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Journal articles on the topic 'GTSE1'

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Author: Grafiati

Published: 11 March 2023

Last updated: 1 April 2023

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1

Zhang, Fan, Jingfei Meng, Hong Jiang, Xing Feng, Dongshan Wei, and Wen Meng. "GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling." Analytical Cellular Pathology 2021 (May 1, 2021): 1–11. http://dx.doi.org/10.1155/2021/5589532.

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The expression of G2 and S phase-expressed-1 (GTSE1) was upregulated in human cancer. However, its expression and roles in lung cancer have not been identified yet. In our study, we reported that GTSE1 expression was statistically higher in lung tissues than in the adjacent noncancerous tissues which might be a consequence of hypomethylation of the GTSE1 promoter. The upregulated expression of GTSE1 mRNA predicted the poorer survival of the lung patients. Ectopic expression of GTSE1 in lung cancer cells significantly increased while knockdown of GTSE1 decreased cell proliferation, cell migration, and cell invasion in H460 and A549 cells. Furthermore, knockdown of GTSE1 regulated the cell cycle and promoted cell apoptosis in H460 and A549 cells. Finally, we presented that GTSE1 was able to activate AKT/mTOR signaling in H460 and A549 cells. In conclusion, these results indicated that the overexpressed GTSE1 was involved in the progress of lung cancer by promoting proliferation migration and invasion and inhibiting apoptosis of lung cancer cells via activating AKT/mTOR signaling.

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2

Zheng, Yongchang, Yue Shi, Si Yu, Yuanyuan Han, Kai Kang, Haifeng Xu, Huajian Gu, Xinting Sang, Yang Chen, and Jingyu Wang. "GTSE1, CDC20, PCNA, and MCM6 Synergistically Affect Regulations in Cell Cycle and Indicate Poor Prognosis in Liver Cancer." Analytical Cellular Pathology 2019 (December 30, 2019): 1–13. http://dx.doi.org/10.1155/2019/1038069.

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GTSE1 is well correlated with tumor progression; however, little is known regarding its role in liver cancer prognosis. By analyzing the hepatocellular carcinoma (HCC) datasets in GEO and TCGA databases, we showed that high expression of GTSE1 was correlated with advanced pathologic stage and poor prognosis of HCC patients. To investigate underlying molecular mechanism, we generated GTSE1 knockdown HCC cell line and explored the effects of GTSE1 deficiency in cell growth. Between GTSE1 knockdown and wild-type HCC cells, we identified 979 differentially expressed genes (520 downregulated and 459 upregulated genes) in the analysis of microarray-based gene expression profiling. Functional enrichment analysis of DEGs suggested that S phase was dysregulated without GTSE1 expression, which was further verified from flow cytometry analysis. Moreover, three other DEGs: CDC20, PCNA, and MCM6, were also found contributing to GTSE1-related cell cycle arrest and to be associated with poor overall survival of HCC patients. In conclusion, GTSE1, together with CDC20, PCNA, and MCM6, may synergistically promote adverse prognosis in HCC by activating cell cycle. Genes like GTSE1, CDC20, PCNA, and MCM6 may be promising prognostic molecular biomarkers in liver cancer.

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3

Bendre, Shweta, Arnaud Rondelet, Conrad Hall, Nadine Schmidt, Yu-Chih Lin, Gary J. Brouhard, and Alexander W. Bird. "GTSE1 tunes microtubule stability for chromosome alignment and segregation by inhibiting the microtubule depolymerase MCAK." Journal of Cell Biology 215, no. 5 (November 23, 2016): 631–47. http://dx.doi.org/10.1083/jcb.201606081.

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The dynamic regulation of microtubules (MTs) during mitosis is critical for accurate chromosome segregation and genome stability. Cancer cell lines with hyperstabilized kinetochore MTs have increased segregation errors and elevated chromosomal instability (CIN), but the genetic defects responsible remain largely unknown. The MT depolymerase MCAK (mitotic centromere-associated kinesin) can influence CIN through its impact on MT stability, but how its potent activity is controlled in cells remains unclear. In this study, we show that GTSE1, a protein found overexpressed in aneuploid cancer cell lines and tumors, regulates MT stability during mitosis by inhibiting MCAK MT depolymerase activity. Cells lacking GTSE1 have defects in chromosome alignment and spindle positioning as a result of MT instability caused by excess MCAK activity. Reducing GTSE1 levels in CIN cancer cell lines reduces chromosome missegregation defects, whereas artificially inducing GTSE1 levels in chromosomally stable cells elevates chromosome missegregation and CIN. Thus, GTSE1 inhibition of MCAK activity regulates the balance of MT stability that determines the fidelity of chromosome alignment, segregation, and chromosomal stability.

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4

Tipton, Aaron R., Jonathan D. Wren, John R. Daum, Joseph C. Siefert, and Gary J. Gorbsky. "GTSE1 regulates spindle microtubule dynamics to control Aurora B kinase and Kif4A chromokinesin on chromosome arms." Journal of Cell Biology 216, no. 10 (August 18, 2017): 3117–32. http://dx.doi.org/10.1083/jcb.201610012.

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In mitosis, the dynamic assembly and disassembly of microtubules are critical for normal chromosome movement and segregation. Microtubule turnover varies among different mitotic spindle microtubules, dictated by their spatial distribution within the spindle. How turnover among the various classes of spindle microtubules is differentially regulated and the resulting significance of differential turnover for chromosome movement remains a mystery. As a new tactic, we used global microarray meta-analysis (GAMMA), a bioinformatic method, to identify novel regulators of mitosis, and in this study, we describe G2- and S phase–expressed protein 1 (GTSE1). GTSE1 is expressed exclusively in late G2 and M phase. From nuclear envelope breakdown until anaphase onset, GTSE1 binds preferentially to the most stable mitotic spindle microtubules and promotes their turnover. Cells depleted of GTSE1 show defects in chromosome alignment at the metaphase plate and in spindle pole integrity. These defects are coupled with an increase in the proportion of stable mitotic spindle microtubules. A consequence of this reduced microtubule turnover is diminished recruitment and activity of Aurora B kinase on chromosome arms. This decrease in Aurora B results in diminished binding of the chromokinesin Kif4A to chromosome arms.

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5

Short, Ben. "GTSE1 leads cancer cells into CIN." Journal of Cell Biology 215, no. 5 (November 25, 2016): 593. http://dx.doi.org/10.1083/jcb.2155if.

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6

Li, Ke. "MiR-509-3-5p inhibits colon cancer malignancy by suppressing GTSE1." Biochemical and Biophysical Research Communications 570 (September 2021): 175–83. http://dx.doi.org/10.1016/j.bbrc.2021.07.008.

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7

Yao, Chengjiao, Yilin Li, Lihong Luo, Qin Xiong, Xiaowu Zhong, Fengjiao Xie, and Peimin Feng. "Identification of miRNAs and genes for predicting Barrett’s esophagus progressing to esophageal adenocarcinoma using miRNA-mRNA integrated analysis." PLOS ONE 16, no. 11 (November 24, 2021): e0260353. http://dx.doi.org/10.1371/journal.pone.0260353.

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Barrett’s esophagus (BE) is defined as any metaplastic columnar epithelium in the distal esophagus, which predisposes to esophageal adenocarcinoma (EAC). Yet, the mechanism through which BE develops to EAC still remain unclear. Moreover, the miRNA-mRNA regulatory network in distinguishing BE from EAC still remains poorly understood. To identify differentially expressed miRNAs (DEMs) and genes (DEGs) between EAC and BE from tissue samples, gene expression microarray datasets GSE13898, GSE26886, GSE1420 and miRNA microarray datasets GSE16456, GSE20099 were downloaded from Gene Expression Omnibus (GEO) database. GEO2R was used to screen the DEMs and DEGs. Pathway and functional enrichment analysis were performed by DAVID database. The protein–protein interaction (PPI) network was constructed by STRING and been visualized by Cytoscape software. Finnal, survival analysis was performed basing TCGA database. A total of 21 DEMs were identified. The enriched functions and pathways analysis inclued Epstein-Barr virus infection, herpesvirus infection and TRP channels. GART, TNFSF11, GTSE1, NEK2, ICAM1, PSMD12, CTNNB1, CDH1, PSEN1, IL1B, CTNND1, JAG1, CDH17, ITCH, CALM1 and ITGA6 were considered as the hub-genes. Hsa-miR-143 and hsa-miR-133b were the highest connectivity target gene. JAG1 was predicted as the largest number of target miRNAs. The expression of hsa-miR-181d, hsa-miR-185, hsa-miR-15b, hsa-miR-214 and hsa-miR-496 was significantly different between normal tissue and EAC. CDH1, GART, GTSE1, NEK2 and hsa-miR-496, hsa-miR-214, hsa-miR-15b were found to be correlated with survival.

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8

Scolz, Massimilano, Per O. Widlund, Silvano Piazza, Debora Rosa Bublik, Simone Reber, Leticia Y. Peche, Yari Ciani, et al. "GTSE1 Is a Microtubule Plus-End Tracking Protein That Regulates EB1-Dependent Cell Migration." PLoS ONE 7, no. 12 (December 7, 2012): e51259. http://dx.doi.org/10.1371/journal.pone.0051259.

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9

Lei, Xiao, Lehui Du, Pei Zhang, Na Ma, Yanjie Liang, Yanan Han, and Baolin Qu. "Knockdown GTSE1 enhances radiosensitivity in non–small‐cell lung cancer through DNA damage repair pathway." Journal of Cellular and Molecular Medicine 24, no. 9 (March 22, 2020): 5162–67. http://dx.doi.org/10.1111/jcmm.15165.

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10

Stelitano, Debora, Yamila Peche Leticia, Emiliano Dalla, Martin Monte, Silvano Piazza, and Claudio Schneider. "GTSE1: a novel TEAD4-E2F1 target gene involved in cell protrusions formation in triple-negative breast cancer cell models." Oncotarget 8, no. 40 (June 27, 2017): 67422–38. http://dx.doi.org/10.18632/oncotarget.18691.

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11

Wiseman, B. R., N. W. Widstrom, and W. W. McMillian. "INSECT RESISTANCE IN TWO RECENTLY RELEASED SWEET CORN INBREDS, GTS1 AND GTS21." Journal of Entomological Science 20, no. 1 (January 1, 1985): 16–19. http://dx.doi.org/10.18474/0749-8004-20.1.16.

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Two recently released sweet corn inbreds, ‘GTS1’ and ‘GTS2,’ were evaluated as inbreds and in hybrid combination for their resistance to the corn earworm, Heliothis zea (Boddie). Based on the weight of 6-day-old larvae and on damage to corn ears in the field at 15 days after silking, the level of resistance to the corn earworm was slightly altered from the original ‘471-U6’ and ‘81-1.’ A slight change in the mechanisms of resistance was shown in that GTS1 showed a slight antibiotic effect which apparently enhanced the performance of its hybrid.

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12

Apostolidis, Pani A., Stephan Lindsey, William M. Miller, and Eleftherios T. Papoutsakis. "Proposed megakaryocytic regulon of p53: the genes engaged to control cell cycle and apoptosis during megakaryocytic differentiation." Physiological Genomics 44, no. 12 (June 15, 2012): 638–50. http://dx.doi.org/10.1152/physiolgenomics.00028.2012.

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During endomitosis, megakaryocytes undergo several rounds of DNA synthesis without division leading to polyploidization. In primary megakaryocytes and in the megakaryocytic cell line CHRF, loss or knock-down of p53 enhances cell cycling and inhibits apoptosis, leading to increased polyploidization. To support the hypothesis that p53 suppresses megakaryocytic polyploidization, we show that stable expression of wild-type p53 in K562 cells (a p53-null cell line) attenuates the cells' ability to undergo polyploidization during megakaryocytic differentiation due to diminished DNA synthesis and greater apoptosis. This suggested that p53's effects during megakaryopoiesis are mediated through cell cycle- and apoptosis-related target genes, possibly by arresting DNA synthesis and promoting apoptosis. To identify candidate genes through which p53 mediates these effects, gene expression was compared between p53 knock-down (p53-KD) and control CHRF cells induced to undergo terminal megakaryocytic differentiation using microarray analysis. Among substantially downregulated p53 targets in p53-KD megakaryocytes were cell cycle regulators CDKN1A (p21) and PLK2, proapoptotic FAS, TNFRSF10B, CASP8, NOTCH1, TP53INP1, TP53I3, DRAM1, ZMAT3 and PHLDA3, DNA-damage-related RRM2B and SESN1, and actin component ACTA2, while antiapoptotic CKS1B, BCL2, GTSE1, and p53 family member TP63 were upregulated in p53-KD cells. Additionally, a number of cell cycle-related, proapoptotic, and cytoskeleton-related genes with known functions in megakaryocytes but not known to carry p53-responsive elements were differentially expressed between p53-KD and control CHRF cells. Our data support a model whereby p53 expression during megakaryopoiesis serves to control polyploidization and the transition from endomitosis to apoptosis by impeding cell cycling and promoting apoptosis. Furthermore, we identify a putative p53 regulon that is proposed to orchestrate these effects.

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13

Wang, Shuaiqun, Xiaoling Xu, and Wei Kong. "Identification of Hub Genes Associated with Lung Adenocarcinoma Based on Bioinformatics Analysis." Computational and Mathematical Methods in Medicine 2021 (April 16, 2021): 1–12. http://dx.doi.org/10.1155/2021/5550407.

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Lung adenocarcinoma (LUAD) is one of the malignant lung tumors. However, its pathology has not been fully understood. The purpose of this study is to identify the hub genes associated with LUAD by bioinformatics methods. Three gene expression datasets including GSE116959, GSE74706, and GSE85841 downloaded from the Gene Expression Omnibus (GEO) database were used in this study. The differentially expressed genes (DEGs) related to LUAD were screened by using the limma package. Gene Ontology (GO) and KEGG analysis of DEGs were carried out through the DAVID website. The protein-protein interaction (PPI) of differentially expressed genes was drawn by the STRING website, and the results were imported into Cytoscape for visualization. Then, the PPI network was analyzed by using MCODE, and the modules with a score greater than 5 were found by using cytoHubba. Finally, the GEPIA database and UALCAN database were used to verify and analyze the survival of hub genes. We identified 67 upregulated genes and 277 downregulated genes from three LUAD datasets. The results of GO analysis showed that the downregulated genes were significantly enriched in matrix adhesion and angiogenesis and upregulated differential genes were significantly enriched in cell adhesion and vascular development. KEGG pathway analysis showed that the differential genes of LUAD were significantly enriched in viral carcinogenesis and adhesion spots. The PPI network of differentially expressed genes consists of 269 nodes and 625 interactions. In addition, three modules with scores greater than 5 and seven hub genes, namely, MCM4, BIRC5, CDC20, CDC25C, FOXM1, GTSE1, and RFC4, playing an important role in the PPI network were screened out. In this study, we obtained the hub genes and pathways related to LUAD, revealing the molecular mechanism and pathogenesis of LUAD, which is helpful for the early detection of LUAD and provides a new idea for the treatment of LUAD.

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14

Fernández, Ester Calvo, Junqiang Wang, Aaron Griffin, Hanna Minns, Hong-Jian Wei, Xu Zhang, Luca Szalontay, et al. "DIPG-57. A systems biology approach to defining and targeting master regulator dependencies from bulk and single-Cell RNA-seq in diffuse midline glioma (DMG)." Neuro-Oncology 24, Supplement_1 (June 1, 2022): i31—i32. http://dx.doi.org/10.1093/neuonc/noac079.114.

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Abstract Diffuse midline glioma (DMG) are fatal pediatric brain tumors with no effective systemic therapies. Molecular profiling demonstrates epigenetic dysregulation and heterogeneity, and novel approaches are needed to identify promising drugs and drug combinations. We used network-based computational analysis of RNA-seq to discover Master Regulator (MR) proteins that represent targetable, mechanistic determinants of distinct DMG cell states. We reverse-engineered the first DMG-specific regulatory network from 122 publicly available DMG RNA-seq profiles with ARACNe. Using this network, we measured sample-specific protein activity based on differential expression of their targets via VIPER. Activity-based clustering identified two clusters showing a trend in survival differences (>1 year, by χ2). The most activated MRs (i.e., TOP2A, CENPF, BUB1B, FOXM1, GTSE1, MKI67, E2F8), relative to normal caudate tissue, were enriched in cell cycle regulation members. The cluster with worse outcomes had significantly higher activity. Targetable MRs activated in subsets of patients () included TOP2A, CHEK1, CDK2, and EZH2. RNA-seq profiles were generated in two DMG cell lines following perturbation with ~400 oncology drugs, and used to identify drugs that invert MR activity profiles with the OncoTreat algorithm. We identified four pharmacotypes, and predicted sensitivity to HDAC, proteosome, EGFR, MEK, and PI3K inhibitors (), amongst others, consistent with published DMG high-throughput drug screens. To dissect intra-tumor heterogeneity, we measured protein activity from published single-cell RNA-seq profiles of 6 DMG patients, using single-cell based regulatory networks. Preliminary activity-based analysis identified 6 cell states representing distinct stages of differentiation/proliferation, including an oligodendrocyte precursor cell-like proliferative state whose MRs overlapped with bulk data (i.e. TOP2A, CENPF, FOXM1, E2F8, ZWINT, CCNA2), suggesting this as a key regulatory module. We are identifying cell state-specific MR-inverter drugs with OncoTreat to ultimately suggest drugs and drug combinations that collapse the transcriptional program and induce tumor kill for validation in MR-matched preclinical DMG models.

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15

Arıkan, Burcu, Aslı Semercі, Ozgur Cakır, and Kara Turgut. "Arabidopsis thaliana GTS1 transcripts are activated by yeast extract." Botanica Serbica 45, no. 2 (2021): 195–201. http://dx.doi.org/10.2298/botserb2102195a.

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WD40 repeat-containing proteins participate in DNA-protein and protein-protein interactions and positively regulate plant stress responses. GTS1, known as a WD40 repeat-containing protein, works as a scaffold protein and is important in ribosome biogenesis and also biomass accumulation. In this study, we evaluated the GIGANTUS1 (GTS1) gene expression in response to biotic and abiotic stress factors in Arabidopsis thaliana plants. In addition, we grew and characterized A. thaliana gts1 mutant (T-DNA SALK_010647) in order to observe the effects of its absence on plants. According to our results, 100-200 mM abscisic acid (ABA) and 100-200 mM sodium chloride (NaCl) treatment did not cause any changes in GTS1 gene expression, while only 6 h of 1 g/l and 2 g/l yeast extract (YE) treatment negatively affected GTS1 expression in 10-day-old plant explants. After 10 and 30 days of YE treatment, GTS1 gene expression was upregulated, and as a consequence plant growth efficiency was reduced. We thus concluded that through the downregulation of GTS1 transcripts, we could obtain better growth and/or higher biomass, which seems to be a good option for agricultural recruitments.

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16

Singh, Prerna, John Eley, Nayab Mahmood, Binny Bhandary, Tijana Dukic, Kevin J. Tu, Jerimy Polf, et al. "Therapeutic Efficacy of Variable Biological Effectiveness of Proton Therapy in U-CH2 and MUG-Chor1 Human Chordoma Cell Death." Cancers 13, no. 23 (December 4, 2021): 6115. http://dx.doi.org/10.3390/cancers13236115.

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Background: Chordoma is a cancer of spinal cord, skull base, and sacral area. Currently, the standard of care to treat chordoma is resection followed by radiation therapy. Since, chordoma is present in the spinal cord and these are very sensitive structures and often complete removal by surgery is not possible. As a result, chordoma has a high chance of recurrence and developing resistance to radiation therapy. In addition, treatment of chordoma by conventional radiation therapy can also damage normal tissues surrounding chordoma. Thus, current therapeutic options to treat chordoma are insufficient and novel therapies are desperately needed to treat locally advanced and metastatic chordoma. (2) Methods: In the present investigation, human chordoma cell lines of sacral origin MUG-Chor1 and U-CH2 were cultured and irradiated with Proton Beam Radiation using the clinical superconducting cyclotron and pencil-beam (active) scanning at Middle and End of the Spread-Out Bragg Peak (SOBP). Proton radiation was given at the following doses: Mug-Chor1 at 0, 1, 2, 4, and 8 Gy and U-CH2 at 0, 4, 8, 12, and 16 Gy. These doses were selected based on a pilot study in our lab and attempted to produce approximate survival fractions in the range of 1, 0.9, 0.5, 0.1, and 0.01, respectively, chosen for linear quadratic model fitting of the dose response. (3) Results: In this study, we investigated relative biological effectiveness (RBE) of proton radiation at the end of Spread Out Bragg Peak assuming that the reference radiation is a proton radiation in the middle of the SOBP. We observed differences in the survival of both Human chordoma cell lines, U-CH2 and MUG-Chor1. The data showed that there was a significantly higher cell death at the end of the Bragg peak as compared to middle of the Bragg peak. Based on the linear quadratic (LQ) fit for cell survival we calculated the RBE between M-SOBP and E-SOBP at 95% CI level and it was observed that RBE was higher than 1 at E-SOBP and caused significantly higher cell killing. Proton field at E-SOBP caused complex DNA damage in comparison to M-EOBP and the genes such as DNA topoisomerase 1, GTSE1, RAD51B were downregulated in E-SOBP treated cells. Thus, we conclude that there seems to be substantial variation in RBE (1.3–1.7) at the E-SOBP compared with the M-SOBP.

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17

Mitsui, K., S. Yaguchi, and K. Tsurugi. "The GTS1 gene, which contains a Gly-Thr repeat, affects the timing of budding and cell size of the yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 14, no. 8 (August 1994): 5569–78. http://dx.doi.org/10.1128/mcb.14.8.5569-5578.1994.

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A gene with an open reading frame encoding a protein of 417 amino acid residues with a Gly-Thr repeat was isolated from the yeast Saccharomyces cerevisiae by using synthetic oligonucleotides encoding three Gly-Thr dimers as probes. The deduced amino acid sequence showed partial homology to the clock-affecting gene, per, of Drosophila melanogaster in the regions including the GT repeat. The function of the gene, named GTS1, was examined by characterizing the phenotypes of transformants with different copy numbers of the GTS1 gene produced either by inactivating the GTS1 gene by gene disruption (TM delta gts1) or by transformation with multicopy plasmid pPER119 (TMpGTS1). They grew at similar rates during the exponential growth phase, but the lag phases were shorter for TM delta gts1 and longer for TMpGTS1 cells than that for the wild type. Analyses of their cell cycle parameters using synchronized cells revealed that the unbudding period changed as a function of gene dosage; that is, the periods of TM delta gts1 and TMpGTS1 were about 20% shorter and longer, respectively, than that of the wild-type. Another significant change in the transformants was detected in the distribution of the cell size. The mean cell volume of the TM delta gts1 cells in the unbudded period (single cells) was 27% smaller than that of single wild-type cells, whereas that of single TMpGTS1 cells was 48% larger. Furthermore, in the temperature-sensitive cdc4 mutant, the GTS1 gene affected the timing of budding at the restrictive temperature. Thus, the GTS1 gene product appears to modulate the timing of budding to obtain an appropriate cell size independent of the DNA replication cycle.

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18

Mitsui, K., S. Yaguchi, and K. Tsurugi. "The GTS1 gene, which contains a Gly-Thr repeat, affects the timing of budding and cell size of the yeast Saccharomyces cerevisiae." Molecular and Cellular Biology 14, no. 8 (August 1994): 5569–78. http://dx.doi.org/10.1128/mcb.14.8.5569.

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A gene with an open reading frame encoding a protein of 417 amino acid residues with a Gly-Thr repeat was isolated from the yeast Saccharomyces cerevisiae by using synthetic oligonucleotides encoding three Gly-Thr dimers as probes. The deduced amino acid sequence showed partial homology to the clock-affecting gene, per, of Drosophila melanogaster in the regions including the GT repeat. The function of the gene, named GTS1, was examined by characterizing the phenotypes of transformants with different copy numbers of the GTS1 gene produced either by inactivating the GTS1 gene by gene disruption (TM delta gts1) or by transformation with multicopy plasmid pPER119 (TMpGTS1). They grew at similar rates during the exponential growth phase, but the lag phases were shorter for TM delta gts1 and longer for TMpGTS1 cells than that for the wild type. Analyses of their cell cycle parameters using synchronized cells revealed that the unbudding period changed as a function of gene dosage; that is, the periods of TM delta gts1 and TMpGTS1 were about 20% shorter and longer, respectively, than that of the wild-type. Another significant change in the transformants was detected in the distribution of the cell size. The mean cell volume of the TM delta gts1 cells in the unbudded period (single cells) was 27% smaller than that of single wild-type cells, whereas that of single TMpGTS1 cells was 48% larger. Furthermore, in the temperature-sensitive cdc4 mutant, the GTS1 gene affected the timing of budding at the restrictive temperature. Thus, the GTS1 gene product appears to modulate the timing of budding to obtain an appropriate cell size independent of the DNA replication cycle.

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19

Suryawijaya, Anita Natalia, Tutiek Purwanti, Djoko Agus Purwanto, and Widji Soeratri. "Characteristic and Physical Stability of Anti-Aging Green Tea Extract (GTE) on NLC with Argan Oil as Liquid Lipid." JURNAL FARMASI DAN ILMU KEFARMASIAN INDONESIA 9, no. 2 (August 31, 2022): 115–24. http://dx.doi.org/10.20473/jfiki.v9i22022.115-124.

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Background: Green tea extract is a hydrophilic antioxidant that is difficult to penetrate. A nanostructured lipid carrier (NLC) delivers a system consisting of solid-liquid lipids that can improve penetration. Argan oil is a vegetable oil that can be used as a liquid lipid in NLC, reducing particle size and increasing penetration by hydrating the skin. Objective: To determine the formula of NLC green tea extract (NLC-GTE) with liquid lipid argan oil, which has good characteristics and is stable. Methods: Preparation of NLC-GTE used the High Shear Homogenization with solid lipids (cetyl palmitate-glyceryl stearate) - liquid lipids (argan oil) NLC-GTE1 (50:50), NLC-GTE2 (70:30), and NLC-GTE3 (90:10). Characteristic tests included organoleptic, pH, particle size (PS), and polydispersity index (PI). The physical stability test (organoleptic, pH, PS, and PI) used the thermal cycling method (3 cycles six days). Result: NLC-GTE1 – NLC-GTE2 has an odor of argan oil. NLC-GTE3 has odorless. NLC-GTE1 – NLC-GTE3 has a pH scale from 5.782-5.784; PS ranges from 359.73–432.56 nm; PI ranges from 0.175-0.257. The statistical analysis results showed no significant difference between NLC-GTE1 – NLC-GTE3 in pH and PI, there was a significant difference in PS NLC-GTE1; NLC-GTE2 against NLC-GTE3. Physical stability test NLC-GTE2 – NLC-GTE3 phase separation occurs. The statistical analysis results showed no significant difference in pH values NLC-GTE1 – NLC-GTE3 before and after storage; there was a significant difference in NLC-GTE3 before and after storage. Conclusion: NLC-GTE1 was a formula with good characteristics and stability.

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20

Onishi, Ryo, Kaoru Sato, Kensaku Murano, Lumi Negishi, Haruhiko Siomi, and Mikiko C. Siomi. "Piwi suppresses transcription of Brahma-dependent transposons via Maelstrom in ovarian somatic cells." Science Advances 6, no. 50 (December 2020): eaaz7420. http://dx.doi.org/10.1126/sciadv.aaz7420.

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Drosophila Piwi associates with PIWI-interacting RNAs (piRNAs) and represses transposons transcriptionally through heterochromatinization; however, this process is poorly understood. Here, we identify Brahma (Brm), the core adenosine triphosphatase of the SWI/SNF chromatin remodeling complex, as a new Piwi interactor, and show Brm involvement in activating transcription of Piwi-targeted transposons before silencing. Bioinformatic analyses indicated that Piwi, once bound to target RNAs, reduced the occupancies of SWI/SNF and RNA polymerase II (Pol II) on target loci, abrogating transcription. Artificial piRNA-driven targeting of Piwi to RNA transcripts enhanced repression of Brm-dependent reporters compared with Brm-independent reporters. This was dependent on Piwi cofactors, Gtsf1/Asterix (Gtsf1), Panoramix/Silencio (Panx), and Maelstrom (Mael), but not Eggless/dSetdb (Egg)–mediated H3K9me3 deposition. The λN-box B–mediated tethering of Mael to reporters repressed Brm-dependent genes in the absence of Piwi, Panx, and Gtsf1. We propose that Piwi, via Mael, can rapidly suppress transcription of Brm-dependent genes to facilitate heterochromatin formation.

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21

Nain, Caroline Waingeh, Eric Mignolet, Marie-France Herent, Joëlle Quetin-Leclercq, Cathy Debier, Melissa M. Page, and Yvan Larondelle. "The Catechins Profile of Green Tea Extracts Affects the Antioxidant Activity and Degradation of Catechins in DHA-Rich Oil." Antioxidants 11, no. 9 (September 19, 2022): 1844. http://dx.doi.org/10.3390/antiox11091844.

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This study investigated the effect of the catechins profile on the antioxidant activity of green tea extracts (GTEs) by comparing the antioxidant activity of an EGC-rich GTE (GTE1, catechin content: 58% EGC, 30.1% EGCG, 7.9% EC, and 3.9% ECG) and an EGCG-rich GTE (GTE2, catechin content: 60.6% EGCG, 17.7% EGC, 11.8% ECG, and 9.8% EC) in a DHA-rich oil. The effects of the individual catechins (EGC, EC, EGCG, and ECG) and reconstituted catechins mixtures (CatMix), prepared to contain the same amount of major catechins as in the GTEs, were also measured. All treatments (GTE1, CatMix1, GTE2, CatMix2, EGC250, EC250, EGCG250, and ECG250), each containing epistructured catechins at a concentration of 250 ppm, as well as the control (oil with no added antioxidant), were stored at 30 °C for 21 days with sampling intervals of 7 days. The antioxidant activity was assessed by measuring the peroxide value (PV) and p-anisidine value (p-AV) of oils. Changes in fatty acid content and catechins content were also monitored. Both GTEs enhanced the oxidative stability of the DHA-rich oil, but GTE1 demonstrated a stronger antioxidant activity than GTE2. No significant difference was observed between the PV of treatments with GTE1 and CatMix1 during storage, whereas the PV of oil with GTE2 was significantly higher than that with CatMix2 after 21 days. Among the individual catechins, EGC was the strongest antioxidant. Overall, the antioxidant activities of the extracts and catechins were observed in the decreasing order GTE1 ≈ EGC250 ≈ CatMix1 > GTE2 > EGCG250 ≈ CatMix2 > ECG250 > EC250. A significant change in fatty acid content was observed for the control and EC250 samples, and the catechins were most stable in GTE1-supplemented oil. Our results indicate that the EGC-rich GTE is a more potent antioxidant in DHA-rich oil than the EGCG-rich GTE.

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Fernández, Ester Calvo, Junqiang Wang, Aaron T. Griffin, Luca Szalontay, Stergios Zacharoulis, Jovana Pavisic, and Andrea Califano. "Abstract 486: A systems biology approach to defining tumor heterogeneity, prognostic and targetable master regulator protein signatures from bulk and single cell RNA-seq in diffuse midline glioma (DMG)." Cancer Research 82, no. 12_Supplement (June 15, 2022): 486. http://dx.doi.org/10.1158/1538-7445.am2022-486.

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Abstract Despite major advances in molecular profiling and numerous clinical trials, diffuse midline glioma (DMG) remains a fatal disease with median survival of only ~9 months and no identified effective drugs. To address this challenge, we leveraged network-based methodologies to dissect the heterogeneity of DMG tumors and to discover Master Regulator (MR) proteins representing pharmacologically accessible, mechanistic determinants of molecularly distinct DMG cell states. The study has produced the first DMG-specific regulatory network, reverse-engineered from 122 publicly available pediatric DMG RNA-seq profiles with ARACNe (Basso et al. Nat Genet 2005). Using this network, we measured protein activity for each sample via VIPER (Alvarez et al., Nat Genet 2016). Activity-based clustering identified 2 clusters, characterized by significant overall survival difference (>1 year, p-val=0.02 by χ2 analysis). Protein activity signatures were not significantly associated with tumor location and Histone3 mutation status. The most aberrantly activated MR proteins across all DMG patients (i.e., TOP2A, CENPF, BUB1B, FOXM1, GTSE1, MKI67, and E2F8), relative to normal caudate tissue from GTEx, were highly enriched in cell cycle regulation members, with samples in the worst outcome cluster showing significantly higher activity. Pharmacologically accessible MRs found to be significantly activated in subsets of patients (p-val<10E-5) include TOP2A, CHEK1, CDK2, and EZH2. To dissect DMG intra-tumor heterogeneity, we measured protein activity from published single-cell RNA-seq profiles of 6 DMG patients, using single-cell based regulatory networks. Activity-based analysis of tumor cells identified 8 clusters representing distinct differentiation and proliferation stages—i.e. astrocyte-like, oligodendrocyte-like, and multiple oligodendrocyte precursor cell (OPC)-like subpopulations. Consistent with bulk-based findings, these included an OPC-like-cycling population presenting highly aberrant activity of proliferative MRs (i.e. TOP2A, CENPF, FOXM1, E2F8, ZWINT, and CCNA2), suggesting this as a key DMG regulatory module (Tumor Checkpoint). We are working to define targetable MRs in these subpopulations, and generating RNA-seq profiles of SU-DIPG-VI and SF8628, two DMG cell lines showing protein activity similarity to >95% of patient samples by enrichment analysis (p-val < 10E-5), following perturbation with ~400 oncology drugs. This will allow us to identify drugs capable of inducing tumor demise by inverting the activity of the MRs of each tumor subpopulation, using the NY Dept. of Health approved OncoTreat algorithm (Alvarez et al., Nat Genet 2018). We are currently finalizing and validating both MR and drug predictions to nominate novel, much-needed therapeutic strategies. Citation Format: Ester Calvo Fernández, Junqiang Wang, Aaron T. Griffin, Luca Szalontay, Stergios Zacharoulis, Jovana Pavisic, Andrea Califano. A systems biology approach to defining tumor heterogeneity, prognostic and targetable master regulator protein signatures from bulk and single cell RNA-seq in diffuse midline glioma (DMG) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 486.

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BAUDE, C., T. RIANT, and B. RIOULT. "GTS11 - Les autres infiltrations au niveau pelvien." Douleurs: Evaluation - Diagnostic - Traitement 6 (November 2005): 56–57. http://dx.doi.org/10.1016/s1624-5687(05)80341-5.

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Hose, Dirk, Thierry Rème, Thomas Hielscher, Jérôme Moreaux, Tobias Meißner, Anja Seckinger, Axel Benner, et al. "A Gene Expression Based Proliferation Index as Independent Prognostic Factor in Multiple Myeloma." Blood 112, no. 11 (November 16, 2008): 1667. http://dx.doi.org/10.1182/blood.v112.11.1667.1667.

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Abstract BACKGROUND. The proliferation-rate of primary myeloma cells is a strong adverse prognostic factor in various trials, but not routinely assessed, partially due to effort in obtaining it. AIM. As gene-expression profiling is increasingly considered a standard diagnostics in myeloma, we investigated the possibility to develop a prognostically relevant gene-expression based proliferation index (GPI). PATIENTS AND METHODS. Gene expression was determined by Affymetrix DNA-microarrays in 784 samples including two independent sets of 233 and 345 CD138-purified myeloma cells from previously untreated patients. The GPI was derived by selecting genes associated with proliferation (in terms of gene ontology) differentially expressed in proliferating malignant (human myeloma cell lines) and benign (plasmablastic) cells compared to non-proliferating, non-malignant cells (normal plasma cells and memory B-cells). The GPI comprises the sum of the expression values of 50 genes (ASPM, AURKA, AURKB, BIRC5, BRCA1, BUB1, BUB1B, CCNA2, CCNB1, CCNB2, CDC2, CDC20, CDC25C, CDC6, CDCA8, CDKN3, CEP55, CHEK1, CKS1B, CKS2, DLG7, ESPL1, GINS1, GTSE1, KIAA1794, KIF11, KIF15, KIF20A, KIF2C, KNTC2, MAD2L1, MCM10, MCM6, MKI67, NCAPD3, NCAPG, NCAPG2, NEK2, NPM1, PAK3, PCNA, PGAM1, PLK4, PTTG1, RACGAP1, SMC2, SPAG5. STIL, TPX2, ZWINT). Proliferation of primary myeloma cells was assessed by propidium iodinestaining (n=67). Chromosomal aberrations were assessed by comprehensive iFISH using a set of probes for the chromosomal regions 1q21, 6q21, 8p21, 9q34, 11q23, 11q13, 13q14.3, 14q32, 15q22, 17p13, 19q13, 22q11, as well as the translocations t(4;14)(p16.3;q32.3) and t(11;14)(q13;q32.3). RESULTS. In the two groups, 39 and 32 percent of primary myeloma cells show a GPI above the median plus three standard deviations of normal bone marrow plasma cells, respectively. The GPI is significantly higher in advanced- compared to early-stage myeloma (P=.001) and in patients harboring a gain of 1q21 (n=95, P<0.001). It correlates significantly with proliferation as determined by propidium iodine in primary myeloma cells (rs=.52, P<.001, n=67). The GPI as continuous variable is significantly predictive for event-free survival (EFS, n=120, P<.001, n=345, P<.001, respectively) and overall survival (OAS, n=345, P<.001) in patients treated with high-dose chemotherapy, independent of serum-β2-microglobulin (B2M) or ISS-stage. A GPI above the median (GPIhigh) delineated significantly inferior EFS (n=168, 41.6 vs. 26 months, P=.04, HR 1.57, CI [1.02,2.42]; n=345, 68.6 vs. 45.2 months, HR 1.55, CI [1.16,2.09], P=.003) and OAS (n=345, P<.001) in two independent cohorts of patients undergoing high-dose chemotherapy. By using B2M above 3.5 mg/l and GPI as staging variables, four groups with difference in median EFS (n=345, B2M <3.5mg/l, GPIhigh/low 76.1 months; B2M < 3.5mg/l, GPIhigh 62.4 months, B2M ≥3.5mg/l, GPIlow 41.8 months, B2M ≥3.5mg/l, GPI 36.1 months, P<.001) and OAS can be delineated. CONCLUSION. The GPI represents a validated tool for the assessment of proliferation in multiple myeloma patients, allows a risk stratification in terms of proliferation either alone or in combination with B2M or ISS, respectively, and has the potential to be used within a risk adapted targeting of anti-proliferative treatment.

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Ipsaro, Jonathan J., Paul A. O’Brien, Shibani Bhattacharya, Arthur G. Palmer, and Leemor Joshua-Tor. "Asterix/Gtsf1 links tRNAs and piRNA silencing of retrotransposons." Cell Reports 34, no. 13 (March 2021): 108914. http://dx.doi.org/10.1016/j.celrep.2021.108914.

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Zhang, Weixing, Yidong Lou, Jennifer S. Haase, Rui Zhang, Gang Zheng, Jinfang Huang, Chuang Shi, and Jingnan Liu. "The Use of Ground-Based GPS Precipitable Water Measurements over China to Assess Radiosonde and ERA-Interim Moisture Trends and Errors from 1999 to 2015." Journal of Climate 30, no. 19 (August 30, 2017): 7643–67. http://dx.doi.org/10.1175/jcli-d-16-0591.1.

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Abstract Global positioning system (GPS) data from over 260 ground-based permanent stations in China covering the period from 1 March 1999 to 30 April 2015 were used to estimate precipitable water (PW) above each site with an accuracy of about 0.75 mm. Four types of radiosondes (referred to as GZZ2, GTS1, GTS1-1, and GTS1-2) were used in China during this period. Instrumentation type changes in radiosonde records were identified by comparing PW calculated from GPS and radiosonde data. Systematic errors in different radiosonde types introduced significant biases to the estimated PW trends at stations where more than one radiosonde type was used. Estimating PW trends from reanalysis products (ERA-Interim), which assimilate the unadjusted radiosonde humidity data, resulted in an artificial downward PW trend at almost all stations in China. The statistically significant GPS PW trends are predominantly positive, consistent in sign with the increase in moisture expected from the Clausius–Clapeyron relation due to a global temperature increase. The standard deviations of the differences between ERA-Interim and GPS PW in the summer were 3 times larger than the observational error of GPS PW, suggesting that potentially significant improvements to the reanalysis could be achieved by assimilating denser GPS PW observations over China. This work, based on an entirely independent GPS PW dataset, confirms previously reported significant differences in radiosonde PW trends when using corrected data. Furthermore, the dense geographical coverage of the all-weather GPS PW observations, especially in remote areas in western China, provides a valuable resource for calibrating regional trends in reanalysis products.

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Adams, Claire A., Hiroshi Kuriyama, David Lloyd, and Douglas B. Murray. "The Gts1 protein stabilizes the autonomous oscillator in yeast." Yeast 20, no. 6 (2003): 463–70. http://dx.doi.org/10.1002/yea.976.

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Bublik, Débora Rosa, Massimiliano Scolz, Gianluca Triolo, Martín Monte, and Claudio Schneider. "Human GTSE-1 Regulates p21CIP1/WAF1Stability Conferring Resistance to Paclitaxel Treatment." Journal of Biological Chemistry 285, no. 8 (December 14, 2009): 5274–81. http://dx.doi.org/10.1074/jbc.m109.045948.

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Bian, Jianchun, Hongbin Chen, Holger Vömel, Yunjun Duan, Yuejian Xuan, and Daren Lü. "Intercomparison of humidity and temperature sensors: GTS1, Vaisala RS80, and CFH." Advances in Atmospheric Sciences 28, no. 1 (December 30, 2010): 139–46. http://dx.doi.org/10.1007/s00376-010-9170-8.

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Zhang, Jinqiang, Hongbin Chen, Jianchun Bian, Yuejian Xuan, Yunjun Duan, and Maureen Cribb. "Development of cloud detection methods using CFH, GTS1, and RS80 radiosondes." Advances in Atmospheric Sciences 29, no. 2 (February 19, 2012): 236–48. http://dx.doi.org/10.1007/s00376-011-0215-4.

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Donertas, D., G. Sienski, and J. Brennecke. "Drosophila Gtsf1 is an essential component of the Piwi-mediated transcriptional silencing complex." Genes & Development 27, no. 15 (August 1, 2013): 1693–705. http://dx.doi.org/10.1101/gad.221150.113.

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Chen, Chao, Xiaoquan Song, Zhangjun Wang, Wenyan Wang, Xiufen Wang, Quanfeng Zhuang, Xiaoyan Liu, et al. "Observations of Atmospheric Aerosol and Cloud Using a Polarized Micropulse Lidar in Xi’an, China." Atmosphere 12, no. 6 (June 21, 2021): 796. http://dx.doi.org/10.3390/atmos12060796.

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A polarized micropulse lidar (P-MPL) employing a pulsed laser at 532 nm was developed by the Institute of Oceanographic Instrumentation, Qilu University of Technology (Shandong Academy of Sciences). The optomechanical structure, technical parameters, detection principle, overlap factor calculation method, and inversion methods of the atmospheric boundary layer (ABL) depth and depolarization ratio (DR) were introduced. Continuous observations using the P-MPL were carried out at Xi’an Meteorological Bureau, and the observation data were analyzed. In this study, we gleaned much information on aerosols and clouds, including the temporal and spatial variation of aerosols and clouds, aerosol extinction coefficient, DR, and the structure of ABL were obtained by the P-MPL. The variation of aerosols and clouds before and after a short rainfall was analyzed by combining time-height-indication (THI) of range corrected signal (RCS) and DR was obtained by the P-MPL with profiles of potential temperature (PT) and relative humidity (RH) detected by GTS1 Digital Radiosonde. Then, the characteristics of tropopause cirrus cloud were discussed using the data of DR, PT, and RH. Finally, a haze process from January 1st to January 5th was studied by using aerosol extinction coefficients obtained by the P-MPL, PT, and RH profiles measured by GTS1 Digital Radiosonde and the time-varying of PM2.5 and PM10 observed by ambient air quality monitor. The source of the haze was simulated by using the NOAA HYSPLIT Trajectory Model.

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Guo, Lei, Shumin Zhang, Bo Zhang, Wanyong Chen, Xiaoqiang Li, Wentao Zhang, Chenhao Zhou, Jubo Zhang, Ning Ren, and Qinghai Ye. "Silencing GTSE-1 expression inhibits proliferation and invasion of hepatocellular carcinoma cells." Cell Biology and Toxicology 32, no. 4 (May 30, 2016): 263–74. http://dx.doi.org/10.1007/s10565-016-9327-z.

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Chen, Kai, Ye Yu, Dehong Yang, Xu Yang, Linmeng Tang, Yujia Liu, Xingyu Luo, et al. "Gtsf1 is essential for proper female sex determination and transposon silencing in the silkworm, Bombyx mori." PLOS Genetics 16, no. 11 (November 2, 2020): e1009194. http://dx.doi.org/10.1371/journal.pgen.1009194.

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Sex determination pathways are astoundingly diverse in insects. For instance, the silk moth Bombyx mori uniquely use various components of the piRNA pathway to produce the Fem signal for specification of the female fate. In this study, we identified BmGTSF1 as a novel piRNA factor which participates in B. mori sex determination. We found that BmGtsf1 has a distinct expression pattern compared to Drosophila and mouse. CRISPR/Cas9 induced mutation in BmGtsf1 resulted in partial sex reversal in genotypically female animals by shifting expression of the downstream targets BmMasc and Bmdsx to the male pattern. As levels of Fem piRNAs were substantially reduced in female mutants, we concluded that BmGtsf1 plays a critical role in the biogenesis of the feminizing signal. We also demonstrated that BmGTSF1 physically interacted with BmSIWI, a protein previously reported to be involved in female sex determination, indicating BmGTSF1 function as the cofactor of BmSIWI. BmGtsf1 mutation resulted in piRNA pathway dysregulation, including piRNA biogenesis defects and transposon derepression, suggesting BmGtsf1 is also a piRNA factor in the silkworm. Furthermore, we found that BmGtsf1 mutation leads to gametogenesis defects in both male and female. Our data suggested that BmGtsf1 is a new component involved in the sex determination pathway in B. mori.

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Ralph, Paul, Pontus Johnson, and Howell Jordan. "Report on the first SEMAT workshop on general theory of software engineering (GTSE 2012)." ACM SIGSOFT Software Engineering Notes 38, no. 2 (March 23, 2013): 26–28. http://dx.doi.org/10.1145/2439976.2439999.

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Johnson, Pontus, Paul Ralph, Michael Goedicke, Pan-Wei Ng, Klaas-Jan Stol, Kari Smolander, Iaakov Exman, and Dewayne E. Perry. "Report on the Second SEMAT Workshop on General Theory of Software Engineering (GTSE 2013)." ACM SIGSOFT Software Engineering Notes 38, no. 5 (August 26, 2013): 47–50. http://dx.doi.org/10.1145/2507288.2529923.

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Chen, Kai, Ye Yu, Dehong Yang, Xu Yang, Linmeng Tang, Yujia Liu, Xingyu Luo, et al. "Correction: Gtsf1 is essential for proper female sex determination and transposon silencing in the silkworm, Bombyx mori." PLOS Genetics 17, no. 5 (May 17, 2021): e1009572. http://dx.doi.org/10.1371/journal.pgen.1009572.

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Tonozuka, H., J. Wang, K. Mitsui, T. Saito, Y. Hamada, and K. Tsurugi. "Analysis of the Upstream Regulatory Region of the GTS1 Gene Required for Its Oscillatory Expression." Journal of Biochemistry 130, no. 5 (November 1, 2001): 589–95. http://dx.doi.org/10.1093/oxfordjournals.jbchem.a003023.

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Soares, Pamela de Oliveira, Patrícia Maluf Cury, Rossana Verónica Mendoza López, Cláudio Roberto Cernea, Erika Erina Fukuyama, David Livingstone Alves Figueiredo, Francisco Gorgonio da Nobrega, et al. "GTSP1 expression in non-smoker and non-drinker patients with squamous cell carcinoma of the head and neck." PLOS ONE 12, no. 8 (August 17, 2017): e0182600. http://dx.doi.org/10.1371/journal.pone.0182600.

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Monte, M., L. Collavin, D. Lazarevic, R. Utrera, T. A. Dragani, and C. Schneider. "Cloning, chromosome mapping and functional characterization of a human homologue of murine Gtse-1 (B99) gene." Gene 254, no. 1-2 (August 2000): 229–36. http://dx.doi.org/10.1016/s0378-1119(00)00260-2.

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Yang, Yi, Na Li, Tongshuai Chen, Chunmei Zhang, Jingyuan Li, Lingxin Liu, Yan Qi, Xuehui Zheng, Chen Zhang, and Peili Bu. "Sirt3 promotes sensitivity to sunitinib-induced cardiotoxicity via inhibition of GTSP1/JNK/autophagy pathway in vivo and in vitro." Archives of Toxicology 93, no. 11 (September 24, 2019): 3249–60. http://dx.doi.org/10.1007/s00204-019-02573-9.

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Huntriss, John, Jianping Lu, Karen Hemmings, Rosemary Bayne, Richard Anderson, Anthony Rutherford, Adam Balen, Kay Elder, and Helen M. Picton. "Isolation and expression of the human gametocyte-specific factor 1 gene (GTSF1) in fetal ovary, oocytes, and preimplantation embryos." Journal of Assisted Reproduction and Genetics 34, no. 1 (September 19, 2016): 23–31. http://dx.doi.org/10.1007/s10815-016-0795-0.

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Monte, Martin, Roberta Benetti, Giacomo Buscemi, Peter Sandy, Giannino Del Sal, and Claudio Schneider. "The Cell Cycle-regulated Protein Human GTSE-1 Controls DNA Damage-induced Apoptosis by Affecting p53 Function." Journal of Biological Chemistry 278, no. 32 (May 15, 2003): 30356–64. http://dx.doi.org/10.1074/jbc.m302902200.

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Geng, Shuang, Jing Wang, Mingyi Chen, Wenming Wang, Yuhong Pang, Yuanyuan Liu, Yanyi Huang, and Hongmei Jing. "Single Cell RNA-Seq Reveals Clonal Consistency and Differential Malignancy in Extramedullary Plasmacytoma of Multiple Myeloma." Blood 126, no. 23 (December 3, 2015): 4808. http://dx.doi.org/10.1182/blood.v126.23.4808.4808.

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Abstract Extramedullary Plasmacytoma (EMP) is a minor yet devastating metastatic form of Multiple Myeloma (MM), shortening patients' survival from 10 years to 6 months on average. Genetic cause of EMP in MM is yet to be defined. Transcriptome difference between EMP+ patients and EMP- patients is studied here on single cell level by RNA Sequencing (RNA-Seq). We sorted CD38+CD138+ malignant plasma cells from bone marrow and peripheral blood samples by flow cytometry, then picked up single malignant plasma cell and performed single cell RNA-Seq with SmartSeq2 protocol followed by Tn5-based library preparation from bone marrow, peripheral blood and extramedullary tissue of EMP patients. From the single cell RNA-Seq results, in bone marrow we found differential gene expression between EMP+ and EMP- samples, such as CTAG2, STMN1 and RRM2. By comparing circulating malignant plasma cells in PBMC and malignant plasma cell from the sample EMP+ patient, we observed metastatic clone in blood with the same VDJ immunoglobulin heavy chain as in bone marrow. Several genes' expression of these metastatic cells are down-regulated than in bone marrow, such as PAGE2, GTSF1, DICER1. These genes may correlate with egress capability of MM cells into peripheral to become circulating plasma cells (cPCs), and EMP eventually. Disclosures No relevant conflicts of interest to declare.

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Pruekprasert, Napat, Qinghe Meng, and Robert N. Cooney. "Activation of Alpha7 Nicotinic Acetylcholine Receptor by GTS21 Regulates Nuclear Factor Kappa-Light-Chain-Enhancer of Activated B Cells Inflammatory Pathway in Hepatocytes." Journal of the American College of Surgeons 227, no. 4 (October 2018): S79. http://dx.doi.org/10.1016/j.jamcollsurg.2018.07.109.

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Jiang, Jianping, Xiang Yuan, Qingqing Qiu, Guanghua Huang, Qinyang Jiang, Penghui Fu, Yu Zhang, Yinhai Jia, Xiurong Yang, and Hesheng Jiang. "Comparative Transcriptome Analysis of Gonads for the Identification of Sex-Related Genes in Giant Freshwater Prawns (Macrobrachium Rosenbergii) Using RNA Sequencing." Genes 10, no. 12 (December 11, 2019): 1035. http://dx.doi.org/10.3390/genes10121035.

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The giant freshwater prawn (Macrobrachium rosenbergii) exhibits sex dimorphism between the male and female individuals. To date, the molecular mechanism governing gonadal development was unclear, and limited data were available on the gonad transcriptome of M. rosenbergii. Here, we conducted comprehensive gonadal transcriptomic analysis of female (ZW), super female (WW), and male (ZZ) M. rosenbergii for gene discovery. A total of 70.33 gigabases (Gb) of sequences were generated. There were 115,338 unigenes assembled with a mean size of 1196 base pair (bp) and N50 of 2195 bp. Alignment against the National Center for Biotechnology Information (NCBI) non-redundant nucleotide/protein sequence database (NR and NT), the Kyoto Encyclopedia of Genes and Genomes (KEGG) database, SwissProt database, Protein family (Pfam), Gene ontology (GO), and the eukaryotic orthologous group (KOG) database, 36,282 unigenes were annotated at least in one database. Comparative transcriptome analysis observed that 10,641, 16,903, and 3393 genes were significantly differentially expressed in ZW vs. ZZ, WW vs. ZZ, and WW vs. ZW samples, respectively. Enrichment analysis of differentially expressed genes (DEGs) resulted in 268, 153, and 42 significantly enriched GO terms, respectively, and a total of 56 significantly enriched KEGG pathways. Additionally, 23 putative sex-related genes, including Gtsf1, IR, HSP21, MRPINK, Mrr, and other potentially promising candidate genes were identified. Moreover, 56,241 simple sequence repeats (SSRs) were identified. Our findings provide a valuable archive for further functional analyses of sex-related genes and future discoveries of underlying molecular mechanisms of gonadal development and sex determination.

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Wada, Tsutomu, Maiko Naito, Hiroki Kenmochi, Hiroshi Tsuneki, and Toshiyasu Sasaoka. "Chronic Nicotine Exposure Enhances Insulin-Induced Mitogenic Signaling via Up-Regulation of α7 Nicotinic Receptors in Isolated Rat Aortic Smooth Muscle Cells." Endocrinology 148, no. 2 (February 1, 2007): 790–99. http://dx.doi.org/10.1210/en.2006-0907.

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Insulin resistance and smoking are significant risk factors for cardiac and cerebral vascular diseases. Because vascular smooth muscle cells play a key role in the development and progression of atherosclerosis, we investigated the effect of nicotine on insulin-induced mitogenic signaling in aortic vascular smooth muscle cells isolated from Sprague Dawley rats. RT-PCR revealed the expression of α2–7, α10, β1–3, δ, and ε subunits of the nicotinic acetylcholine receptor (nAChR) in the cells. Short-term nicotine treatment stimulated phosphorylation of p44/42-MAPK, p38-MAPK, and signal transducer and activator of transcription 3. However, an additive effect of nicotine pretreatment on insulin stimulation was only observed on p44/42-MAPK. The nicotine-induced phosphorylation of p44/42-MAPK and [methyl-3H]thymidine incorporation were effectively suppressed by a α7-nAChR-selective antagonist, methyllycaconitine, and the phosphorylation of p44/42-MAPK was stimulated by a α7-nAChR-specific agonist, GTS21. Furthermore, the phosphorylation was mediated via calmodulin kinase II, Src, and Shc. Interestingly, long-term (48-h) pretreatment with nicotine increased the amount of α7-AChR in the plasma membrane and insulin-induced phosphorylation of p44/42-MAPK. These results provide the first evidence that acute exposure to nicotine enhances insulin-induced mitogenesis predominantly by affecting the phosphorylation of p44/42-MAPK and that chronic exposure further augments the insulin signal via up-regulation of α7-nAChR, which may be crucial for the development and progression of atherosclerosis in large vessels.

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Ramirez, Dorian, Edward J. Lammer, David M. Iovannisci, Cecile Laurent, Richard H. Finnell, and Gary M. Shaw. "Maternal Smoking during Early Pregnancy, GSTP1 and EPHX1 Variants, and Risk of Isolated Orofacial Clefts." Cleft Palate-Craniofacial Journal 44, no. 4 (July 2007): 366–73. http://dx.doi.org/10.1597/06-011.1.

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Objective: To examine the interactions between four fetal xenobiotic metabolizing gene polymorphisms, maternal cigarette smoking, and risk for oral cleft defects. Design and Participants: California population–based case-control study of 431 infants born with isolated orofacial clefts and 299 nonmalformed controls. Main Outcome Measures: Infants were genotyped for functional polymorphisms of the detoxification enzymes microsomal epoxide hydrolase-1 (EPHX1 T→C [Tyr113His], and A→G [His139Arg]), and glutathione-S transferase Pi-1 (GSTP1 A→G [Ile105Val] and C→T [Ala114Val]), and risks for cleft outcomes were measured for gene only and gene-maternal smoking effects. Results: Although smoking was associated with an increased risk for isolated cleft lip ± palate, we found no independent associations of genotypes of EPHX1-codon 113 or GSTP1-codon 105 polymorphisms for either isolated cleft lip ± palate or isolated cleft palate. The heterozygote genotype for the EPHX1-codon 139 polymorphism was associated with an increased risk of isolated cleft palate (odds ratio = 1.6 [95% confidence interval, 1.0 to 2.6]). Infant EPHX1 and GTSP1 polymorphic variants did not appreciably alter the risks for clefts associated with maternal smoking, nor were any EPHX1 combined genotype-specific risks found. Infant genotypes of the GSTP1-codon 105 polymorphism, combined with glutathione-S-transferase-μ-1 null genotypes, did not appreciably alter the risk of orofacial clefts. Conclusions: Our results suggest that genetic variation of the detoxification enzymes EPHX1 and GSTP1 did not increase the risks of orofacial clefting, nor do they influence the risks associated with maternal smoking.

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Krakowski, I., D. Baylot, F. Barral, M. Navez, B. Fergane, and N. Vuillemin. "GTS01 - La circulaire N° DHOS/SDO/2005/100 du 22 février 2005 relative à l’organisation des soins en cancérologie dans le cadre du plan cancer." Douleurs : Evaluation - Diagnostic - Traitement 6 (November 2005): 51. http://dx.doi.org/10.1016/s1624-5687(05)80331-2.

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Yoshimura, Takuji, Shuichi Toyoda, Satomi Kuramochi-Miyagawa, Tatsushi Miyazaki, Satsuki Miyazaki, Fumi Tashiro, Eiji Yamato, Toru Nakano, and Jun-ichi Miyazaki. "Gtsf1/Cue110, a gene encoding a protein with two copies of a CHHC Zn-finger motif, is involved in spermatogenesis and retrotransposon suppression in murine testes." Developmental Biology 335, no. 1 (November 2009): 216–27. http://dx.doi.org/10.1016/j.ydbio.2009.09.003.

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