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1
Meluh, P. B., and D. Koshland. "Evidence that the MIF2 gene of Saccharomyces cerevisiae encodes a centromere protein with homology to the mammalian centromere protein CENP-C." Molecular Biology of the Cell 6, no. 7 (July 1995): 793–807. http://dx.doi.org/10.1091/mbc.6.7.793.
Повний текст джерелаАнотація:
The MIF2 gene of Saccharomyces cerevisiae has been implicated in mitosis. Here we provide genetic evidence that MIF2 encodes a centromere protein. Specifically, we found that mutations in MIF2 stabilize dicentric minichromosomes and confer high instability (i.e., a synthetic acentric phenotype) to chromosomes that bear a cis-acting mutation in element I of the yeast centromeric DNA (CDEI). Similarly, we observed synthetic phenotypes between mutations in MIF2 and trans-acting mutations in three known yeast centromere protein genes-CEP1/CBF1/CPF1, NDC10/CBF2, and CEP3/CBF3B. In addition, the mif2 temperature-sensitive phenotype can be partially rescued by increased dosage of CEP1. Synthetic lethal interactions between a cep1 null mutation and mutations in either NDC10 or CEP3 were also detected. Taken together, these data suggest that the Mif2 protein interacts with Cep1p at the centromere and that the yeast centromere indeed exists as a higher order protein-DNA complex. The Mif2 and Cep1 proteins contain motifs of known transcription factors, suggesting that assembly of the yeast centromere is analogous to that of eukaryotic enhancers and origins of replication. We also show that the predicted Mif2 protein shares two short regions of homology with the mammalian centromere Ag CENP-C and that two temperature-sensitive mutations in MIF2 lie within these regions. These results provide evidence for structural conservation between yeast and mammalian centromeres.
2
Baker, Richard E., Kendra Harris, and Keming Zhang. "Mutations Synthetically Lethal with cep1 Target S. cerevisiae Kinetochore Components." Genetics 149, no. 1 (May 1, 1998): 73–85. http://dx.doi.org/10.1093/genetics/149.1.73.
Повний текст джерелаАнотація:
Abstract CP1 (encoded by CEP1) is a Saccharomyces cerevisiae chromatin protein that binds a DNA element conserved in centromeres and in the 5′-flanking DNA of methionine biosynthetic (MET) genes. Strains lacking CP1 are defective in chromosome segregation and MET gene transcription, leading to the hypothesis that CP1 plays a general role in assembling higher order chromatin structures at genomic sites where it is bound. A screen for mutations synthetically lethal with a cep1 null allele yielded five recessive csl (cep1 synthetic lethal) mutations, each defining a unique complementation group. Four of the five mutations synergistically increased the loss rate of marker chromosomes carrying a centromere lacking the CP1 binding site, suggesting that the cep1 synthetic lethality was due to chromosome segregation defects. Three of these four CSL genes were subsequently found to be known or imputed kinetochore genes: CEP3, NDC10, and CSE4. The fourth, CSL4, corresponded to ORF YNL232w on chromosome XIV, and was found to be essential. A human cDNA was identified that encoded a protein homologous to Csl4 and that complemented the csl4-1 mutation. The results are consistent with the view that the major cellular role of CP1 is to safeguard the biochemical integrity of the kinetochore.
3
O'Connell, K. F., and R. E. Baker. "Possible cross-regulation of phosphate and sulfate metabolism in Saccharomyces cerevisiae." Genetics 132, no. 1 (September 1, 1992): 63–73. http://dx.doi.org/10.1093/genetics/132.1.63.
Повний текст джерелаАнотація:
Abstract CP1 (encoded by the gene CEP1) is a sequence-specific DNA binding protein of Saccharomyces cerevisiae that recognizes a sequence element (CDEI) found in both yeast centromeres and gene promoters. Strains lacking CP1 exhibit defects in growth, chromosome segregation and methionine biosynthesis. A YEp24-based yeast genomic library was screened for plasmids which suppressed the methionine auxotrophy of a cep1 null mutant. The suppressing plasmids contained either CEP1 or DNA derived from the PHO4 locus. Subcloning experiments confirmed that suppression correlated with increased dosage of PHO4. PHO4c, pho80 and pho84 mutations, all of which lead to constitutive activation of the PHO4 transcription factor, also suppressed cep1 methionine auxotrophy. The suppression appeared to be a direct effect of PHO4, not a secondary effect of PHO regulon derepression, and was PHO2-dependent. Spontaneously arising extragenic suppressors of cep1 methionine auxotrophy were also isolated; approximately one-third of them were alleles of pho80. While PHO4 overexpression suppressed the methionine auxotrophy of a cep1 mutant, CEP1 overexpression failed to suppress the phenotype of a pho4 mutant; however, a cep1 null mutation suppressed the low inorganic phosphate growth deficiency of a pho84 mutant. The results may suggest that phosphate and sulfate metabolism are cross-regulated.
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Masison, D. C., and R. E. Baker. "Meiosis in Saccharomyces cerevisiae mutants lacking the centromere-binding protein CP1." Genetics 131, no. 1 (May 1, 1992): 43–53. http://dx.doi.org/10.1093/genetics/131.1.43.
Повний текст джерелаАнотація:
Abstract CP1 (encoded by the CEP1 gene) is a centromere binding protein of Saccharomyces cerevisiae that binds to the conserved DNA element I (CDEI) of yeast centromeres. To investigate the function of CP1 in yeast meiosis, we analyzed the meiotic segregation of CEN plasmids, nonessential chromosome fragments (CFs) and chromosomes in cep1 null mutants. Plasmids and CFs missegregated in 10-20% of meioses with the most frequent type of aberrant event being precocious sister segregation at the first meiotic division; paired and unpaired CFs behaved similarly. An unpaired chromosome I homolog (2N + 1) also missegregated at high frequency in the cep1 mutant (7.6%); however, missegregation of other chromosomes was not detected by tetrad analysis. Spore viability of cep1 tetrads was significantly reduced, and the pattern of spore death was nonrandom. The inviability could not be explained solely by chromosome missegregation and is probably a pleiotropic effect of cep1. Mitotic chromosome loss in cep1 strains was also analyzed. Both simple loss (1:0 segregation) and nondisjunction (2:0 segregation) were increased, but the majority of loss events resulted from nondisjunction. We interpret the results to suggest that CP1 generally promotes chromatid-kinetochore adhesion.
5
Alunno, A., O. Bistoni, F. Pratesi, F. Topini, I. Puxeddu, V. Valentini, G. Cafaro, E. Bartoloni, P. Migliorini, and R. Gerli. "Association between anti-citrullinated alpha enolase antibodies and clinical features in a cohort of patients with rheumatoid arthritis: a pilot study." Reumatismo 70, no. 2 (July 6, 2018): 67. http://dx.doi.org/10.4081/reumatismo.2018.1028.
Повний текст джерелаАнотація:
In recent years several antibodies against citrullinated peptides (ACPAs) have been identified in patients with rheumatoid arthritis (RA) and their pathogenic, diagnostic and prognostic significance is under intense investigation. Among ACPAs, those targeting citrullinated alpha enolase (anti-CEP1) have been identified in RA but data about their ability to predict the development of erosive disease are conflicting. Furthermore, no data are currently available concerning their possible association with extra-articular manifestations (EAMs) in RA. The aim of this study was to investigate the prevalence and significance of anti-CEP1 from a prognostic point of view. In this pilot study we confirmed that anti-CEP1 Abs are associated with higher prevalence of bone erosions, but we also provided the first evidence of an association between anti-CEP1 Abs and RA interstitial lung disease (ILD). These results provide the basis to investigate the association between anti-CEP1 Abs and EAMs in larger cohorts of RA patients to possibly confirm its role as biomarker for RA-ILD.
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Baker, R. E., and D. C. Masison. "Isolation of the gene encoding the Saccharomyces cerevisiae centromere-binding protein CP1." Molecular and Cellular Biology 10, no. 6 (June 1990): 2458–67. http://dx.doi.org/10.1128/mcb.10.6.2458-2467.1990.
Повний текст джерелаАнотація:
CP1 is a sequence-specific DNA-binding protein of the yeast Saccharomyces cerevisiae which recognizes the highly conserved DNA element I (CDEI) of yeast centromeres. We cloned and sequenced the gene encoding CP1. The gene codes for a protein of molecular weight 39,400. When expressed in Escherichia coli, the CP1 gene directed the synthesis of a CDEI-binding protein having the same gel mobility as purified yeast CP1. We have given the CP1 gene the genetic designation CEP1 (centromere protein 1). CEP1 was mapped and found to reside on chromosome X, 2.0 centimorgans from SUP4. Strains were constructed in which most of CEP1 was deleted. Such strains lacked detectable CP1 activity and were viable; however, CEP1 gene disruption resulted in a 35% increase in cell doubling time and a ninefold increase in the rate of mitotic chromosome loss. An unexpected consequence of CP1 gene disruption was methionine auxotrophy genetically linked to cep1. This result and the recent finding that CDEI sites in the MET25 promoter are required to activate transcription (D. Thomas, H. Cherest, and Y. Surdin-Kerjan, J. Mol. Biol. 9:3292-3298, 1989) suggest that CP1 is both a kinetochore protein and a transcription factor.
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Baker, R. E., and D. C. Masison. "Isolation of the gene encoding the Saccharomyces cerevisiae centromere-binding protein CP1." Molecular and Cellular Biology 10, no. 6 (June 1990): 2458–67. http://dx.doi.org/10.1128/mcb.10.6.2458.
Повний текст джерелаАнотація:
CP1 is a sequence-specific DNA-binding protein of the yeast Saccharomyces cerevisiae which recognizes the highly conserved DNA element I (CDEI) of yeast centromeres. We cloned and sequenced the gene encoding CP1. The gene codes for a protein of molecular weight 39,400. When expressed in Escherichia coli, the CP1 gene directed the synthesis of a CDEI-binding protein having the same gel mobility as purified yeast CP1. We have given the CP1 gene the genetic designation CEP1 (centromere protein 1). CEP1 was mapped and found to reside on chromosome X, 2.0 centimorgans from SUP4. Strains were constructed in which most of CEP1 was deleted. Such strains lacked detectable CP1 activity and were viable; however, CEP1 gene disruption resulted in a 35% increase in cell doubling time and a ninefold increase in the rate of mitotic chromosome loss. An unexpected consequence of CP1 gene disruption was methionine auxotrophy genetically linked to cep1. This result and the recent finding that CDEI sites in the MET25 promoter are required to activate transcription (D. Thomas, H. Cherest, and Y. Surdin-Kerjan, J. Mol. Biol. 9:3292-3298, 1989) suggest that CP1 is both a kinetochore protein and a transcription factor.
8
Alunno, A., F. Carubbi, O. Bistoni, M. Antonucci, E. Bartoloni Bocci, R. Giacomelli, and R. Gerli. "FRI0565 PREVALENCE AND SIGNIFICANCE OF ANTIBODIES AGAINST CITRULLINATED ALPHA-ENOLASE (ANTI-CEP1) IN CONNECTIVE TISSUE DISEASES." Annals of the Rheumatic Diseases 79, Suppl 1 (June 2020): 885.2–885. http://dx.doi.org/10.1136/annrheumdis-2020-eular.4549.
Повний текст джерелаАнотація:
Background:Anti-cyclic citrullinated peptide (anti-CCP) auto-antibodies represent the current gold standard for the diagnosis of rheumatoid arthritis (RA). However, growing evidence suggests that a variety of other citrullinated self-proteins may act as autoantigens and lead to the production of autoantibodies (1). Furthermore, autoantibodies believed to be RA-specific have been detected also in patients with connective tissue diseases (CTDs). We recently demonstrated that antibodies against citrullinated alpha-enolase (anti-CEP1) are a biomarker of erosive disease and RA-associated interstitial lung disease (2).Objectives:The purpose of this study was to investigate the prevalence and possible prognostic value of anti-CEP-1 in patients with CTDs.Methods:Two hundred and twelve consecutive patients with CTDs (51 systemic lupus erythematosus (SLE), 85 primary Sjogren’s syndrome (pSS) and 76 systemic sclerosis (SSc)) were studied and compared to 97 sex and age matched normal controls (NC) and 267 patients with RA. Anti-CEP1 IgG were detected in serum samples with a commercial ELISA kit (Euroimmun).Results:The overall prevalence of anti-CEP1 in CTDs was 7% (15/212 patients). In detail, these antibodies were detectable in 4 out of 85 pSS (5%), 5 out of 51 SLE (10%) and 6/76 SSc (8%). The prevalence and the titer of anti-CEP1 in CTDs was significantly higher compared to NC and significantly lower compared to RA. Anti-CEP1 positive patients did not display a specific clinical and serological picture. Unlike in RA, anti-CEP1 did not correlate with CTD-associated ILD.Conclusion:This is the first study assessing anti-CEP1 in a large cohort of patients with CTDs. We demonstrated that the association of these autoantibodies with ILD is specific for RA since it is not observed in SLE, pSS and SSc. Furthermore, although being significantly more prevalent and at higher titer compared to NC, anti-CEP1 do not allow to discriminate different patient subsets displaying peculiar clinical or serological phenotypes. Based on our results, the application of anti-CEP1 in CTDs is not advisable, however larger studies may possibly identify correlations not evident in our cohort.References:[1] Bonifacio AF, Alunno A, La Paglia GMC, Valentini E, Leone MC, Bartoloni E, Gerli R. Novel autoantibodies in rheumatoid arthritis. Reumatismo 2019;71(1):1-12[2] Alunno A, Bistoni O, Pratesi F, La Paglia GMC, Puxeddu I, Migliorini P, Gerli R. Anti-citrullinated alpha enolase antibodies, interstitial lung disease and bone erosion in rheumatoid arthritis. Rheumatology (Oxford). 2018;57(5):850-855Disclosure of Interests:Alessia Alunno: None declared, Francesco Carubbi Speakers bureau: Francesco Carubbi received speaker honoraria from Abbvie and Celgene outside this work., Onelia Bistoni: None declared, Matteo Antonucci: None declared, Elena Bartoloni Bocci: None declared, Roberto Giacomelli Grant/research support from: Actelion, Pfizer, Speakers bureau: Abbvie, Roche, Actelion, BMS, MSD, Ely Lilly, SOBI, Pfizer, Roberto Gerli: None declared
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Alunno, A., O. Bistoni, F. Carubbi, M. Antonucci, S. Calvacchi, E. Bartoloni Bocci, M. Zen, et al. "POS0755 PREVALENCE AND RELEVANCE OF ANTIBODIES AGAINST CITRULLINATED ALPHA ENOLASE (ANTI-CEP1) IN CONNECTIVE TISSUE DISEASES." Annals of the Rheumatic Diseases 80, Suppl 1 (May 19, 2021): 630.1–630. http://dx.doi.org/10.1136/annrheumdis-2021-eular.2825.
Повний текст джерелаАнотація:
Background:Anti-citrullinated alpha enolase antibodies have been investigated in rheumatoid arthritis and associated with bone erosion and interstitial lung disease but little is known about their prevalence and role in connective tissue diseases (CTDs).Objectives:The aim of this study was to investigate the prevalence and relevance of anti-CEP1 antibodies in CTDs.Methods:Serum samples from five independent patient cohorts were assessed: 1) established (est) primary Sjogren’s syndrome (pSS) N=78, 2) est-systemic lupus erythematosus (SLE) N=52, 3) est-systemic sclerosis (SSc) N=71, 4) pSS at disease onset N=30, 5) SLE at disease onset N=46 (cohorts 4 and 5 had at least 3 years of follow-up). Samples from ninety sex and age matched healthy donors (HD) and 200 patients with est-RA (disease controls) were also tested. Anti-CEP1 IgG antibodies were measured with a commercially available ELISA kit (Euroimmun, Luebeck, Germany).Results:Anti-CEP1 titer was significantly higher in est-pSS, est-SLE and est-SSc compared to HD, significantly lower in est-pSS and est-SSc compared to est-RA and comparable in est-SLE versus est-RA. We divided patients in every CTD group based on whether their anti-CEP1 titer was below or above the 25th, 50th and 75th percentile. In est-SLE anti-CEP1 values over the 25th percentile were associated with articular involvement (odds ratio, OR (95% confidence interval, CI)=11.5; 1.9-70.6, p=0.008). In est-pSS, no relationship between anti-CEP1>25th percentile and articular involvement was found but rather an association with rheumatoid factor positivity (OR (95% CI)=4.8, 1.6-14.1, p=0.004) and salivary gland swelling (OR (95% CI)=6.2, 1.3-29.1, p=0.021). In est-SSc no difference could be detected across the 3 groups. Anti-CEP-1 titers in pSS and SLE at onset did not differ from each other, were comparable also to those of HD and significantly lower than those of est-pSS, est-SLE and est-RA patients (all p<0.0001).). Of interest, we could retrieve a serum sample collected at the time of diagnosis for 5 patients from the cohort of established pSS and we observed that anti-CEP1 titers were significantly lower at pSS onset than during follow up (at least 12 months after the diagnosis, p=0.0024). No difference was observed in the clinical presentation at disease onset according to different anti-CEP1 titer and they did not predict the development of new clinical manifestations during follow-up.Conclusion:Anti-CEP-1 antibodies can be detected in CTDs at different title during the disease course and may increase overtime, at least in pSS. Although anti-CEP1 antibodies are associated with specific clinical manifestation in est-CTDs, such as articular involvement in est-SLE, they seem to lack a predictive value for future manifestations when measured at disease onset.References:[1]Alunno A, Bistoni O, Pratesi F et al Rheumatology (Oxford) 2018.[2]Manca ML, Alunno A, D’Amato C et al. Joint Bone Spine 2018.Disclosure of Interests:None declared
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Guo, Xiaorui, Lihong Li, Xiatong Liu, Chong Zhang, Xiaoyun Yao, Zhili Xun, Zhijing Zhao, et al. "MYB2 Is Important for Tapetal PCD and Pollen Development by Directly Activating Protease Expression in Arabidopsis." International Journal of Molecular Sciences 23, no. 7 (March 24, 2022): 3563. http://dx.doi.org/10.3390/ijms23073563.
Повний текст джерелаАнотація:
Tapetal programmed cell death (PCD) is a complex biological process that plays an important role in pollen formation and reproduction. Here, we identified the MYB2 transcription factor expressed in the tapetum from stage 5 to stage 11 that was essential for tapetal PCD and pollen development in Arabidopsis thaliana. Downregulation of MYB2 retarded tapetal degeneration, produced defective pollen, and decreased pollen vitality. EMSA and transcriptional activation analysis revealed that MYB2 acted as an upstream activator and directly regulated expression of the proteases CEP1 and βVPE. The expression of these proteases was lower in the buds of the myb2 mutant. Overexpression of either/both CEP1 or/and βVPE proteases partially recover pollen vitality in the myb2 background. Taken together, our results revealed that MYB2 regulates tapetal PCD and pollen development by directly activating expression of the proteases CEP1 and βVPE. Thus, a transcription factor/proteases regulatory and activated cascade was established for tapetal PCD during another development in Arabidopsis thaliana. Highlight: MYB2 is involved in tapetal PCD and pollen development by directly regulating expression of the protease CEP1 and βVPE and establishes a transcription factor/proteases regulatory and activated cascade.
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Jenkins, R. B., K. V. Ballman, C. Giannini, R. M. Arusell, H. Blair, S. Passe, H. Flynn, P. Brown, E. G. Shaw, and J. C. Buckner. "Diagnostic and prognostic significance of a t(1;19)(q10;p10) in patients (pts) with low-grade oligodendroglioma and astrocytoma: NCCTG 94–72–53." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 1505. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.1505.
Повний текст джерелаАнотація:
1505 Background: Combined deletion of chromosomes 1p and 19q is associated with improved prognosis in pts with anaplastic oligodendroglioma. We recently discovered that the combined deletion is mediated by a chromosome 1;19 translocation: t(1;19)(q10;p10). The prognostic significance of this alteration in pts with low-grade gliomas is not known. Methods: Paraffin-embedded tumor tissue was obtained from 134 pts enrolled in two NCCTG trials for newly-diagnosed low-grade glioma: 86–72–51: a randomized phase III trial of 50.4 Gy vs 64.8 Gy radiation therapy (RT) and 93–72–02: a phase II trial of PCV for 6 cycles followed by RT. Interphase fusion of a CEP1 probe and a BAC contig probe for 19p12 was used to detect the 1;19 translocation. Analysis of 1p and 19q deletions had been previously performed by FISH. Kaplan-Meier distributions of overall survival (OS) and progression-free survival (PFS) for pts whose tumors did or did not exhibit CEP1/19p12 fusion were compared using the Wilcoxon test. Results: Of 134 pts, CEP1/19p12 fusion testing was informative for 92. CEP1/19p12 fusion prevalence was 55% among 42 oligodendrogliomas, 47% among 30 mixed oligoastrocytomas, and 5% among 20 astrocytomas. 91% of gliomas with and 11% without 1p/19q deletion had CEP1/19p12 fusion (p<0.0001, chi-square test). The frequency of the t(1;19) by tumor histology, as well as median and 5-year progression-free and overall survival are provided in the table . Conclusions: Our results strongly suggest that a t(1;19)(q10;p10) mediates the combined deletion of 1p and 19q in human gliomas. Like combined 1p and 19q deletion, the 1;19 translocation is associated with superior progression-free and overall survival in low-grade oligodendroglioma patients. FISH analysis of the t(1;19) will likely be a more sensitive and specific means to assess 1p and 19q status in patients with gliomas. (Supported in part by CA85799, CA108961 and NCCTG grants CA25224 and CA114740) [Table: see text] No significant financial relationships to disclose.
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Cheng, Ziyi, Xiaorui Guo, Jiaxue Zhang, Yadi Liu, Bing Wang, Hui Li та Hai Lu. "βVPE is involved in tapetal degradation and pollen development by activating proprotease maturation in Arabidopsis thaliana". Journal of Experimental Botany 71, № 6 (20 грудня 2019): 1943–55. http://dx.doi.org/10.1093/jxb/erz560.
Повний текст джерелаАнотація:
Abstract Vacuolar processing enzyme (VPE) is responsible for the maturation and activation of vacuolar proteins in plants. We found that βVPE was involved in tapetal degradation and pollen development by transforming proproteases into mature protease in Arabidopsis thaliana. βVPE was expressed specifically in the tapetum from stages 5 to 8 of anther development. The βVPE protein first appeared as a proenzyme and was transformed into the mature enzyme before stages 7–8. The recombinant βVPE protein self-cleaved and transformed into a 27 kDa mature protein at pH 5.2. The mature βVPE protein could induce the maturation of CEP1 in vitro. βvpe mutants exhibited delayed vacuolar degradation and decreased pollen fertility. The maturation of CEP1, RD19A, and RD19C was seriously inhibited in βvpe mutants. Our results indicate that βVPE is a crucial processing enzyme that directly participates in the maturation of cysteine proteases before vacuolar degradation, and is indirectly involved in pollen development and tapetal cell degradation.
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O'Connell, K. F., Y. Surdin-Kerjan, and R. E. Baker. "Role of the Saccharomyces cerevisiae general regulatory factor CP1 in methionine biosynthetic gene transcription." Molecular and Cellular Biology 15, no. 4 (April 1995): 1879–88. http://dx.doi.org/10.1128/mcb.15.4.1879.
Повний текст джерелаАнотація:
Saccharomyces cerevisiae general regulatory factor CP1 (encoded by the gene CEP1) is required for optimal chromosome segregation and methionine prototrophy. MET16-CYC1-lacZ reporter constructs were used to show that MET16 5'-flanking DNA contains a CP1-dependent upstream activation sequence (UAS). Activity of the UAS required an intact CP1-binding site, and the effects of cis-acting mutations on CP1 binding and UAS activity correlated. In most respects, MET16-CYC1-lacZ reporter gene expression mirrored that of chromosomal MET16; however, the endogenous gene was found to be activated in response to amino acid starvation (general control). The latter mechanism was both GCN4 and CP1 dependent. MET25 was also found to be activated by GCN4, albeit weakly. More importantly, MET25 transcription was strongly CP1 dependent in gcn4 backgrounds. The modulation of MET gene expression by GCN4 can explain discrepancies in the literature regarding CP1 dependence of MET gene transcription. Lastly, micrococcal nuclease digestion and indirect end labeling were used to analyze the chromatin structure of the MET16 locus in wild-type and cep1 cells. The results indicated that CP1 plays no major role in configuring chromatin structure in this region, although localized CP1-specific differences in nuclease sensitivity were detected.
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Javerzat, Jean-Paul, Gordon McGurk, Gwen Cranston, Christian Barreau, Pascal Bernard, Colin Gordon, and Robin Allshire. "Defects in Components of the Proteasome Enhance Transcriptional Silencing at Fission Yeast Centromeres and Impair Chromosome Segregation." Molecular and Cellular Biology 19, no. 7 (July 1, 1999): 5155–65. http://dx.doi.org/10.1128/mcb.19.7.5155.
Повний текст джерелаАнотація:
ABSTRACT Fission yeast centromeres are transcriptionally silent and form a heterochromatin-like structure essential for normal centromere function; this appears analogous to heterochromatin and position effect variegation in other eukaryotes. Conditional mutations in three genes designated cep (centromere enhancer of position effect) were found to enhance transcriptional silencing within centromeres. Cloning of the cep1 + andcep2 + genes by functional complementation revealed that they are identical to the previously described genespad1 + and mts2 +, respectively, which both encode subunits of the proteasome 19S cap. Like Mts2 and Mts4, epitope-tagged Cep1/Pad1 localizes to or near the nuclear envelope throughout the cell cycle. The cep mutants display a range of phenotypes depending on the temperature. Silencing within the central domain of centromeres is increased at 36°C. This suggests that the proteasome is involved in regulating silencing and thus centromeric chromatin architecture, possibly by lowering the level of some chromatin-associated protein by ubiquitin-dependent degradation. This is the first report of defective proteasome function affecting heterochromatin-mediated transcriptional silencing. At 36 and 32°C, the cep mutants lose chromosomes at an elevated rate, and at 18°C, the mutants are cryosensitive for growth. Cytological analysis at 18°C revealed a defect in sister chromatid separation while other mitotic events occurred normally, indicating that cep mutations might interfere specifically with the degradation of inhibitor(s) of sister chromatid separation. These observations suggest that 19S subunits confer a level of substrate specificity on the proteasome and raise the possibility of a link between components involved in centromere architecture and sister chromatid cohesion.
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Yamamoto, Katsuya, Hiroki Kawano, Shinichiro Nishikawa, Kimikazu Yakushijin, Atsuo Okamura, and Toshimitsu Matsui. "A biphenotypic transformation of 8p11 myeloproliferative syndrome with CEP1/FGFR1 fusion gene." European Journal of Haematology 77, no. 4 (October 2006): 349–54. http://dx.doi.org/10.1111/j.1600-0609.2006.00723.x.
Повний текст джерела
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Imin, N., N. A. Mohd-Radzman, H. A. Ogilvie, and M. A. Djordjevic. "The peptide-encoding CEP1 gene modulates lateral root and nodule numbers in Medicago truncatula." Journal of Experimental Botany 64, no. 17 (November 20, 2013): 5395–409. http://dx.doi.org/10.1093/jxb/ert369.
Повний текст джерела
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Jilani, A. A., and C. G. Mackworth-Young. "The Role of Citrullinated Protein Antibodies in Predicting Erosive Disease in Rheumatoid Arthritis: A Systematic Literature Review and Meta-Analysis." International Journal of Rheumatology 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/728610.
Повний текст джерелаАнотація:
Background. Autoantibodies to citrullinated peptides have been shown to be valuable in the diagnosis of rheumatoid arthritis (RA). The expanding repertoire of antibodies to citrullinated peptide antigens (ACPA) has been a topic of great interest in recent reviews and research studies, as has the ability of these autoantibodies to predict disease outcome.Objectives. The aim of this review was to provide an update on the relevance of ACPA as prognostic markers in RA. The ability to identify patients predisposed to an aggressive outcome at the time of initial diagnosis greatly facilitates the selection of appropriate and cost-effective treatment.Methods. A systematic review of the literature was carried out. Studies from 1967 up to June 2014 with data on prognostic value of ACPA were included. Quality assessment was done by using the modified Hayden list for prognostic studies. Meta-analysis was performed using BioStat software.Results. The results of 25 studies were selected for the final review. A total of 6421 patients with RA were included, mainly in inception cohorts, with follow-up duration ranging from one year to ten years. All studies carried prognostic data on all available isotypes of anticyclic citrullinated protein (CCP), while four had data on antimutated citrullinated vimentin (MCV). There was a single relevant study each on anticitrullinated enolase peptide 1 (CEP1) and antichimaeric fibrin/filaggrin citrullinated peptide 1 (CFFCP1). All studies showed ACPA to be strong predictors of joint erosions in RA. Other factors, particularly baseline erosions, showed an additive effect. Anti-MCV appeared to be a marker of a more aggressive form of disease. Ten studies had data on which a meta-analysis could be performed. This gave an overall odds ratio of 4.85 for ACPA (anti-CCP/MCV) positivity being predictive for the development of joint erosions. Two studies with data on anti-CEP1 and anti-CFFCP1 also showed this positive predictive role of ACPA for joint erosions.Conclusions. ACPA are strong predictors of severity in RA. Their use should be part of routine rheumatology practice.
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Feki, S., A. Turki, R. Ben Salah, H. Hachicha, F. Frikha, L. Chakroun, Z. Bahloul та H. Masmoudi. "Les anticorps anti-peptides α-énolase citrullinés (anti-CEP1) : nouveaux marqueurs diagnostiques pour la polyarthrite rhumatoïde séronégative". La Revue de Médecine Interne 38 (грудень 2017): A170—A171. http://dx.doi.org/10.1016/j.revmed.2017.10.130.
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Zhang, Dandan, Di Liu, Xiaomeng Lv, Ying Wang, Zhili Xun, Zhixiong Liu, Fenglan Li, and Hai Lu. "The Cysteine Protease CEP1, a Key Executor Involved in Tapetal Programmed Cell Death, Regulates Pollen Development in Arabidopsis." Plant Cell 26, no. 7 (July 2014): 2939–61. http://dx.doi.org/10.1105/tpc.114.127282.
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Singh, Arun D., Raymond Tubbs, Charles Biscotti, Lynn Schoenfield, and Pierre Trizzoi. "Chromosomal 3 and 8 Status Within Hepatic Metastasis of Uveal Melanoma." Archives of Pathology & Laboratory Medicine 133, no. 8 (August 1, 2009): 1223–27. http://dx.doi.org/10.5858/133.8.1223.
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Abstract Context.—Several studies have evaluated clinical, histopathologic, cytogenetic, and molecular prognostic variables in uveal melanoma. However, it is not known whether the primary tumor cells maintain these aggressive attributes at the metastatic sites. Objective.—To determine the status of chromosomes 3 and 8q and c-myc amplification using fluorescence in situ hybridization on hepatic metastatic lesions of primary uveal melanoma. Design.—Ten patients with uveal melanoma with needle core biopsy–confirmed hepatic metastasis. Representative paraffin blocks were selected based on review of hematoxylin-eosin–stained sections. Fluorescence in situ hybridization was performed for detection of monosomy 3 and amplification at the 8q24 MYC locus using standard methods. The tricolor chromosome enumeration probe 8 (CEP8)/ IGH/MYC and the Urovysion probe consisting of CEP3, CEP7, CEP17, and 9P21 probes were used. A total of 200 interphase cells were scored. Results.—Hepatic metastasis was confirmed in each case by needle core biopsy. Fluorescence in situ hybridization analysis revealed chromosome 3 monosomy in 5 of the 8 cases that could be satisfactorily evaluated. Aneusomy of chromosome 8 was observed in 2 cases. MYC amplification was observed in 5 samples. In a single case where the primary tumor was treated by enucleation, the chromosomal monosomy 3 and aneusomy of chromosome 8 were present both in the primary tumor and its hepatic metastatic lesion. Conclusions.—The presence of cytogenetic changes within the metastatic lesions confirms that chromosome 3 monosomy and aneusomy of chromosome 8 are not just markers of metastatic potential of the primary tumor but are also present within the hepatic metastatic lesions.
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Han, Jingyi, Hui Li, Bin Yin, Yongzhuo Zhang, Yadi Liu, Ziyi Cheng, Di Liu, and Hai Lu. "The papain-like cysteine protease CEP1 is involved in programmed cell death and secondary wall thickening during xylem development in Arabidopsis." Journal of Experimental Botany 70, no. 1 (October 30, 2018): 205–15. http://dx.doi.org/10.1093/jxb/ery356.
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Cheng, Ziyi, Jiaxue Zhang, Bin Yin, Yadi Liu, Bing Wang, Hui Li та Hai Lu. "γVPE plays an important role in programmed cell death for xylem fiber cells by activating protease CEP1 maturation in Arabidopsis thaliana". International Journal of Biological Macromolecules 137 (вересень 2019): 703–11. http://dx.doi.org/10.1016/j.ijbiomac.2019.07.017.
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Zhao, Xiaorong, Ronald Thomason, and Xiao-Xiang Zhang. "Comparison of Immunophenotypic and Genotypic Profiles of Neoplastic Plasma Cells by Use of Flow Cytometric Immunophenotyping and FISH Analysis Following Plasma Cell Enrichment,." Blood 118, no. 21 (November 18, 2011): 3925. http://dx.doi.org/10.1182/blood.v118.21.3925.3925.
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Abstract Abstract 3925 According to The European Myeloma Network(1), FISH analysis of plasma cell myeloma (multiple myeloma, or MM) should be performed on samples enriched for plasma cells or an assay that allows for identification and study of plasma cells apart from other cells should be utilized. We enriched 400 bone marrow samples sent to our laboratory from May-September 2010 using CD138 antibody microbeads for plasma cells and then performed FISH utilizing probes for CEP3, CEP7, CEP9, CEP11, IgH breakapart, IgH/CCND1 (11;14), IgH/MAF (14;16), IgH/FGFR3(4;14), Rb1/13q, and TP53/CEP17. The genotypic profiles were then compared to the immunophenotypic profiles of monoclonal plasma cells derived from flow cytometric immunophenotyping for the following antibodies: CD38, CD19, CD56, CD117, CD20, HLA DR, CD45 and CD10. We identified genetic abnormalities in 90.6% (184/203) of the samples with monoclonal plasma cell percentages of 0.1% or more as detected by concurrent flow cytometric analysis. The most common identified genetic abnormality was aneuploidy {55.5% (222/400)}, either as a sole finding or in combination with translocations or gene loss. The aneuploid samples were further found to be hyperdipoid {23.75% (95/400)}, hypodiploid {15.75% (63/400)}, or polypoid {16.00% (64/400)}. IgH rearrangement was the seond most common abnormality and was seen in 30.2% of the 400 cases. The IgH rearrangements and frequencies were as follows: 11.25% (45/400) with t(11;14), 5.5% (22/400) with t(4;14), 3.0% (12/400) with 14;16, and 10.5% (42/100) with IgH translocation with partners unknown. Deletion of chromosome 13q/monosomy 13 was observed in 26% (104/400) of cases. This was an isolated finding in 3/400 (0.75%), observed with aneuploidy in 71/400 (17.75%), and seen in combination with IgH rearrangement in 64/400 (16.0%). There was a strong association between del (13q14) and IgH rearrangement, especially with t(4;14) and t(14;16). Loss of TP53 was observed in 3.8% (15/400) of cases. This was an isolated finding in 0/400 (0%), observed with aneuploidy in 14/400 (3.5%), and seen in combination with IgH rearrangement in 8/400 (2%). We explored the relationship between identified genetic abnormalities and respective immunophenotypic findings for the cases. Our results showed that t(4;14) was significantly associated with expression of CD56 (17/17 positive, 100%) and the absence of CD117 (76.5% negative, 13/17) and CD20 (82.4% negative, 14/17). On the other hand, t(14;16) was only rarely seen in combination with CD56 expression (88.9% negative, 8/9) or CD20 expression (100% negative, 9/9), but was highly associated with CD117 expression (66.7% positive, 6/9). t(11;14) was associated with CD20 expression (21.9% positive, 7/32), CD56 expression (34.4% positive, 11/32), and CD117 expression (37.5% positive, 12/32). Additionally, our results found that both CD56 and CD117 expression correlate with aneuploidy. Disclosures: No relevant conflicts of interest to declare.
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Xuan, Ying, Qizhong Gao, Chenhu Wang, and Dongyan Cai. "Positive peritoneal lavage fluid cytology based on isolation by size of epithelial tumor cells indicates a high risk of peritoneal metastasis." PeerJ 12 (June 28, 2024): e17602. http://dx.doi.org/10.7717/peerj.17602.
Повний текст джерелаАнотація:
Background Peritoneal metastasis (PM) is the most prevalent type of metastasis in patients with gastric cancer (GC) and has an extremely poor prognosis. The detection of free cancer cells (FCCs) in the peritoneal cavity has been demonstrated to be one of the worst prognostic factors for GC. However, there is a lack of sensitive detection methods for FCCs in the peritoneal cavity. This study aimed to use a new peritoneal lavage fluid cytology examination to detect FCCs in patients with GC, and to explore its clinical significance on diagnosing of occult peritoneal metastasis (OPM) and prognosis. Methods Peritoneal lavage fluid from 50 patients with GC was obtained and processed via the isolation by size of epithelial tumor cells (ISET) method. Immunofluorescence and fluorescence in situ hybridization (FISH) were used to identify FCCs expressing chromosome 8 (CEP8), chromosome 17 (CEP17), and epithelial cell adhesion molecule (EpCAM). Results Using a combination of the ISET platform and immunofluorescence-FISH, the detection of FCCs was higher than that by light microscopy (24.0% vs. 2.0%). Samples were categorized into positive and negative groups, based on the expressions of CEP8, CEP17, and EpCAM. Statistically significant relationships were demonstrated between age (P = 0.029), sex (P = 0.002), lymphatic invasion (P = 0.001), pTNM stage (P = 0.001), and positivity for FCCs. After adjusting for covariates, patients with positive FCCs had lower progression-free survival than patients with negative FCCs. Conclusion The ISET platform highly enriched nucleated cells from peritoneal lavage fluid, and indicators comprising EpCAM, CEP8, and CEP17 confirmed the diagnosis of FCCs. As a potential detection method, it offers an opportunity for early intervention of OPM and an extension of patient survival.
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Du, Jiang, Li Xu, Yun Cui, Zhaoxia Liu, Yujin Su, and Guilin Li. "Benign notochordal cell tumour: clinicopathology and molecular profiling of 13 cases." Journal of Clinical Pathology 72, no. 1 (October 24, 2018): 66–74. http://dx.doi.org/10.1136/jclinpath-2018-205441.
Повний текст джерелаАнотація:
AimsTo study the clinicopathological and molecular features of benign notochordal cell tumours (BNCTs) and their differential diagnosis from chordoma.Methods13 cases of BNCT were investigated. The genome-wide copy number imbalances were performed using Oncoscan CNV array in three cases and fluorescence in situ hybridisation (FISH) detection of epidermal growth factor receptor (EGFR)/chromosome 7 enumeration probe (CEP7), LSI1p36/1q21, LSI19p13/19q13, CEP3/CEP12 and Telvysion 6 P was performed in 13 cases.ResultsAll 13 BNCTs were symptomatic and eight cases showed a close relationship with the bones of the skull base. The important histological character for differential diagnosis with chordoma was the absence of extracellular matrix and eosinophil cells and the presence of vacuoles in most tumour cells. Immunohistochemical staining of AE1/AE3, vimentin, epithelial membrane antigen, S-100 and brachyury (100% each) were positive in BNCTs. Gain of chromosome 7 occurred in 10 cases (76.9%), gain of 1p in four (30.8%), gain of 1q in five (38.5%), gain of 19p and 19q in five (38.5%), gain of chromosome 12 in 11 cases (84.6%), gain of 6p in eight (61.5%) and gain of chromosome 3 in four cases (30.8%).ConclusionsIn contrast to chordoma, chromosome gain or normal copy number was more common while chromosome loss was infrequent in BNCTs. This may be a differential diagnosis clue for chordoma and may be an important characteristic in the progression of notochordal cell tumours.
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Roberts, Ianto, Stephanie Smith, Elisabeth Stes, Bert De Rybel, An Staes, Brigitte van de Cotte, Maria Fransiska Njo, et al. "CEP5 and XIP1/CEPR1 regulate lateral root initiation in Arabidopsis." Journal of Experimental Botany 67, no. 16 (June 13, 2016): 4889–99. http://dx.doi.org/10.1093/jxb/erw231.
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Strunnikov, A. V., J. Kingsbury, and D. Koshland. "CEP3 encodes a centromere protein of Saccharomyces cerevisiae." Journal of Cell Biology 128, no. 5 (March 1, 1995): 749–60. http://dx.doi.org/10.1083/jcb.128.5.749.
Повний текст джерелаАнотація:
We have designed a screen to identify mutants specifically affecting kinetochore function in the yeast Saccharomyces cerevisiae. The selection procedure was based on the generation of "synthetic acentric" minichromosomes. "Synthetic acentric" minichromosomes contain a centromere locus, but lack centromere activity due to combination of mutations in centromere DNA and in a chromosomal gene (CEP) encoding a putative centromere protein. Ten conditional lethal cep mutants were isolated, seven were found to be alleles of NDC10 (CEP2) encoding the 110-kD protein of yeast kinetochore. Three mutants defined a novel essential gene CEP3. The CEP3 product (Cep3p) is a 71-kD protein with a potential DNA-binding domain (binuclear Zn-cluster). At nonpermissive temperature the cep3 cells arrest with an undivided nucleus and a short mitotic spindle. At permissive temperature the cep3 cells are unable to support segregation of minichromosomes with mutations in the central part of element III of yeast centromere DNA. These minichromosomes, when isolated from cep3 cultures, fail to bind bovine microtubules in vitro. The sum of genetic, cytological and biochemical data lead us to suggest that the Cep3 protein is a DNA-binding component of yeast centromere. Molecular mass and sequence comparison confirm that Cep3p is the p64 component of centromere DNA binding complex Cbf3 (Lechner, 1994).
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Hédé-Haüy, Benoît, and Nicolas Ciaravola. "CEPA et CEPN, au service de l’innovation opérationnelle dans la Marine." Revue Défense Nationale N° 809, no. 4 (April 1, 2018): 65–71. http://dx.doi.org/10.3917/rdna.809.0065.
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Lopes, Jeane Cândida, Aloisio Freitas Chagas Junior, Gessiel Newton Scheidt, Layssah Passos Soares, and Lillian França Borges Chagas. "Biomassa e extração de quitina e quitosana a partir de isolados de Cunninghamella sp." Semina: Ciências Biológicas e da Saúde 38, no. 1 (December 18, 2017): 25. http://dx.doi.org/10.5433/1679-0367.2017v38n1p25.
Повний текст джерелаАнотація:
O estudo objetivou avaliar a produção de biomassa de nove isolados de Cunninghamella sp. e da cepa referência de Cunninghamella elegans (CBMAI 0843) e estabelecer a capacidade de produção de quitina e quitosana por estas cepas. Assim como, caracterizar a quitosana fúngica obtida por parâmetros como massa molar, grau de desacetilação e distribuição dos grupos funcionais ao longo da cadeia polimérica. Para a maioria das cepas avaliadas, o período de maior crescimento foi em 48 horas de cultivo, sendo que, neste período, o isolado UFT Ce08 apresentou a maior quantidade de biomassa, 20,17 g L-1. Os rendimentos de quitina ficaram entre 15,64 a 30,33% e os rendimentos de quitosana entre 0,94 a 7,43%. A cepa UFT Ce11 apresentou o melhor quantitativo de quitina e a cepa UFT Ce09, mesmo apresentando o segundo menor quantitativo de biomassa, 9,34 g L-1, teve o melhor rendimento de quitosana. Sete cepas isoladas no presente estudo apresentaram maior rendimento de quitosana comparada à cepa referência. O grau médio de desacetilação foi de 83,7% para quitosana obtida do isolado UFT Ce09 e 80,5% para quitosana obtida da cepa referência. As massas molares para a quitosana do isolado UFT Ce09 e da cepa referência foram de 43,031 e 19,215 g mol-1, respetivamente. A espectrometria de infravermelho apresentou bandas com comprimentos de onda e grupos funcionais coincidentes com a literatura e com a quitosana comercial. A quitosana fúngica deste estudo apresentou propriedades que atestam sua qualidade e características de interesse biotecnológico e comercial.
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Matos, Ignacio, Rebeca Lozano, Emilio Fonseca, Jesus MariÂa Hernandez, Arantxa Amores, Lina Lopez, Carolina Lopez, Maria Angeles Hernandez, Juan Luis Hernandez, and Juan J. Cruz. "Isolation of circulating tumor cells in colon cancer patients by size and chromosomal abnormalities." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e22058-e22058. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e22058.
Повний текст джерелаАнотація:
e22058 Background: Determining the number of circulating tumor cells (CTCs) in patients with metastatic colorectal cancer (CRC) has shown to be a prognostic factor, recent studies have proven the existence of EpCAM and cytokeratin negative CTCs. These cells present morphological and genetic alterations. Our study is based on an algorithm determined by the selection of the size of the cells and the genetic alterations detected by FISH which enables the isolation of CTCs in CRC patients by an automated system of fluorescence. Methods: Patients with metastatic CRC with normal blood differential and healthy controls between June 2011 and June 2012 were chosen. The objective was to show the differences between the quantification of morphogenetically altered cells in peripheral blood obtained from control and patients. The selected cells were over 7 micra in size and presented two or more genetic alterations. A combination of four probe sets was used: centromeric probe for CEP3, CEP7 and CEP17 and LSI p16INK4A 9p21.3. Fluorescent signals in specimens were quantified using an automated fluorescent system (Metafer) that is capable of scanning and classifying hundreds of cells under fluorescent illumination and allows for detection of cells according to nuclear size > 7 um and FISH pattern based on the algorithm that we have developed. Results: We selected 28 healthy individuals and 45 patients with CRC. In all the cases, 1,000 cells were analyzed in each individual. Only 30 cells >7 micra being found in the controls out of the 28,000 cells analyzed (0.1%). In the case of the patients, 640 cells were found (1.42%), the difference becoming statistically relevant after the T-test (p=0.003). None of the controls presented cells with two or more genetic alterations and over 7 micra in size, whereas 38% of the patients presented these characteristics despite having received treatment. The most frequent chromosomal changes were trisomy 3 and 17 (26% and 18%, respectively). Conclusions: This method allows us to select genetically abnormal circulating cells in a simple and automatic way. This opens the door for future studies to analyze the prognostic factor and the response rate to treatment under this method.
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NIYAZ, MADINIYAT, ABLAJAN ABDURAHMAN, ABDUGHENI TURGHUN, and IDIRIS AWUT. "CEP3 and CEP17 DNA probe potential in the genetic diagnosis and prognostic prediction of esophageal squamous cell cancer." Experimental and Therapeutic Medicine 11, no. 4 (February 16, 2016): 1375–80. http://dx.doi.org/10.3892/etm.2016.3080.
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Bernasconi, Paolo, Celeste Calvello, Catherine Klersy, Irene Dambruoso, Marina Boni, Stefania Casarin, Giovanni Paladini, Vittorio Perfetti, and Giampaolo Merlini. "FISH reveals chromosomal abnormalities in 41 Patients with Systemic Amyloidosis (AL)." Blood 116, no. 21 (November 19, 2010): 1197. http://dx.doi.org/10.1182/blood.v116.21.1197.1197.
Повний текст джерелаАнотація:
Abstract Abstract 1197 Over the past fifteen years FISH has considerably improved our ability to reveal consistent chromosomal changes in M-GUS, MM and plasma cell leukaemia (PCL), providing evidence of common genetic disease mechanisms and parameters to guide therapeutic decisions. In contrast, this information is still limited in AL due to the rarity of the disease, the low burden and the low proliferative index of clonal PCs. However, recent studies have suggested that in AL FISH, either combined with cytoplasmic staining of specific IgL (cIg-FISH) or performed on immuno-selected PCs, can reveal aneuploidies and translocations involving the immunoglobulin heavy chain locus (IGH). Based on these data we applied FISH to study 41 consecutive AL patients in order to establish the incidence of chromosomal abnormalities and their possible correlation with clinical parameters and outcome. In addition, since in every patient FISH was carried out on immuno-selected and immuno-stained PCs a comparison between these two FISH methods ((iFISH and cIg-FISH respectively) was made. The diagnosis of primary AL was based on the demonstration of amyloid deposits in tissues and organs, the identification of a monoclonal protein in serum or urine, the predominance of a monoclonal k or λ plasma cell population in the bone marrow. iFISH and cIg-FISH were carried out with the FGFR3/IGH [t(4;14)] dual color dual fusion, the CCND1/IGH [t(11;14)] dual color dual fusion, the IgH/c-MAF [t(14;16)] dual color dual fusion, the CEP7, the CEP9, the LSI D13S319+LSI 13q34, the LSI ATM+CEP11, the LSI p53+CEP17 probes (Vysis, Downers Grove, IL, USA) and with the ON MM 1q21/8p21.1 and the 4q21 tricolor probes (Kreated, Amsterdam, The Netherlands). Probes cut-off values were calculated by applying a one tail binomial distribution with a 95% confidence interval to the results obtained from the analysis of 1500 nuclei from five normal controls. For monosomies cut-off values were fixed at 8.3%, for trisomies at 3%, for translocations at 10%. The Mann Whitney U test and the Fisher exact test were used to make statistical comparisons. A 2-sided p-value <0.05 was considered statistically significant. Karyotype defects had an incidence of 87.8% on iFISH and of 80.4% on cIg-FISH. An insufficient PCs number in cytospin preparation was the major drawback of cIg-FISH. However, the two FISH approaches revealed similar percentages of abnormal cells. IGH rearrangements were the most frequent karyotype alterations and their incidence was 51.2%. The CCND1 locus was the most common IGH partner being involved in 41.5% of patients and was followed by the c-MAF locus involved in two patients (4.8%). No patient with the t(11;14) translocation presented a FISH pattern suggestive of a 11q13 (CCND1 locus) gain which, instead, was observed in ten t(11;14) negative patients. Monosomy 13/13q deletion and 1q21 amplification were revealed in 34.1% and 31.7% of patients respectively. Hyperdiploidy had a frequency of 24.4%. The t(11;14) was rare in patients with major peripheral nervous system involvement (p=0.027) and was not correlated with cardiac involvement (p=0.5). Moreover, t(11;14) positive patients presented a median bone marrow PCs percentage similar to that of patients with amp1q21 and higher than that of 13q-/-13 patients. No defect correlated with an increased bone marrow PCs infiltration. In conclusion: i) iFISH and cIg-FISH provided very similar results; ii) chromosomal defects had an incidence of 80–88%; iii) the t(11;14) was significantly correlated with absence of peripheral nervous system involvement; iv) no chromosomal defect was associated with a significant increase of median BM PCs infiltration. Our data confirm the relevant role of CCDN1 in AL pathogenesis. Disclosures: Merlini: Millennium: Honoraria; Ortho-Biotech: Honoraria.
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Reichenbecher, Marisa, Friedrich Lottspeich, and Karin Bronnenmeier. "Purification and Properties of a Cellobiose Phosphorylase (CepA) and a Cellodextrin Phosphorylase (CepB) from the Cellulolytic Thermophile Clostridium Stercorarium." European Journal of Biochemistry 247, no. 1 (July 1997): 262–67. http://dx.doi.org/10.1111/j.1432-1033.1997.00262.x.
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Lian, Defu, Xing Xie, Vincent W. Zheng, Nicholas Jing Yuan, Fuzheng Zhang, and Enhong Chen. "CEPR." ACM Transactions on Intelligent Systems and Technology 6, no. 1 (March 11, 2015): 1–27. http://dx.doi.org/10.1145/2629557.
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Abdellatif, Ahmed A. H., Amer Mahmood, Mansour Alsharidah, Hamdoon A. Mohammed, Salman Khalaf Alenize, Abdellatif Bouazzaoui, Osamah Al Rugaie, et al. "Bioactivities of the Green Synthesized Silver Nanoparticles Reduced Using Allium cepa L Aqueous Extracts Induced Apoptosis in Colorectal Cancer Cell Lines." Journal of Nanomaterials 2022 (February 4, 2022): 1–13. http://dx.doi.org/10.1155/2022/1746817.
Повний текст джерелаАнотація:
Allium cepa L (A. cepa) extract is frequently used as an adjuvant food in cancer treatment. We hypothesized that it contains a source of anticancer activity. There is a need to synthesize the silver nanoparticles (AgNPs) using an environment-friendly green synthesis reduction method using an aqueous extract of A. cepa. The AgNPs-CEPA were prepared by reduction method using the aqueous extract of A. cepa. The formed AgNPs-CEPA were characterized for their sizes and charge distribution. The AgNP-CEPA was investigated for its antioxidant and anticancer properties. Cell viability was evaluated by MTT assay. Gene expression was evaluated by real-time polymerase chain reaction (RT-PCR), and apoptosis measurement was carried out by flow cytometry in AgNP-CEPA-treated cells. The results showed a uniform size for AgNPs-CEPA of 155 ± 2.1 nm with a zeta potential of − 37.3 ± − 2.92 mv. The produced AgNPs-CEPA are biocompatible with anticancer action and a moderate level of antioxidant reactivity. AgNPs-CEPA showed better reducing activity for A. cepa extract compared to the AgNPs-CEPA. AgNP-CEPA treatment of human colorectal cancer cell lines (HT-29 and SW620) inhibited cell proliferation and altered Bcl2 family gene expression. Moreover, exposure of cell lines to AgNPs-CEPA resulted in the significant induction of apoptosis compared to A. cepa and AgNO3. These findings indicate that AgNP-CEPA induces apoptosis by inhibiting Bcl2 family gene expression, suggesting that this formula is a promising anticancer agent for treating colorectal cancer.
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De la Fuente, Juan Ramón. "El CEPE." Decires 5, no. 5 (December 1, 2001): 15–18. http://dx.doi.org/10.22201/cepe.14059134e.2001.5.5.91.
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Pulido González, Guillermo. "El CEPE." Decires 5, no. 5 (December 1, 2001): 21–24. http://dx.doi.org/10.22201/cepe.14059134e.2001.5.5.93.
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Cann, Howard M. "CEPH maps." Current Opinion in Genetics & Development 2, no. 3 (January 1992): 393–99. http://dx.doi.org/10.1016/s0959-437x(05)80148-0.
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Cann, Howard M. "CEPH maps." Current Biology 2, no. 6 (June 1992): 321. http://dx.doi.org/10.1016/0960-9822(92)90889-i.
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Tica, Yvanna Vien. "Cepi Corpus." Prairie Schooner 97, no. 2 (June 2023): 21–23. http://dx.doi.org/10.1353/psg.2023.a920337.
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Rohani, A. S., S. N. Rudang, R. N. Daulay, T. I. Hanum, and N. A. Juwita. "Characterization, phytochemistry screening and acute toxicity of Allium cepa fermented." IOP Conference Series: Earth and Environmental Science 1241, no. 1 (September 1, 2023): 012093. http://dx.doi.org/10.1088/1755-1315/1241/1/012093.
Повний текст джерелаАнотація:
Abstract The health benefit of Allium cepa could be obtained through processing using fermentation technique. This study aimed to obtain standardized fermented onion extract as raw material for medicinal preparations. In addition, this study determined the different content of secondary metabolites of unfermented and fermented Allium cepa then the acute toxicity was conducted to know the LD50.of Allium cepa fermented extract. Fermentation was done by saving the Allium cepa in a fermentation machine for 15 days at a temperature of 50-80°C. Allium cepa fermented was extracted by maceration using ethanol. Allium cepa fermented extract was characterized and tested for phytochemical screening. The characterization showed that the fermented extract of Allium cepa contained 3.47% of total ash, 0.39% of acid-insoluble ash, 15.51% of water-soluble, and 18.14% of ethanol-soluble. Phytochemical studies showed alkaloids, flavonoids, saponins, glycosides, and terpenoids in the unfermented Allium cepa extract while the Allium cepa fermented extract contained Flavonoids, Glycosides, and Triterpenoids. The LD50 of Allium cepa fermented extract was included as the preparations with a toxicity level of 6 (non-toxic). It showed that Allium cepa fermented extract has a stability-tested extract and included non-toxic criteria.
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Irisarri, P. "Un plasmido de Rhizobium loti involucrado en la competencia por la nodulación." Agrociencia 1, no. 1 (June 1997): 44–49. http://dx.doi.org/10.31285/agro.01.1081.
Повний текст джерелаАнотація:
La cepa U226 de Rhizobium loti posee un único plásmido críptico de 220 Mdal. Con el objetivo de estudiar funciones codificados por este plásmido, se lo marcó con Tn5-mob-sac y se sometió a la cepa a un tratamiento de cura de plásmido. Se evaluó el comportamiento de la cepa curada y la cepa salvaje en simbiosis con Lotus corniculatus. La eliminación del plásmido no afectó la inefectividad ni la efectividad de la fijación de nitrógeno. Sin embargo, en plántulas de lotus inoculadas con diferentes proporciones de la cepa con el plásmido y la cepa curada, se encontró que la cepa portadora del plásmido ocupaba la mayoría de los nódulos. Esto indicaría que el plásmido de la cepa de R. loti U226 está involucrado en la competencia por la ocupación de los nódulos.
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Gao, Jie. "CEPC and SppC Status — From the completion of CDR towards TDR." International Journal of Modern Physics A 36, no. 22 (August 10, 2021): 2142005. http://dx.doi.org/10.1142/s0217751x21420057.
Повний текст джерелаАнотація:
In November 2018, CEPC CDR was announced and since then, CEPC accelerator entered TDR phase towards its planned completion at the end of 2022. In this paper, we give status review of CEPC optimization design, hardware TDR R&D progresses, CEPC-SppC compatibility relation, civil engineering design, site selection, CIPC and international collaborations, etc. CEPC plan is also presented.
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Fuller, Kathy, Henry Hui, Jason Stanley, and Wendy N. Erber. "FISH By Imaging Flow Cytometry in CLL for Diagnosis and MRD Assessment." Blood 138, Supplement 1 (November 5, 2021): 2619. http://dx.doi.org/10.1182/blood-2021-152266.
Повний текст джерелаАнотація:
Abstract Chronic lymphocytic leukaemia is a genetically heterogeneous disease with treatment and prognosis varying based on chromosomal abnormalities. These are detectable in up to 80% of cases when tested on the nuclei of interphase cells by fluorescence in situ hybridisation (FISH). Despite the clinical importance of FISH in management, as only up to 200 nuclei are generally assessed, it is not suitable for minimal residual disease (MRD) assessment. Since clinical decisions are based on detection thresholds of 10 -4, MRD assays are restricted to flow cytometry and molecular based assessment. Here we have explored the utility of a cutting-edge automated imaging flow cytometry method that incorporates cell immunophenotype and FISH ("immuno-flowFISH") to detect chromosomal abnormalities in CLL. Aims: Our aim was to determine the capability of immuno-flowFISH using imaging flow cytometry to detect del(17p) and +12 in CLL, and, the lowest limit of detection. We hypothesized that this integrated automated immuno-flowFISH method would be suitable for MRD assessment of CLL. Methods: Blood from 75 patients with CLL, at diagnosis or on therapy, was analysed. For MRD studies, cells from the CI cell line were spiked into normal blood at concentrations of 0.001 - 10%. After red cell lysis, samples were incubated with CD3, CD5 and CD19 fluorophore-conjugated antibodies (fluorophores: BV480, BV605, AF647). Following fixation and membrane permeabilization, DNA was denatured at 78 oC for 5 mins. FISH probes to 17p12 and centromeres of chromosomes 12 and 17 were added and hybridized for 24 hours at 42 oC. Nuclei were then stained with SYTOX AADvanced and up to 600,000 cells acquired on the Amnis ® ImageStream ®XMk II imaging flow cytometer. Digital images (x60 objective) and quantitative data derived from computational algorithms (IDEAS software) were used to assess FISH signals overlying cell nuclei. IDEAS was then used to assess the number and percent CD19/CD5-positive CLL cells with FISH abnormalities. Results: Between 10,000 and 600,000 cells (mean 60,000) were acquired. CLL (CD19/CD5-positive) and T- (CD3/CD5-positive) cells could be clearly identified by their immunophenotype and assessed individually for probe signals. FISH signals were identifiable on the digital images as specific "spots" overlying the SYTOX AADvanced nuclear stain. The IDEAS software could enumerate the number of FISH spots per cell and this was confirmed by quantitative mean channel fluorescence intensity for each probe. A chromosome 12 or 17 abnormality was detected in 23 of the 75 CLL cases. Of these, 10 cases had only one 17p signal (but 2 for the centromere of chromosome 17), indicative of del(17p). Del(17p) was detected in 2-35% of CD19/CD5-positive cells (i.e. 0.4-23% or 270-35,441 of all cells), the lowest seen in a patient on cytoreductive therapy. In 13/75 cases, there were 3 FISH signals for CEP12, consistent with trisomy 12 (+12) in 0.1-46% of all cells analysed; the lowest number of 0.1% was when 26 out of 26,000 cells analysed were CD19/CD5-positive and had +12. We also performed multi-FISH, incorporating CEP12, CEP17 and 17p probes together with the CD3, CD5 and CD19 antibodies. This required 7-fluorophores (antibodies, probes and nucleus) and confirmed the ability to detect del(17p) and chromosome 12 copy number simultaneously in a single analysis. Spiking of CI CLL cells into normal blood demonstrated that +12 could be detected to a lowest limit of 10 -5. In all analyses, CLL cells had normal diploid spots for the control CEP17 probe, and the CD3/CD5-positive T cells had dual signals for CEP12, CEP17 and 17p12 probes on numerical analysis and on digital imagery. Conclusion: This study of confirms that high-throughput automated imaging flow cytometry, integrating FISH and immunophenotyping, can detect chromosomal defects in CLL. The lowest limit of detection for a FISH-detectable abnormality was 10 -5. This high sensitivity and specificity exceeds current clinical practice (10 -4), and was achieved through the analysis of many thousands of cells and positive identification of CLL cells based on their phenotype. This immuno-flowFISH method does not require any prior cell separation and is automated. It adds a new dimension to chromosomal analysis in CLL, both at diagnosis and for MRD monitoring. The high precision and specificity of immuno-flowFISH illustrates that this has a real place as a new MRD assessment tool for CLL. Disclosures No relevant conflicts of interest to declare.
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Arroyo, Rita, Sonia López, Enrique Romo, Gonzalo Montoya, Lía Hoz, Claudia Pedraza, Yonathan Garfias та Higinio Arzate. "Carboxy-Terminal Cementum Protein 1-Derived Peptide 4 (cemp1-p4) Promotes Mineralization through wnt/β-catenin Signaling in Human Oral Mucosa Stem Cells". International Journal of Molecular Sciences 21, № 4 (15 лютого 2020): 1307. http://dx.doi.org/10.3390/ijms21041307.
Повний текст джерелаАнотація:
Human cementum protein 1 (CEMP1) is known to induce cementoblast and osteoblast differentiation and alkaline phosphatase (ALP) activity in human periodontal ligament-derived cells in vitro and promotes bone regeneration in vivo. CEMP1′s secondary structure analysis shows that it has a random-coiled structure and is considered an Intrinsic Disordered Protein (IDP). CEMP1′s short peptide sequences mimic the biological capabilities of CEMP1. However, the role and mechanisms of CEMP1′s C-terminal-derived synthetic peptide (CEMP1-p4) in the canonical Wnt/β-catenin signaling pathway are yet to be described. Here we report that CEMP1-p4 promotes proliferation and differentiation of Human Oral Mucosa Stem Cells (HOMSCs) by activating the Wnt/β-catenin pathway. CEMP1-p4 stimulation upregulated the expression of β-catenin and glycogen synthase kinase 3 beta (GSK-3B) and activated the transcription factors TCF1/7 and Lymphoid Enhancer binding Factor 1 (LEF1) at the mRNA and protein levels. We found translocation of β-catenin to the nucleus in CEMP1-p4-treated cultures. The peptide also penetrates the cell membrane and aggregates around the cell nucleus. Analysis of CEMP1-p4 secondary structure revealed that it has a random-coiled structure. Its biological activities included the induction to nucleate hydroxyapatite crystals. In CEMP1-p4-treated HOMSCs, ALP activity and calcium deposits increased. Expression of Osterix (OSX), Runt-related transcription factor 2 (RUNX2), Integrin binding sialoproptein (IBSP) and osteocalcin (OCN) were upregulated. Altogether, these data show that CEMP1-p4 plays a direct role in the differentiation of HOMSCs to a “mineralizing-like” phenotype by activating the β-catenin signaling cascade.
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Mangum, Paul, and Ellen Peffley. "Analysis of (Allium cepa × A. fistulosum) × A. cepa Fourth-generation Backcross Populations for A. fistulosum Introgression." HortScience 35, no. 4 (July 2000): 568C—568b. http://dx.doi.org/10.21273/hortsci.35.4.568c.
Повний текст джерелаАнотація:
(Allium cepa × A. fistulosum) × A. cepa breeding lines have been established to the fourth generation. The aim is to develop an A. cepa-like bulbing onion carrying A. fistulosum genes. Seven populations were characterized for morphological traits and three isozyme markers. Each bulb from the populations was characterized for maturity, soluble solids content, bulb shape, and bulb color. All the populations produced A. cepa-like bulbs. Significant variation was observed within each population for each morphological trait. All the bulbs were screened for the presence of A. cepa and A. fistulosum alleles of alcohol dehydrogenase (Adh-1), esterase (Est), and phosphoglucoisomerase (Pgi-1). Allium cepa Adh-1, Est, and Pgi-1 alleles were observed in all the populations. One population, 951026-8, contained plants heterozygous for A. cepa and A. fistulosum Pgi-1 alleles. Recovery of these fourth generation Allium backcross plants demonstrates introgression of the A. fistulosum genome into an A. cepa-like bulbing onion.
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Gao, J. "CEPC-SPPC accelerator status towards CDR." International Journal of Modern Physics A 32, no. 34 (December 10, 2017): 1746003. http://dx.doi.org/10.1142/s0217751x17460034.
Повний текст джерелаАнотація:
In this paper we will give an introduction to the Circular Electron Positron Collider (CEPC). The scientific background, physics goal, the collider design requirements and the conceptual design principle of the CEPC are described. On the CEPC accelerator, the optimization of parameter designs for the CEPC with different energies, machine lengths, single ring and crab-waist collision partial double ring, advanced partial double ring and fully partial double ring options, etc. have been discussed systematically, and compared. The CEPC accelerator baseline and alternative designs have been proposed based on the luminosity potential in relation with the design goals. The CEPC sub-systems, such as the collider main ring, booster, electron positron injector, etc. have also been introduced. The detector and the MAchine-Detector Interface (MDI) design have been briefly mentioned. Finally, the optimization design of the Super Proton–Proton Collider (SppC), its energy and luminosity potentials, in the same tunnel of the CEPC are also discussed. The CEPC-SppC Progress Report (2015–2016) has been published.
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Ige, Serah Funke, and Aminat Aderayo Adekola. "Potential of Allium cepa in thromboembolism in Ulcerative Colitis in Rats." Journal of Drug Delivery and Therapeutics 11, no. 3-S (June 15, 2021): 74–80. http://dx.doi.org/10.22270/jddt.v11i3-s.4879.
Повний текст джерелаАнотація:
Colitis and coagulation influence each other and patients with colitis have been reported to have an increased risk of thromboembolic events. Allium cepa has been reported to have anti-coagulative activity and anti-inflammatory activity. This research was carried out to investigate the effect of Allium cepa on coagulation changes in colitis
Twenty eight rats weighed 180 ± 20g were used for this study. They were divided into four groups; Control group, Colitis group, Allium Cepa + Colitis group and Allium Cepa group. Allium Cepa + Colitis group and Allium Cepa were given 1ml/100g body weight of Allium cepa extract daily for 28days orally. Colitis was induced by a single dose of intra-rectal administration of 1ml/100g body weight of 6% acetic acid. Forty eight hours after the colitis induction, blood was taken by cardiac puncture for clotting time test, Prothrombin time (PT), Partial thromboplastin time with kaolin test (PTT.K), platelet count, Calcium ion and Potassium ion test.
Calcium ion was significantly decreased while potassium ion, platelet count, significantly increased and partial thromboplastin time shortened in colitis animals when compared with control. Calcium ion, potassium ion, platelet count and partial thromboplastin time showed no significant difference in Allium Cepa + Colitis group when compared with control. It can be concluded that Allium cepa has potential to reduced the risk of thromboembolism in colitis
Keywords: Colitis, Allium cepa, thromboembolism
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Santana, Maricela, Gonzalo Montoya, Raúl Herrera, Lía Hoz, Enrique Romo, Claudia Zamora, Ana Wintergerst, and Higinio Arzate. "Cemp1-p3 Peptide Promotes the Transformation of Octacalcium Phosphate into Hydroxyapatite Crystals." Crystals 10, no. 12 (December 11, 2020): 1131. http://dx.doi.org/10.3390/cryst10121131.
Повний текст джерелаАнотація:
Dental cementum contains unique molecules that regulate the mineralization process in vitro and in vivo, such as cementum protein 1 (CEMP1). This protein possesses amino acid sequence motifs like the human recombinant CEMP1 with biological activity. This novel cementum protein 1-derived peptide (CEMP1-p3, from the CEMP1’s N-terminal domain: (QPLPKGCAAVKAEVGIPAPH), consists of 20 amino acids. Hydroxyapatite (HA) crystals could be obtained through the combination of the amorphous precursor phase and macromolecules such as proteins and peptides. We used a simple method to synthesize peptide/hydroxyapatite nanocomposites using OCP and CEMP1-p3. The characterization of the crystals through scanning electron microscopy (SEM), powder X-ray diffraction (XRD), high--resolution transmission electron microscopy (HRTEM), and Raman spectroscopy revealed that CEMP1-p3 transformed OCP into hydroxyapatite (HA) under constant ionic strength and in a buffered solution. CEMP1-p3 binds and highly adsorbs to OCP and is a potent growth stimulator of OCP crystals. CEMP1-p3 fosters the transformation of OCP into HA crystals with crystalline planes (300) and (004) that correspond to the cell of hexagonal HA. Octacalcium phosphate crystals treated with CEMP1-p3 grown in simulated physiological buffer acquired hexagonal arrangement corresponding to HA. These findings provide new insights into the potential application of CEMP1-p3 on possible biomimetic approaches to generate materials for the repair and regeneration of mineralized tissues, or restorative materials in the orthopedic field.
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Delay, Christina, Kelly Chapman, Michael Taleski, Yaowei Wang, Sonika Tyagi, Yan Xiong, Nijat Imin, and Michael A. Djordjevic. "CEP3 levels affect starvation-related growth responses of the primary root." Journal of Experimental Botany 70, no. 18 (June 6, 2019): 4763–74. http://dx.doi.org/10.1093/jxb/erz270.
Повний текст джерелаАнотація:
AbstractCEPs (C-TERMINALLY ENCODED PEPTIDEs) inhibit Arabidopsis primary root growth by unknown mechanisms. We investigated how CEP3 levels control primary root growth. CEP3 peptide application decreased cell division, S-phase cell number, root meristematic cell number, and meristem zone (MZ) size in a dose- and CEP RECEPTOR1-dependent manner. Grafting showed that CEP3-dependent growth inhibition requires root and shoot CEPR1. CEP3 induced mitotic quiescence in MZ cells significantly faster than that induced by nutrient limitation alone. CEP3 also inhibited the restoration of S-phase to mitotically quiescence cells by nutrient resupply without quantitatively reducing TARGET OF RAPAMYCIN (TOR) kinase activity. In contrast, cep3-1 had an increased meristem size and S-phase cell number under nitrogen (N)-limited conditions, but not under N-sufficient conditions. Furthermore, cep3-1 meristematic cells remained in S-phase longer than wild-type cells during a sustained carbon (C) and N limitation. RNA sequencing showed that CEP3 peptide down-regulated genes involved in S-phase entry, cell wall and ribosome biogenesis, DNA replication, and meristem expansion, and up-regulated genes involved in catabolic processes and proteins and peptides that negatively control meristem expansion and root growth. Many of these genes were reciprocally regulated in cep3-1. The results suggest that raising CEP3 induces starvation-related responses that curtail primary root growth under severe nutrient limitation.