cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.13272894.v2
title: GLIPR2 is a negative regulator of autophagy and the BECN1-ATG14-containing phosphatidylinositol 3-kinase complex

description: A key mediator of macroautophagy/autophagy induction is the class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) consisting of PIK3C3/VPS34, PIK3R4/VPS15, BECN1, and ATG14. Although several proteins are known to enhance or decrease PtdIns3K-C1 activity, our understanding of the molecular regulation of PtdIns3K-C1 is still incomplete. Previously, we identified a Golgi-associated protein, GLIPR2, in a screen for proteins that interact with amino acids 267–284 of BECN1, a region of BECN1 sufficient to induce autophagy when fused to a cell penetrating leader sequence. In this study, we used CRISPR-Cas9-mediated depletion of GLIPR2 in cells and mice to investigate the role of GLIPR2 in the regulation of autophagy and PtdIns3K-C1 activity. Depletion of GLIPR2 in HeLa cells increased autelophagic flux and generation of phosphatidylinositol 3-phosphate (PtdIns3P). <i>GLIPR2</i> knockout resulted in less compact Golgi structures, which was also observed in autophagy-inducing conditions such as amino acid starvation or Tat-BECN1 peptide treatment. Importantly, the binding of GLIPR2 to purified PtdIns3K-C1 inhibited the in vitro lipid kinase activity of PtdIns3K-C1. Moreover, the tissues of <i>glipr2</i> knockout mice had increased basal autophagic flux as well as increased recruitment of the PtdIns3P-binding protein, WIPI2. Taken together, our findings demonstrate that GLIPR2 is a negative regulator of PtdIns3K-C1 activity and basal autophagy. <b>Abbreviations:</b> ATG14: autophagy related 14; Baf A1: bafilomycin A<sub>1</sub>; BARA: β-α repeated, autophagy-specific; CQ: chloroquine; GFP: green fluorescent protein; GLIPR2: GLI pathogenesis related 2; HBSS: Hanks’ balanced salt solution; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PBS: phosphate-buffered saline; PtdIns3K-C1: phosphatidylinositol 3-kinase complex I; PtdIns3P: phosphatidylinositol-3-phosphate; SEM: standard error of the mean; WIPI2: WD repeat domain, phosphoinositide interacting 2
DOI: 10.6084/m9.figshare.21137119.v1
title: Additional file 8 of Quality control recommendations for RNASeq using FFPE samples based on pre-sequencing lab metrics and post-sequencing bioinformatics metrics

description: Additional file 8. All sample related metrics including pre-sequencing lab metrics and post sequencing bioinformatics metrics.
DOI: 10.6084/m9.figshare.21137354.v1
title: Sunitinib induced resistance of endothelial cells by up-regulating P-glycoprotein and PI3K/Akt pathway

description: Abstract Drug resistance is a crucial obstacle to achieve satisfactory chemotherapeutic effects. Numerous studies have shown that the PI3K/Akt signaling pathway plays a significant role in various processes of cellular events and tumor progression, while few studies have focused on the PI3K/Akt signaling pathway in drug resistance of endothelial cells. The present study aims to explore the relationship of PI3K/Akt signaling and cellular resistance to anticancer drugs in human microvessel endothelial cells (HMEC-1). We established stable sunitinib-resiatant human microvessel endothelial cells (HMEC-su) after long-term exposure to sunitinib (a small-molecule tyrosine kinase receptor inhibitor) for 12 months. HMEC-su showed significant alternations of cell morphology and exhibited a 2.32-fold higher IC50 of sunitinib than parental HMEC-1 cells. Expression of P-glycoprotein (P-gp) and breast cancer-resistance protein (ABCG2) which mediates drug efflux, increased significantly in HMEC-su lines compared with HMEC-1 cells by western blots assay. Our study further demonstrates that LY294002 (blocking the PI3K/Akt pathway) enhances the sensibility of HMEC-su to suntinib and inhibits the gene transcription and protein expression of P-gp, ABCG2 in HMEC-su cells. In conclusion, these results indicate that LY294002 could reverse P-gp and ABCG2 mediated-drug resistance to sunitinib in HMEC-su cells by inhibiting PI3K/Akt signaling.
DOI: 10.6084/m9.figshare.13272894.v1
title: GLIPR2 is a negative regulator of autophagy and the BECN1-ATG14-containing phosphatidylinositol 3-kinase complex

description: A key mediator of macroautophagy/autophagy induction is the class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) consisting of PIK3C3/VPS34, PIK3R4/VPS15, BECN1, and ATG14. Although several proteins are known to enhance or decrease PtdIns3K-C1 activity, our understanding of the molecular regulation of PtdIns3K-C1 is still incomplete. Previously, we identified a Golgi-associated protein, GLIPR2, in a screen for proteins that interact with amino acids 267–284 of BECN1, a region of BECN1 sufficient to induce autophagy when fused to a cell penetrating leader sequence. In this study, we used CRISPR-Cas9-mediated depletion of GLIPR2 in cells and mice to investigate the role of GLIPR2 in the regulation of autophagy and PtdIns3K-C1 activity. Depletion of GLIPR2 in HeLa cells increased autophagic flux and generation of phosphatidylinositol 3-phosphate (PtdIns3P). <i>GLIPR2</i> knockout resulted in less compact Golgi structures, which was also observed in autophagy-inducing conditions such as amino acid starvation or Tat-BECN1 peptide treatment. Importantly, the binding of GLIPR2 to purified PtdIns3K-C1 inhibited the in vitro lipid kinase activity of PtdIns3K-C1. Moreover, the tissues of <i>glipr2</i> knockout mice had increased basal autophagic flux as well as increased recruitment of the PtdIns3P-binding protein, WIPI2. Taken together, our findings demonstrate that GLIPR2 is a negative regulator of PtdIns3K-C1 activity and basal autophagy. <b>Abbreviations:</b> ATG14: autophagy related 14; Baf A1: bafilomycin A<sub>1</sub>; BARA: β-α repeated, autophagy-specific; CQ: chloroquine; GFP: green fluorescent protein; GLIPR2: GLI pathogenesis related 2; HBSS: Hanks’ balanced salt solution; KO: knockout; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; PBS: phosphate-buffered saline; PtdIns3K-C1: phosphatidylinositol 3-kinase complex I; PtdIns3P: phosphatidylinositol-3-phosphate; SEM: standard error of the mean; WIPI2: WD repeat domain, phosphoinositide interacting 2
DOI: 10.6084/m9.figshare.7505918.v1
title: Additional file 1: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: RNA-seq analysis. (XLSX 8372 kb)
DOI: 10.6084/m9.figshare.21137354
title: Sunitinib induced resistance of endothelial cells by up-regulating P-glycoprotein and PI3K/Akt pathway

description: Abstract Drug resistance is a crucial obstacle to achieve satisfactory chemotherapeutic effects. Numerous studies have shown that the PI3K/Akt signaling pathway plays a significant role in various processes of cellular events and tumor progression, while few studies have focused on the PI3K/Akt signaling pathway in drug resistance of endothelial cells. The present study aims to explore the relationship of PI3K/Akt signaling and cellular resistance to anticancer drugs in human microvessel endothelial cells (HMEC-1). We established stable sunitinib-resiatant human microvessel endothelial cells (HMEC-su) after long-term exposure to sunitinib (a small-molecule tyrosine kinase receptor inhibitor) for 12 months. HMEC-su showed significant alternations of cell morphology and exhibited a 2.32-fold higher IC50 of sunitinib than parental HMEC-1 cells. Expression of P-glycoprotein (P-gp) and breast cancer-resistance protein (ABCG2) which mediates drug efflux, increased significantly in HMEC-su lines compared with HMEC-1 cells by western blots assay. Our study further demonstrates that LY294002 (blocking the PI3K/Akt pathway) enhances the sensibility of HMEC-su to suntinib and inhibits the gene transcription and protein expression of P-gp, ABCG2 in HMEC-su cells. In conclusion, these results indicate that LY294002 could reverse P-gp and ABCG2 mediated-drug resistance to sunitinib in HMEC-su cells by inhibiting PI3K/Akt signaling.
DOI: 10.6084/m9.figshare.7505903.v1
title: Additional file 3: of Prevalence of pathogenic/likely pathogenic variants in the 24 cancer genes of the ACMG Secondary Findings v2.0 list in a large cancer cohort and ethnicity-matched controls

description: Table S2. InterVar classification of ACMG SF v2.0 cancer genes after expert review. (XLSX 30 kb)
DOI: 10.6084/m9.figshare.7505918
title: Additional file 1: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: RNA-seq analysis. (XLSX 8372 kb)
DOI: 10.6084/m9.figshare.7505951.v1
title: Additional file 6: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: pEZG paralogs and phylogeny trees. (FASTA 212 kb)
DOI: 10.6084/m9.figshare.7505903
title: Additional file 3: of Prevalence of pathogenic/likely pathogenic variants in the 24 cancer genes of the ACMG Secondary Findings v2.0 list in a large cancer cohort and ethnicity-matched controls

description: Table S2. InterVar classification of ACMG SF v2.0 cancer genes after expert review. (XLSX 30 kb)
DOI: 10.6084/m9.figshare.7505927.v1
title: Additional file 2: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: stringent pEZGs. (XLSX 85 kb)
DOI: 10.6084/m9.figshare.7505936
title: Additional file 3: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: relaxed (MHT 482 kb)
DOI: 10.6084/m9.figshare.7505936.v1
title: Additional file 3: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: relaxed (MHT 482 kb)
DOI: 10.6084/m9.figshare.7505927
title: Additional file 2: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: stringent pEZGs. (XLSX 85 kb)
DOI: 10.6084/m9.figshare.7505945
title: Additional file 4: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: Figure S1. (XLSX 13 kb)
DOI: 10.6084/m9.figshare.7505945.v1
title: Additional file 4: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: Figure S1. (XLSX 13 kb)
DOI: 10.6084/m9.figshare.7505954
title: Additional file 7: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: the GT-rich motif. (XLSX 14 kb)
DOI: 10.6084/m9.figshare.7505954.v1
title: Additional file 7: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: the GT-rich motif. (XLSX 14 kb)
DOI: 10.6084/m9.figshare.7505951
title: Additional file 6: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: pEZG paralogs and phylogeny trees. (FASTA 212 kb)
DOI: 10.6084/m9.figshare.7505975.v1
title: Additional file 9: of Pure early zygotic genes in the Asian malaria mosquito Anopheles stephensi

description: Table S2. (FASTA 82 kb)
DOI: 10.6084/m9.figshare.16418797
title: Provenance and Palaeogeomorphology study of the southwestern North China Craton during Middle-Late Triassic and its geological implication

description: The study of tectonic, provenance, and paleogeomorphologic systems is important for defining the basin evolution and it is also the basis for the accurate evaluation of oil and gas potential of a basin. The provenance and paleogeomorphology of the western Ordos Basin and the Hexi Corridor in the southwestern North China Craton(sw-NCC) have long been debated. In this study, detrital zircon geochronology, petrography and geochemistry methods are used to analyse the evolution of provenance and paleogeomorphology in the sw-NCC during the Middle–Late Triassic, and the provenance and paleogeomorphic relationships with tectonic events are discussed. The U–Pb detrital zircon geochronology of the Yaoshan samples in the western Ordos Basin are clear and consistent, and shows that there are three major age populations, 2700–2200 Ma, 2150–1650 Ma and 450–220 Ma. While the age spectrums of the samples from different formations in the Hexi Corridor are complex, showing significant differences. The whole results imply that the Hexi Corridor and the west margin of the Ordos Basin had a unified source during the Middle Triassic, which is the western NCC. However, in the Late Triassic, the sediment of the Hexi Corridor was mainly from the Qilian–Qaidam Terrane while the source of the western Ordos Basin remained unchanged. Besides the provenance analysis, the stratigraphic correlation, petrology and geochemistry analyses also support that the Hexi Corridor was temporarily connected with the Ordos Basin during the Middle Triassic but was separated from the Ordos Basin by a small-scale, underwater paleo-uplift during the Late Triassic. The evolution of the provenance and paleogeomorphology in the southwestern Ordos Basin was related to the closure of the shallow shelf of the Paleo-Tethys Ocean.
DOI: 10.6084/m9.figshare.16418797.v1
title: Provenance and Palaeogeomorphology study of the southwestern North China Craton during Middle-Late Triassic and its geological implication

description: The study of tectonic, provenance, and paleogeomorphologic systems is important for defining the basin evolution and it is also the basis for the accurate evaluation of oil and gas potential of a basin. The provenance and paleogeomorphology of the western Ordos Basin and the Hexi Corridor in the southwestern North China Craton(sw-NCC) have long been debated. In this study, detrital zircon geochronology, petrography and geochemistry methods are used to analyse the evolution of provenance and paleogeomorphology in the sw-NCC during the Middle–Late Triassic, and the provenance and paleogeomorphic relationships with tectonic events are discussed. The U–Pb detrital zircon geochronology of the Yaoshan samples in the western Ordos Basin are clear and consistent, and shows that there are three major age populations, 2700–2200 Ma, 2150–1650 Ma and 450–220 Ma. While the age spectrums of the samples from different formations in the Hexi Corridor are complex, showing significant differences. The whole results imply that the Hexi Corridor and the west margin of the Ordos Basin had a unified source during the Middle Triassic, which is the western NCC. However, in the Late Triassic, the sediment of the Hexi Corridor was mainly from the Qilian–Qaidam Terrane while the source of the western Ordos Basin remained unchanged. Besides the provenance analysis, the stratigraphic correlation, petrology and geochemistry analyses also support that the Hexi Corridor was temporarily connected with the Ordos Basin during the Middle Triassic but was separated from the Ordos Basin by a small-scale, underwater paleo-uplift during the Late Triassic. The evolution of the provenance and paleogeomorphology in the southwestern Ordos Basin was related to the closure of the shallow shelf of the Paleo-Tethys Ocean.
DOI: 10.6084/m9.figshare.14322171
title: Predictive performance of 12 equations for estimating glomerular filtration rate in severely obese patients

description: ABSTRACT Objective: Considering that the Cockcroft-Gault formula and the equation of diet modification in renal disease are amply used in clinical practice to estimate the glomerular filtration rate, although they seem to have low accuracy in obese patients, the present study intends to evaluate the predictive performance of 12 equations used to estimate the glomerular filtration rate in obese patients. Methods: This is a cross-sectional retrospective study, conducted between 2007 and 2008 and carried out at a university, of 140 patients with severe obesity (mean body mass index 44 ± 4.4 kg/m2). The glomerular filtration rate was determined by means of 24-hour urine samples. Patients were classified into one or more of the four subgroups: impaired glucose tolerance (n = 43), diabetic (n = 24), metabolic syndrome (n = 76), and/or hypertension (n = 66). We used bias, precision, and accuracy to assess the predictive performance of each equation in the entire group and in the subgroups. Results: In renal disease, Cockcroft-Gault's formula and the diet modification equation are not precise in severely obese patients (precision: 40.9 and 33.4, respectively). Sobh's equation showed no bias in the general group or in two subgroups. Salazar-Corcoran's and Sobh's equations showed no bias for the entire group (Bias: −5.2, 95% confidence interval (CI) = −11.4, 1.0, and 6. 2; 95%CI = −0.3, 12.7, respectively). All the other equations were imprecise for the entire group. Conclusion: Of the equations studied, those of Sobh and Salazar-Corcoran seem to be the best for estimating the glomerular filtration rate in severely obese patients analyzed in our study.
DOI: 10.6084/m9.figshare.6981992.v1
title: Additional file 1: of Functional CRISPR screen identifies AP1-associated enhancer regulating FOXF1 to modulate oncogene-induced senescence

description: Table S1. OIS-responsive bi-directional transcriptional units. Table S2. sgRNA oligo list. Table S3. CRISPR screen analysis. Table S4. Primer list. (XLSX 728 kb)
DOI: 10.6084/m9.figshare.6981767
title: Transcriptional Profile and Integrative Analyses of Long Noncoding RNAs in Primary Human Corneal Epithelial Cells in Response to HSV-1 Infection

description: Long noncoding RNAs (lncRNAs) have been demonstrated to have important regulatory functions in diverse cellular processes; however, the role of lncRNAs in the pathogenesis of herpes simplex keratitis (HSK) remains poorly understood. Primary human corneal epithelial cells (HCECs) were infected with herpes simplex virus-1 (HSV-1) and the total RNAs extracted from both the infected group and the mock-infected group subjected to microarray analysis to identify the differential expression of lncRNAs and mRNAs. We also performed bioinformatic analysis including gene ontology (GO) analysis, pathway analysis and co-expression network analysis. Compared with mock-infected group, the expression of thousands of lncRNAs and mRNAs were significantly changed, and the microarray results were validated by qRT-PCR. The most enriched GOs targeted by up-regulated transcripts were defense response, intrinsic component of plasma membrane and cytokine activity，and the most enriched GOs targeted by the down-regulated transcripts were cellular metabolic process, intracellular part and poly (A) RNA binding. Pathway analysis indicated that the most correlated pathways for up- and down-regulated transcripts were cytokine-cytokine receptor interaction and RNA transport, respectively. Our study identified the genome-wide profile of lncRNAs and mRNAs expression in primary corneal epithelial cells with HSV-1 infection. These transcriptomic data together with subsequent bioinformatic analysis will provide us with novel clue to the insight into molecular mechanism and potential therapeutic targets of HSK. Further studies are expected to verify the potentially functional genes and pathways and explore the critical lncRNAs. Long noncoding RNAs: lncRNAs; herpes simplex virus-1: HSV-1; herpes simplex virus keratitis: HSK; human corneal epithelial cells: HCECs
DOI: 10.6084/m9.figshare.6981767.v1
title: Transcriptional Profile and Integrative Analyses of Long Noncoding RNAs in Primary Human Corneal Epithelial Cells in Response to HSV-1 Infection

description: Long noncoding RNAs (lncRNAs) have been demonstrated to have important regulatory functions in diverse cellular processes; however, the role of lncRNAs in the pathogenesis of herpes simplex keratitis (HSK) remains poorly understood. Primary human corneal epithelial cells (HCECs) were infected with herpes simplex virus-1 (HSV-1) and the total RNAs extracted from both the infected group and the mock-infected group subjected to microarray analysis to identify the differential expression of lncRNAs and mRNAs. We also performed bioinformatic analysis including gene ontology (GO) analysis, pathway analysis and co-expression network analysis. Compared with mock-infected group, the expression of thousands of lncRNAs and mRNAs were significantly changed, and the microarray results were validated by qRT-PCR. The most enriched GOs targeted by up-regulated transcripts were defense response, intrinsic component of plasma membrane and cytokine activity，and the most enriched GOs targeted by the down-regulated transcripts were cellular metabolic process, intracellular part and poly (A) RNA binding. Pathway analysis indicated that the most correlated pathways for up- and down-regulated transcripts were cytokine-cytokine receptor interaction and RNA transport, respectively. Our study identified the genome-wide profile of lncRNAs and mRNAs expression in primary corneal epithelial cells with HSV-1 infection. These transcriptomic data together with subsequent bioinformatic analysis will provide us with novel clue to the insight into molecular mechanism and potential therapeutic targets of HSK. Further studies are expected to verify the potentially functional genes and pathways and explore the critical lncRNAs. Long noncoding RNAs: lncRNAs; herpes simplex virus-1: HSV-1; herpes simplex virus keratitis: HSK; human corneal epithelial cells: HCECs
DOI: 10.6084/m9.figshare.6981992
title: Additional file 1: of Functional CRISPR screen identifies AP1-associated enhancer regulating FOXF1 to modulate oncogene-induced senescence

description: Table S1. OIS-responsive bi-directional transcriptional units. Table S2. sgRNA oligo list. Table S3. CRISPR screen analysis. Table S4. Primer list. (XLSX 728 kb)
DOI: 10.6084/m9.figshare.12218885
title: Additional file 3 of Wheat chromatin architecture is organized in genome territories and transcription factories

description: Additional file 3:Table S2. With odds ratios (OR) and effect size (Cramer’s V) for all combinations of features of interacting genes pairs.
DOI: 10.6084/m9.figshare.12218891
title: Additional file 4 of Wheat chromatin architecture is organized in genome territories and transcription factories

description: Additional file 4:Table S3. With a summary of Hi-C and HiChIP libraries statistics.
DOI: 10.6084/m9.figshare.6982139
title: Additional file 1: of Tip110/SART3 regulates IL-8 expression and predicts the clinical outcomes in melanoma

description: Supplementary materials. (ZIP 3620 kb)
DOI: 10.6084/m9.figshare.6982139.v1
title: Additional file 1: of Tip110/SART3 regulates IL-8 expression and predicts the clinical outcomes in melanoma

description: Supplementary materials. (ZIP 3620 kb)