Статті в журналах: "Sugp1"

1

Liu, Zhaoqi, Jian Zhang, Yiwei Sun, Tomin E. Perea-Chamblee, James L. Manley, and Raul Rabadan. "Pan-cancer analysis identifies mutations in SUGP1 that recapitulate mutant SF3B1 splicing dysregulation." Proceedings of the National Academy of Sciences 117, no. 19 (April 24, 2020): 10305–12. http://dx.doi.org/10.1073/pnas.1922622117.

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The gene encoding the core spliceosomal protein SF3B1 is the most frequently mutated gene encoding a splicing factor in a variety of hematologic malignancies and solid tumors. SF3B1 mutations induce use of cryptic 3′ splice sites (3′ss), and these splicing errors contribute to tumorigenesis. However, it is unclear how widespread this type of cryptic 3′ss usage is in cancers and what is the full spectrum of genetic mutations that cause such missplicing. To address this issue, we performed an unbiased pan-cancer analysis to identify genetic alterations that lead to the same aberrant splicing as observed with SF3B1 mutations. This analysis identified multiple mutations in another spliceosomal gene, SUGP1, that correlated with significant usage of cryptic 3′ss known to be utilized in mutant SF3B1 expressing cells. Remarkably, this is consistent with recent biochemical studies that identified a defective interaction between mutant SF3B1 and SUGP1 as the molecular defect responsible for cryptic 3′ss usage. Experimental validation revealed that five different SUGP1 mutations completely or partially recapitulated the 3′ss defects. Our analysis suggests that SUGP1 mutations in cancers can induce missplicing identical or similar to that observed in mutant SF3B1 cancers.

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2

Alsafadi, Samar, Stephane Dayot, Malcy Tarin, Alexandre Houy, Dorine Bellanger, Michele Cornella, Michel Wassef, et al. "Genetic alterations of SUGP1 mimic mutant-SF3B1 splice pattern in lung adenocarcinoma and other cancers." Oncogene 40, no. 1 (October 14, 2020): 85–96. http://dx.doi.org/10.1038/s41388-020-01507-5.

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AbstractGenes involved in 3′-splice site recognition during mRNA splicing constitute an emerging class of oncogenes. SF3B1 is the most frequently mutated splicing factor in cancer, and SF3B1 mutants corrupt branchpoint recognition leading to usage of cryptic 3′-splice sites and subsequent aberrant junctions. For a comprehensive determination of alterations leading to this splicing pattern, we performed a pan-TCGA screening for SF3B1-specific aberrant acceptor usage. While the most of aberrant 3′-splice patterns were explained by SF3B1 mutations, we also detected nine SF3B1 wild-type tumors (including five lung adenocarcinomas). Genomic profile analysis of these tumors identified somatic mutations combined with loss-of-heterozygosity in the splicing factor SUGP1 in five of these cases. Modeling of SUGP1 loss and mutations in cell lines showed that both alterations induced mutant-SF3B1-like aberrant splicing. Our study provides definitive evidence that genetic alterations of SUGP1 genocopy SF3B1 mutations in lung adenocarcinoma and other cancers.

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3

Benbarche, Salima, Jose Maria Bello Pineda, Laura Baquero Galvis, Bo Liu, Jeetayu Biswas, Eric Wang, K. Ashley Lyttle, et al. "Synthetic Introns Identify the Novel RNA Splicing Factor GPATCH8 As Required for Mis-Splicing Induced By SF3B1 Mutations." Blood 142, Supplement 1 (November 28, 2023): 3. http://dx.doi.org/10.1182/blood-2023-179848.

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Disclosures Mutations in the core RNA splicing factor SF3B1 are common across MDS, CLL, and clonal hematopoiesis. Prior studies have elucidated that mutations in SF3B1 result in neomorphic widespread changes in splicing due to usage of aberrant intronic branchpoint nucleotides. However, the molecular basis by which mutant SF3B1 induces mis-splicing is not established and therapeutic means to correct mis-splicing due to mutant SF3B1 do not exist. Recently, the aberrant gain-of-function splicing activity of mutant SF3B1 was harnessed to regulate expression of proteins in a mutant selective manner using synthetic version of endogenous mRNA sequences uniquely recognized by mutant SF3B1. Here, we utilized this technology to engineer a synthetic intron derived from MAP3K7 that interrupts the coding sequence of the fluorescent protein mEmerald such that mutant SF3B1 produces lower mEmerald expression than SF3B1 wild-type (WT) cells (Fig.A). This fluorescent splicing reporter was then used to perform positive enrichment whole genome CRISPR screens to identify genes whose deletion corrects SF3B1 mutant aberrant splicing. GPATCH8 was the single most robust hit. GPATCH8 knockout strongly corrected mis-splicing of both synthetic and endogenous MAP3K7 introns (Fig.A). A previously unexplored protein, GPATCH8 has domains characteristic of RNA splicing factors including a G-patch motif, thought to be important in activating RNA helicases. Interestingly, recent work suggests that mutations in SF3B1 result in mis-splicing by disrupting physical interaction of SF3B1 to the RNA helicase DHX15 via the G-patch domain containing protein SUGP1. We therefore compared SUGP1 to GPATCH8 activity, evaluating first their transcriptome-wide binding sites using TRIBE-seq. We found that both proteins predominantly target intronic sequences over other genomic regions suggesting roles in splicing. RNA-seq of SF3B1 mutant and WT cells with or without GPATCH8/SUGP1 deletion revealed that ~33% of SF3B1 mutant splicing alterations are corrected by GPATCH8 deletion, while ~60% of SF3B1 mutant splicing alterations are recapitulated upon SUGP1 deletion. GPATCH8 regulated splicing events have stronger branchpoints indicating a potential role for GPATCH8 in 3' splice site recognition. To further understand the connection between GPATCH8 and mutant SF3B1, we performed mass spectrometry studies of immunoprecipitated endogenous GPATCH8 in SF3B1 WT and mutant knockin cells. This revealed strong interaction between GPATCH8 and DHX15. GPATCH8 interacts with DHX15 at the same sites previously shown to be occupied by SUGP1 in crystal structures of the SUGP1/DHX15 interaction. These data and further biochemical studies elucidated that GPATCH8 competes with SUGP1 for interaction to DHX15. As such, deletion of GPATCH8 corrects SF3B1 mutant mis-splicing by enhancing the interaction of SUGP1 and DHX15 to the mutant SF3b complex. Given that GPATCH8 is required for a large proportion of the splicing alterations induced by mutant SF3B1, we next evaluated the phenotypic effect of correcting SF3B1 mutant mis-splicing. We first tested the impact of anti-Gpatch8 shRNAs in bone marrow from WT mice as well as animals with conditional knockin of Sf3b1 K700E, K666N, or R625H mutations. While each Sf3b1 mutation results in impaired colony formation of hematopoietic precursors in methylcellulose assays, silencing of Gpatch8 rescued colony formation from hematopoietic precursors of each of the different Sf3b1 mutant mice and was tolerated by normal hematopoietic precursors (Fig.B). Moreover, while CRISPR base-edited knockin of the SF3B1 K700E mutation in adult CD34 + cells impaired erythroid development, this erythroid differentiation defect was rescued by GPATCH8 deletion in the same cells (Fig.B). These data identify GPATCH8 as a novel RNA splicing factor involved in quality control of RNA branchpoint selection whose expression is required for mis-splicing by the different mutant forms of SF3B1. GPATCH8 antagonizes the activity of SUGP1 by competing for interaction with DHX15. These findings suggest that disrupting GPATCH8/DHX15 interaction could have important therapeutic benefit for the multitude of SF3B1 mutant hematopoietic diseases. This study also demonstrates the power of synthetic intronic splicing assays for discovery of trans factors and druggable proteins required by leukemia-associated mutant RNA splicing factors. Abdel-Wahab: AbbVie, Inc.: Consultancy, Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Loxo/Lilly: Consultancy; Nurix Therapeutics: Research Funding; Minovia Therapeutics: Research Funding; Amphista Therapeutics: Consultancy; AstraZeneca: Consultancy; Harmonic Discovery: Current holder of stock options in a privately-held company. Figure 1

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4

Zhang, Jian, Abdullah M. Ali, Yen K. Lieu, Zhaoqi Liu, Jianchao Gao, Raul Rabadan, Azra Raza, Siddhartha Mukherjee, and James L. Manley. "Disease-Causing Mutations in SF3B1 Alter Splicing by Disrupting Interaction with SUGP1." Molecular Cell 76, no. 1 (October 2019): 82–95. http://dx.doi.org/10.1016/j.molcel.2019.07.017.

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5

Feng, Qing, Keegan Krick, Jennifer Chu, and Christopher B. Burge. "Splicing quality control mediated by DHX15 and its G-patch activator SUGP1." Cell Reports 42, no. 10 (October 2023): 113223. http://dx.doi.org/10.1016/j.celrep.2023.113223.

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6

Deng, Guo-Xiong, Rui-Xing Yin, Yao-Zong Guan, Chun-Xiao Liu, Peng-Fei Zheng, Bi-Liu Wei, Jin-Zhen Wu, and Liu Miao. "Association of the NCAN-TM6SF2-CILP2-PBX4-SUGP1-MAU2 SNPs and gene-gene and gene-environment interactions with serum lipid levels." Aging 12, no. 12 (June 22, 2020): 11893–913. http://dx.doi.org/10.18632/aging.103361.

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7

Liu, Xinglin, Zengchun Wang, Yanping Jiang, Libo Huang, Xuejun Yuan, Yang Li, Ning Jiao, Weiren Yang, and Shuzhen Jiang. "Quantitative Proteomic Analysis of Zearalenone Exposure on Uterine Development in Weaned Gilts." Toxins 14, no. 10 (October 9, 2022): 692. http://dx.doi.org/10.3390/toxins14100692.

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The aim of this study was to explore the effect of zearalenone (ZEA) exposure on uterine development in weaned gilts by quantitative proteome analysis with tandem mass spectrometry tags (TMT). A total of 16 healthy weaned gilts were randomly divided into control (basal diet) and ZEA3.0 treatments groups (basal diet supplemented with 3.0 mg/kg ZEA). Results showed that vulva size and uterine development index were increased (p < 0.05), whereas serum follicle stimulation hormone, luteinizing hormone and gonadotropin-releasing hormone were decreased in gilts fed the ZEA diet (p < 0.05). ZEA, α-zearalenol (α-ZOL) and β-zearalenol (β-ZOL) were detected in the uteri of gilts fed a 3.0 mg/kg ZEA diet (p < 0.05). The relative protein expression levels of creatine kinase M-type (CKM), atriopeptidase (MME) and myeloperoxidase (MPO) were up-regulated (p < 0.05), whereas aldehyde dehydrogenase 1 family member (ALDH1A2), secretogranin-1 (CHGB) and SURP and G-patch domain containing 1 (SUGP1) were down-regulated (p < 0.05) in the ZEA3.0 group by western blot, which indicated that the proteomics data were dependable. In addition, the functions of differentially expressed proteins (DEPs) mainly involved the cellular process, biological regulation and metabolic process in the biological process category. Some important signaling pathways were changed in the ZEA3.0 group, such as extracellular matrix (ECM)-receptor interaction, focal adhesion and the phosphoinositide 3-kinase–protein kinase B (PI3K-AKT) signaling pathway (p < 0.01). This study sheds new light on the molecular mechanism of ZEA in the uterine development of gilts.

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8

Arslanow, A., C. S. Stokes, F. Grünhage, F. Lammert, and M. Krawczyk. "P1048 : Effects of prosteatogenic TM6SF2 and NCAN/SUGP1 variants on hepatic steatosis and non-invasive markers of liver injury in patients with chronic liver diseases." Journal of Hepatology 62 (April 2015): S741—S742. http://dx.doi.org/10.1016/s0168-8278(15)31246-0.

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9

Ghodsian, Nooshin, Erik Abner, Émilie Gobeil, Nele Taba, Alexis St Amand, Nicolas Perrot, Christian Couture, et al. "Electronic Health Record-Based Genome-Wide Meta-Analysis Identifies New Susceptibility Loci for Non-Alcoholic Fatty Liver Disease." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A501. http://dx.doi.org/10.1210/jendso/bvab048.1024.

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Abstract Background: Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of liver disease. Observational studies documented associations of NAFLD with several chronic and infectious diseases but whether these associations underlie causal effects is unknown. The molecular mechanisms and genetic architecture of NAFLD are poorly understood. Our objectives were to identify genetic loci associated with NAFLD and determine whether the presence of NAFLD was causally associated with human diseases. Methods: We created a NAFLD genetic instrument through the identification of independent single-nucleotide polymorphisms (SNPs) associated with NAFLD in a meta-analysis of genome-wide association study (GWAS) (6715 cases and 682,748 controls). Using inverse-variance weighted Mendelian Randomization (MR), we investigated the impact of NAFLD on human disease-related phenotypes in the UK Biobank and FinnGen cohorts as well as in the COVID-19 host genetics initiative. Results: We first performed a GWAS meta-analysis of four cohorts and found variants significantly associated with NAFLD (p<5.0E-8) at six genetic loci (MTARC1, GCKR, TRIB1, LMO3, SUGP1 [TM6SF2] and PNPLA3). Using a risk factor informed Bayesian approach (bGWAS), we identify variants at three additional loci (LPL, FTO, and APOE). To determine if the association between NAFLD and human diseases shows evidence of causality, we performed MR across the human disease-related phenome (>800 diseases) using a genetic instrument for NAFLD. Results of these analyses suggest that NAFLD was not causally associated with diseases outside the spectrum of liver diseases. We also found no causal association between genetically predicted NAFLD and COVID-19-related outcomes. Conclusions: This study identified several new genetic loci associated with NAFLD. NAFLD was not causally associated with diseases outside those of the spectrum of liver diseases. This finding suggests that the resolution of NAFLD might not prevent other diseases previously associated with NAFLD.

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10

Patterton, D., and J. Hapgood. "suGF1 binds in the major groove of its oligo(dG).oligo(dC) recognition sequence and is excluded by a positioned nucleosome core." Molecular and Cellular Biology 14, no. 2 (February 1994): 1410–18. http://dx.doi.org/10.1128/mcb.14.2.1410-1418.1994.

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We have elsewhere reported the purification of a poly(dG).poly(dC)-binding nuclear protein (suGF1) from sea urchin embryos (J. Hapgood and D. Patterton, Mol. Cell. Biol. 14:this issue, 1994). We proposed that suGF1 may be a member of a family of G-string factors involved in developmental gene regulation, possibly via alterations in chromatin structure. In this article, we characterize the binding of purified suGF1 to 11 contiguous Gs in the H1-H4 intergenic region of a sea urchin early histone gene battery in vitro. It is shown that suGF1-DNA binding is dependent on ionic strength and requires divalent cations. Purified suGF1 forms discrete protein-DNA multimers, consistent with suGF1-suGF1 interactions. In a model for the suGF1-DNA complex derived from our footprinting and methylation interference data, suGF1 contacts the Gs in the major groove as well as one of the bordering phosphate backbones. The data are consistent with the direction of curvature of the DNA in the suGF1-DNA complex being the same as that preferred by the free DNA and exhibited by the DNA when bent around a positioned nucleosome core in vitro. However, on the basis of steric considerations, the binding of suGF1 and that of the histone octamer are predicted to be mutually exclusive. We show that suGF1 is indeed unable to bind to the G string when occupied by a histone octamer located in the major in vitro positioning frame in the H1-H4 intergenic region.

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11

Patterton, D., and J. Hapgood. "suGF1 binds in the major groove of its oligo(dG).oligo(dC) recognition sequence and is excluded by a positioned nucleosome core." Molecular and Cellular Biology 14, no. 2 (February 1994): 1410–18. http://dx.doi.org/10.1128/mcb.14.2.1410.

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We have elsewhere reported the purification of a poly(dG).poly(dC)-binding nuclear protein (suGF1) from sea urchin embryos (J. Hapgood and D. Patterton, Mol. Cell. Biol. 14:this issue, 1994). We proposed that suGF1 may be a member of a family of G-string factors involved in developmental gene regulation, possibly via alterations in chromatin structure. In this article, we characterize the binding of purified suGF1 to 11 contiguous Gs in the H1-H4 intergenic region of a sea urchin early histone gene battery in vitro. It is shown that suGF1-DNA binding is dependent on ionic strength and requires divalent cations. Purified suGF1 forms discrete protein-DNA multimers, consistent with suGF1-suGF1 interactions. In a model for the suGF1-DNA complex derived from our footprinting and methylation interference data, suGF1 contacts the Gs in the major groove as well as one of the bordering phosphate backbones. The data are consistent with the direction of curvature of the DNA in the suGF1-DNA complex being the same as that preferred by the free DNA and exhibited by the DNA when bent around a positioned nucleosome core in vitro. However, on the basis of steric considerations, the binding of suGF1 and that of the histone octamer are predicted to be mutually exclusive. We show that suGF1 is indeed unable to bind to the G string when occupied by a histone octamer located in the major in vitro positioning frame in the H1-H4 intergenic region.

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12

Xu, Q., R. A. Singer, and G. C. Johnston. "Sug1 modulates yeast transcription activation by Cdc68." Molecular and Cellular Biology 15, no. 11 (November 1995): 6025–35. http://dx.doi.org/10.1128/mcb.15.11.6025.

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The Cdc68 protein is required for the transcription of a variety of genes in the yeast Saccharomyces cerevisiae. In a search for proteins involved in the activity of the Cdc68 protein, we identified four suppressor genes in which mutations reverse the temperature sensitivity caused by the cdc68-1 allele. We report here the molecular characterization of mutations in one suppressor gene, the previously identified SUG1 gene. The Sug1 protein has been implicated in both transcriptional regulation and proteolysis. sug1 suppressor alleles reversed most aspects of the cdc68-1 mutant phenotype but did not suppress the lethality of a cdc68 null allele, indicating that sug1 suppression is by restoration of Cdc68 activity. Our evidence suggests that suppression by sug1 is unlikely to be due to increased stability of mutant Cdc68 protein, despite the observation that Sug1 affected proteolysis of mutant Cdc68. We report here that attenuated Sug1 activity strengthens mutant Cdc68 activity, whereas increased Sug1 activity further inhibits enfeebled Cdc68 activity, suggesting that Sug1 antagonizes the activator function of Cdc68 for transcription. Consistent with this hypothesis, we find that Sug1 represses transcription in vivo.

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13

Mukhopadhyay, Debaditya, Ferhan Ayaydin, Nagamalleswari Kolli, Shyh-Han Tan, Tadashi Anan, Ai Kametaka, Yoshiaki Azuma, Keith D. Wilkinson, and Mary Dasso. "SUSP1 antagonizes formation of highly SUMO2/3-conjugated species." Journal of Cell Biology 174, no. 7 (September 21, 2006): 939–49. http://dx.doi.org/10.1083/jcb.200510103.

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Small ubiquitin-related modifier (SUMO) processing and deconjugation are mediated by sentrin-specific proteases/ubiquitin-like proteases (SENP/Ulps). We show that SUMO-specific protease 1 (SUSP1), a mammalian SENP/Ulp, localizes within the nucleoplasm. SUSP1 depletion within cell lines expressing enhanced green fluorescent protein (EGFP) fusions to individual SUMO paralogues caused redistribution of EGFP-SUMO2 and -SUMO3, particularly into promyelocytic leukemia (PML) bodies. Further analysis suggested that this change resulted primarily from a deficit of SUMO2/3-deconjugation activity. Under these circumstances, PML bodies became enlarged and increased in number. We did not observe a comparable redistribution of EGFP-SUMO1. We have investigated the specificity of SUSP1 using vinyl sulfone inhibitors and model substrates. We found that SUSP1 has a strong paralogue bias toward SUMO2/3 and that it acts preferentially on substrates containing three or more SUMO2/3 moieties. Together, our findings argue that SUSP1 may play a specialized role in dismantling highly conjugated SUMO2 and -3 species that is critical for PML body maintenance.

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14

Hapgood, J., and D. Patterton. "Purification of an oligo(dG).oligo(dC)-binding sea urchin nuclear protein, suGF1: a family of G-string factors involved in gene regulation during development." Molecular and Cellular Biology 14, no. 2 (February 1994): 1402–9. http://dx.doi.org/10.1128/mcb.14.2.1402-1409.1994.

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Contiguous deoxyguanosine residues (G strings) have been implicated in regulation of gene expression in several organisms via the binding of G-string factors. Regulation of expression of the chicken adult beta-globin gene may involve the interplay between binding of an erythrocyte-specific G-string factor, BGP1, and the stability of a positioned nucleosome (C. D. Lewis, S. P. Clark, G. Felsenfeld, and H. Gould, Genes Dev. 2:863-873, 1988). We have purified a 59.5-kDa nuclear protein (suGF1) from sea urchin embryos by DNA affinity chromatography. suGF1 has high binding affinity and specificity for oligo(dG).oligo(dC). The identity of the purified protein was confirmed by renaturation of sequence-specific DNA-binding activity from a sodium dodecyl sulfate-polyacrylamide gel slice and by Southwestern (DNA-protein) blotting. suGF1 binds in vitro to a G11 string present in the H1-H4 intergenic region of a sea urchin early histone gene battery. This suGF1 DNA recognition site occurs within a homopurine-homopyrimidine stretch previously shown to be incorporated into a positioned nucleosome core in vitro. DNase I footprinting shows that suGF1 protects the same base pairs on the promoter of the chicken beta A-globin gene as does BGP1. We show that a G-string cis-regulatory element of a sea urchin cell lineage-specific gene LpS1 (M. Xiang, S.-Y. Lu, M. Musso, G. Karsenty, and W. H. Klein, Development 113:1345-1355, 1991) also represents a high-affinity recognition site for suGF1. suGF1 may be a member of a family of G-string factors involved in the regulation of expression of unrelated genes during development of a number of different organisms.

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15

Hapgood, J., and D. Patterton. "Purification of an oligo(dG).oligo(dC)-binding sea urchin nuclear protein, suGF1: a family of G-string factors involved in gene regulation during development." Molecular and Cellular Biology 14, no. 2 (February 1994): 1402–9. http://dx.doi.org/10.1128/mcb.14.2.1402.

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Contiguous deoxyguanosine residues (G strings) have been implicated in regulation of gene expression in several organisms via the binding of G-string factors. Regulation of expression of the chicken adult beta-globin gene may involve the interplay between binding of an erythrocyte-specific G-string factor, BGP1, and the stability of a positioned nucleosome (C. D. Lewis, S. P. Clark, G. Felsenfeld, and H. Gould, Genes Dev. 2:863-873, 1988). We have purified a 59.5-kDa nuclear protein (suGF1) from sea urchin embryos by DNA affinity chromatography. suGF1 has high binding affinity and specificity for oligo(dG).oligo(dC). The identity of the purified protein was confirmed by renaturation of sequence-specific DNA-binding activity from a sodium dodecyl sulfate-polyacrylamide gel slice and by Southwestern (DNA-protein) blotting. suGF1 binds in vitro to a G11 string present in the H1-H4 intergenic region of a sea urchin early histone gene battery. This suGF1 DNA recognition site occurs within a homopurine-homopyrimidine stretch previously shown to be incorporated into a positioned nucleosome core in vitro. DNase I footprinting shows that suGF1 protects the same base pairs on the promoter of the chicken beta A-globin gene as does BGP1. We show that a G-string cis-regulatory element of a sea urchin cell lineage-specific gene LpS1 (M. Xiang, S.-Y. Lu, M. Musso, G. Karsenty, and W. H. Klein, Development 113:1345-1355, 1991) also represents a high-affinity recognition site for suGF1. suGF1 may be a member of a family of G-string factors involved in the regulation of expression of unrelated genes during development of a number of different organisms.

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16

Kumar, Yatender, Vegesna Radha, and Ghanshyam Swarup. "Interaction with Sug1 enables Ipaf ubiquitination leading to caspase 8 activation and cell death." Biochemical Journal 427, no. 1 (March 15, 2010): 91–104. http://dx.doi.org/10.1042/bj20091349.

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Activation of initiator caspases is dependent on interacting proteins, and Ipaf [ICE (interleukin-1β-converting enzyme)-protease activating factor] {NLRC4 [NLR (Nod-like receptor) family CARD (caspase activation and recruitment domain)-containing 4]} an inflammasome component, is involved in caspase 1 activation and apoptosis. Investigating the mechanisms of Ipaf activation, we found that the C-terminal LRR (leucine-rich repeat) domain of Ipaf, through intramolecular interaction, negatively regulates its apoptosis-inducing function. In A549 lung carcinoma cells, expression of Ac-Ipaf (LRR-domain-deleted Ipaf) induced cell death that was dependent on caspase 8, but not on caspase 1. A yeast two-hybrid screen using Ac-Ipaf as bait identified human Sug1 (suppressor of gal 1), a component of the 26S proteasome, as an interacting protein. In mammalian cells Sug1 interacts and co-localizes with Ipaf. Sug1 binds to amino acids 91–253 of Ipaf, which is also the region that the LRR domain binds to. It potentiates cell death induced by Ipaf and Ac-Ipaf, and co-expression of Sug1 and Ipaf induces caspase-8-dependent cell death. Cellular complexes formed by Ipaf and Sug1 contain caspase 8. Expression of Ac-Ipaf or co-expression of Sug1 with Ipaf results in the formation of cytoplasmic aggregates and caspase 8 activation. Sug1 co-expression enabled modification of Ipaf by ubiquitination. Tagging ubiquitin molecules to Ipaf led to aggregate formation, enhanced caspase 8 interaction and activation, resulting in induction of cell death. Using RNAi (RNA interference) and dominant-negative approaches, we have shown that cell death induced by Ac-Ipaf expression or by treatment with TNF-α (tumour necrosis factor α) or doxorubicin is dependent on Sug1. Our results suggest a role for ubiquitination of Ipaf that is enabled by its interaction with Sug1, leading to caspase 8 activation and cell death.

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17

Koues, Olivia I., R. Kyle Dudley, Agnieszka D. Truax, Dawson Gerhardt, Kavita P. Bhat, Sam McNeal, and Susanna F. Greer. "Regulation of Acetylation at the Major Histocompatibility Complex Class II Proximal Promoter by the 19S Proteasomal ATPase Sug1." Molecular and Cellular Biology 28, no. 19 (July 28, 2008): 5837–50. http://dx.doi.org/10.1128/mcb.00535-08.

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ABSTRACT Recent studies have made evident the fact that the 19S regulatory component of the proteasome has functions that extend beyond degradation, particularly in the regulation of transcription. Although 19S ATPases facilitate chromatin remodeling and acetylation events in yeast (Saccharomyces cerevisiae), it is unclear if they play similar roles in mammalian cells. We have recently shown that the 19S ATPase Sug1 positively regulates the transcription of the critical inflammatory gene for major histocompatibility complex class II (MHC-II) by stabilizing enhanceosome assembly at the proximal promoter. We now show that Sug1 is crucial for regulating histone H3 acetylation at the MHC-II proximal promoter. Sug1 binds to acetylated histone H3 and, in the absence of Sug1, histone H3 acetylation is dramatically decreased at the proximal promoter, with a preferential loss of acetylation at H3 lysine 18. Sug1 also binds to the MHC-II histone acetyltransferase CREB-binding protein (CBP) and is critical for the recruitment of CBP to the MHC-II proximal promoter. Our current study strongly implicates the 19S ATPase Sug1 in modifying histones to initiate MHC-II transcription and provides novel insights into the role of the proteasome in the regulation of mammalian transcription.

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18

Dagkesamanskaya, A. R., and M. D. Ter-Avanesyan. "Interaction of the yeast omnipotent suppressors SUP1(SUP45) and SUP2(SUP35) with non-mendelian factors." Genetics 128, no. 3 (July 1, 1991): 513–20. http://dx.doi.org/10.1093/genetics/128.3.513.

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Abstract The SUP1 and SUP2 genes code for protein factors intimately involved in the control of translational accuracy. The disrupted alleles of these genes confer a recessive lethal phenotype in both [psi+] and [psi-] genetic backgrounds, indicating an essential function for the corresponding proteins. In [psi+] diploids, heterozygous for the SUP1 null allele, several dominant phenotypes were evident with slow growth and inability to sporulate. These dominant phenotypes disappear after transformation with the multicopy plasmid carrying the wild-type allele of the SUP1 gene. Such dominant phenotypes were not observed for the SUP2 null allele. The incompatibility of multicopy plasmids carrying the SUP2 gene with guanidine hydrochloride-curable cytoplasmic factor(s) was also demonstrated. The possible mechanisms of interaction of the SUP1 and SUP2 genes with the [psi] determinant are discussed.

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19

Kostyunina, O., A. Filipchenko, M. Fornara, A. Sermyagin, and N. Zinovieva. "328 Polymorphism in TMEM95, SUGT1." Journal of Animal Science 96, suppl_3 (December 2018): 125. http://dx.doi.org/10.1093/jas/sky404.275.

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20

Barbosa, F. A., D. S. Graça, P. H. S. Guimarães, and F. V. Silva Júnior. "Análise econômica da suplementação protéico-energética de novilhos durante o período de transição entre água-seca." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 60, no. 4 (August 2008): 911–16. http://dx.doi.org/10.1590/s0102-09352008000400021.

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Avaliou-se economicamente o efeito da suplementação protéico-energética em dois níveis de ingestão diária, 0,17% e 0,37% do peso vivo, sobre o desempenho de novilhos, em pastagens de Brachiaria brizantha cv. Marandu utilizando-se 14 animais por tratamento. Os tratamentos foram: SM - suplementação mineral (controle), SUP1 - suplementação protéico-energética com média de ingestão diária de 0,17% do peso vivo e SUP2 - suplementação protéico-energética com média de ingestão diária de 0,37% do peso vivo. Novilhos que receberam a suplementação protéico-energética SUP1 e SUP2 apresentaram maiores ganhos de peso, 0,655 e 0,746kg/animal/dia, respectivamente em relação aos que receberam apenas suplementação mineral, 0,535kg/animal/dia. Os maiores lucros operacionais, observados para os animais dos tratamentos SUP1 e SUP2. 67,12 e 72,08 R$/animal/período, respectivamente, em relação aos do tratamento controle, 66,67 R$/animal/período; os resíduos para remuneração foram de R$59,92, R$55,10 e R$54,85/animal/período, para novilhos que receberam SUP2, SUP1 e SM, respectivamente e sugerem que a suplementação protéico-energética possibilitou maior retorno econômico.

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21

Cheng, Guojun, Ramakrishnan Karunakaran, Alison K. East, and Philip S. Poole. "Multiplicity of Sulfate and Molybdate Transporters and Their Role in Nitrogen Fixation in Rhizobium leguminosarum bv. viciae Rlv3841." Molecular Plant-Microbe Interactions® 29, no. 2 (February 2016): 143–52. http://dx.doi.org/10.1094/mpmi-09-15-0215-r.

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Rhizobium leguminosarum Rlv3841 contains at least three sulfate transporters, i.e., SulABCD, SulP1 and SulP2, and a single molybdate transporter, ModABC. SulABCD is a high-affinity transporter whose mutation prevented growth on a limiting sulfate concentration, while SulP1 and SulP2 appear to be low-affinity sulfate transporters. ModABC is the sole high-affinity molybdate transport system and is essential for growth with NO3− as a nitrogen source on limiting levels of molybdate (<0.25 μM). However, at 2.5 μM molybdate, a quadruple mutant with all four transporters inactivated, had the longest lag phase on NO3−, suggesting these systems all make some contribution to molybdate transport. Growth of Rlv3841 on limiting levels of sulfate increased sulB, sulP1, modB, and sulP2 expression 313.3-, 114.7-, 6.2-, and 4.0-fold, respectively, while molybdate starvation increased only modB expression (three- to 7.5-fold). When grown in high-sulfate but not low-sulfate medium, pea plants inoculated with LMB695 (modB) reduced acetylene at only 14% of the wild-type rate, and this was not further reduced in the quadruple mutant. Overall, while modB is crucial to nitrogen fixation at limiting molybdate levels in the presence of sulfate, there is an unidentified molybdate transporter also capable of sulfate transport. [Formula: see text] Copyright © 2016 The Author(s). This is an open access article distributed under the CC BY Attribution 4.0 International license .

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22

Barbosa, F. A., D. S. Graça, W. E. Maffei, F. V. Silva Júnior, and G. M. Souza. "Desempenho e consumo de matéria seca de bovinos sob suplementação protéico-energética, durante a época de transição água-seca." Arquivo Brasileiro de Medicina Veterinária e Zootecnia 59, no. 1 (February 2007): 160–67. http://dx.doi.org/10.1590/s0102-09352007000100027.

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Анотація:

Avaliou-se o efeito da suplementação protéico-energética em dois níveis de ingestão diária, 0,17 e 0,37% do peso vivo médio, sobre o no desempenho e consumo de matéria seca por bovinos, em pastagens de Brachiaria brizantha cv. Marandu. Para avaliação do desempenho foram utilizados 42 novilhos (Holandês x Gir - HG), com média de 211kg de peso vivo inicial (PVI) e para a avaliação do consumo de matéria seca total (CMST) e de forragem (CMSF) foram usados 15 novilhos inteiros HG, com 239kg de PVI. Os tratamentos foram: SM - controle; SUP1 - suplementação protéico-energética com ingestão média diária de 0,17% do peso vivo e SUP2 - suplementação protéico-energética com ingestão média diária de 0,37% do peso vivo (PV). Os valores do CMSF foram de 2,6, 2,4 e 2,3% PV, e os de CMST 2,6, 2,6 e 2,6% PV, para SM, SUP1 e SUP2, respectivamente. Esses valores não diferiram entre si (P>0,05). A suplementação protéico-energética proporcionou maior ganho de peso, 0,54, 0,66 e 0,75kg/cabeça/dia para SM, SUP1 e SUP2, respectivamente.

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23

Lv, Tingxia, Wei Zhang, Anjian Xu, Yanmeng Li, Donghu Zhou, Bei Zhang, Xiaojin Li, et al. "Non-HFE mutations in haemochromatosis in China: combination of heterozygous mutations involving HJV signal peptide variants." Journal of Medical Genetics 55, no. 10 (August 30, 2018): 650–60. http://dx.doi.org/10.1136/jmedgenet-2018-105348.

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IntroductionHereditary haemochromatosis (HH) caused by a homozygous p.C282Y mutation in haemochromatosis (HFE) gene has been well documented. However, less is known about the causative non-HFE mutation. We aimed to assess mutation patterns of haemochromatosis-related genes in Chinese patients with primary iron overload.MethodsPatients were preanalysed for mutations in the classic HH-related genes: HFE, HJV, HAMP, TFR2 and SLC40A1. Whole exome sequencing was conducted for cases with variants in HJV signal peptide region. Representative variants were analysed for biological function.ResultsNone of the cases analysed harboured the HFE p.C282Y; however, 21 of 22 primary iron-overload cases harboured at least one non-synonymous variant in the non-HFE genes. Specifically, p.E3D or p.Q6H variants in the HJV signal peptide region were identified in nine cases (40.9%). In two of three probands with the HJV p.E3D, exome sequencing identified accompanying variants in BMP/SMAD pathway genes, including TMPRSS6 p.T331M and BMP4 p.R269Q, and interestingly, SUGP2 p.R639Q was identified in all the three cases. Pedigree analysis showed a similar pattern of combination of heterozygous mutations in cases with HJV p.E3D or p.Q6H, with SUGP2 p.R639Q or HJV p.C321X being common mutation. In vitro siRNA interference of SUGP2 showed a novel role of downregulating the BMP/SMAD pathway. Site-directed mutagenesis of HJV p.Q6H/p.C321X in cell lines resulted in loss of membrane localisation of mutant HJV, and downregulation of p-SMAD1/5 and HAMP.ConclusionCompound heterozygous mutations of HJV or combined heterozygous mutations of BMP/SMAD pathway genes, marked by HJV variants in the signal peptide region, may represent a novel aetiological factor for HH.

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24

Carvalho, Cristina Dos Santos, Antonio Ralf Da Cunha Carneiro, and Wesley Da Silva Magalhães. "Construções parentéticas epistêmicas no português angolano e moçambicano (Epistemic parenthetical constructions in Angolan and Mozambican Portuguese: convergences and divergences)." Estudos da Língua(gem) 18, no. 1 (April 30, 2020): 105. http://dx.doi.org/10.22481/el.v18i1.6100.

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Este artigo pretende analisar, quanto à propriedade esquematicidade, construções parentéticas epistêmicas quase-asseverativas de base clausal verbal portuguesas, instanciadas por microconstruções como (eu) creio que, (eu) acho que, (eu) penso que, de um lado, e (eu) creio, (eu) acho, (eu) penso, do outro. Para análise dessas construções, assume-se como orientação teórico-metodológica a Linguística Funcional Centrada no Uso, com ênfase na abordagem construcional da gramática e mudança linguística. A investigação se baseia em ocorrências empíricas das variedades angolana e moçambicana do português contemporâneo, extraídas do banco de dados do Corpus do Português. Os resultados mostram que: (i) a rede construcional dos parentéticos analisados apresenta dois subesquemas: [(SUJP1)VEpist Compl]Parent e [(SUJP1)VEpist]Parent; (ii) os dois subesquemas ocorrem no português angolano e moçambicano, havendo diferença quanto à produtividade; (iii) nas microconstruções, os verbos epistêmicos que mais ocorrem são achar (português moçambicano) e crer (português angolano e moçambicano).

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25

Vielitz, Arne. "Aufbruch in eine Welt jenseits von p < 0,05." manuelletherapie 24, no. 01 (February 2020): 5. http://dx.doi.org/10.1055/a-1085-7676.

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26

Chen, Mei-xiang, Qing-hua Chen, Qiao-xin Li, and Zhong-peng Yang. "On the Open Problem Related to Rank Equalities for the Sum of Finitely Many Idempotent Matrices and Its Applications." Scientific World Journal 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/702413.

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Tian and Styan have shown many rank equalities for the sum of two and three idempotent matrices and pointed out that rank equalities for the sumP1+⋯+PkwithP1,…,Pkbe idempotent (k>3) are still open. In this paper, by using block Gaussian elimination, we obtained rank equalities for the sum of finitely many idempotent matrices and then solved the open problem mentioned above. Extensions to scalar-potent matrices and some related matrices are also included.

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27

ZHANG, Xian, Roger J. A. GRAND, Christopher J. McCABE, Jayne A. FRANKLYN, Phillip H. GALLIMORE та Andrew S. TURNELL. "Transcriptional regulation of the human glycoprotein hormone common α subunit gene by cAMP-response-element-binding protein (CREB)-binding protein (CBP)/p300 and p53". Biochemical Journal 368, № 1 (15 листопада 2002): 191–201. http://dx.doi.org/10.1042/bj20020634.

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We have investigated the functional interactions between adenovirus early region 1A (AdE1A) protein, the co-activators cAMP-response-element-binding protein (CREB)-binding protein (CBP)/p300 and SUG1, and the transcriptional repressor retinoblastoma (Rb) in mediating T3-dependent repression. Utilizing the human glycoprotein hormone common α-subunit (α-subunit) promoter and AdE1A mutants with selective binding capacity to these molecules we have determined an essential role for CBP/p300. In normal circumstances, wild-type 12S AdE1A inhibited α-subunit activity. In contrast, adenovirus mutants that retain both the SUG1- and Rb-binding sites, but lack the CBP/p300-binding site, were unable to repress promoter activity. We have also identified a role for the tumour-suppressor gene product p53 in regulation of the α-subunit promoter. Akin to 12S AdE1A, exogenous p53 expression repressed α-subunit activity. This function resided in the ability of p53 to interact with CBP/p300; an N-terminal mutant incapable of interacting with CBP/p300 did not inhibit α-subunit activity. Stabilization of endogenous p53 by UV irradiation also correlated positively with reduced α-subunit activity. Intriguingly, T3 stimulated endogenous p53 transcriptional activity, implicating p53 in T3-dependent signalling pathways. These data indicate that CBP/p300 and p53 are key regulators of α-subunit activity.

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28

Kazankov, Vyacheslav, and Vladimir Gubin. "Psychology of ustoychivost': numerical scale for assessing human’s ustoychivost' according to the golden ratio rule." E3S Web of Conferences 210 (2020): 20018. http://dx.doi.org/10.1051/e3sconf/202021020018.

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Exploring man, the modern psychology of Europe and America began to actively apply the concepts stability and/or resistance that, in Russia psychology, are combined into one concept — ustoychivost’. In modern psychology, there is no methodology for numerically assessing human ustoychivost’. The article presents the author’s scale of numerical evaluation of ustoychivost ’person and outlines an approach to the formation of its road map. Human ustoychivost ’refers to his ability to maintain health at the psychophysiological, psychological and psychosocial levels of life, forming the unity of the individual, personality and the subject of work in a person. Three hypotheses are put forward. Hypothesis 1: it is possible to numerically establish human ustoychivost ' if you create a scale for assessing it by applying the golden ratio rule — the stability scale for the golden ratio (SUGP). Hypothesis 2: if a person subjectively evaluates his ustoychivost ’in the range from 0.382 to 0.618, then objectively he is stability; if a person subjectively evaluates his ustoychivost ’in the intervals from 0.382 to 0 or from 0.618 to 1, then objectively he is resistance. To test the hypotheses put forward, an experiment on a sample of firefighters is presented, which confirms their fidelity, and also indicates the appropriateness of using SUGP in extreme psychology, labor psychology.

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29

Tax, Frans E., James H. Thomas, Edwin L. Ferguson, and H. Robert Horvitzt. "Identification and Characterization of Genes That Interact With lin-12 in Caenorhabditis elegans." Genetics 147, no. 4 (December 1, 1997): 1675–95. http://dx.doi.org/10.1093/genetics/147.4.1675.

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Abstract We identified and characterized 14 extragenic mutations that suppressed the dominant egg-laying defect of certain lin-12 gain-of-function mutations. These suppressors defined seven genes: sup-l7, lag-2, sel-4, sel-5, sel-6, sel-7 and sel-8. Mutations in six of the genes are recessive suppressors, whereas the two mutations that define the seventh gene, lag-2, are semi-dominant suppressors. These suppressor mutations were able to suppress other lin-12 gain-of-function mutations. The suppressor mutations arose at a very low frequency per gene, 10-50 times below the typical loss-of-function mutation frequency. The suppressor mutations in sup1 7 and lag-2 were shown to be rare non-null alleles, and we present evidence that null mutations in these two genes cause lethality. Temperature-shift studies for two suppressor genes, sup1 7and lag-2, suggest that both genes act at approximately the same time as lin-12in specifying a cell fate. Suppressor alleles of six of these genes enhanced a temperature-sensitive loss-of-function allele of glp-1, a gene related to lin-12 in structure and function. Our analysis of these suppressors suggests that the majority of these genes are part of a shared lin-12/glp-1 signal transduction pathway, or act to regulate the expression or stability of lin-12 and glp-1.

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30

Wang, W., P. M. Chevray, and D. Nathans. "Mammalian Sug1 and c-Fos in the nuclear 26S proteasome." Proceedings of the National Academy of Sciences 93, no. 16 (August 6, 1996): 8236–40. http://dx.doi.org/10.1073/pnas.93.16.8236.

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31

Ibrahim, S. P. Syed, K. R. Chandran, and C. J. Kabila Kanthasamy. "CHISC-AC: Compact Highest Subset Confidence-Based Associative Classification^|^sup1;." Data Science Journal 13 (2014): 127–37. http://dx.doi.org/10.2481/dsj.14-035.

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32

Allouch, Awatef, Cristina Di Primio, Audrey Paoletti, Gabrielle Lê-Bury, Frédéric Subra, Valentina Quercioli, Roberta Nardacci, et al. "SUGT1 controls susceptibility to HIV-1 infection by stabilizing microtubule plus-ends." Cell Death & Differentiation 27, no. 12 (June 8, 2020): 3243–57. http://dx.doi.org/10.1038/s41418-020-0573-5.

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33

Cheng, L., N. Roemer, K. A. Smyth, J. Belote, J. R. Nambu, and L. M. Schwartz. "Cloning and characterization of Pros45, the Drosophila SUG1 proteasome subunit homolog." Molecular and General Genetics MGG 259, no. 1 (July 1998): 13–20. http://dx.doi.org/10.1007/s004380050783.

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34

Ivins, K. J., R. R. Luedtke, R. P. Artymyshyn, and P. B. Molinoff. "Regulation of dopamine D2 receptors in a novel cell line (SUP1)." Molecular Pharmacology 39, no. 4 (April 1991): 531–39. https://doi.org/10.1016/s0026-895x(25)11002-x.

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35

Carvalho, Cristina dos Santos, Antonio Ralf da Cunha A Carneiro, and Wesley da Silva Magalhães. "Um estudo sociofuncional dos parentéticos epistêmicos quase-asseverativos em variedades do português (A sociofunctional study of quasi-assertive epistemic parentheticals in Portuguese varieties)." Estudos da Língua(gem) 19, no. 4 (December 30, 2021): 109–32. http://dx.doi.org/10.22481/el.v19i4.8651.

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Neste trabalho, descrevemos, no português angolano e moçambicano, parentéticos epistêmicos quase-asseverativos de base clausal verbal, instanciados, no padrão construcional [(SUJP1)VEpist (Compl)]Parent, por microconstruções como (eu) acho (que), (eu) creio (que), (eu) suponho (que) etc. Para tanto, fundamentamo-nos nos pressupostos teórico-metodológicos da Linguística Funcional Centrada no Uso (BYBEE, 2010; TRAUGOTT; TROUSDALE, 2013, dentre outros) e da Sociolinguística Quantitativa (LABOV, 2008 [1972]), no que tem sido denominado de orientação sociofuncionalista. Sob essa perspectiva, procedemos à análise de ocorrências empíricas do português contemporâneo extraídas do banco de dados Corpus do Português. Nossa análise, baseada nos graus de esquematicidade das construções (TRAUGOTT; TROUSDALE, 2013) e em parâmetros formais e funcionais, mostra que, nas duas variedades do português, os parentéticos epistêmicos quase-asseverativos estão correlacionados a distintos usos e níveis construcionais.

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36

SU, Kaihong, Xiaoyong YANG, Mark D. ROOS, Andrew J. PATERSON, and Jeffrey E. KUDLOW. "Human Sug1/p45 is involved in the proteasome-dependent degradation of Sp1." Biochemical Journal 348, no. 2 (June 1, 2000): 281. http://dx.doi.org/10.1042/0264-6021:3480281.

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37

SU, Kaihong, Xiaoyong YANG, Mark D. ROOS, Andrew J. PATERSON, and Jeffrey E. KUDLOW. "Human Sug1/p45 is involved in the proteasome-dependent degradation of Sp1." Biochemical Journal 348, no. 2 (May 23, 2000): 281–89. http://dx.doi.org/10.1042/bj3480281.

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The transcription factor Sp1 was previously shown to undergo proteasome-dependent degradation when cells were glucose-starved and stimulated with the adenylate cyclase inducer, forskolin. However, the control of the Sp1 degradation process is largely unknown. Using in vitro and in vivo interaction studies, we show in the present study that Sp1 interacts with human Sug1 [hSug1, also known as p45 or thyroid-hormone-receptor interacting protein (‘TRIP1’)], an ATPase subunit of the 26 S proteasome and a putative transcriptional modulator. This interaction with Sp1 occurs through the C-terminus of hSug1, the region that contains the conserved ATPase domain in this protein. Both in vitro studies, in reconstituted degradation assays, and in vivo experiments, in which hSug1 is overexpressed in normal rat kidney cells, show that full-length hSug1 is able to stimulate the proteasome-dependent degradation of Sp1. However, hSug1 truncations that lack either the N- or C-terminal domain of hSug1 act as dominant negatives, inhibiting Sp1 degradation in vitro. Also, an ATPase mutant of hSug1, while still able to bind Sp1, acts as a dominant negative, blocking Sp1 degradation both in vitro and in vivo. These results demonstrate that hSug1 is involved in the degradation of Sp1 and that ATP hydrolysis by hSug1 is necessary for this process. Our findings indicate that hSug1 is an exchangeable proteasomal component that plays a critical regulatory role in the proteasome-dependent degradation of Sp1. However, hSug1 is not the factor limiting Sp1 degradation in the cells treated with glucosamine. This and other considerations suggest that hSug1 co-operation with other molecules is necessary to target Sp1 for proteasome degradation.

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38

Pazynina, Galina V., Svetlana V. Tsygankova, Marina A. Sablina, Nadezhda V. Shilova, Alexander S. Paramonov, Alexander O. Chizhov та Nicolai V. Bovin. "Synthesis of Sug1-4GalNAcα disaccharides and their interaction with human blood antibodies". Mendeleev Communications 33, № 1 (січень 2023): 107–8. http://dx.doi.org/10.1016/j.mencom.2023.01.033.

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39

Kim, Keun Il, Sung Hee Baek, Young-Joo Jeon, Shigeki Nishimori, Toshiaki Suzuki, Sanae Uchida, Naoki Shimbara, Hisato Saitoh, Keiji Tanaka, and Chin Ha Chung. "A New SUMO-1-specific Protease, SUSP1, That Is Highly Expressed in Reproductive Organs." Journal of Biological Chemistry 275, no. 19 (May 5, 2000): 14102–6. http://dx.doi.org/10.1074/jbc.275.19.14102.

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40

van Witteloostuijn, Arjen. "New-day statistical thinking: A bold proposal for a radical change in practices." Journal of International Business Studies 51, no. 2 (December 2, 2019): 274–78. http://dx.doi.org/10.1057/s41267-019-00288-8.

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AbstractIn this commentary, I argue why we should stop engaging in null hypothesis statistical significance testing altogether. Artificial and misleading it may be, but we know how to play the p value threshold and null hypothesis-testing game. We feel secure; we love the certainty. The fly in the ointment is that the conventions have led to questionable research practices. Wasserstein, Schirm, & Lazar (Am Stat 73(sup1):1–19, 2019. 10.1080/00031305.2019.1583913) explain why, in their thought-provoking editorial introducing a special issue of The American Statistician: “As ‘statistical significance’ is used less, statistical thinking will be used more.” Perhaps we empirical researchers can together find a way to work ourselves out of the straitjacket that binds us.

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41

Kushwaha, Nidhi, and O. P. Vyas. "Leveraging Bibliographic RDF Data for Keyword Prediction with Association Rule Mining (ARM)^|^sup1;." Data Science Journal 13 (2014): 119–26. http://dx.doi.org/10.2481/dsj.14-033.

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42

CIOFFI, Anna Valentina, Diana FERRARA, Maria Vittoria CUBELLIS, Francesco ANIELLO, Marcella CORRADO, Francesca LIGUORI, Alessandro AMOROSO, Laura FUCCI, and Margherita BRANNO. "An open reading frame in intron seven of the sea urchin DNA-methyltransferase gene codes for a functional AP1 endonuclease." Biochemical Journal 365, no. 3 (August 1, 2002): 833–40. http://dx.doi.org/10.1042/bj20011857.

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Analysis of the genome structure of the Paracentrotus lividus (sea urchin) DNA methyltransferase (DNA MTase) gene showed the presence of an open reading frame, named METEX, in intron 7 of the gene. METEX expression is developmentally regulated, showing no correlation with DNA MTase expression. In fact, DNA MTase transcripts are present at high concentrations in the early developmental stages, while METEX is expressed at late stages of development. Two METEX cDNA clones (Met1 and Met2) that are different in the 3′ end have been isolated in a cDNA library screening. The putative translated protein from Met2 cDNA clone showed similarity with Escherichia coli endonuclease III on the basis of sequence and predictive three-dimensional structure. The protein, overexpressed in E. coli and purified, had functional properties similar to the endonuclease specific for apurinic/apyrimidinic (AP) sites on the basis of the lyase activity. Therefore the open reading frame, present in intron 7 of the P. lividus DNA MTase gene, codes for a functional AP endonuclease designated SuAP1.

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Tassan, J. P., K. Le Guellec, M. Kress, M. Faure, J. Camonis, M. Jacquet, and M. Philippe. "In Xenopus laevis, the product of a developmentally regulated mRNA is structurally and functionally homologous to a Saccharomyces cerevisiae protein involved in translation fidelity." Molecular and Cellular Biology 13, no. 5 (May 1993): 2815–21. http://dx.doi.org/10.1128/mcb.13.5.2815-2821.1993.

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We have performed a differential screen of a Xenopus egg cDNA library and selected two clones (Cl1 and Cl2) corresponding to mRNA which are specifically adenylated and recruited into polysomes after fertilization. Sequence analysis of Cl1 reveals that the corresponding protein is 67.5% identical (83% similar) to the product of the Saccharomyces cerevisiae SUP45 (also called SUP1 or SAL4) gene. This gene, when mutated, is an omnipotent suppressor of nonsense codons. When expressed in a sup45 mutant, the Xenopus Cl1 cDNA was able to suppress sup45-related phenotypes, showing that the structural homology reflects a functional homology. Our discovery of a structural and functional homolog in Xenopus cells implies that the function of SUP45 is not restricted to lower eukaryotes and that the SUP45 protein may perform a crucial cellular function in higher eukaryotes.

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44

Tassan, J. P., K. Le Guellec, M. Kress, M. Faure, J. Camonis, M. Jacquet, and M. Philippe. "In Xenopus laevis, the product of a developmentally regulated mRNA is structurally and functionally homologous to a Saccharomyces cerevisiae protein involved in translation fidelity." Molecular and Cellular Biology 13, no. 5 (May 1993): 2815–21. http://dx.doi.org/10.1128/mcb.13.5.2815.

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We have performed a differential screen of a Xenopus egg cDNA library and selected two clones (Cl1 and Cl2) corresponding to mRNA which are specifically adenylated and recruited into polysomes after fertilization. Sequence analysis of Cl1 reveals that the corresponding protein is 67.5% identical (83% similar) to the product of the Saccharomyces cerevisiae SUP45 (also called SUP1 or SAL4) gene. This gene, when mutated, is an omnipotent suppressor of nonsense codons. When expressed in a sup45 mutant, the Xenopus Cl1 cDNA was able to suppress sup45-related phenotypes, showing that the structural homology reflects a functional homology. Our discovery of a structural and functional homolog in Xenopus cells implies that the function of SUP45 is not restricted to lower eukaryotes and that the SUP45 protein may perform a crucial cellular function in higher eukaryotes.

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45

Rubin, David M., Olivier Coux, Inge Wefes, Christoph Hengartner, Richard A. Young, Alfred L. Goldberg, and Daniel Daniel Finley. "Identification of the gal4 suppressor Sug1 as a subunit of the yeast 26S proteasome." Nature 379, no. 6566 (February 1996): 655–57. http://dx.doi.org/10.1038/379655a0.

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46

Grand, Roger JA, Andrew S. Turnell, Grant GF Mason, Wenlan Wang, Anne E. Milner, Joe S. Mymryk, Susan M. Rookes, A. Jennifer Rivett, and Phillip H. Gallimore. "Adenovirus early region 1A protein binds to mammalian SUG1-a regulatory component of the proteasome." Oncogene 18, no. 2 (January 1999): 449–58. http://dx.doi.org/10.1038/sj.onc.1202304.

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47

Makino, Yasutaka, Kazuya Yamano, Masato Kanemaki, Kiyoshi Morikawa, Toshihiko Kishimoto, Naoki Shimbara, Keiji Tanaka, and Taka-aki Tamura. "SUG1, a Component of the 26 S Proteasome, Is an ATPase Stimulated by Specific RNAs." Journal of Biological Chemistry 272, no. 37 (September 12, 1997): 23201–5. http://dx.doi.org/10.1074/jbc.272.37.23201.

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48

Bhat, Kavita P., Jonathan D. Turner, Sarah E. Myers, Austin D. Cape, Jenny P. Y. Ting, and Susanna F. Greer. "The 19S proteasome ATPase Sug1 plays a critical role in regulating MHC class II transcription." Molecular Immunology 45, no. 8 (April 2008): 2214–24. http://dx.doi.org/10.1016/j.molimm.2007.12.001.

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49

Inoue, Takeshi, Takahide Kon, Rieko Ajima, Reiko Ohkura, Masachika Tani, Jun Yokota, and Kazuo Sutoh. "MYO18B interacts with the proteasomal subunit Sug1 and is degraded by the ubiquitin–proteasome pathway." Biochemical and Biophysical Research Communications 342, no. 3 (April 2006): 829–34. http://dx.doi.org/10.1016/j.bbrc.2006.02.025.

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50

Barhite, Steven, Christelle Thibault та Michael F. Miles. "Phosducin-like protein (PhLP), a regulator of Gβγ function, interacts with the proteasomal protein SUG1". Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1402, № 1 (березень 1998): 95–101. http://dx.doi.org/10.1016/s0167-4889(97)00141-9.

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