding proliferating cell nuclear antigen, confirming previous biochemical evidence of their functional interaction in DNA replication.
3

Cui, Kan, Lei Qin, Xianyu Tang, Jieying Nong, Jin Chen, Nan Wu, Xin Gong, Lixiong Yi, Chenghuizi Yang, and Shitou Xia. "A Single Amino Acid Substitution in RFC4 Leads to Endoduplication and Compromised Resistance to DNA Damage in Arabidopsis thaliana." Genes 13, no. 6 (June 9, 2022): 1037. http://dx.doi.org/10.3390/genes13061037.

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Replication factor C (RFC) is a heteropentameric ATPase associated with the diverse cellular activities (AAA+ATPase) protein complex, which is composed of one large subunit, known as RFC1, and four small subunits, RFC2/3/4/5. Among them, RFC1 and RFC3 were previously reported to mediate genomic stability and resistance to pathogens in Arabidopsis. Here, we generated a viable rfc4e (rfc4−1/RFC4G54E) mutant with a single amino acid substitution by site-directed mutagenesis. Three of six positive T2 mutants with the same amino acid substitution, but different insertion loci, were sequenced to identify homozygotes, and the three homozygote mutants showed dwarfism, early flowering, and a partially sterile phenotype. RNA sequencing revealed that genes related to DNA repair and replication were highly upregulated. Moreover, the frequency of DNA lesions was found to be increased in rfc4e mutants. Consistent with this, the rfc4e mutants were very sensitive to DSB-inducing genotoxic agents. In addition, the G54E amino acid substitution in AtRFC4 delayed cell cycle progression and led to endoduplication. Overall, our study provides evidence supporting the notion that RFC4 plays an important role in resistance to genotoxicity and cell proliferation by regulating DNA damage repair in Arabidopsis thaliana.
4

Gong, Maokai, James Yess, Tatiana Connolly, S. Percy Ivy, Takao Ohnuma, Kenneth H. Cowan, and Jeffrey A. Moscow. "Molecular Mechanism of Antifolate Transport-Deficiency in a Methotrexate-Resistant MOLT-3 Human Leukemia Cell Line." Blood 89, no. 7 (April 1, 1997): 2494–99. http://dx.doi.org/10.1182/blood.v89.7.2494.

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Abstract Ohnuma et al reported a series of methotrexate-resistant MOLT-3 human T-cell acute lymphoblastic leukemia cell lines that showed decreasing methotrexate (MTX) uptake as the sublines acquired increasing MTX resistance (Cancer Res 45:1815, 1985). The alteration of MTX uptake kinetics in these cells, the intermediately resistant MOLT-3/MTX200 and the highly resistant MOLT-3/MTX10,000 cell lines, was attributed to a change in Vmax for methotrexate transport, without an apparent change in affinity of the transporter for MTX. We studied these cell lines to determine whether alteration of transcription or translation of the recently isolated reduced folate carrier gene (RFC1) was the cause of MTX transport deficiency in these cell lines. Reconstitution of RFC activity in MOLT-3/MTX10,000 cells by transduction with a murine RFC retroviral vector reversed MTX resistance and trimetrexate sensitivity. Although RFC1 RNA levels were unchanged in the resistant cell lines, FACS analysis using a polyclonal anti-RFCl antibody showed no detectable RFCl protein in the MOLT-3/MTX10,000 cells. Determination of the nucleotide sequence of RFC1 genes from MOLT-3/MTX10,000 cells revealed that this cell line contained 3 RFC1 alleles: a wild-type allele, an allele containing the premature stop codon at codon 40 and a third allele containing another mutation, which resulted in a premature stop codon at codon 25. We examined the relative expression of these alleles by determining the nucleotide sequence of 24 RFC1 cDNA subclones from MOLT-3/MTX10,000 cells and found that only one-third of these clones contained the wild-type sequence. Determination of the genomic sequence of RFC1 in MOLT-3/MTX200 cells demonstrated that these cells were heterozygous for a mutation at codon 40, but were homozygous for the wild-type sequence at codon 25. Thus, the acquisition of MTX transport-deficiency in MOLT-3/MTX10,000 cells results from inactivating mutations of RFC1 gene alleles.
5

Naiki, Takahiro, Tae Kondo, Daisuke Nakada, Kunihiro Matsumoto, and Katsunori Sugimoto. "Chl12 (Ctf18) Forms a Novel Replication Factor C-Related Complex and Functions Redundantly with Rad24 in the DNA Replication Checkpoint Pathway." Molecular and Cellular Biology 21, no. 17 (September 1, 2001): 5838–45. http://dx.doi.org/10.1128/mcb.21.17.5838-5845.2001.

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ABSTRACT RAD24 has been identified as a gene essential for the DNA damage checkpoint in budding yeast. Rad24 is structurally related to subunits of the replication factor C (RFC) complex, and forms an RFC-related complex with Rfc2, Rfc3, Rfc4, and Rfc5. Therad24Δ mutation enhances the defect ofrfc5-1 in the DNA replication block checkpoint, implicating RAD24 in this checkpoint.CHL12 (also called CTF18) encodes a protein that is structurally related to the Rad24 and RFC proteins. We show here that although neither chl12Δ norrad24Δ single mutants are defective, chl12Δ rad24Δ double mutants become defective in the replication block checkpoint. We also show that Chl12 interacts physically with Rfc2, Rfc3, Rfc4, and Rfc5 and forms an RFC-related complex which is distinct from the RFC and RAD24 complexes. Our results suggest that Chl12 forms a novel RFC-related complex and functions redundantly with Rad24 in the DNA replication block checkpoint.
6

Panda, Debasis, Daniel J. Fernandez, Madhu Lal, Eugen Buehler, and Bernard Moss. "Triad of human cellular proteins, IRF2, FAM111A, and RFC3, restrict replication of orthopoxvirus SPI-1 host-range mutants." Proceedings of the National Academy of Sciences 114, no. 14 (March 20, 2017): 3720–25. http://dx.doi.org/10.1073/pnas.1700678114.

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Viruses and their hosts can reach balanced states of evolution ensuring mutual survival, which makes it difficult to appreciate the underlying dynamics. To uncover hidden interactions, virus mutants that have lost defense genes may be used. Deletion of the gene that encodes serine protease inhibitor 1 (SPI-1) of rabbitpox virus and vaccinia virus, two closely related orthopoxviruses, prevents their efficient replication in human cells, whereas certain other mammalian cells remain fully permissive. Our high-throughput genome-wide siRNA screen identified host factors that prevent reproduction and spread of the mutant viruses in human cells. More than 20,000 genes were interrogated with individual siRNAs and those that prominently increased replication of the SPI-1 deletion mutant were subjected to a secondary screen. The top hits based on the combined data—replication factor C3 (RFC3), FAM111A, and interferon regulatory factor 2 (IRF2)—were confirmed by custom assays. The siRNAs to RFC1, RFC2, RFC4, and RFC5 mRNAs also enhanced spread of the mutant virus, strengthening the biological significance of the RFC complex as a host restriction factor for poxviruses. Whereas association with proliferating cell nuclear antigen and participation in processive genome replication are common features of FAM111A and RFC, IRF2 is a transcriptional regulator. Microarray analysis, quantitative RT-PCR, and immunoblotting revealed that IRF2 regulated the basal level expression of FAM111A, suggesting that the enhancing effect of depleting IRF2 on replication of the SPI-1 mutant was indirect. Thus, the viral SPI-1 protein and the host IRF2, FAM111A, and RFC complex likely form an interaction network that influences the ability of poxviruses to replicate in human cells.
7

Kai, Mihoko, Hiroyuki Tanaka, and Teresa S. F. Wang. "Fission Yeast Rad17 Associates with Chromatin in Response to Aberrant Genomic Structures." Molecular and Cellular Biology 21, no. 10 (May 15, 2001): 3289–301. http://dx.doi.org/10.1128/mcb.21.10.3289-3301.2001.

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ABSTRACT Fission yeast checkpoint protein Rad17 is required for the DNA integrity checkpoint responses. A fraction of Rad17 is chromatin bound independent of the other checkpoint proteins throughout the cell cycle. Here we show that in response to DNA damage induced by either methyl methanesulfonate treatment or ionizing radiation, increased levels of Rad17 bind to chromatin. Following S-phase stall induced by hydroxyurea or a cdc22 mutation, the chromatin-bound Rad17 progressively dissociates from the chromatin. After S-phase arrest by hydroxyurea in cds1Δ or rad3Δ cells or by replication mutants, Rad17 remains chromatin bound. Rad17 is able to complex in vivo with an Rfc small subunit, Rfc2, but not with Rfc1. Furthermore, cells with rfc1Δ are checkpoint proficient, suggesting that Rfc1 does not have a role in checkpoint function. A checkpoint-defective mutant protein, Rad17(K118E), which has similar nuclear localization to that of the wild type, is unable to bind ATP and has reduced ability in chromatin binding. Mutant Rad17(K118E) protein also has reduced ability to complex with Rfc2, suggesting that Lys118 of Rad17 plays a role in Rad17-Rfc small-subunit complex formation and chromatin association. However, in therad17.K118E mutant cells, Cds1 can be activated by hydroxyurea. Together, these results suggest that Rad17 binds to chromatin in response to an aberrant genomic structure generated from DNA damage, replication mutant arrest, or hydroxyurea arrest in the absence of Cds1. Rad17 is not required to bind chromatin when genomic structures are protected by hydroxyurea-activated Cds1. The possible checkpoint events induced by chromatin-bound Rad17 are discussed.
8

Ma, David W. L., Richard H. Finnell, Laurie A. Davidson, Evelyn S. Callaway, Ofer Spiegelstein, Jorge A. Piedrahita, J. Michael Salbaum, et al. "Folate Transport Gene Inactivation in Mice Increases Sensitivity to Colon Carcinogenesis." Cancer Research 65, no. 3 (February 1, 2005): 887–97. http://dx.doi.org/10.1158/0008-5472.887.65.3.

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Abstract Low dietary folate intake is associated with an increased risk for colon cancer; however, relevant genetic animal models are lacking. We therefore investigated the effect of targeted ablation of two folate transport genes, folate binding protein 1 (Folbp1) and reduced folate carrier 1 (RFC1), on folate homeostasis to elucidate the molecular mechanisms of folate action on colonocyte cell proliferation, gene expression, and colon carcinogenesis. Targeted deletion of Folbp1 (Folbp1+/− and Folbp1−/−) significantly reduced (P < 0.05) colonic Folbp1 mRNA, colonic mucosa, and plasma folate concentration. In contrast, subtle changes in folate homeostasis resulted from targeted deletion of RFC1 (RFC1+/−). These animals had reduced (P < 0.05) colonic RFC1 mRNA and exhibited a 2-fold reduction in the plasma S-adenosylmethionine/S-adenosylhomocysteine. Folbp1+/− and Folbp1−/− mice had larger crypts expressed as greater (P < 0.05) numbers of cells per crypt column relative to Folbp1+/+ mice. Colonic cell proliferation was increased in RFC1+/− mice relative to RFC1+/+ mice. Microarray analysis of colonic mucosa showed distinct changes in gene expression specific to Folbp1 or RFC1 ablation. The effect of folate transporter gene ablation on colon carcinogenesis was evaluated 8 and 38 weeks post-azoxymethane injection in wild-type and heterozygous mice. Relative to RFC1+/+ mice, RFC1+/− mice developed increased (P < 0.05) numbers of aberrant crypt foci at 8 weeks. At 38 weeks, RFC1+/− mice developed local inflammatory lesions with or without epithelial dysplasia as well as adenocarcinomas, which were larger relative to RFC1+/+ mice. In contrast, Folbp1+/− mice developed 4-fold (P < 0.05) more lesions relative to Folbp1+/+ mice. In conclusion, Folbp1 and RFC1 genetically modified mice exhibit distinct changes in colonocyte phenotype and therefore have utility as models to examine the role of folate homeostasis in colon cancer development.
9

Xie, Yali, Chris Counter, and Eric Alani. "Characterization of the Repeat-Tract Instability and Mutator Phenotypes Conferred by a Tn3 Insertion in RFC1, the Large Subunit of the Yeast Clamp Loader." Genetics 151, no. 2 (February 1, 1999): 499–509. http://dx.doi.org/10.1093/genetics/151.2.499.

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Abstract The RFC1 gene encodes the large subunit of the yeast clamp loader (RFC) that is a component of eukaryotic DNA polymerase holoenzymes. We identified a mutant allele of RFC1 (rfc1::Tn3) from a large collection of Saccharomyces cerevisiae mutants that were inviable when present in a rad52 null mutation background. Analysis of rfc1::Tn3 strains indicated that they displayed both a mutator and repeat-tract instability phenotype. Strains bearing this allele were characterized in combination with mismatch repair (msh2Δ, pms1Δ), double-strand break repair (rad52), and DNA replication (pol3-01, pol30-52, rth1Δ/rad27Δ) mutations in both forward mutation and repeat-tract instability assays. This analysis indicated that the rfc1::Tn3 allele displays synthetic lethality with pol30, pol3, and rad27 mutations. Measurement of forward mutation frequencies in msh2Δ rfc1:Tn3 and pms1Δ rfc1:Tn3 strains indicated that the rfc1::Tn3 mutant displayed a mutation frequency that appeared nearly multiplicative with the mutation frequency exhibited by mismatch-repair mutants. In repeat-tract instability assays, however, the rfc1::Tn3 mutant displayed a tract instability phenotype that appeared epistatic to the phenotype displayed by mismatch-repair mutants. From these data we propose that defects in clamp loader function result in DNA replication errors, a subset of which are acted upon by the mismatch-repair system.
10

Zhao, Rongbao, Feng Gao, and I. David Goldman. "Reduced folate carrier transports thiamine monophosphate: an alternative route for thiamine delivery into mammalian cells." American Journal of Physiology-Cell Physiology 282, no. 6 (June 1, 2002): C1512—C1517. http://dx.doi.org/10.1152/ajpcell.00547.2001.

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Although the reduced folate carrier RFC1 and the thiamine transporters THTR-1 and THTR-2 share ∼40% of their identity in protein sequence, RFC1 does not transport thiamine and THTR-1 and THTR-2 do not transport folates. In the present study, we demonstrate that transport of thiamine monophosphate (TMP), an important thiamine metabolite present in plasma and cerebrospinal fluid, is mediated by RFC1 in L1210 murine leukemia cells. Transport of TMP was augmented by a factor of five in cells (R16) that overexpress RFC1 and was markedly inhibited by methotrexate, an RFC1 substrate, but not by thiamine. At a near-physiological concentration (50 nM), TMP influx mediated by RFC1 in wild-type L1210 cells was ∼50% of thiamine influx mediated by thiamine transporter(s). Within 1 min, the majority of TMP transported into R16 cells was hydrolyzed to thiamine with a component metabolized to thiamine pyrophosphate, the active enzyme cofactor. These data suggest that RFC1 may be one of the alternative transport routes available for TMP in some tissues when THTR-1 is mutated in the autosomal recessive disorder thiamine-responsive megaloblastic anemia.
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Статті в журналах Дисертації Книги

Дисертації з теми "Rfc1":

1

Breitenbücher, Frank. "Allgemeine und funktionelle Untersuchungen zur grossen Untereinheit des humanen Replikationsfaktors C (RFC1), sowie initiale Untersuchungen zur Regulation der Expression von RFC1 durch das BCR-ABLp210-Onkogen." [S.l.] : [s.n.], 2005. http://archiv.ub.uni-marburg.de/diss/z2005/0114/.

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2

Hinken, Matthias. "Gewebeverteilung und Lokalisation des Transportproteins für reduzierte Folate (RFC1) der Ratte." Doctoral thesis, Universitätsbibliothek Leipzig, 2007. http://nbn-resolving.de/urn:nbn:de:bsz:15-20071107-143055-8.

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Der Folsäureantagonist Methotrexat (MTX) wird zur Behandlung onkologischer und rheumatoider Erkrankungen eingesetzt. Die Aufnahme des Methotrexats in die Zielzelle ist dabei Vorraussetzung für die Bindung an seine intrazellulären Zielstrukturen und erfolgt über verschiedene Transportsysteme. In diesem Zusammenhang ist bei entsprechenden Plasma-konzentrationen von MTX der Reduced Folate Carrier (RFC1) von besonderer Bedeutung. 1994 konnte erstmals die cDNA dieses Transporters aus Maus- und Hamstergewebe isoliert werden. Die cDNA für einen mit dem RFC1 identischen hepatozellulären MTX-Transporter der Ratte wurde 2000 kloniert. Vorhergehende Gen-Expressionsstudien zeigten, dass die RFC1-mRNA ubiquitär gebildet wird. Die Proteinexpression wurde jedoch bisher nur in ausgewählten Geweben der Maus untersucht. Systematische Arbeiten, in denen in vergleichender Weise sowohl die RFC1 Gen- als auch die Proteinexpression in allen Geweben mit einer möglichen Relevanz für die Folat- und Antifolataufnahme, Speicherung und Eliminierung untersucht werden, fehlten bisher. Insbesondere die Expression des RFC1-Proteins der Ratte (rRFC1) mittels immunologischer Verfahren ist bisher nicht beschrieben worden. Ziel dieser Arbeit war es daher, die Gen- und Proteinexpression des rRFC1 in ausgewählten Geweben der Ratte darzustellen. Dieses schließt die Generierung spezifischer Antiseren gegen den rRFC1 als ersten Schritt mit ein. Es wurden geeignete antigene Aminosäuresequenzen des rRFC1 bestimmt und die entsprechenden cDNA Sequenzen wurden amplifiziert und in einen geeigneten Expressionsvektor kloniert. Rekombinante rRFC1 Fusionsproteine konnten mittels E. coli Zellen hergestellt und anschließend aufgereinigt werden. Nachfolgend wurden entweder die rRFC1 Fusionsproteine oder die rRFC1 spezifischen Peptide, welche von dem Affinitätspeptid separiert worden waren, für die Immunisierung von Kaninchen verwendet Drei Antiseren mit ausreichender Reaktivität und Spezifität konnten gewonnen und mittels Affinitätschromatographie aufgereinigt werden. Die erhaltenen Antiseren sind gegen die intrazellulären N- und C-terminalen Regionen (ID1, ID7) bzw. gegen die erste extrazelluläre Schleife (OD1) gerichtet. In Western-Blot Studien konnte mittels dieser Antiseren für den rRFC1, der in transfizierten Nierenepithelzellen (MDCK-rRFC-HA) stabil exprimiert wurde, ein Molekulargewicht von 71 kD für die glykosylierte Form und von 53 kD für die unglykosylierte Form ermittelt werden. Weiter konnte belegt werden, dass das Protein in MDCK-rRFC1-HA Zellen überwiegend in der glycosylierten Form vorliegt. Mittels RT-PCR Analysen wurde die Genexpression des rRFC1 in allen untersuchten Geweben nachgewiesen. Besonders hohe mRNA-Gehalte waren in Thymus, Niere und Milz vorhanden, während in Herz- und Muskelgewebe sowie in Leukozyten nur ein Signal nahe der Nachweisgrenze detektierbar war. Durch immunhistologische Untersuchungen konnten die rRFC1 Proteinexpression und beträchtliche Unterschiede in der Signalintensität bestätigt werden. Zusätzlich konnten neue Informationen über die unterschiedliche subzelluläre Lokalisation gewonnen werden: so konnte eine starke Expression des Transporters in der apikalen Membran von Dünn- und Dickdarmmukosa dargestellt werden, während die ebenfalls starke Färbung in der Niere auf den Bereich der basolateralen Membran der Tubuli beschränkt war. In der Leber war eine Expression mittlerer Intensität im Bereich der Lebertrias erkennbar. Während in der Milz nur in der roten Pulpa das RFC1-Protein detektiert wurde, konnten im Thymus sowohl in der Rinde als auch im Mark positive Zellen nachgewiesen werden. Im Hoden konnte der Transporter in den Sertoli-Zellen dargestellt werden. Eine starke Expression des Transporters wurde im Gehirn im Bereich der apikalen Membran der Ependymzellen des Plexus choroideus nachgewiesen. In der Skelettmuskulatur und im Herzgewebe beschränkte sich die Expression des rRFC1 auf das Perimysium des Muskelgewebes und auf kleinere Gefäße des Muskel- und Herzgewebes. In dieser Arbeit konnte somit gezeigt werden, dass der RFC1 der Ratte ubiquitär exprimiert wird, wobei die Expressionsstärke jedoch stark variiert. Die beobachtete Gewebslokalisation des RFC1 belegt sowohl dessen zentrale Rolle in der Folathomöostase als auch in der MTX vermittelten Organtoxizität und Pharmakokinetik, insbesondere bei der intestinalen Resorption sowie der hepatischen und renalen Exkretion.
3

Chazelas, Pauline. "Syndrome de CANVAS – Analyse moléculaire des répétitions pentanucléotidiques du gène RFC1 et étude de leurs conséquences physiopathologiques." Electronic Thesis or Diss., Limoges, 2024. http://www.theses.fr/2024LIMO0006.

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Le syndrome de CANVAS définie un ensemble d’entités cliniques que sont l’ataxie cérébelleuse, la neuronopathie sensitive et l’aréflexie vestibulaire, responsable conjointement ou individuellement de différents symptômes dont le plus majoritaire est un trouble de l’équilibre. De façon intéressante, il est maintenant établi que la majorité des patients présentent, des dizaines d’années avant les troubles neurologiques, une toux chronique réfractaire. En 2019, la cause génétique de ce syndrome a été décrite. Elle intéresse le gène RFC1 au sein duquel une expansion biallélique de répétitions du pentanucléotide AAGGG situé dans l’intron 2 du gène a pu être mise en cause chez les patients cliniquement atteint. Ce motif AAGGG de grande taille remplace la conformation AAAAG classiquement répétée 11 fois en population générale. La cause physiopathologique responsable de cette maladie n’est pas encore connue. Plusieurs études ont montré une variabilité de la zone répétée qu’elles soient en termes de conformations du motif qu’en termes de nombre de répétitions. Leurs implications dans la pathologie ne sont pas toujours évidentes.Dans ce travail, nous nous sommes intéressés à trois axes concernant ce syndrome : (a) décrire la variabilité de la zone répétée dans une cohorte de témoins et dans une cohorte de patients adressée pour neuropathie, (b) étudier histologiquement l’atteinte nerveuse périphérique en particulier celle des petites fibres nerveuses, non décrites antérieurement, (c) étudier la prévalence de l’expansion biallélique du pentanucléotide AAGGG dans une cohorte de patients tousseurs chroniques réfractaires.Nos résultats ont permis de mettre en évidence de nouveaux motifs répétés complexes à la fois chez des témoins mais aussi chez des patients avec neuropathie. L’atteinte des petites fibres nerveuses dans le CANVAS a pu être objectivée pour la première fois. Notre étude de cohorte de 68 patients tousseurs chroniques réfractaires a permis de mettre en évidence 16% des patients porteurs d’une expansion biallélique AAGGG pathogène et nous conduit à suggérer que la toux des patients CANVAS serait une toux neurogène.L’ensemble de ces résultats de thèse a permis une avancée dans les connaissances moléculaires et physiopathologiques du syndrome de CANVAS. Des travaux complémentaires permettront de comprendre les mécanismes physiopathologiques sous-jacents afin d’envisager in fine d’éventuelles thérapeutiques personnalisées
The CANVAS syndrome defines a group of clinical entities - cerebellar ataxia, sensory neuronopathy and vestibular areflexia - that together or separately are responsible for a variety of symptoms, the most common of which is a disturbance of balance. Interestingly, it has now been shown that the majority of patients present with a chronic refractory cough decades before the onset of neurological disorders. In 2019, the genetic cause of this syndrome was described. It involves the RFC1 gene, in which a biallelic expansion of AAGGG pentanucleotide repeats in intron 2 of the gene has been implicated in clinically affected patients. This large AAGGG motif replaces the AAAAG conformation, which is classically repeated 11 times in the general population. The pathophysiological cause of the disease is still unknown. Several studies have shown variability in the repeat zone, both in terms of motif conformation and number of repeats. The implications for pathology are not always clear.In this study, we focused on three aspects of this syndrome: (a) description of the variability of the repeated zone in a cohort of controls and in a cohort of patients referred for neuropathy, (b) histological study of peripheral nerve damage, particularly that of small nerve fibers, which has not been previously described, (c) study of the prevalence of biallelic expansion of the pentanucleotide AAGGG in a cohort of refractory chronic cough patients.Our results revealed novel complex repeats in both controls and patients with neuropathy. The involvement of small nerve fibers in CANVAS was objectified for the first time. Our cohort study of 68 patients with refractory chronic cough identified 16% of patients with a pathogenic AAGGG biallelic expansion, leading us to suggest that the cough of CANVAS patients is neurogenic.Taken together, the results of this thesis represent a breakthrough in the molecular and pathophysiological knowledge of CANVAS syndrome. Further work is required to understand the underlying pathophysiological mechanisms with a view to developing personalized therapies
4

Halwachs, Sandra. "Regulation des Reduced Folate Carrier (RFC1) in HPCT-1E3-Ratten-Hepatocytoma-Zellen durch Cytochrom P450-Induktoren vom Phenobarbital-Typ." Doctoral thesis, Universitätsbibliothek Leipzig, 2006. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-34397.

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The sodium dependent reduced folate carrier (Rfc1; Slc19a1) provides the major route for cellular uptake of antifolate chemotherapeutic drugs such as methotrexate (MTX) and reduced folates into liver, kidneys and other tissues. Despite its essential role in cancer treatment and for the body’s folate homeostasis, little is known about Rfc1 regulation. In rat hepatocytes, the 5´ untranslated region of this carrier exhibits, amongst other regulatory elements, a barbiturate recognition box which as yet has only been found in the promotor region of xenobiotic metabolizing enzymes, particularly those of the CYP450 enzyme family. We have therefore investigated the issue of Rfc1 regulation by phenobarbital (PB)-type CYP450 inducers on the functional, transcriptional and translational level using an adequate in vitro model for rat liver. A significant decrease in Rfc1 activity was observed following treatment (48 h) with 1-10 times therapeutic plasma concentrations of PB-type CYP450 inducers like PB, carbamazepine, chlorpromazine, clotrimazole and with the constitutive androstane receptor agonist TCPOBOP. This was not associated with reduced mRNA and protein levels. Further mechanistic investigations revealed that short-term treatment (2 h) of cells with protein phosphatase 2A inhibitor okadaic acid and proteinkinase C inductor PMA was related to a significant reduction of Rfc1 mediated MTX uptake. Finally, the reduction in Rfc1 activity caused by PB, TCPOBOP and PMA was almost completely reversed by simultaneous incubation with the specific PKC inhibitor bisindolylmaleimide. These results demonstrate, that clinical relevant concentrations of PB-type CYP450 inducers cause a significant PKC-dependent reduction in Rfc1 uptake activity on the posttranscriptional level.
5

Lopes, Tairine Zara. "Avaliação de polimorfismos nos genes MTHFR, MTR, RFC1 e CßS envolvidos no metabolismo do folato em pacientes com câncer de tireoide." Faculdade de Medicina de São José do Rio Preto, 2015. http://hdl.handle.net/tede/272.

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Introduction: Thyroid cancer is the most common malignancy of the endocrine system and has been presenting continuous increase in the last years. Studies suggest that folate deficiency in the body decrease DNA repair, resulting in malignant cells changes that alter expression of genes, and may induce several kinds of cancer development. Polymorphisms in genes involved in folate pathway have been investigated as risk factors for susceptibility to cancer, among them MTHFR, MTR, RFC1 and CßS. Objectives: To investigate association of polymorphisms in the MTHFR (C677T), MTR (A2756G), RFC1 (A80G) and CßS (844ins68) genes in risk thyroid cancer in a case-control study; to evaluate the association of polymorphisms with gender, age, alcohol and tobacco consumption, body-mass index in thyroid cancer development; and to evaluated the association between polymorphisms and clinical-histopathological parameters. Methods: This study included 462 individuals (151 patients with thyroid cancer and 311 controls). The peripheral blood was collected and genomic DNA was extracted. The MTHFR (C677T), MTR (A2756G) and RFC1 (A80G) were evaluated by PCR-RFLP and CßS (844ins68) by conventional PCR without enzymatic digestion. For statistical analysis chi-square and multiple logistic regression were used. Results: The results showed that MTHFR C677T (OR=2.87, 95% CI=1.50-5.48, p< 0.01, codominant model), (OR=1.76, 95% CI=1.18-2.64, p< 0.01, dominant model), (OR=2.37, 95% CI=1.28-4.39, p< 0.01, recessive model) and RFC1 A80G (OR: 1.55; 95% CI: 1.02-2.38; p=0.04, recessive model) were associated with thyroid cancer. The alcohol (OR=1.56, 95% CI=1.36-1.89, p< 0.01) and tobacco consumption (OR=1.97, 95% CI=1.28-3.04, p< 0.01) were statistically significant, being associated with increased risk. The MTR A2756G is associated with tumor extension (OR=2.69, 95% CI=1.27-5.71, p< 0.01) and aggressiveness (OR= 4.51, 95% CI=1.67-12.1, p< 0.01). Conclusions: The MTHFR (C677T) and RFC1 (A80G) polymorphisms were involved in risk for thyroid cancer. Additionally, alcohol and tobacco consumption increase risk for disease development.
Introdução: O câncer de tireoide é a neoplasia maligna mais comum do sistema endócrino e vem apresentando contínuo aumento nos últimos anos. Estudos sugerem que a deficiência de folato no organismo diminui a reparação do DNA, resultando em alterações celulares malignas que modulam a expressão gênica, podendo levar ao desenvolvimento de vários tipos de câncer. Polimorfismos em genes envolvidos na via do folato têm sido investigados como fatores de risco para suscetibilidade ao câncer, entre eles, polimorfismos nos genes MTHFR, MTR, RFC1 e CßS. Objetivos: Investigar a associação dos polimorfismos nos genes MTHFR (C677T), MTR (A2756G), RFC1 (A80G) e CßS (844ins68) no risco de câncer de tireoide em um estudo caso-controle; Avaliar a associação dos polimorfismos com o gênero, idade, consumo de álcool e tabaco, índice de massa corpórea (IMC) no desenvolvimento do câncer de tireoide; Avaliar a associação entre os polimorfismos e os parâmetros clínico-histopatológicos do câncer de tireoide. Casuística e Método: Este estudo incluiu 462 indivíduos (151 pacientes com câncer de tireoide e 311 indivíduos controles). Foi coletado sangue periférico e extraído o DNA genômico. Os polimorfismos MTHFR (C677T), MTR (A2756G) e RFC1 (A80G) foram avaliados por meio da PCR-RFLP e o polimorfismo CßS (844ins68) foi analisado por PCR convencional sem corte enzimático. Para análise estatística utilizou-se o teste do qui-quadrado e regressão logística múltipla. Resultados: Os resultados mostraram que os polimorfismos MTHFR C677T (OR=2.87, 95% IC=1.50-5.48, p< 0.01, modelo codominante), (OR=1.76, 95% IC=1.18-2.64, p< 0.01, modelo dominante), (OR=2.37, 95% IC=1.28-4.39, p< 0.01, modelo recessivo) e RFC1 A80G (OR: 1.55; 95% IC: 1.02-2.38; p=0.04, modelo recessivo) estão associados ao câncer de tireoide. O consumo de álcool (OR=1.56, 95% IC=1.36-1.89, p< 0.01) e tabaco (OR=1.97, 95% IC=1.28-3.04, p< 0.01) foram estatisticamente significantes, sendo associados ao aumento do risco. O polimorfismo MTR A2756G está associado à extensão do tumor (OR=2.69, 95% IC=1.27-5.71, p< 0.01) e à agressividade (OR= 4.51, 95% IC=1.67-12.1, p< 0.01). Conclusões: Os polimorfismos MTHFR (C677T) e RFC1 (A80G) estão envolvidos no risco de câncer de tireoide. Adicionalmente, o consumo de álcool e tabaco aumenta o risco de desenvolvimento da doença.
6

Tomida, Junya. "DNA damage induced ubiquitylation of RFC2 subunit of RFC complex." Kyoto University, 2008. http://hdl.handle.net/2433/135870.

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7

Ng, Chin Chin. "Performance analysis of the mobile IP protocol (RFC 3344 and related RFCS)." Thesis, Monterey, Calif. : Naval Postgraduate School, 2006. http://bosun.nps.edu/uhtbin/hyperion.exe/06Dec%5FNg%5FChin.pdf.

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Thesis (M.S. in Computer Science)--Naval Postgraduate School, December 2006.
Thesis Advisor(s): George W. Dinolt, J. D. Fulp. "December 2006." Includes bibliographical references (p. 121-125). Also available in print.
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Hakim, Chantal DDS MSD, Marie M. MD PhD DrSc Tolarová, and Miroslav MD PhD Tolar. "Association of Type and Severity of Nonsyndromic Orofacial Clefts with Combined Genotypes of RFC1 80 GA, MTHFR 677 CT, IRF6 (rs642961) and IRF6 (rs2235371) Gene Polymorphisms in an Indian Population." Scholarly Commons, 2020. https://scholarlycommons.pacific.edu/dugoni_etd/2.

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Association of type and severity of nonsyndromic OROFACIAL CLEFTS with combined genotypes of RFC1 80 GA, MTHFR 677 CT, IRF6 rs642961 and rs2235371 gene polymorphisms in an Indian population Abstract By Chantal Hakim University of the Pacific. Arthur Dugoni School of Dentistry 2020 Introduction. Genetic etiology of nonsyndromic orofacial clefts comprises many genes acting together. However, little is known about their interactions. The purpose of our study was to analyze associations of phenotypic subtypes of nonsyndromic orofacial clefts with combinations of four genotypes involving candidate gene polymorphisms. Materials and Methods. We analyzed a large dataset of cases and controls collected in one location (Karaikal in India) and genotyped for four gene polymorphisms: RFC1 G80A, MTHFR C677T, IRF6 GA rs642961 and IRF6 CT rs2235371 (IRB approval Nr. 17-118 for existing data). The samples were tested for Hardy-Weinberg genetic equilibrium. Combinations of genotypes in cleft subsamples were compared with controls using Odds Ratio and Confidence Interval (95% significance level) calculations. Results. The Hardy-Weinberg equilibrium test showed that all samples were in genetic equilibrium. Some combinations of RFC1 G80A, MTHFR C677T, IRF6 GA rs642961 and IRF6 CT rs2235371 yielded increased or decreased Odds Ratio (OR>1 or OR<1).This means that subtypes of orofacial clefts were differentially determined by genotype combinations of four gene polymorphisms. Conclusions. Our results suggest that combinations of gene polymorphisms may modulate genetic risk in subtypes of nonsyndromic orofacial clefts. Such studies seem to be important for development of a general procedure and how a prevention plan for a specific location needs to be prepared, which data needs to be collected and which analyses need to be performed.
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Giusti, Kelma Cordeiro da Silva. "Associação entre polimorfismos em genes relacionados ao metabolismo de folato (RFC1, GCP2, MTHFR e MTHFD1) e alterações nas concentrações de folato, cobalamina e homocisteína em mulheres com história de abortos espontâneos recorrentes." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-08032013-115754/.

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O aborto espontâneo recorrente (AER) é caracterizado pela ocorrência de três ou mais abortos consecutivos e acomete 2-4% das mulheres em idade fértil. A etiologia está associada a vários fatores de risco, tais como anomalias uterinas, aberrações cromossômicas, autoimunidade, trombofilias, elevação na concentração de homocisteína (tHcy), porém cerca de 40% dos casos permanece sem causa definida. O metabolismo de unidades de carbono desempenha papel fundamental na disponibilidade de folato na célula, sendo essencial para o desenvolvimento placentário e fetal. Deficiência de vitaminas que regulam este metabolismo, como o ácido fólico, e polimorfismos em genes que codificam enzimas relacionadas ao metabolismo de folato (MTHFR, RFC1, GCP2 e MTHFD1) podem levar à redução das concentrações desta vitamina e ao aumento das concentrações de tHcy. Objetivo foi avaliar a associação entre polimorfismos em genes relacionados ao metabolismo do folato (RFC1, GCP2, MTHFR e MTHFD1) e o risco de se ter AER, bem como avaliar a associação entre estes polimorfismos e as alterações nas concetranções de folato, cobalamina e homocisteína. Foram constituídos três grupos: AER primário: 117 mulheres com AER e nenhum feto viável; AER secundário: 139 mulheres com AER e pelo menos um feto viável; e Controle: 264 mulheres sem história de aborto espontâneo. Nenhuma das mulheres estava grávida no momento da coleta do sangue. Amostras de sangue foram obtidas para dosagens bioquímicas (folato, Cbl, tHcy, entre outras), imunológicas e extração de DNA genômico. As genotipagens foram feitas por PCR-RFLP ou PCR em tempo real. As concentrações séricas de folato e Cbl foram maiores no AER primário e secundário (p<0,05). A distribuição dos genótipos de todos os polimorfismos foi semelhante nos três grupos. O aumento nas concentrações de folato sérico (OR: 1,05, 95% IC: 1,03 - 1,07, p<0,001), Cbl (OR: 1,00, 95% IC: 1,00 - 1,00, p= 0,016), tHcy (OR: 1,03, 95% IC: 0,97 - 1,11, p= 0,033) e T4 (OR: 1,02, 95% IC: 1,00 - 1,03, p= 0,006) e a presença de FAN reagente (1:160) (OR: 2,90, 95% IC: 1,25 - 6,75, p= 0,013) foram considerados fatores de risco para aborto primário. Para o aborto secundário, foram considerados fatores de risco o aumento nas concentrações de folato sérico (OR: 1,04, 95% IC: 1,02 - 1,05, p<0,001), Cbl (OR: 1,00, 95% IC: 1,00 - 1,00, p= 0,019) e tHcy (OR: 1,05, 95% IC: 1,00 - 1,09, p= 0,039), maiores idades (OR: 1,02, 95% IC: 0,98 - 1,06, p= 0,031), hábito de fumar (OR: 2,54, 95% IC: 1,41 - 4,60, p= 0,002) e ter maior IMC (OR:1,42, 95% IC: 1,07 - 1,88, p= 0,015). Os polimorfismos estudados não foram associados ao maior risco de se ter AER, quando analisados isoladamente, e também não foram associados a alterações nas concentrações séricas de folato, Cbl e tHcy, com exceção do genótipo MTHFR 677TT, cujas portadoras apresentaram maior concentração de tHcy, quando comparadas com as portadoras de genótipos 677CC e 677CT nos três grupos. As variáveis concentrações de folato, Cbl, tHcy e T4 e presença de FAN reagente foram associadas ao maior risco de se ter aborto primário. As variáveis idade, IMC, tabagismo, concentrações de folato, Cbl e tHcy foram associadas ao maior risco de aborto secundário.
The recurrent spontaneous abortion (RSA) is characterized by the occurrence of three or more consecutive miscarriages and affects 2-4% of women of childbearing age. The etiology is associated with several risk factors such as uterine abnormalities, chromosomal aberrations, autoimmunity, thrombophilia, increased concentration of homocysteine (tHcy). About 40% of cases remains unknown cause. The units of carbon metabolism plays an essential role in the availability of the cell folate, is essential for the placental and fetal development. A deficiency of the vitamins that regulate this metabolism, like folic acid, and polymorphisms in genes encoding enzymes related to folate metabolism (MTHFR, RFC1, and GCP2 MTHFD1) may lead to decreased concentrations of this vitamin and increased concentrations of tHcy. Objective was to evaluate the association between polymorphisms in genes related to folate metabolism (RFC1, GCP2, MTHFD1 and MTHFR) and the risk of having AER, and to evaluate the association between these polymorphisms and changes in concetranções folate, cobalamin, and homocysteine. Three groups were divided: AER primary: 117 women with RSA and no viable fetus, AER secondary: 139 women with RSA and at least one viable fetus and Control: 264 women with no history of miscarriage. None of the women was pregnant at time of blood collection. Blood samples were taken for biochemical (folate, Cbl, tHcy, etc.), immunological and genomic DNA extraction. The genotyping were carried out by PCR-RFLP or real time PCR. Serum concentrations of folate and Cbl were higher in groups 1 and 2 (p <0.05). The distribution of genotypes of MTHFR c.677C> T, MTHFR c.1298A> C, MTHFD1 c.1958G> A, RFC1 c.80G>GCP2 A and c.1561C> T was similar among the three groups. The increased concentrations of serum folate (OR: 1.05, 95% CI: 1.03 - 1.07, p <0.001), Cbl (OR: 1.00, 95% CI: 1.00 to 1.00, p = 0.016), tHcy (OR: 1.03, 95% CI: 0.97 to 1.11, p = 0.033) and T4 (OR: 1.02, 95% CI: 1.00 to 1.03, p = 0.006) and the presence of ANA (1:160) (OR: 2.90, 95% CI: 1.25 - 6.75, p = 0.013) were considered risk factors primary for abortion. For secondary abortion, were considered risk factors increased the concentrations of serum folate (OR: 1.04, 95% CI: 1.02 - 1.05, p <0.001), cobalamin (OR: 1.00, 95 % CI: 1.00 to 1.00, p = 0.019) and tHcy (OR: 1.05, 95% CI: 1.00 to 1.09, p = 0.039), higher age (OR: 1.02, 95% CI: 0.98 to 1.06, p = 0.031), cigarette smoking (OR: 2.54, 95% CI: 1.41 to 4.60, p = 0.002) and had a higher BMI (OR : 1,42,95% CI: 1.07 to 1.88, p = 0.015). The studied polymorphisms were not associated with increased risk of having RSA when analyzed separately, and were not associated with changes in serum folate, Cbl and tHcy, with the exception of the MTHFR 677TT genotype, whose patients had a higher concentration of total tHcy compared with those with 677CC and 677CT genotypes in the three groups. The variable concentrations of folate, Cbl, tHcy, and T4, presence of ANA and have been associated with increased risk for miscarriage primary. The variables age, BMI, smoking, concentrations of folate, Cbl and tHcy were associated with increased risk of secondary miscarriage.
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Alata, Jimenez Nagif. "La deficiencia en los transportadores de folato (FOLR1 y RFC1) causa cambios epigenéticos que afectan el desarrollo neural y de las células de la cresta neural en embriones de pollo Gallus gallus." Bachelor's thesis, Universidad Nacional Mayor de San Marcos, 2019. https://hdl.handle.net/20.500.12672/10342.

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El desarrollo neural ocurre mediante el proceso de neurulación originando el sistema nervioso central y la médula espinal. Durante este proceso las células de la cresta neural (CCN) son especificadas en la región más dorsal del tubo neural; posteriormente, las CCN delaminan del epitelio neural, migran a diferentes regiones del embrión y se diferencian en diversos tipos celulares. Defectos en el desarrollo del tubo neural y de las CCN generan desórdenes congénitos como espina bífida, encefalocelia, y neurocristopatías (paladar-labio hendido, albinismo, entre otras). Una vitamina importante durante el desarrollo embrionario temprano es el folato, el cual se encuentra en el sistema circulatorio en forma de 5-metiltetrahidrofolato (5-MTHF) e ingresa a la célula por medio del receptor de membrana FOLR1 y el transportador RFC1. El 5-MTHF participa en la síntesis de nucleótidos y en la generación de Sadenosilmetionina (SAM) para la metilación de ácidos nucleicos y proteínas. La metilación de ácidos nucleicos y proteínas son importantes mecanismos de regulación epigenética durante el normal desarrollo embrionario de los vertebrados. Considerando lo dicho se plantea determinar el efecto epigenético de la deficiencia del folato en el desarrollo del tubo neural y de las CCN. Para esto realizamos la pérdida de función del receptor FOLR1 y transportador RFC1 mediante el uso de los morfolinos FolR1spMO y RFC1spMO en embriones de pollo. Posteriormente se evalúan los niveles de 5mC en el ADN y 6mA en el ARN mediante dot blots, observando una clara disminución en ambas marcas epigenéticas. El análisis de expresión del marcador de CCN Sox10 en embriones inyectados evidenció una disminución en el número de CCN. Adicionalmente, el marcador neural Sox2 presentó una expresión ectópica en el territorio de las CCN. Estos resultados muestran que la deficiencia de folato afecta la metilación global del ADN y ARN generando un cambio en el destino celular de los progenitores de las CCN hacia un destino neural. Los resultados obtenidos pueden sentar las bases para un mejor entendimiento y desarrollo de tratamientos capaces de prevenir o disminuir las anomalías ocasionadas por la deficiencia de folato en mujeres embarazadas.
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Книги з теми "Rfc1":

1

Peter, Loshin, ed. Big book of FYI RFCs. San Francisco, Calif: Morgan Kaufmann, 2000.

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2

Loshin, Peter. Big book of IPsec RFCs. San Diego, CA: Morgan Kaufmann, 2000.

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3

Salus, Peter H. Big book of IPv6 addressing RFCs. San Diego: Morgan Kaufmann, 2000.

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4

Peter, Loshin, ed. Big book of terminal emulation RFCs. San Francisco: Morgan Kaufmann, 2000.

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5

Lin, Tan. Heath course pak rfc. 2nd ed. Denver: Counterpath, 2012.

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Loshin, Peter. Big book of Internet file transfer RFCs. San Diego: Morgan Kaufmann, 2000.

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Peter, Loshin, ed. Big book of World Wide Web RFCs. San Francisco, Calif: Morgan Kaufmann, 2000.

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8

Revell, Alex. No 56 Sqn RAF/RFC. Oxford: Osprey, 2009.

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Revell, Alex. No 60 Sqn RFC/RAF. Oxford: Osprey Pub., 2011.

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Loshin, Peter. Essential Ethernet standards: RFCs and protocols made practical. New York: John Wiley & Sons, 2000.

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Частини книг з теми "Rfc1":

1

Angeli, Axeö, Ulrich Streit, and Robi Gonfalonieri. "RFC Remote Function Call." In The SAP R/3® Guide to EDI and Interfaces, 79–85. Wiesbaden: Vieweg+Teubner Verlag, 2000. http://dx.doi.org/10.1007/978-3-663-01091-3_12.

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2

Stubbs, David A., and Wally C. Hoppe. "RFC Automated Inspection Overview." In Review of Progress in Quantitative Nondestructive Evaluation, 901–10. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7763-8_97.

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3

Karimi, Kamran, and Howard J. Hamilton. "RFCT: An Association-Based Causality Miner." In Advances in Artificial Intelligence, 334–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/3-540-47922-8_29.

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4

Jin, Feng, and Duruo Huang. "Design of RFC Arch Dam." In Hydroscience and Engineering, 179–203. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8298-8_6.

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5

Jin, Feng, and Duruo Huang. "Design of RFC Gravity Dam." In Hydroscience and Engineering, 135–77. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8298-8_5.

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6

Hoppe, Wally C., and David A. Stubbs. "RFC Eddy Current Probe Tests." In Review of Progress in Quantitative Nondestructive Evaluation, 893–900. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4615-7763-8_96.

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7

Oke, Muse, Manal S. Zaher, and Samir M. Hamdan. "Mechanism of PCNA Loading by RFC." In Molecular Life Sciences, 1–6. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-6436-5_137-1.

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8

Oke, Muse, Manal S. Zaher, and Samir M. Hamdan. "PCNA Loading by RFC, Mechanism of." In Molecular Life Sciences, 861–66. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4614-1531-2_137.

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9

Do, Cao-Phan, Thien-Phuc Nguyen, and Anh-Thang Le. "Study on Adhesive Characteristics of RFCC Asphalt Mastic." In Lecture Notes in Civil Engineering, 926–36. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-99-7434-4_97.

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10

Wörfel, René, and Hans Dodel†. "Antragsbeispiele API bzw. RfC (CR/C)/ITU." In Satellitenfrequenzkoordinierung, 391–99. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-29203-3_13.

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Тези доповідей конференцій з теми "Rfc1":

1

Hirons, B., K. Rhatigan, R. Curro, B. Rugginini, J. Shaw, H. Abubakar-Waziri, H. Kesavan, et al. "P215 RFC1 disorder; a genetic, neuropathic cause of chronic cough." In British Thoracic Society Winter Meeting 2023, QEII Centre, Broad Sanctuary, Westminster, London SW1P 3EE, 22 to 24 November 2023, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2023. http://dx.doi.org/10.1136/thorax-2023-btsabstracts.365.

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2

Laury, John, Lars Abrahamsson, and Math Bollen. "Transient Stability of Rotary Frequency Converter Fed Low Frequency Railway Grids: The Impact of Different Grid Impedances and Different Converter Station Configurations." In 2018 Joint Rail Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/jrc2018-6247.

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Анотація:
One method of strengthening low frequency AC railway grids is to upgrade Booster Transformer (BT) catenary systems, to Auto Transformer (AT) catenary systems. An AT catenary system has lower equivalent impedance compared to a BT system. Thus, an upgrade makes the existing converter stations electrically closer. Converter stations may have different types of Rotary Frequency Converters (RFCs) installed in them, and it is not well explored how different RFCs behaves and interact during and after a large disturbance. Using the Anderson-Fouad model of synchronous machines to describe the dynamics of RFCs, several case studies have been performed through numerical simulations. The studies investigate the interactions within and between converter stations constituted with different RFC types, for BT as well AT catenary systems. The numerical studies reveal that replacing BT with AT catenary systems, results in a more oscillatory system behaviour. This is seen for example in the power oscillations between and inside converter stations, after fault clearance.
3

Xu, Chang, Jie Zhang, and Zhu Sun. "Online Reputation Fraud Campaign Detection in User Ratings." In Twenty-Sixth International Joint Conference on Artificial Intelligence. California: International Joint Conferences on Artificial Intelligence Organization, 2017. http://dx.doi.org/10.24963/ijcai.2017/541.

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Reputation fraud campaigns (RFCs) distort the reputations of rated items, by generating fake ratings through multiple spammers. One effective way of detecting RFCs is to characterize their collective behaviors based on rating histories.However, these campaigns are constantly evolving and changing tactics to evade detection.For example, they can launch early attacks on the items to quickly dominate the reputations.They can also whitewash themselves through creating new accounts for subsequent attacks.It is thus challenging for existing approaches working on historical data to promptly react to such emerging fraud activities.In this paper, we conduct RFC detection in online fashion, so as to spot campaign activities as early as possible.This leads to a unified and scalable optimization framework, FraudScan, that can adapt to emerging fraud patterns over time.Empirical analysis on two real-world datasets validates the effectiveness and efficiency of the proposed framework.
4

Kolling, Maikel L., Felipe A. Kuentzer, Cristiano Battisti, Cristiano B. Both, Rafael R. dos Santos, and Tatiana G. S. dos Santos. "Verificação em Hardware de Componentes de Comunicação." In Simpósio em Sistemas Computacionais de Alto Desempenho. Sociedade Brasileira de Computação, 2008. http://dx.doi.org/10.5753/wscad.2008.17678.

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Nas últimas décadas, a transformação nos meios e formas de comunicação vêm impulsionando uma grande diversificação de dispositivos na área de comunicação de dados. Essa transformação é possível, sobretudo, em decorrência do desenvolvimento da microeletrônica e dos sistemas embarcados. Apesar da grande evolução ocorrida nos equipamentos em si, ainda existe uma carência no que diz respeito aos testes e validações dos mesmos. Várias RFCs (Request for Comments) já foram escritas objetivando a definição de uma metodologia para benchmarking, mas a maioria são tipicamente implementadas através de software e os equipamentos para esse fim, disponíveis no mercado, possuem um alto custo agregado. Porém, com a necessidade crescente de aumento da vazão, muitos desses testes ficam restritos, já que o software não consegue atingir os requisitos de vazão e latência necessários. Assim, esse trabalho tem como principal objetivo implementar os testes descritos na RFC 2544 em hardware. Os resultados mostram que essa abordagem é bastante eficiente e flexível, tendo em vista que não é necessário o uso de um sistema operacional e aplicativos de alto nível.
5

Yen, Jane, Ramesh Govindan, and Barath Raghavan. "Tools for disambiguating RFCs." In ANRW '21: Applied Networking Research Workshop. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3472305.3472314.

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6

Meriem, B. "Performance of self-compacting concrete based on fine recycled concrete aggregate incorporating polyethylene terephtalate fibers." In Advanced Topics in Mechanics of Materials, Structures and Construction. Materials Research Forum LLC, 2023. http://dx.doi.org/10.21741/9781644902592-17.

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Abstract. This experimental research aims to investigate the effect of adding polyethylene terephthalate plastic fibers (PETF) on the behavior of recycled self-compacting concrete (RSCC) based on recycled fine concrete aggregates (RFCA). Twenty RSCC mixes were made for this study. RFCA was obtained from the laboratory demolition of a moderate concrete slab and substituted by natural fine aggregates (NFA) at various mass fractions (0%, 25%, 50%, 75%, and 100%). Furthermore, four volumetric fractions (Vf) of plastic fibers (0.3%, 0.5%, 1%, and 1.2%) were added and sorted from plastic bottle recycling. The properties of the fresh and hardened new composite (RSCC made with PETF and RFCA contents) are analyzed and compared. The results showed that the mechanical performances of RSCC in terms of flexural strength and elasticity modulus were improved, where the compressive strength decreased with an increase in the Vf content of PETF and RFCA. The incorporation of 100% RFCA combined with 1.2% of PETF can enhance both flexural strength and modulus of elasticity of concrete up to 9% and 24%. This type of concrete can be recommended for structural repair applications.
7

Ahn, HyeongJoon. "Design Procedure of an Eddy Current Damper Type Reaction Force Compensation (RFC) Mechanism for a Linear Motor Motion Stage." In ASME 2015 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/detc2015-48080.

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Base vibration of a linear motor motion stage has been reduced with passive RFC mechanism based on movable magnet track and springs. This paper presents design procedure of an eddy-current damper (ECD) type RFC mechanism for a linear motor motion stage. The RFC mechanism with a movable magnet track and an ECD can overcome disadvantages of the spring based RFC mechanism such as resonance and difficulty of assembly due to spring. A lumped parameter model for the ECD type RFC mechanism is derived considering sinusoidal magnetic flux density and effective width of the ECD according to magnet track motion. Then, a design procedure for ECD type RFC mechanism is proposed to meet system requirements such as transmission ratio of reaction force and maximum magnet track motion. Design example illustrates the effectiveness of the proposed design procedure for ECD type RFC mechanism.
8

Wirasbawa, Nicholas Dwiarto, Yaman Khaeruzzaman, and Alexander Waworuntu. "Modern, Secure Application Programming Interface Implementation using RFC 6238 and RFC 7617." In 2023 International Conference on Smart Computing and Application (ICSCA). IEEE, 2023. http://dx.doi.org/10.1109/icsca57840.2023.10087735.

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9

Elkacimi, Younes, and Norbert Mu¨ller. "Regenerative Flow Pumps and Compressors (RFP/RFC) Applications for Water as Refrigerant." In ASME 2006 International Mechanical Engineering Congress and Exposition. ASMEDC, 2006. http://dx.doi.org/10.1115/imece2006-13486.

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This paper presents some preliminary design consideration of Regenerative Flow Pumps and Compressors (RFP/RFC) and their application in chillers that use water (R718) as the sole refrigerant. A brief overview of the fundamentals and hypothesis of the operation of RFP/RFC is presented. A one-dimensional (1-D) performance prediction code of an RFP/RFC model is developed using geometric parameters as input. Results of a sensitivity analysis are briefly discussed as they are validated using CFD analysis and suggest design changes for performance enhancement. Finally the RFC may be considered as an interesting alternative solution for R718-chiller application especially for smaller capacities and operation with lower speed.
10

Laury, John, Lars Abrahamsson, and Math Bollen. "Impact of Reduced Share of Rotary Frequency Converters in a Low Frequency Synchronous Railway Grid: A Transient Stability Study." In 2019 Joint Rail Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/jrc2019-1238.

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Анотація:
Most low-frequency AC single-phase railway grids have both power-electronic based Static Frequency Converters (SFCs) and electrical-machine based Rotary Frequency Converters (RFCs) connecting them to the three-phase public grid. Already today, in some such grids, a majority of the power conversion is from SFCs. As railway traffic (and thus power demand) increases, more SFCs are installed for capacity increase, while the number of RFCs remains (almost) constant. Thus, the share of SFCs is expected to increase, and the ratio of installed rotational inertia over installed power to decrease. This paper investigates how different shares of SFCs affect the transient stability of low-frequency AC railway grids when having a mix of RFCs and SFCs converting three-phase AC power to single-phase AC power. Results from numerical simulations of the interactions that occur between converters when and after the grid is subject to a fault are presented. The numerical studies show that with an increased share of SFCs there is an increased oscillatory behavior, for example in the voltage magnitude and active power after fault clearance.

Звіти організацій з теми "Rfc1":

1

Brownlee, N. SVG Drawings for RFCs: SVG 1.2 RFC. RFC Editor, December 2016. http://dx.doi.org/10.17487/rfc7996.

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2

Eggert, L. Moving the Undeployed TCP Extensions RFC 1072, RFC 1106, RFC 1110, RFC 1145, RFC 1146, RFC 1379, RFC 1644, and RFC 1693 to Historic Status. RFC Editor, May 2011. http://dx.doi.org/10.17487/rfc6247.

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3

Daigle, L., ed. The RFC Series and RFC Editor. RFC Editor, July 2007. http://dx.doi.org/10.17487/rfc4844.

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4

Housley, R., and L. Daigle, eds. The RFC Series and RFC Editor. RFC Editor, February 2020. http://dx.doi.org/10.17487/rfc8729.

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5

Hoffman, P. HTML Format for RFCs. Edited by J. Hildebrand. RFC Editor, December 2016. http://dx.doi.org/10.17487/rfc7992.

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6

Masinter, L., and M. Hardy. PDF Format for RFCs. Edited by T. Hansen. RFC Editor, December 2016. http://dx.doi.org/10.17487/rfc7995.

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7

Flanagan, H., ed. Fifty Years of RFCs. RFC Editor, December 2019. http://dx.doi.org/10.17487/rfc8700.

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8

Huitema, C., J. Postel, and S. Crocker. Not All RFCs are Standards. RFC Editor, April 1995. http://dx.doi.org/10.17487/rfc1796.

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9

Flanagan, H. Requirements for Plain-Text RFCs. RFC Editor, December 2016. http://dx.doi.org/10.17487/rfc7994.

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10

Flanagan, H., and S. Ginoza. RFC Style Guide. RFC Editor, September 2014. http://dx.doi.org/10.17487/rfc7322.

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