cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.25549/one-ouc17554235
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.6084/m9.figshare.8159468
title: Consumption substitution and change of household indirect energy consumption in China from 1997 to 2012: A two-tier structural decomposition analysis.xlsx

description: The data contains the input-output data of China, and the price index as comparable to 1997, the sectoral energy consumption data of China
DOI: 10.25549/one-ouc17554238
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554239
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.6084/m9.figshare.21261604
title: Additional file 2 of Comprehensive characterization of ubiquitinome of human colorectal cancer and identification of potential survival-related ubiquitination

description: Additional file 2. Table S1. Ubiquitination annotation. Table S2. Protein annotation. Table S3. 42 proteins having ten or more than ten ubiquitination modifications. Table S4. 20 ubiquitin-binding motifs. Table S5. 2242 proteins with an upregulated ubiquitination and 1204 proteins with a down-regulated ubiquitination. Table S6. 1172 up-regulated proteins and 1700 down-regulated proteins. Table S7. 646 Secretory proteins. Table S8. 53 proteins having an upregulated expression simultaneously with a down-regulated ubiquitination and 116 proteins having down-regulated expression simultaneously with an up-regulated ubiquitination. Table S9. 7 proteins having an up-regulated expression simultaneously with a down-regulated ubiquitination. Table S10. 52 proteins having a down-regulated expression simultaneously with an up-regulated ubiquitination. Table S11. 101 proteins which were probably associated with the overall survival rates of CRC patients.
DOI: 10.25549/one-ouc17554240
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.25549/one-ouc17554241
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554242
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554247
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.25549/one-ouc17554243
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554245
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.25549/one-ouc17554941
title: Mattachine Society, Police-Community Relations, San Francisco (1967)
DOI: 10.25549/one-ouc17554246
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554938
title: Mattachine Society, Police-Community Relations, San Francisco (1967)
DOI: 10.25549/one-ouc17554250
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.25549/one-ouc17554253
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.6084/m9.figshare.19164455
title: Additional file 4 of Engineered exosomes as an in situ DC-primed vaccine to boost antitumor immunity in breast cancer

description: Additional file 4: Table 3. List of antibodies for this study.
DOI: 10.25549/one-ouc17554252
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554254
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554255
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.25549/one-ouc17554256
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.6084/m9.figshare.19164455.v1
title: Additional file 4 of Engineered exosomes as an in situ DC-primed vaccine to boost antitumor immunity in breast cancer

description: Additional file 4: Table 3. List of antibodies for this study.
DOI: 10.25549/one-ouc17554258
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554257
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554259
title: Mattachine Society, reports given at ONE, Incorporated Midwinter Institute (1956)
DOI: 10.25549/one-ouc17556037
title: Mattachine Society, Long Beach (Harbor) Area Council correspondence and memoranda (1953-1956)
DOI: 10.25549/one-ouc17556040
title: Mattachine Society, Long Beach (Harbor) Area Council correspondence and memoranda (1953-1956)
DOI: 10.25549/one-ouc17556036
title: Mattachine Society, Long Beach (Harbor) area council meeting minutes (1954-1955)
DOI: 10.25549/one-ouc17556041
title: Mattachine Society, Long Beach (Harbor) Area Council correspondence and memoranda (1953-1956)
DOI: 10.25549/one-ouc17556042
title: Mattachine Society, Tavern Guild (1964-1967)
DOI: 10.25549/one-ouc17556045
title: Mattachine Society, Long Beach (Harbor) area council meeting minutes (1954-1955)
DOI: 10.25549/one-ouc17554263
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554261
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.25549/one-ouc17554262
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554956
title: Mattachine Society, Paul Coates incident (1953-1954)
DOI: 10.6084/m9.figshare.19164452
title: Additional file 3 of Engineered exosomes as an in situ DC-primed vaccine to boost antitumor immunity in breast cancer

description: Additional file 3: Table 2. List of primers used.
DOI: 10.6084/m9.figshare.19164458.v1
title: Additional file 5 of Engineered exosomes as an in situ DC-primed vaccine to boost antitumor immunity in breast cancer

description: Additional file 5: Table 4. Human breast cancer organoids medium recipe.
DOI: 10.25549/one-ouc17554264
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554266
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.6084/m9.figshare.11300186
title: MOESM6 of Identification and expression analysis of GRAS transcription factors in the wild relative of sweet potato Ipomoea trifida

description: Additional file 6: Table S5. The expression data of the GRAS genes under four abiotic stress conditions in I.trifida. (XLS 33 kb)
DOI: 10.6084/m9.figshare.19164584
title: Expression and SNP dataset used for expression quantitative loci mapping

description: The expression profiled from 340 distinct maize genotypes used for an eGWAS analysis. In the file named 'eGWAS340_repMerged_Untransformed_fpkm.csv' , FPKM of 19,565 genes profiled from the root tissues of 340 maize genotypes, replicated genotypes were averaged. <br><br>'eGWAS340_repUnmerged_Untransformed_fpkm.csv': FPKM of 19,565 genes profiled from the root tissues of 340 maize genotypes, replicated genotypes were kept raw for heritability calculation. <br>'eGWAS340_maf05het02.hmp.txt.gz': the SNP genotype data used for eQTL mapping and visible phenotype GWAS <br><br><br>
DOI: 10.25549/one-ouc17554265
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.6084/m9.figshare.21261604.v1
title: Additional file 2 of Comprehensive characterization of ubiquitinome of human colorectal cancer and identification of potential survival-related ubiquitination

description: Additional file 2. Table S1. Ubiquitination annotation. Table S2. Protein annotation. Table S3. 42 proteins having ten or more than ten ubiquitination modifications. Table S4. 20 ubiquitin-binding motifs. Table S5. 2242 proteins with an upregulated ubiquitination and 1204 proteins with a down-regulated ubiquitination. Table S6. 1172 up-regulated proteins and 1700 down-regulated proteins. Table S7. 646 Secretory proteins. Table S8. 53 proteins having an upregulated expression simultaneously with a down-regulated ubiquitination and 116 proteins having down-regulated expression simultaneously with an up-regulated ubiquitination. Table S9. 7 proteins having an up-regulated expression simultaneously with a down-regulated ubiquitination. Table S10. 52 proteins having a down-regulated expression simultaneously with an up-regulated ubiquitination. Table S11. 101 proteins which were probably associated with the overall survival rates of CRC patients.
DOI: 10.25549/one-ouc17554268
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554267
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554269
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17555064
title: Mattachine Society, Society for Individual Rights (1964-1967)
DOI: 10.6084/m9.figshare.19688938.v2
title: LINC00173 promotes Wilms’ tumor progression through MGAT1-mediated MUC3A <i>N</i>-glycosylation

description: Recent studies have unveiled that LINC00173 promotes small cell lung cancer progression. However, LINC00173 has not been studied in Wilms’ tumor (WT). <i>N</i>-glycosylation is a complex post-translational protein modification, and alterations of protein glycosylation have been identified to affect the development of multiple tumors, including WT. MGAT1, known as <i>N</i>-acetylglucosaminyltransferase I (GlcNAcT-1), could initiate synthesis of complex <i>N-</i>glycans, but it has never been related to LINC00173 in WT. This study aimed to explore if LINC00173 could impact WT progression via MGAT1. RT-qPCR and western blot were done to measure the expression and protein levels. Functional assays, as well as animal experiments were conducted to evaluate the function of genes <i>in vivo</i> and <i>in vitro</i>. Additionally, RNA pull-down, RIP, and dual-luciferase reporter assays were carried out to determine the molecular bindings. <i>In vitro</i> experiments proved that sh-LINC00173 inhibited WT cell invasion and promoted WT cell apoptosis, while <i>in vivo</i> experiments indicated sh-LINC00173 restrained WT progression. LINC00173 stabilized MGAT1 mRNA by recruiting HNRNPA2B1. Meanwhile, MGAT1 was verified to stabilize MUC3A protein by inducing <i>N</i>-glycosylation. In summary, our study first discovered that LINC00173 promoted WT progression through MGAT1-mediated MUC3A <i>N</i>-glycosylation, giving new clues to further understanding the mechanism underlying WT progression.
DOI: 10.6084/m9.figshare.19688938
title: LINC00173 promotes Wilms’ tumor progression through MGAT1-mediated MUC3A <i>N</i>-glycosylation

description: Recent studies have unveiled that LINC00173 promotes small cell lung cancer progression. However, LINC00173 has not been studied in Wilms’ tumor (WT). <i>N</i>-glycosylation is a complex post-translational protein modification, and alterations of protein glycosylation have been identified to affect the development of multiple tumors, including WT. MGAT1, known as <i>N</i>-acetylglucosaminyltransferase I (GlcNAcT-1), could initiate synthesis of complex <i>N-</i>glycans, but it has never been related to LINC00173 in WT. This study aimed to explore if LINC00173 could impact WT progression via MGAT1. RT-qPCR and western blot were done to measure the expression and protein levels. Functional assays, as well as animal experiments were conducted to evaluate the function of genes <i>in vivo</i> and <i>in vitro</i>. Additionally, RNA pull-down, RIP, and dual-luciferase reporter assays were carried out to determine the molecular bindings. <i>In vitro</i> experiments proved that sh-LINC00173 inhibited WT cell invasion and promoted WT cell apoptosis, while <i>in vivo</i> experiments indicated sh-LINC00173 restrained WT progression. LINC00173 stabilized MGAT1 mRNA by recruiting HNRNPA2B1. Meanwhile, MGAT1 was verified to stabilize MUC3A protein by inducing <i>N</i>-glycosylation. In summary, our study first discovered that LINC00173 promoted WT progression through MGAT1-mediated MUC3A <i>N</i>-glycosylation, giving new clues to further understanding the mechanism underlying WT progression.
DOI: 10.6084/m9.figshare.19688938.v1
title: LINC00173 Promotes Wilms’ Tumor Progression Through MGAT1-mediated MUC3A N-glycosylation

description: Recent studies have unveiled that LINC00173 promotes small cell lung cancer progression. However, LINC00173 has not been studied in Wilms’ tumor (WT). N-glycosylation is a complex post-translational protein modification, and alterations of protein glycosylation have been identified to affect the development of multiple tumors, including WT. MGAT1, known as N-acetylglucosaminyltransferase I (GlcNAcT-1), could initiate synthesis of complex N-glycans, but it has never been related to LINC00173 in WT. This study aimed to explore if LINC00173 could impact WT progression via MGAT1. RT-qPCR and western blot were done to measure the expression and protein levels. Functional assays, as well as animal experiments were conducted to evaluate function of genes <i>in vivo</i> and <i>in vitro</i>. Additionally, RNA pull-down, RIP, and dual luciferase reporter assays were carried out to determine the molecular bindings. <i>In vitro</i> experiments proved that sh-LINC00173 inhibited WT cell invasion and promoted WT cell apoptosis, while <i>in vivo</i> experiments indicated sh-LINC00173 restrained WT progression. LINC00173 stabilized MGAT1 mRNA by recruiting HNRNPA2B1. Meanwhile, MGAT1 was verified to stabilize MUC3A protein by inducing N-glycosylation. In summary, our study first discovered that LINC00173 promoted WT progression through MGAT1-mediated MUC3A N-glycosylation, giving new clues to further understanding the mechanism underlying WT progression.
DOI: 10.25549/one-ouc17554270
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17554271
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.25549/one-ouc17554273
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.25549/one-ouc17555077
title: Mattachine Society, Police-Community Relations, San Francisco (1967)
DOI: 10.25549/one-ouc17554275
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.6084/m9.figshare.21259545
title: Additional file 1 of Effect and mechanisms of kaempferol against endometriosis based on network pharmacology and in vitro experiments

description: Additional file 1.
DOI: 10.25549/one-ouc17554276
title: Mattachine Society, ONE, Incorporated correspondence (1960-1963)
DOI: 10.6084/m9.figshare.19689184
title: Analysis of the different characteristics between omental preadipocytes and differentiated white adipocytes using bioinformatics methods

description: Obesity is emerging as an epidemiological issue, being associated with the onset and progress of various metabolism-related disorders. Obesity is characterized by the white adipose expansion, which encounters white adipocyte hypertrophy and hyperplasia. White adipocyte hyperplasia is defined as adipogenesis with the increase in the number of the white adipocytes from the preadipocytes. Adipogenesis contributes to distributing excess triglycerides among the smaller newly formed adipocytes, reducing the number of hypertrophic adipocytes and secreting anti-inflammatory factor. Therefore, adipogenesis is emerging as a new therapeutic target for the treatment of obesity. In the present study, for a better understanding of the contribution of the alteration of the omental differentiated white adipocytes to the systemic metabolic disorders, we downloaded the mRNA expression profiles from GEO database GSE1657, 328 differentially expressed genes (DEGs) were screened between the undifferentiated preadipocytes (UNDIF) and omental differentiated white adipocytes (DIF). The contributions of the upregulated and downregulated DEGs to the system were performed via the Gene Ontology (GO) analysis, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Protein–Protein Interaction (PPI) network, respectively. The potential contribution of the whole altered genes in the differentiated white adipocytes was explored with the performance of Gene Set Enrichment Analysis (GSEA), especially on the GO analysis, KEGG analysis, hallmark analysis, oncogenic analysis and related miRNA analysis. The output of the current study will shed light on the new targets for the treatment of obesity and obesity-related disorders.
DOI: 10.6084/m9.figshare.14446346.v1
title: HBx induces hepatocellular carcinogenesis through ARRB1-mediated autophagy to drive the G<sub>1</sub>/S cycle

description: The hepatitis B virus X protein (HBx) is involved in the process of hepatocellular carcinoma via the activation of various oncogenes. Our previous study indicated that ARBB1 (arrestin beta 1) promotes hepatocellular carcinogenesis (HCC). However, the role of ARRB1 in HBx-related HCC remains unclear. Herein, we identified that ARRB1 was upregulated by HBx <i>in vivo</i> and <i>in vitro. Arrb1</i> deficiency suppressed HBx-induced hepatocellular carcinogenesis in several mouse models. Furthermore, knockdown of <i>ARRB1</i> blocked HBx-induced macroautophagic/autophagic flux and disrupted the formation of autophagosomes. ARRB1 interacted with HBx, and the autophagic core protein MAP1LC3/LC3, a scaffolding protein, was essential for complete autophagy. Inhibition of autophagy by 3-methyladenine or interference of <i>ATG5</i> or <i>ATG7</i> attenuated HBx-induced cell cycle acceleration and the subsequent proliferative response via the induction of G<sub>1</sub>/S arrest. The absence of autophagy abolished the phosphorylation of CDK2 and the activity of the CDK2-CCNE1 complex. Our results demonstrate that ARRB1 plays a critical role in HBV-related HCC via modulating autophagy and the CDKN1B-CDK2-CCNE1-E2F1 axis and indicate that ARRB1 may be a potential therapeutic target for HCC. <b>Abbreviations:</b> ARRB1: arrestin beta 1; ACTB: actin beta; AMPK: adenosine monophosphate (AMP)-activated protein kinase; ATG5: autophagy related 5; ATG7: autophagy related 7; Baf A1: bafilomycin A<sub>1</sub>; CDK2: cyclin dependent kinase 2; CDKN1B/p27Kip1: cyclin dependent kinase inhibitor 1B; CQ: chloroquine; E2F1: E2F transcription factor 1; FBS: fetal bovine serum; GPCRs: G protein-coupled receptors; GST: glutathione S-transferase; HCC: hepatocellular carcinoma; HBV: hepatitis B virus; HBx: hepatitis B virus X protein; HMGB1: high mobility group box 1; HIF1A/HIF-1α: hypoxia inducible factor 1 subunit alpha; IHC: immunohistochemistry; JAK1: Janus kinase 1; LOX: lysyl oxidase; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; MKI67: marker of proliferation Ki-67; MTOR: mechanistic target of rapamycin kinase; MAPK: mitogen-activated protein kinase; 3-MA: 3-methyladenine; NFKB/NF-κB: nuclear factor kappa B; PIK3CA: phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha; PIK3C3: phosphatidylinositol 3-kinase catalytic subunit type 3; PHHs: primary human hepatocytes; RB1: RB transcriptional corepressor 1; SQSTM1/p62: sequestosome 1; STAT: signal transducer and activator of transcription; TACR1/NK1R: tachykinin receptor 1
DOI: 10.6084/m9.figshare.21259545.v1
title: Additional file 1 of Effect and mechanisms of kaempferol against endometriosis based on network pharmacology and in vitro experiments

description: Additional file 1.
DOI: 10.25549/one-ouc17554278
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)
DOI: 10.6084/m9.figshare.19689184.v2
title: Analysis of the different characteristics between omental preadipocytes and differentiated white adipocytes using bioinformatics methods

description: Obesity is emerging as an epidemiological issue, being associated with the onset and progress of various metabolism-related disorders. Obesity is characterized by the white adipose expansion, which encounters white adipocyte hypertrophy and hyperplasia. White adipocyte hyperplasia is defined as adipogenesis with the increase in the number of the white adipocytes from the preadipocytes. Adipogenesis contributes to distributing excess triglycerides among the smaller newly formed adipocytes, reducing the number of hypertrophic adipocytes and secreting anti-inflammatory factor. Therefore, adipogenesis is emerging as a new therapeutic target for the treatment of obesity. In the present study, for a better understanding of the contribution of the alteration of the omental differentiated white adipocytes to the systemic metabolic disorders, we downloaded the mRNA expression profiles from GEO database GSE1657, 328 differentially expressed genes (DEGs) were screened between the undifferentiated preadipocytes (UNDIF) and omental differentiated white adipocytes (DIF). The contributions of the upregulated and downregulated DEGs to the system were performed via the Gene Ontology (GO) analysis, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and Protein–Protein Interaction (PPI) network, respectively. The potential contribution of the whole altered genes in the differentiated white adipocytes was explored with the performance of Gene Set Enrichment Analysis (GSEA), especially on the GO analysis, KEGG analysis, hallmark analysis, oncogenic analysis and related miRNA analysis. The output of the current study will shed light on the new targets for the treatment of obesity and obesity-related disorders.
DOI: 10.6084/m9.figshare.9203459
title: Reconstruction of nearshore chemical conditions in the Mesoproterozoic: evidence from red and grey beds of the Yangzhuang formation, North China Craton

description: Mesoproterozoic red beds near ancient coasts have not aroused extensive interest. A new geochemical study of the alternating red and grey dolostones from the Yangzhuang Formation provides a better understanding of the redox conditions of nearshore sedimentary environments. In this contribution, whole-rock samples are characterized by positive correlations of rare earth elements (REE) vs. Th and Fe<sub>T</sub> vs. Th and flat-type REE distribution patterns, indicating massive terrigenous input, which is considered to be inherited from felsic rocks. Relatively high (Fe<sub>mag</sub>+Fe<sub>ox</sub>)/Fe<sub>T</sub> and Fe<sup>3+</sup>/Fe<sup>2+</sup> ratios in red beds indicate more oxidized conditions in supratidal environments compared with the lower oxygen contents in intertidal environments. Under these two distinct chemical sedimentary conditions, acetic acid-leached red and grey samples both have HREE-depleted distributions, suggesting significant freshwater invasion. Moreover, limited terrigenous redox-sensitive elements (RSEs) can reach the coast where the red beds are deposited, whereas relatively high RSE enrichment factors originating from shallow oceans are recorded in grey beds. In the Mesoproterozoic, limited oxidative weathering, shallow seawater desalination, and low organic production occurred near the coast. Meanwhile, a prolonged period of low Mo and U availability preserved in carbonate minerals confirmed that marine oxygen levels failed to satisfy the deposition of offshore red beds. During the regression, potentially exposed sediments connected to atmospheric oxygen guaranteed the oxidation of iron and the formation of red beds, and these events were coupled with negative δ<sup>13</sup>C<sub>carb</sub> shifts in the Yanliao rift zone.
DOI: 10.25549/one-ouc17554277
title: Mattachine Society, ONE, Incorporated correspondence (1952-1960)