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Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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1

Fukunaga, Kenzo, Yukinori Hirano, and Katsunori Sugimoto. "Subtelomere-binding protein Tbf1 and telomere-binding protein Rap1 collaborate to inhibit localization of the Mre11 complex to DNA ends in budding yeast." Molecular Biology of the Cell 23, no. 2 (January 15, 2012): 347–59. http://dx.doi.org/10.1091/mbc.e11-06-0568.

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Chromosome ends, known as telomeres, have to be distinguished from DNA double-strand breaks that activate DNA damage checkpoints. In budding yeast, the Mre11-Rad50-Xrs2 (MRX) complex associates with DNA ends and promotes checkpoint activation. Rap1 binds to double-stranded telomeric regions and recruits Rif1 and Rif2 to telomeres. Rap1 collaborates with Rif1 and Rif2 and inhibits MRX localization to DNA ends. This Rap1-Rif1-Rif2 function becomes attenuated at shortened telomeres. Here we show that Rap1 acts together with the subtelomere-binding protein Tbf1 and inhibits MRX localization to DNA ends. The placement of a subtelomeric sequence or TTAGGG repeats together with a short telomeric TG repeat sequence inhibits MRX accumulation at nearby DNA ends in a Tbf1-dependent manner. Moreover, tethering of both Tbf1 and Rap1 proteins decreases MRX and Tel1 accumulation at nearby DNA ends. This Tbf1- and Rap1-dependent pathway operates independently of Rif1 or Rif2 function. Depletion of Tbf1 protein stimulates checkpoint activation in cells containing short telomeres but not in cells containing normal-length telomeres. These data support a model in which Tbf1 and Rap1 collaborate to maintain genomic stability of short telomeres.
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2

Craven, Rolf J., and Thomas D. Petes. "Dependence of the Regulation of Telomere Length on the Type of Subtelomeric Repeat in the Yeast Saccharomyces cerevisiae." Genetics 152, no. 4 (August 1, 1999): 1531–41. http://dx.doi.org/10.1093/genetics/152.4.1531.

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Abstract In the yeast Saccharomyces cerevisiae, chromosomes terminate with ∼400 bp of a simple repeat poly(TG1-3). Based on the arrangement of subtelomeric X and Y′ repeats, two types of yeast telomeres exist, those with both X and Y′ (Y′ telomeres) and those with only X (X telomeres). Mutations that result in abnormally short or abnormally long poly(TG1-3) tracts have been previously identified. In this study, we investigated telomere length in strains with two classes of mutations, one that resulted in short poly(TG1-3) tracts (tel1) and one that resulted in elongated tracts (pif1, rap1-17, rif1, or rif2). In the tel1 pif1 strain, Y′ telomeres had about the same length as those in tel1 strains and X telomeres had lengths intermediate between those in tel1 and pif1 strains. Strains with either the tel1 rap1-17 or tel1 rif2 genotypes had short tracts for all chromosome ends examined, demonstrating that the telomere elongation characteristic of rap1-17 and rif2 strains is Tel1p-dependent. In strains of the tel1 rif1 or tel1 rif1 rif2 genotypes, telomeres with Y′ repeats had short terminal tracts, whereas most of the X telomeres had long terminal tracts. These results demonstrate that the regulation of telomere length is different for X and Y′ telomeres.
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3

Bonetti, Diego, Carlo Rinaldi, Jacopo Vertemara, Marco Notaro, Paolo Pizzul, Renata Tisi, Giuseppe Zampella, and Maria Pia Longhese. "DNA binding modes influence Rap1 activity in the regulation of telomere length and MRX functions at DNA ends." Nucleic Acids Research 48, no. 5 (December 27, 2019): 2424–41. http://dx.doi.org/10.1093/nar/gkz1203.

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Abstract The cellular response to DNA double-strand breaks (DSBs) is initiated by the Mre11–Rad50–Xrs2 (MRX) complex that has structural and catalytic functions. MRX association at DSBs is counteracted by Rif2, which is known to interact with Rap1 that binds telomeric DNA through two tandem Myb-like domains. Whether and how Rap1 acts at DSBs is unknown. Here we show that Rif2 inhibits MRX association to DSBs in a manner dependent on Rap1, which binds to DSBs and promotes Rif2 association to them. Rap1 in turn can negatively regulate MRX function at DNA ends also independently of Rif2. In fact, a characterization of Rap1 mutant variants shows that Rap1 binding to DNA through both Myb-like domains results in formation of Rap1-DNA complexes that control MRX functions at both DSBs and telomeres primarily through Rif2. By contrast, Rap1 binding to DNA through a single Myb-like domain results in formation of high stoichiometry complexes that act at DNA ends mostly in a Rif2-independent manner. Altogether these findings indicate that the DNA binding modes of Rap1 influence its functional properties, thus highlighting the structural plasticity of this protein.
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4

Hirano, Yukinori, Kenzo Fukunaga, and Katsunori Sugimoto. "Rif1 and Rif2 Inhibit Localization of Tel1 to DNA Ends." Molecular Cell 33, no. 3 (February 2009): 312–22. http://dx.doi.org/10.1016/j.molcel.2008.12.027.

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5

Shi, Tianlai, Richard D. Bunker, Stefano Mattarocci, Cyril Ribeyre, Mahamadou Faty, Heinz Gut, Andrea Scrima, et al. "Rif1 and Rif2 Shape Telomere Function and Architecture through Multivalent Rap1 Interactions." Cell 153, no. 6 (June 2013): 1340–53. http://dx.doi.org/10.1016/j.cell.2013.05.007.

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6

Pobiega, Sabrina, Olivier Alibert, and Stéphane Marcand. "A new assay capturing chromosome fusions shows a protection trade-off at telomeres and NHEJ vulnerability to low-density ionizing radiation." Nucleic Acids Research 49, no. 12 (June 14, 2021): 6817–31. http://dx.doi.org/10.1093/nar/gkab502.

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Abstract Chromosome fusions threaten genome integrity and promote cancer by engaging catastrophic mutational processes, namely chromosome breakage–fusion–bridge cycles and chromothripsis. Chromosome fusions are frequent in cells incurring telomere dysfunctions or those exposed to DNA breakage. Their occurrence and therefore their contribution to genome instability in unchallenged cells is unknown. To address this issue, we constructed a genetic assay able to capture and quantify rare chromosome fusions in budding yeast. This chromosome fusion capture (CFC) assay relies on the controlled inactivation of one centromere to rescue unstable dicentric chromosome fusions. It is sensitive enough to quantify the basal rate of end-to-end chromosome fusions occurring in wild-type cells. These fusions depend on canonical nonhomologous end joining (NHEJ). Our results show that chromosome end protection results from a trade-off at telomeres between positive effectors (Rif2, Sir4, telomerase) and a negative effector partially antagonizing them (Rif1). The CFC assay also captures NHEJ-dependent chromosome fusions induced by ionizing radiation. It provides evidence for chromosomal rearrangements stemming from a single photon–matter interaction.
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7

Li, Bibo, and Titia de Lange. "Rap1 Affects the Length and Heterogeneity of Human Telomeres." Molecular Biology of the Cell 14, no. 12 (December 2003): 5060–68. http://dx.doi.org/10.1091/mbc.e03-06-0403.

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Telomere length is controlled in part by cis-acting negative regulators that limit telomere extension by telomerase. In budding yeast, the major telomere length regulator scRap1 binds to telomeric DNA and acts to inhibit telomere elongation in cis. Because the human Rap1 ortholog hRap1 does not bind to telomeric DNA directly but is recruited to telomeres by TRF2, we examined its role in telomere length control. The data are consistent with hRap1 being a negative regulator of telomere length, indicating functional conservation. Deletion mapping confirmed that hRap1 is tethered to telomeres through interaction of its C terminus with TRF2. The telomere length phenotypes of hRap1 deletion mutants implicated both the BRCT and Myb domain as protein interaction domains involved in telomere length regulation. By contrast, scRap1 binds to telomeres with its Myb domains and uses its C terminus to recruit the telomere length regulators Rif1 and Rif2. Together, our data show that although the role of Rap1 at telomeres has been largely conserved, the domains of Rap1 have undergone extensive functional changes during eukaryotic evolution. Surprisingly, hRap1 alleles lacking the BRCT domain diminished the heterogeneity of human telomeres, indicating that hRap1 also plays a role in the regulation of telomere length distribution.
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8

Bradley, Gregory W., John H. Holloway, Han Joong Koh, David G. Morris, and Paul G. Watson. "4-(Difluoroiodo)tricyclene, an isolable compound of type RIF2 from an aliphatic iodide." Journal of the Chemical Society, Perkin Transactions 1, no. 22 (1992): 3001. http://dx.doi.org/10.1039/p19920003001.

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9

Poschke, Heiko, Martina Dees, Michael Chang, Sandeep Amberkar, Lars Kaderali, Rodney Rothstein, and Brian Luke. "Rif2 Promotes a Telomere Fold-Back Structure through Rpd3L Recruitment in Budding Yeast." PLoS Genetics 8, no. 9 (September 20, 2012): e1002960. http://dx.doi.org/10.1371/journal.pgen.1002960.

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10

Zhang, Ling-Li, Zhenfang Wu, and Jin-Qiu Zhou. "Tel1 and Rif2 oppositely regulate telomere protection at uncapped telomeres in Saccharomyces cerevisiae." Journal of Genetics and Genomics 45, no. 9 (September 2018): 467–76. http://dx.doi.org/10.1016/j.jgg.2018.09.001.

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11

Kaizer, Hannah, Carla J. Connelly, Kelsey Bettridge, Christopher Viggiani, and Carol W. Greider. "Regulation of Telomere Length Requires a Conserved N-Terminal Domain of Rif2 inSaccharomyces cerevisiae." Genetics 201, no. 2 (August 20, 2015): 573–86. http://dx.doi.org/10.1534/genetics.115.177899.

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12

Martina, M., M. Clerici, V. Baldo, D. Bonetti, G. Lucchini, and M. P. Longhese. "A Balance between Tel1 and Rif2 Activities Regulates Nucleolytic Processing and Elongation at Telomeres." Molecular and Cellular Biology 32, no. 9 (February 21, 2012): 1604–17. http://dx.doi.org/10.1128/mcb.06547-11.

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13

Marsella, Antonio, Elisa Gobbini, Corinne Cassani, Renata Tisi, Elda Cannavo, Giordano Reginato, Petr Cejka, and Maria Pia Longhese. "Sae2 and Rif2 regulate MRX endonuclease activity at DNA double-strand breaks in opposite manners." Cell Reports 34, no. 13 (March 2021): 108906. http://dx.doi.org/10.1016/j.celrep.2021.108906.

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14

Bonetti, Diego, Michela Clerici, and Maria Pia Longhese. "Interplay between Sae2 and Rif2 in the regulation of Mre11-Rad50 activities at DNA ends." Current Opinion in Genetics & Development 71 (December 2021): 72–77. http://dx.doi.org/10.1016/j.gde.2021.07.001.

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15

Bonetti, Diego, Michela Clerici, Nicola Manfrini, Giovanna Lucchini, and Maria Pia Longhese. "The MRX Complex Plays Multiple Functions in Resection of Yku- and Rif2-Protected DNA Ends." PLoS ONE 5, no. 11 (November 30, 2010): e14142. http://dx.doi.org/10.1371/journal.pone.0014142.

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16

BRADLEY, G. W., J. H. HOLLOWAY, H. J. KOH, D. G. MORRIS, and P. G. WATSON. "ChemInform Abstract: 4-(Difluoroiodo)tricyclene, an Isolable Compound of Type RIF2 from an Aliphatic Iodide." ChemInform 24, no. 13 (August 20, 2010): no. http://dx.doi.org/10.1002/chin.199313155.

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17

Cassani, Corinne, Elisa Gobbini, Weibin Wang, Hengyao Niu, Michela Clerici, Patrick Sung, and Maria Pia Longhese. "Tel1 and Rif2 Regulate MRX Functions in End-Tethering and Repair of DNA Double-Strand Breaks." PLOS Biology 14, no. 2 (February 22, 2016): e1002387. http://dx.doi.org/10.1371/journal.pbio.1002387.

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18

McGee, Jean S., Jane A. Phillips, Angela Chan, Michelle Sabourin, Katrin Paeschke, and Virginia A. Zakian. "Reduced Rif2 and lack of Mec1 target short telomeres for elongation rather than double-strand break repair." Nature Structural & Molecular Biology 17, no. 12 (November 7, 2010): 1438–45. http://dx.doi.org/10.1038/nsmb.1947.

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19

Hailemariam, Sarem, Paolo De Bona, Roberto Galletto, Marcel Hohl, John H. Petrini, and Peter M. Burgers. "The telomere-binding protein Rif2 and ATP-bound Rad50 have opposing roles in the activation of yeast Tel1ATM kinase." Journal of Biological Chemistry 294, no. 49 (October 22, 2019): 18846–52. http://dx.doi.org/10.1074/jbc.ra119.011077.

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20

Viscardi, Valeria, Enrico Baroni, Michele Romano, Giovanna Lucchini, and Maria Pia Longhese. "Sudden Telomere Lengthening Triggers a Rad53-dependent Checkpoint inSaccharomyces cerevisiae." Molecular Biology of the Cell 14, no. 8 (August 2003): 3126–43. http://dx.doi.org/10.1091/mbc.e02-11-0719.

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Telomeres are specialized functional complexes that ensure chromosome stability by protecting chromosome ends from fusions and degradation and avoiding chromosomal termini from being sensed as DNA breaks. Budding yeast Tel1 is required both for telomere metabolism and for a Rad53-dependent checkpoint responding to unprocessed double-strand breaks. We show that overexpression of a GAL1-TEL1 fusion causes transient telomere lengthening and activation of a Rad53-dependent G2/M checkpoint in cells whose telomeres are short due to the lack of either Tel1 or Yku70. Sudden telomere elongation and checkpoint-mediated cell cycle arrest are also triggered in wild-type cells by overproducing a protein fusion between the telomeric binding protein Cdc13 and the telomerase-associated protein Est1. Checkpoint activation by GAL1-TEL1 requires ongoing telomere elongation. In fact, it is turned off concomitantly with telomeres reaching a new stable length and is partially suppressed by deletion of the telomerase EST2 gene. Moreover, both telomere length rebalancing and checkpoint inactivation under galactose-induced conditions are accelerated by high levels of either the Sae2 protein, involved in double-strand breaks processing, or the negative telomere length regulator Rif2. These data suggest that sudden telomere lengthening elicits a checkpoint response that inhibits the G2/M transition.
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21

Evers, J. L. H. (Hans). "Is RIF rife?" Human Reproduction 31, no. 12 (November 5, 2016): 2661. http://dx.doi.org/10.1093/humrep/dew277.

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22

Rios-Avila, Fernando. "Recentered influence functions (RIFs) in Stata: RIF regression and RIF decomposition." Stata Journal: Promoting communications on statistics and Stata 20, no. 1 (March 2020): 51–94. http://dx.doi.org/10.1177/1536867x20909690.

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Recentered influence functions (RIFs) are statistical tools popularized by Firpo, Fortin, and Lemieux (2009 , Econometrica 77: 953–973) for analyzing unconditional partial effects on quantiles in a regression analysis framework (unconditional quantile regressions). The flexibility and simplicity of these tools have opened the possibility to extend the analysis to other distributional statistics using linear regressions or decomposition approaches. In this article, I introduce one function and two commands to facilitate the use of RIFs in the analysis of outcome distributions: rifvar() is an egen extension used to create RIFs for a large set of distributional statistics, rifhdreg facilitates the estimation of RIF regressions enabling the use of high-dimensional fixed effects, and oaxaca_rif implements Oaxaca–Blinder decomposition analysis (RIF decompositions).
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23

Grandjeat, Yves-Charles. "Brother Figures: The Rift and Riff in John E. Wideman's Fiction." Callaloo 22, no. 3 (1999): 615–22. http://dx.doi.org/10.1353/cal.1999.0119.

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24

Rachek, Lyudmila I., Aimee M. Tucker, Herbert H. Winkler, and David O. Wood. "Transformation of Rickettsia prowazekiito Rifampin Resistance." Journal of Bacteriology 180, no. 8 (April 15, 1998): 2118–24. http://dx.doi.org/10.1128/jb.180.8.2118-2124.1998.

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ABSTRACT Rickettsia prowazekii, the causative agent of epidemic typhus, is an obligate intracellular parasitic bacterium that grows directly within the cytoplasm of the eucaryotic host cell. The absence of techniques for genetic manipulation hampers the study of this organism’s unique biology and pathogenic mechanisms. To establish the feasibility of genetic manipulation in this organism, we identified a specific mutation in the rickettsial rpoB gene that confers resistance to rifampin and used it to demonstrate allelic exchange in R. prowazekii. Comparison of the rpoB sequences from the rifampin-sensitive (Rifs) Madrid E strain and a rifampin-resistant (Rifr) mutant identified a single point mutation that results in an arginine-to-lysine change at position 546 of theR. prowazekii RNA polymerase β subunit. A plasmid containing this mutation and two additional silent mutations created in codons flanking the Lys-546 codon was introduced into the Rifs Madrid E strain of R. prowazekii by electroporation, and in the presence of rifampin, resistant rickettsiae were selected. Transformation, via homologous recombination, was demonstrated by DNA sequencing of PCR products containing the three mutations in the Rifrregion of rickettsial rpoB. This is the first successful demonstration of genetic transformation of Rickettsia prowazekii and represents the initial step in the establishment of a genetic system in this obligate intracellular pathogen.
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25

Filipenko, ML, IP Oscorbin, EA Khrapov, DA Shamovskaya, AG Cherednichenko, and YaSh Shvartz. "Detection of Ser450Leu mutation in rpoB gene of Mycobacterium tuberculosis by allele-specific loop-mediated isothermal DNA amplification method." Laboratory diagnostics, no. 1 (March 9, 2019): 34–40. http://dx.doi.org/10.24075/brsmu.2019.007.

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To identify genetic mutations a rather time-consuming and expensive method of polymerase chain reaction (PCR) is widely used. The aim of the present work was to evaluate the possibility of using the two schemes of the method of allele-specific isothermal loop amplification (LAMP) to detect the TCG/TTG (S450L) mutation in the rpoB gene of Mycobacterium tuberculosis. 48 clinical isolates of M. tuberculosis and 11 samples of sputum were used, randomized and obtained in the microbiological laboratory of the city of Novosibirsk from incident patients. It is shown that the use of an analysis scheme using the allele-specific primer FIP compared to F3 has the best resolution: the difference between the amplification time of the mutation and the wild type allele was 22 ± 2,4 versus 13 ± 4,1 minutes (p = 0,0011). When using 100 DNA genomic equivalents a true positive signal (amplification of the rpoB gene with a mutation using the corresponding allele-specific primer) was detected after 29,4 ± 3,4 minutes. A positive signal was visualized after adding SYBR Green I to the reaction, both when illuminated with daylight and when using a UV transilluminator. Using the developed method the DNA sample of 20 RIFR isolates from M. tuberculosis was analyzed containing the Ser450Leu mutation in the rpoB gene, 10 RIFR isolates containing other mutations in the rpoB gene and 18 RIFs isolates without any mutations; the presence of mutations in the samples was determined using classical Sanger sequencing. The sensitivity and specificity of LAMP for detecting a Ser450Leu mutation in the rpoB gene was 100%. This approach allows the use of crude lysates of mycobacteria as DNA, which reduces the total analysis time to 1,5 hour.
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26

Lima, Dirce Mary C., Clarice P. Abrantes-Lemos, Sumie Hoshino-Shimizu, Luiz P. C. Valli, Hermínia H. Y. Kanamura, Luiz Caetano da Silva, and Silvia A. G. Vellosa. "Imunodiagnóstico da esquistossomose mansônica com baixa carga parasitária." Revista da Sociedade Brasileira de Medicina Tropical 29, no. 2 (April 1996): 145–52. http://dx.doi.org/10.1590/s0037-86821996000200007.

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Atualmente, a esquistossomose mansônica com baixa carga parasitária é freqüente, e desta forma, ensaios imunológicos de interesse ao diagnóstico populacional de infecção leve por Schistosoma mansoni foram aqui avaliados. Incluíram-se neste estudo ensaios anteriormente não avaliados (grupo I) e pouco avaliados (grupo II) para triagem de infecções leves. No grupo I, destacaram-se as reações de inunofluorescência destinadas à detecção de anticorpos IgM antiverme (RIFv IgM), e de anticorpos IgG anti-ovo (RIFo IgG) por apresentarem níveis elevados de sensibilidade, especificidade, eficiência e valor preditivo positivo. Todavia, os ensaios imunoenzimáticos para a detecção de anticorpos IgM, antiverme (ELISAv IgM) e anti- ovo (ELISAo IgM) revelaram níveis menores que as reações acima. Os ensaios do grupo II, namaioria utilizada para detecção de anticorpos IgG contra os mesmos antígenos, demonstraram desempenhos diagnósticos satisfatórios. Os dados aqui obtidos contribuíram para evidenciar pelo menos três categorias de ensaios imunológicos, e concluímos que os de categoria I são apropriados para estudos soroepidemiológicos de infecção leve por S. mansoni, em vista de suas características diagnosticas permanecerem inalteradas mesmo que a intensidade de infecção por S. mansoni varie significativamente.
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27

Hyett, Barbara Helfgott. "Rift." Prairie Schooner 80, no. 4 (2006): 29–34. http://dx.doi.org/10.1353/psg.2007.0014.

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28

Ganser, A., C. Carlo-Stella, J. Greher, B. Volkers, and D. Hoelzer. "Effect of recombinant interferons alpha and gamma on human bone marrow- derived megakaryocytic progenitor cells." Blood 70, no. 4 (October 1, 1987): 1173–79. http://dx.doi.org/10.1182/blood.v70.4.1173.1173.

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Abstract Interferons (IFNs) have been shown to suppress the proliferation of human pluripotent hematopoietic progenitor cells, CFU-GEMM, and committed erythroid (BFU-E, CFU-E) and granulocyte-macrophage (CFU-GM) progenitor cells. However, no information is yet available concerning the effect of IFNs on human megakaryocytic progenitor cells CFU-Mk. Furthermore the mechanisms underlying the inhibitory activity of IFNs are still controversial. Therefore highly purified recombinant IFN preparations, rIFN-alpha and rIFN-gamma, were assessed for their influence on in vitro growth of human bone marrow-derived CFU-Mk as well as CFU-GEMM. In addition, the role of hematopoietic accessory cells, that is, adherent cells and T lymphocytes, in the mediation of the suppressive effect of rIFNs was examined. When added to unseparated bone marrow cells, both rIFN preparations significantly inhibited colony formation with 50% inhibition of CFU-Mk occurring at 22 U/mL for rIFN-alpha and 59 U/mL for rIFN-gamma, while 50% inhibition of CFU-GEMM occurred at 59 U/mL for rIFN-alpha and 101 U/mL for rIFN-gamma. The suppressive effect of rIFN-alpha and rIFN-gamma was selectively abolished by monoclonal antibodies (MoAbs) against rIFN-alpha and rIFN- gamma, thus confirming that the inhibitory activity was due to the rIFN preparations used. The antiproliferative effect of rIFN-alpha and rIFN- gamma on CFU-GEMM growth was not associated with a decrease in the percentage of mixed colonies containing megakaryocytic cells as assessed by use of the MoAb C17.28 against platelet glycoprotein IIIa. Removal of adherent cells and T lymphocytes from the target bone marrow cells had no influence on the suppressive effect of rIFN-alpha, whereas it significantly reduced the inhibitory effect of rIFN-gamma on the growth of megakaryocytic colonies and the other hematopoietic progenitors. The data indicate that (1) human megakaryocytopoiesis is markedly inhibited by rIFN-alpha and rIFN-gamma, and (2) the inhibitory effect of rIFN-alpha is due to a direct action on hematopoietic progenitor cells, whereas the effect of rIFN-gamma is mediated to a significant degree through accessory cell populations.
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29

Ganser, A., C. Carlo-Stella, J. Greher, B. Volkers, and D. Hoelzer. "Effect of recombinant interferons alpha and gamma on human bone marrow- derived megakaryocytic progenitor cells." Blood 70, no. 4 (October 1, 1987): 1173–79. http://dx.doi.org/10.1182/blood.v70.4.1173.bloodjournal7041173.

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Interferons (IFNs) have been shown to suppress the proliferation of human pluripotent hematopoietic progenitor cells, CFU-GEMM, and committed erythroid (BFU-E, CFU-E) and granulocyte-macrophage (CFU-GM) progenitor cells. However, no information is yet available concerning the effect of IFNs on human megakaryocytic progenitor cells CFU-Mk. Furthermore the mechanisms underlying the inhibitory activity of IFNs are still controversial. Therefore highly purified recombinant IFN preparations, rIFN-alpha and rIFN-gamma, were assessed for their influence on in vitro growth of human bone marrow-derived CFU-Mk as well as CFU-GEMM. In addition, the role of hematopoietic accessory cells, that is, adherent cells and T lymphocytes, in the mediation of the suppressive effect of rIFNs was examined. When added to unseparated bone marrow cells, both rIFN preparations significantly inhibited colony formation with 50% inhibition of CFU-Mk occurring at 22 U/mL for rIFN-alpha and 59 U/mL for rIFN-gamma, while 50% inhibition of CFU-GEMM occurred at 59 U/mL for rIFN-alpha and 101 U/mL for rIFN-gamma. The suppressive effect of rIFN-alpha and rIFN-gamma was selectively abolished by monoclonal antibodies (MoAbs) against rIFN-alpha and rIFN- gamma, thus confirming that the inhibitory activity was due to the rIFN preparations used. The antiproliferative effect of rIFN-alpha and rIFN- gamma on CFU-GEMM growth was not associated with a decrease in the percentage of mixed colonies containing megakaryocytic cells as assessed by use of the MoAb C17.28 against platelet glycoprotein IIIa. Removal of adherent cells and T lymphocytes from the target bone marrow cells had no influence on the suppressive effect of rIFN-alpha, whereas it significantly reduced the inhibitory effect of rIFN-gamma on the growth of megakaryocytic colonies and the other hematopoietic progenitors. The data indicate that (1) human megakaryocytopoiesis is markedly inhibited by rIFN-alpha and rIFN-gamma, and (2) the inhibitory effect of rIFN-alpha is due to a direct action on hematopoietic progenitor cells, whereas the effect of rIFN-gamma is mediated to a significant degree through accessory cell populations.
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30

Arabi, Yaseen M., Sarah Shalhoub, Yasser Mandourah, Fahad Al-Hameed, Awad Al-Omari, Eman Al Qasim, Jesna Jose, et al. "Ribavirin and Interferon Therapy for Critically Ill Patients With Middle East Respiratory Syndrome: A Multicenter Observational Study." Clinical Infectious Diseases 70, no. 9 (June 25, 2019): 1837–44. http://dx.doi.org/10.1093/cid/ciz544.

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Abstract Background The objective of this study was to evaluate the effect of ribavirin and recombinant interferon (RBV/rIFN) therapy on the outcomes of critically ill patients with Middle East respiratory syndrome (MERS), accounting for time-varying confounders. Methods This is a retrospective cohort study of critically ill patients with laboratory-confirmed MERS from 14 hospitals in Saudi Arabia diagnosed between September 2012 and January 2018. We evaluated the association of RBV/rIFN with 90-day mortality and MERS coronavirus (MERS-CoV) RNA clearance using marginal structural modeling to account for baseline and time-varying confounders. Results Of 349 MERS patients, 144 (41.3%) patients received RBV/rIFN (RBV and/or rIFN-α2a, rIFN-α2b, or rIFN-β1a; none received rIFN-β1b). RBV/rIFN was initiated at a median of 2 days (Q1, Q3: 1, 3 days) from intensive care unit admission. Crude 90-day mortality was higher in patients with RBV/rIFN compared to no RBV/rIFN (106/144 [73.6%] vs 126/205 [61.5%]; P = .02]. After adjusting for baseline and time-varying confounders using a marginal structural model, RBV/rIFN was not associated with changes in 90-day mortality (adjusted odds ratio, 1.03 [95% confidence interval {CI}, .73–1.44]; P = .87) or with more rapid MERS-CoV RNA clearance (adjusted hazard ratio, 0.65 [95% CI, .30–1.44]; P = .29). Conclusions In this observational study, RBV/rIFN (RBV and/or rIFN-α2a, rIFN-α2b, or rIFN-β1a) therapy was commonly used in critically ill MERS patients but was not associated with reduction in 90-day mortality or in faster MERS-CoV RNA clearance.
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BURKE, K. "A Continental Rift: Rio Grande Rift." Science 228, no. 4707 (June 28, 1985): 1521. http://dx.doi.org/10.1126/science.228.4707.1521.

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32

Buonomo, Sara B. C., Yipin Wu, David Ferguson, and Titia de Lange. "Mammalian Rif1 contributes to replication stress survival and homology-directed repair." Journal of Cell Biology 187, no. 3 (November 2, 2009): 385–98. http://dx.doi.org/10.1083/jcb.200902039.

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Rif1, originally recognized for its role at telomeres in budding yeast, has been implicated in a wide variety of cellular processes in mammals, including pluripotency of stem cells, response to double-strand breaks, and breast cancer development. As the molecular function of Rif1 is not known, we examined the consequences of Rif1 deficiency in mouse cells. Rif1 deficiency leads to failure in embryonic development, and conditional deletion of Rif1 from mouse embryo fibroblasts affects S-phase progression, rendering cells hypersensitive to replication poisons. Rif1 deficiency does not alter the activation of the DNA replication checkpoint but rather affects the execution of repair. RNA interference to human Rif1 decreases the efficiency of homology-directed repair (HDR), and Rif1 deficiency results in aberrant aggregates of the HDR factor Rad51. Consistent with a role in S-phase progression, Rif1 accumulates at stalled replication forks, preferentially around pericentromeric heterochromatin. Collectively, these findings reveal a function for Rif1 in the repair of stalled forks by facilitating HDR.
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33

Siringoringo, Luhut Pardamean, and Dardji Noeradi. "The Paleogene Tectonostratigraphy Of Northern Part Masalima Trench Basin." Journal of Geoscience, Engineering, Environment, and Technology 1, no. 1 (December 1, 2016): 7. http://dx.doi.org/10.24273/jgeet.2016.11.2.

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Northern part of Masalima Trench Basin is located in the southern part of the Strait of Makassar, which includes Masalima Trough and Massalima High. The area of research is an extension of the South Makassar Basin which extends from South Makassar Basin to the Northeast part of Java Sea. Subsurface data are used such as 2D seismic sections (21 lines) and data drilling wells (2 wells) to understand the tectonic structure in the basin formation and understand the stratigraphic order of basin. Based on well data can be known that Northern part Masalima Trench Basin is aborted rift because marked by post rift phase. Northern part Masalima Trench Basin was formed by normal faults which have trend northeast-southwest with pre rift, early syn rift, late syn rift, and post rift sediment geometry. Early syn rift sediment was Middle Eocene, late syn rift sediment was Middle Eocene till Early Oligocene and post rift sediment was Early Oligocene till Early Miocene. The Depositional environment of early syn rift phase such as beach, shallow marine, and land. The Depositional environment of late syn rift phase such as beach till deep marine, and the depositional environment of post rift is deep marine.
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34

Carlo-Stella, C., M. Cazzola, A. Ganser, G. Bergamaschi, P. Pedrazzoli, D. Hoelzer, and E. Ascari. "Synergistic antiproliferative effect of recombinant interferon-gamma with recombinant interferon-alpha on chronic myelogenous leukemia hematopoietic progenitor cells (CFU-GEMM, CFU-Mk, BFU-E, and CFU-GM)." Blood 72, no. 4 (October 1, 1988): 1293–99. http://dx.doi.org/10.1182/blood.v72.4.1293.1293.

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Abstract Recombinant interferons, alpha (rIFN-alpha) and gamma (rIFN-gamma), have been demonstrated to have significant antitumor activity as single agents in the treatment of chronic myelogenous leukemia (CML). Due to their possible synergistic efficacy, a combination rIFN therapy in CML has been proposed. To establish a biologic basis for this, we have studied the suppressive effects of rIFN-alpha and rIFN-gamma on the in vitro growth of CML-derived progenitor cells (CFU-GEMM, CFU-Mk, BFU-E, CFU-GM), the optimal conditions for rIFN synergism, and the possible role of hematopoietic accessory cells (T-lymphocytes and monocytes- macrophages) in mediating rIFN-induced growth inhibition. When added to unseparated bone marrow cells, rIFN-alpha and rIFN-gamma significantly reduced colony formation, with 50% inhibition occurring at 71 and 186 U/mL for CFU-GEMM, 40 and 152 U/mL for CFU-Mk, 222 and 1,458 U/mL for BFU-E, and 119 and 442 U/mL for CFU-GM, respectively. A small amount of rIFN-gamma (5 U/mL) acted synergistically with increasing doses of rIFN- alpha, and the values of 50% inhibitory concentrations fell outside the lower limit (10 U/mL) used in our experiments. This synergy was evident even when rIFN-gamma was added 72 hours after the initiation of cultures; however, it was completely lost when the target cells were depleted of accessory cells. When a low dose of rIFN-alpha (5 U/mL) was added to rIFN-gamma, the 50% inhibitory concentration values were decreased up to tenfold. These studies (1) confirm that CML-derived hematopoietic progenitors are responsive to the suppressive activity of both rIFN-alpha and rIFN-gamma in vitro, (2) demonstrate that different mechanisms are responsible for the suppressive activity of the two rIFNs, and (3) characterize their synergistic interaction, providing a basis for future clinical trials aimed at investigating combination rIFN therapy in CML.
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35

Carlo-Stella, C., M. Cazzola, A. Ganser, G. Bergamaschi, P. Pedrazzoli, D. Hoelzer, and E. Ascari. "Synergistic antiproliferative effect of recombinant interferon-gamma with recombinant interferon-alpha on chronic myelogenous leukemia hematopoietic progenitor cells (CFU-GEMM, CFU-Mk, BFU-E, and CFU-GM)." Blood 72, no. 4 (October 1, 1988): 1293–99. http://dx.doi.org/10.1182/blood.v72.4.1293.bloodjournal7241293.

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Recombinant interferons, alpha (rIFN-alpha) and gamma (rIFN-gamma), have been demonstrated to have significant antitumor activity as single agents in the treatment of chronic myelogenous leukemia (CML). Due to their possible synergistic efficacy, a combination rIFN therapy in CML has been proposed. To establish a biologic basis for this, we have studied the suppressive effects of rIFN-alpha and rIFN-gamma on the in vitro growth of CML-derived progenitor cells (CFU-GEMM, CFU-Mk, BFU-E, CFU-GM), the optimal conditions for rIFN synergism, and the possible role of hematopoietic accessory cells (T-lymphocytes and monocytes- macrophages) in mediating rIFN-induced growth inhibition. When added to unseparated bone marrow cells, rIFN-alpha and rIFN-gamma significantly reduced colony formation, with 50% inhibition occurring at 71 and 186 U/mL for CFU-GEMM, 40 and 152 U/mL for CFU-Mk, 222 and 1,458 U/mL for BFU-E, and 119 and 442 U/mL for CFU-GM, respectively. A small amount of rIFN-gamma (5 U/mL) acted synergistically with increasing doses of rIFN- alpha, and the values of 50% inhibitory concentrations fell outside the lower limit (10 U/mL) used in our experiments. This synergy was evident even when rIFN-gamma was added 72 hours after the initiation of cultures; however, it was completely lost when the target cells were depleted of accessory cells. When a low dose of rIFN-alpha (5 U/mL) was added to rIFN-gamma, the 50% inhibitory concentration values were decreased up to tenfold. These studies (1) confirm that CML-derived hematopoietic progenitors are responsive to the suppressive activity of both rIFN-alpha and rIFN-gamma in vitro, (2) demonstrate that different mechanisms are responsible for the suppressive activity of the two rIFNs, and (3) characterize their synergistic interaction, providing a basis for future clinical trials aimed at investigating combination rIFN therapy in CML.
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36

Liu, Yong-Bin, Ying Mei, Zheng-Wen Tian, Jing Long, Chen-Hui Luo, and Hong-Hao Zhou. "Downregulation of RIF1 Enhances Sensitivity to Platinum-Based Chemotherapy in Epithelial Ovarian Cancer (EOC) by Regulating Nucleotide Excision Repair (NER) Pathway." Cellular Physiology and Biochemistry 46, no. 5 (2018): 1971–84. http://dx.doi.org/10.1159/000489418.

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Background/Aims: Rap1 interacting factor 1 (RIF1) was deemed to be involved in replication timing regulation and DNA damage response. However, little is known about the role of RIF1 in malignancies. Thus, this study aimed to investigate whether the expression of RIF1 is relevant to the response of epithelial ovarian cancer (EOC) patients to cisplatin chemotherapy and its underlying mechanism. Methods: Immunohistochemistry was used for detecting the expression of RIF1 in 72 human ovarian cancer tissues followed by association analysis of RIF1 expression with patients’ responses to platinum-based chemotherapy. The survival analysis of ovarian patients based on platinum chemotherapy was analyzed using online databases. RNA interference of RIF1 was carried out in OVCAR3 and A2780 cell lines, to determine the effect of lacking RIF1 expression on cellular responses to cisplatin by using MTS assay. The nucleotide excision repair (NER) capacity of these cells was assessed by using host-cell reactivation and UV sensitivity assay. Western Blot analysis was carried out to determine the effect of RIF1 on the proteins of NER and apoptosis signaling pathway by using RIF1 knockdown cells. BALB/c nude mice model was used for detection of response to cisplatin in vivo. Results: RIF1 expression was significantly associated with the response of ovarian patients to platinum-based chemotherapy (P< 0.01). In cohorts from online databases, high expression of RIF1 was associated with higher mortality of EOC patients based on platinum chemotherapy (P < 0.01). RIF1 knockdown increased sensitivity to cisplatin in EOC in vitro and in vivo. Deletion of RIF1 impaired the NER activity by inhibiting the NER proteins in ovarian cancer cells. Besides, knockdown of RIF1 enhanced cisplatin-induced apoptosis. Conclusions: RIF1 plays an important role in regulating the expression of NER proteins, which in turn contributes to cellular response to cisplatin and EOC patients’ response to platinum-based chemotherapy. RIF1 knockdown also promotes cisplatin-induced apoptosis. RIF1 may serve as a novel biomarker for predicting platinum-based chemosensitivity and the prognosis of EOC patients.
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37

Lu, Chafen, Anlai Wang, Marion Dorsch, Jane Tian, Kumiko Nagashima, Anthony J. Coyle, Bruce Jaffee, Timothy D. Ocain, and Yajun Xu. "Participation of Rip2 in Lipopolysaccharide Signaling Is Independent of Its Kinase Activity." Journal of Biological Chemistry 280, no. 16 (February 3, 2005): 16278–83. http://dx.doi.org/10.1074/jbc.m410114200.

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Rip2 (Rick, Cardiak, CCK2, and CARD3) is a serine/threonine kinase containing a caspase recruitment domain (CARD) at the C terminus. Previous reports have shown that Rip2 is involved in multiple receptor signaling pathways that are important for innate and adaptive immune responses. However, it is not known whether Rip2 kinase activity is required for its function. Here we confirm that Rip2 participates in lipopolysaccharide (LPS)/Toll-like receptor (TLR4) signaling and demonstrate that its kinase activity is not required. Upon LPS stimulation, Rip2 was transiently recruited to the TLR4 receptor complex and associated with key TLR signaling mediators IRAK1 and TRAF6. Furthermore, Rip2 kinase activity was induced by LPS treatment. These data indicate that Rip2 is directly involved in the LPS/TLR4 signaling. Whereas macrophages from Rip2-deficient mice showed impaired NF-κB and p38 mitogen-activated protein kinase activation and reduced cytokine production in response to LPS stimulation, LPS signaling was intact in macrophages from mice that express Rip2 kinase-dead mutant. These results demonstrate that Rip2-mediated LPS signaling is independent of its kinase activity. Our findings strongly suggest that Rip2 functions as an adaptor molecule in transducing signals from immune receptors.
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38

Ojok, Tonny, John BK Duot, Majorine Namaganda, Nasra Sadiki, and Michael Msabi. "Analogue Sandbox Scaled Modelling of Oblique and Orthogonal Extension Rifting in Rukwa Rift Basin, Tanzania." Tanzania Journal of Science 47, no. 5 (December 1, 2021): 1660–74. http://dx.doi.org/10.4314/tjs.v47i5.15.

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Fault evolution in oblique and orthogonal rift systems in the brittle upper crust of the Rukwa rift basin was simulated using scaled sandbox modelling by varying the angle between the rift axis and the extension direction, α, through 45° and 90°, over a 10 cm displacement. The 45° oblique model exhibits a half-graben architecture bounded by a planar fault, intra-rift faults and a conjugate fault in some vertical sections. The map view of the model’s basin trends in the NW-SE direction, and is comparable with the Rukwa rift basin orientation. The 90° oblique model forms a basin structure which is orthogonal to the extension direction of the model in aerial photos. Its linear fault remains orthogonal to the extension direction, while the flexural side of the model segments into sinuous normal faults. Planar to slightly curved intra-rift faults are observed in vertical sections. The half-grabens have similar geometries in vertical sections for both models, while intra-rift faults elongate in vertical sections. The results of the oblique model are similar to natural examples of rift fault systems like the Rukwa rift. The fault geometries of the sandbox models can serve as examples for recognizing fault styles in oblique rift systems. Keywords: Analogue Sandbox modelling, Oblique rifting, Orthogonal rifting, Tanganyika-Rukwa-Malawi Rift Segment, Rukwa Rift Basin
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39

Zwaan, Frank, and Guido Schreurs. "How oblique extension and structural inheritance influence rift segment interaction: Insights from 4D analog models." Interpretation 5, no. 1 (February 1, 2017): SD119—SD138. http://dx.doi.org/10.1190/int-2016-0063.1.

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Rifting of the continental lithosphere involves the initial formation of distinct rift segments, often along preexisting crustal heterogeneities resulting from preceding tectonic phases. Progressive extension, either orthogonal or oblique, causes these rift segments to interact and connect, ultimately leading to a full-scale rift system. We study continental rift interaction processes with the use of analog models to test the influence of a range of structural inheritance (seed) geometries and various degrees of oblique extension. The inherited geometry involves main seeds, offset in a right-stepping fashion, along which rift segments form as well as the presence or absence of secondary seeds connecting the main seeds. X-ray computer tomography techniques are used to analyze the 3D models through time, and results are compared with natural examples. Our experiments indicate that the extension direction exerts a key influence on rift segment interaction. Rift segments are more likely to connect through discrete fault structures under dextral oblique extension conditions because they generally propagate toward each other. In contrast, sinistral oblique extension commonly does not result in hard linkage because rift segment tend to grow apart. These findings also hold when the system is mirrored: left-stepping rift segments under sinistral and dextral oblique extension conditions, respectively. However, under specific conditions, when the right-stepping rift segments are laterally far apart, sinistral oblique extension can produce hard linkage in the shape of a strike-slip-dominated transfer zone. A secondary structural inheritance between rift segments might influence rift linkage, but only when the extension direction is favorable for activation. Otherwise, propagating rifts will simply align perpendicularly to the extension direction. When secondary structural grains do reactivate, the resulting transfer zone and the strike of internal faults follow their general orientation. However, these structures can be slightly oblique due to the influence of the extension direction. Several of the characteristic structures observed in our models are also present in natural rift settings such as the Rhine-Bresse Transfer Zone, the Rio Grande Rift, and the East African Rift System.
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40

Ren, Gang, Ji Young Kim, and Cynthia M. Smas. "Identification of RIFL, a novel adipocyte-enriched insulin target gene with a role in lipid metabolism." American Journal of Physiology-Endocrinology and Metabolism 303, no. 3 (August 1, 2012): E334—E351. http://dx.doi.org/10.1152/ajpendo.00084.2012.

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To identify new genes that are important in fat metabolism, we utilized the Lexicon-Genentech knockout database of genes encoding transmembrane and secreted factors and whole murine genome transcriptional profiling data that we generated for 3T3-L1 in vitro adipogenesis. Cross-referencing null models evidencing metabolic phenotypes with genes induced in adipogenesis led to identification of a new gene, which we named RIFL (refeeding induced fat and liver). RIFL-null mice have serum triglyceride levels approximately one-third of wild type. RIFL transcript is induced >100-fold during 3T3-L1 adipogenesis and is also increased markedly during adipogenesis of murine and human primary preadipocytes. siRNA-mediated knockdown of RIFL during 3T3-L1 adipogenesis results in an ∼35% decrease in adipocyte triglyceride content. Murine RIFL transcript is highly enriched in white and brown adipose tissue and liver. Fractionation of WAT reveals that RIFL transcript is exclusive to adipocytes with a lack of expression in stromal-vascular cells. Nutritional and hormonal studies are consistent with a prolipogenic function for RIFL. There is evidence of an approximately eightfold increase in RIFL transcript level in WAT in ob/ob mice compared with wild-type mice. RIFL transcript level in WAT and liver is increased ∼80- and 12-fold, respectively, following refeeding of fasted mice. Treatment of 3T3-L1 adipocytes with insulin increases RIFL transcript ≤35-fold, whereas agents that stimulate lipolysis downregulate RIFL. Interestingly, the 198-amino acid RIFL protein is predicted to be secreted and shows ∼30% overall conservation with the NH2-terminal half of angiopoietin-like 3, a liver-secreted protein that impacts lipid metabolism. In summary, our data suggest that RIFL is an important new regulator of lipid metabolism.
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Desai, Biva, Pamela Haile, Linda Casillas, Peter Gough, John Bertin, and Bart Votta. "Use of novel small molecule inhibitors to investigate the role of endogenous RIP2 kinase activity in modulating NOD2/RIP2-dependent cytokine signaling (172.4)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 172.4. http://dx.doi.org/10.4049/jimmunol.188.supp.172.4.

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Abstract RIP2 is a Ser/Thr protein kinase, which undergoes autophosphorylation and activates NF-κB and MAPKs following stimulation of the upstream NOD1/NOD2 receptors resulting in proinflammatory cytokine production. Previous studies using transient overexpression systems have suggested that RIP2 kinase activity mediates NOD1/2-dependent signaling by regulating cellular RIP2 protein levels. To interrogate whether this is also the case for endogenous RIP2 kinase, we used novel, potent and highly-selective small-molecule RIP2 kinase inhibitors to study MDP-stimulated signaling in both primary human monocytes and human colonic epithelial (HCT116) cells. We demonstrated that inhibition of RIP2 kinase activity blocks proinflammatory cytokine production in monocytes in the absence of detectable changes in total RIP2 protein levels. Using TNFα-primed HCT116 cells, we confirmed these observations and demonstrated a direct correlation between the inhibition of endogenous RIP2 kinase activity (measured as a decrease in pS176-RIPK2 levels) and a reduction in proinflammatory cytokine signaling in response to MDP-stimulation. Our data confirm the importance of endogenous RIP2 kinase activity in modulating proinflammatory cytokine release from both human monocytes and intestinal epithelial cells in response to bacterial ligands. Furthermore, our results suggest that RIP2 kinase inhibition may represent a novel therapeutic strategy for the treatment of intestinal inflammation.
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42

Hasselbalch, Hans, Vibe Skov, Lasse Kjær, Morten Kranker Larsen, Trine A. Knudsen, Marko Lucijanić, and Rajko Kusec. "Recombinant Interferon-β in the Treatment of Polycythemia Vera and Related Neoplasms: Rationales and Perspectives." Cancers 14, no. 22 (November 9, 2022): 5495. http://dx.doi.org/10.3390/cancers14225495.

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About 30 years ago, the first clinical trials of the safety and efficacy of recombinant interferon-α2 (rIFN-α2) were performed. Since then, several single-arm studies have shown rIFN-α2 to be a highly potent anticancer agent against several cancer types. Unfortunately, however, a high toxicity profile in early studies with rIFN-α2 -among other reasons likely due to the high dosages being used-disqualified rIFN-α2, which was accordingly replaced with competitive drugs that might at first glance look more attractive to clinicians. Later, pegylated IFN-α2a (Pegasys) and pegylated IFN-α2b (PegIntron) were introduced, which have since been reported to be better tolerated due to reduced toxicity. Today, treatment with rIFN-α2 is virtually outdated in non-hematological cancers, where other immunotherapies—e.g., immune-checkpoint inhibitors—are routinely used in several cancer types and are being intensively investigated in others, either as monotherapy or in combination with immunomodulatory agents, although only rarely in combination with rIFN-α2. Within the hematological malignancies, rIFN-α2 has been used off-label for decades in patients with Philadelphia-negative chronic myeloproliferative neoplasms (MPNs)—i.e., essential thrombocythemia, polycythemia vera, and myelofibrosis—and in recent years rIFN-α2 has been revived with the marketing of ropeginterferon-α2b (Besremi) for the treatment of polycythemia vera patients. Additionally, rIFN-α2 has been revived for the treatment of chronic myelogenous leukemia in combination with tyrosine kinase inhibitors. Another rIFN formulation-recombinant interferon-β (rIFN-β)—has been used for decades in the treatment of multiple sclerosis but has never been studied as a potential agent to be used in patients with MPNs, although several studies and reviews have repeatedly described rIFN-β as an effective anticancer agent as well. In this paper, we describe the rationales and perspectives for launching studies on the safety and efficacy of rIFN-β in patients with MPNs.
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43

Stephens, Jacqueline M. "RIFL aims to be a new player in lipid metabolism." American Journal of Physiology-Endocrinology and Metabolism 303, no. 3 (August 1, 2012): E332—E333. http://dx.doi.org/10.1152/ajpendo.00169.2012.

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RIFL (refeeding induced in fat and liver) is highly expressed in brown and white fat as well as in liver. In white adipose tissue and liver, RIFL expression is induced by refeeding and is also elevated in ob/ob mice. The function of RIFL is unknown, and there is some evidence to suggest it may be secreted. RIFL expression is induced during adipogenesis in rodent and human model systems, and cellular knockdown and mouse knockout studies demonstrate that RIFL expression correlates with lipid levels. Overall, these studies indicate that RIFL is a new important player in lipid metabolism.
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44

King, E. C. "Observations of a rift in the Ronne Ice Shelf, Antarctica." Journal of Glaciology 40, no. 134 (1994): 187–89. http://dx.doi.org/10.1017/s0022143000003968.

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Abstract During seismic profiling on the northwest Ronne Ice Shelf Antarctica, a rift in the ice shelf was encountered. The rift trends southeast to northwest and is located approximately 30 km inland from the present-day ice front The rift is 340 m wide and the surface elevation of the ice shelf drops by 14.65 m over the axis of the rift. The rift has an asymmetrical base with a near-vertical ice-water interface on its northeast flank and a more gently dipping ice-water interface forming its southeastern flank. The ice shelf thins from a thickness of 350 m away from the rift to a thickness of 225 m at the rift axis. The rift is the probable location of a future major calving event on this section of the Ronne Ice Shelf, an event which would release an iceberg of up to 30 km by 180 km into the Weddell Sea.
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45

King, E. C. "Observations of a rift in the Ronne Ice Shelf, Antarctica." Journal of Glaciology 40, no. 134 (1994): 187–89. http://dx.doi.org/10.3189/s0022143000003968.

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AbstractDuring seismic profiling on the northwest Ronne Ice Shelf Antarctica, a rift in the ice shelf was encountered. The rift trends southeast to northwest and is located approximately 30 km inland from the present-day ice front The rift is 340 m wide and the surface elevation of the ice shelf drops by 14.65 m over the axis of the rift. The rift has an asymmetrical base with a near-vertical ice-water interface on its northeast flank and a more gently dipping ice-water interface forming its southeastern flank. The ice shelf thins from a thickness of 350 m away from the rift to a thickness of 225 m at the rift axis. The rift is the probable location of a future major calving event on this section of the Ronne Ice Shelf, an event which would release an iceberg of up to 30 km by 180 km into the Weddell Sea.
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46

Balter, M. "PALEONTOLOGY: Paleontological Rift in the Rift Valley." Science 292, no. 5515 (April 13, 2001): 198–201. http://dx.doi.org/10.1126/science.292.5515.198.

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47

Ernstoff, M. S., S. Nair, R. R. Bahnson, L. M. Miketic, B. Banner, W. Gooding, R. Day, T. Whiteside, T. Hakala, and J. M. Kirkwood. "A phase IA trial of sequential administration recombinant DNA-produced interferons: combination recombinant interferon gamma and recombinant interferon alfa in patients with metastatic renal cell carcinoma." Journal of Clinical Oncology 8, no. 10 (October 1990): 1637–49. http://dx.doi.org/10.1200/jco.1990.8.10.1637.

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This study investigated the effects of sequentially administered recombinant interferon gamma (rIFN gamma) and recombinant interferon alfa (rIFN alpha) in 36 patients with metastatic renal cell carcinoma (RCC). rIFN alpha was subcutaneously administered daily for 70 days at dosages that varied (2.5, 5, 10, and 20 x 10(6) U/m2) across four cohorts of patients. Within each cohort of patients receiving a given dose of rIFN alpha, three subsets of patients received either 30, 300, or 1,000 micrograms/m2 rIFN gamma. rIFN gamma was administered intravenously for 5 days every third week, 6 hours prior to administration of rIFN alpha. Dose-limiting toxicity (DLT) included constitutional symptoms, leukopenia, nephrotic syndrome with acute renal failure, hypotension associated with death, and congestive heart failure. DLT was related more often to the rIFN alpha dose level than to rIFN gamma dose level. Maximum-tolerated dose (MTD) was 10 x 10(6) U/m2 rIFN alpha and 1,000 micrograms/m2 rIFN gamma. Six patients failed to complete a minimum of 21 days of therapy due to toxicity or rapid progression of disease. Clinical responses were seen in eight of 30 assessable patients. Two patients experienced complete remission and have remained in complete remission 20+ and 22+ months. An additional six patients have shown partial responses for 4 to 18+ months. One patient in partial remission continues to show slow regression of pulmonary and liver lesions off therapy with rIFNs. Clinical responses have remained durable for patients with complete remissions and patients with partial remissions. The results of this study suggest that toxicities associated with combination rIFN therapy can be reduced by administering these agents sequentially as opposed to simultaneously.
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Sohrah, Sohrah. "MEDIA SOSIAL DAN DAMPAKNYA TERHADAP PERCERAIAN." Al-Risalah Jurnal Ilmu Syariah dan Hukum 19, no. 2 (March 4, 2020): 286. http://dx.doi.org/10.24252/al-risalah.v19i2.12839.

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Lately, the use of social media is increasingly prevalent after experiencing the development of its characteristics and uniqueness. The convenience offered by social media for its users also influences one's lifestyle. The results of this study conclude that the presence of social media contributes to the rift of households for some married couples which is marked by an increase in divorce rates triggered by disputes and quarrels for married couples. The results showed that there were several cases as proof of the role of social media as one of the causes of divorce due to the husband or wife so easily covert infidelity because of the use of social media. It is undeniable that the presence of social media as a communication tool has a very important positive side in this modern era to facilitate various interests and needs of human life, but on the other hand there are also negative sides that can affect the morale of its users. One impact that has been rife lately is the high number of divorce cases as reported by the Makassar Religious Court office from 2015-2018. In 2015 there were 493 cases, while in 2018 there were 628 cases. These cases were caused due to ongoing disputes.
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Kanoh, Yutaka, Masaru Ueno, Motoshi Hayano, Satomi Kudo, and Hisao Masai. "Aberrant association of chromatin with nuclear periphery induced by Rif1 leads to mitotic defect." Life Science Alliance 6, no. 4 (February 7, 2023): e202201603. http://dx.doi.org/10.26508/lsa.202201603.

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The architecture and nuclear location of chromosomes affect chromatin events. Rif1, a crucial regulator of replication timing, recognizes G-quadruplex and inhibits origin firing over the 50–100-kb segment in fission yeast,Schizosaccharomyces pombe, leading us to postulate that Rif1 may generate chromatin higher order structures inhibitory for initiation. However, the effects of Rif1 on chromatin localization in nuclei have not been known. We show here that Rif1 overexpression causes growth inhibition and eventually, cell death in fission yeast. Chromatin-binding activity of Rif1, but not recruitment of phosphatase PP1, is required for growth inhibition. Overexpression of a PP1-binding site mutant of Rif1 does not delay the S-phase, but still causes cell death, indicating that cell death is caused not by S-phase problems but by issues in other phases of the cell cycle, most likely the M-phase. Indeed, Rif1 overexpression generates cells with unequally segregated chromosomes. Rif1 overexpression relocates chromatin near nuclear periphery in a manner dependent on its chromatin-binding ability, and this correlates with growth inhibition. Thus, coordinated progression of S- and M-phases may require regulated Rif1-mediated chromatin association with the nuclear periphery.
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50

REY, J. "Extensional Jurassic tectonism of an eastern Subbetic section (southern Spain)." Geological Magazine 135, no. 5 (September 1998): 685–97. http://dx.doi.org/10.1017/s0016756898001277.

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Abstract:
The subsidence and stratigraphic evolution in an eastern section of the Subbetic Zone (External Zones of the Betic Cordilleras, Spain) during Jurassic and early Cretaceous times have been examined. The sediments have been deposited on a passive margin undergoing rifting. The data indicate that the activity was complex and spasmodic, with two distinct rift and post-rift phases. The beginning of the first syn-rift and post-rift phases are recorded by two regional sedimentary breaks, in the Late Carixian and in the Bathonian, respectively. The second rift and post-rift phases began, with less clearly defined limits, during the Oxfordian and at the Jurassic–Cretaceous boundary, respectively.
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