cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.22622767.v1
title: Additional file 1 of The arabinose transporter MtLat-1 is involved in hemicellulase repression as a pentose transceptor in Myceliophthora thermophila

description: Additional file 1. Table S1: List of PCR primers used in this study. Table S2: Profiles of RNA-Seq reads mapped to the genome of M. thermophila. Table S3: Transcriptomic profiles of 26 sugar transporters with robust expression levels (RPKM &gt; 20) in at least one tested condition. Table S4: Genes showing significantly different transcriptional levels in strain ∆Mtlat-1 compared with the WT when grown on 1 × VMM with 2% arabinan for 4 days. Table S5: Transcriptomic profiles of genes encoding major hemicellulases from RNA-Seq data when grown on 1 × VMM with 2% arabinan. Table S6: Gene ontology (GO) analysis of up-regulated genes in strain ΔMtlat-1 compared with the WT when grown on 1 × VMM with 2% arabinan for 4 days. Table S7: Transcriptomic profiles of transcription factor genes with significantly upregulated expression levels in WT M. thermophila grown on l-arabinose, d-xylose, or d-glucose, compared with that under no carbon. Table S8: Genes showing significantly different transcriptional levels in strain ∆Mtara-1 compared with the WT strain when grown on 2% arabinan for the induction of 4 h.
DOI: 10.6084/m9.figshare.22624967.v1
title: Additional file 1 of A novel feedback regulated loop of circRRM2-IGF2BP1-MYC promotes breast cancer metastasis

description: Additional file 1: Fig. S1. Analysis of four candidate circRNAs and enrichment analysis of parent genes. Fig. S2. The mRNA levels of hsa_circ_0052582, hsa_circ_0058113, hsa_circ_0058148, and hsa_circ_0060551 in patients with BC from the GEO dataset (GSE111504). Fig. S3. The mRNA levels of hsa_circ_0052582, hsa_circ_0058113, hsa_circ_0058148, and hsa_circ_0060551 in patients with BC at different T stages from the GEO dataset (GSE111504). Fig. S4. The mRNA levels of hsa_circ_0052582, hsa_circ_0058113, hsa_circ_0058148, and hsa_circ_0060551 in patients with BC at different N stages from the GEO dataset (GSE111504). Fig. S5. CircRNA-miRNA-mRNA ceRNA network. Fig. S6. Expression level of circRRM2/IGF2BP1/MYC in BC and the migration phenotype of miR-27b-3p/miR-31-5p inhibitor in BC cells. Overexpression (A) or knockout (B) efficiency of circRRM2 in BT-549 and MDA-MB-231 was verified by RT qPCR. (C) The levels of IGF2BP1 in BC cells. (D) Expression level of MYC in BC tissues. (E) Correlation analysis of circRRM2 and MYC in BC tissues. (F-G) circRRM2 knockdown abolished the suppression of cell migration treated with miR-27b-3p/miR-31-5p inhibitor. BT-549 cells were transfected with miR-27b-3p (F) or miR-31-5p (G) inhibitor, and the scratch wound healing assay was performed to measure the ability of cell migration. The rescue assay was conducted by co-transfecting the circRRM2 plasmid. *P &lt; 0.05, **P &lt; 0.01, ***P &lt; 0.001. Fig. S7. Prediction and prognostic value of target genes binding with both miR-27b-3p and miR-31-5p. Fig. S8. Prognostic value of target genes binding with both miR-27b-3p and miR-31-5p. *P &lt; 0.05, **P &lt; 0.01, ***P &lt; 0.001. Fig. S9. The transwell assay in BC cell transfected with circRRM2 plasmid and IGF2BP1 siRNA. The transwell assay was performed to detect the rescue effect of overexpression of circRRM2 on IGF2BP1 knockdown in BT-549 (A) or MDA-MB-231 (B) cells. Fig. S10. Calibration plot of the nomogram to predict the probability of the OS in patients with BC at 1, 3, and 5 years. Fig. S11. Analysis of immune cell infiltration related to IGF2BP1 in patients with BC. (A) Lollipop plot shows the correlation between IGF2BP1 level and immunocytes infiltration. (B) Correlations between IGF2BP1 and immune checkpoint-related genes. (C) Scatter plot of correlation between IGF2BP1 and immunocytes infiltration. (D) KM curve of immunocytes infiltration status and OS in patients with BC. (E) Comparison of immunocytes infiltration related with copy number variation of IGF2BP1. *P &lt; 0.05, **P &lt; 0.01, ***P &lt; 0.001. Fig. S12. Mutational analysis of IGF2BP1. (A) The oncoprint of IGF2BP1 was obtained using cBioPortal. (B) Analysis of PTM sites in IGF2BP1. Fig. S13. Network of candidates binding to IGF2BP1 constructed using the BioGRID database. Table S1. Primers used for qRT-PCR. Table S2. The sequences of siRNAs.
DOI: 10.6084/m9.figshare.20003545
title: Additional file 9 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in Huntington’s disease

description: Additional file 9. Differential Gene Expression analyses across the four different genotypes WT, zQ175, CK2α’(+/-) and zQ175:CK2α’(+/-).
DOI: 10.6084/m9.figshare.22625036.v1
title: Additional file 7 of Comparison of long-term outcomes of stereotactic body radiotherapy (SBRT) via Helical tomotherapy for early-stage lung cancer with or without pathological proof

description: Additional file 7: Table S3. Patterns of failure.
DOI: 10.6084/m9.figshare.22624936.v1
title: Additional file 2 of circMMD reduction following tumor treating fields inhibits glioblastoma progression through FUBP1/FIR/DVL1 and miR-15b-5p/FZD6 signaling

description: Additional file 2: Table S1. Information of the primers, siRNAs/shRNAs and antibodies used in the study.
DOI: 10.6084/m9.figshare.22625021
title: Additional file 2 of Comparison of long-term outcomes of stereotactic body radiotherapy (SBRT) via Helical tomotherapy for early-stage lung cancer with or without pathological proof

description: Additional file 2: Table S1. Probability of malignancy.
DOI: 10.6084/m9.figshare.20003545.v1
title: Additional file 9 of CK2 alpha prime and alpha-synuclein pathogenic functional interaction mediates synaptic dysregulation in huntington’s disease

description: Additional file 9. Differential Gene Expression analyses across the four different genotypes WT, zQ175, CK2α’(+/-) and zQ175:CK2α’(+/-).
DOI: 10.6084/m9.figshare.22624942
title: Additional file 4 of circMMD reduction following tumor treating fields inhibits glioblastoma progression through FUBP1/FIR/DVL1 and miR-15b-5p/FZD6 signaling

description: Additional file 4: Table S3. Correlation between circMMD expression and clinical features of glioma patients.
DOI: 10.6084/m9.figshare.23156073
title: Retrieval and validation of vertical LAI profile derived from airborne and spaceborne LiDAR data at a deciduous needleleaf forest site

description: Leaf area index (LAI) is defined as one half of the total green leaf area per unit ground surface area. Its vertical profile is critical for understanding the remote sensing radiative transfer processes. LAI profile has been derived from airborne and spaceborne LiDAR data, such as the Global Ecosystem Dynamics Investigation (GEDI) installed on the International Space Station. However, the capability of various algorithms for the LAI profile estimation with airborne LiDAR is not clearly evaluated, and the estimated LAI profiles, including the GEDI LAI products, are not been fully validated. This study conducted a quantitative retrieval and validation of the LAI profiles using terrestrial and airborne laser scanning (TLS and ALS) and spaceborne GEDI data over a deciduous needleleaf forest site in northern China. The vertical LAI profile was estimated in the field using an upward digital hemispherical photography (DHP) attached to a portable measurement system in 2020 and 2021. A suite of new LiDAR indices combining both LiDAR return number and return intensity was explored for the LAI profile estimation. All LAI profiles obtained from the DHP, TLS, ALS, and GEDI during the leaf-on season and leaf-off season were compared. The DHP shows a good agreement with the TLS LAI profiles (R<sup>2</sup> = 0.97). The LAI profile derived from the ALS data using the combined light penetration index (LPI<sub>RI</sub>) agrees well (R<sup>2</sup> ≥0.86) with the DHP, TLS, and GEDI estimates. In general, the LPI<sub>RI</sub> is advantageous for regional LAI profile mapping from ALS. The GEDI cumulative LAI corresponds well with the DHP during the leaf-on season (R<sup>2</sup> = 0.90, RMSE = 0.23), but underestimates during the leaf-off season (R<sup>2</sup> = 0.70, RMSE = 0.14, bias=−0.13). The underestimation is attributed to the higher canopy and ground reflectance ratio (ρ<sub>v</sub>/ρ<sub>g</sub>) assigned in the algorithm and the height discrepancy between the GEDI and field measurements. For the GEDI LAI profile product, further validation and improvement are necessary for other biome types and landscape conditions, especially during the leaf-off season.
DOI: 10.6084/m9.figshare.23156073.v1
title: Retrieval and validation of vertical LAI profile derived from airborne and spaceborne LiDAR data at a deciduous needleleaf forest site

description: Leaf area index (LAI) is defined as one half of the total green leaf area per unit ground surface area. Its vertical profile is critical for understanding the remote sensing radiative transfer processes. LAI profile has been derived from airborne and spaceborne LiDAR data, such as the Global Ecosystem Dynamics Investigation (GEDI) installed on the International Space Station. However, the capability of various algorithms for the LAI profile estimation with airborne LiDAR is not clearly evaluated, and the estimated LAI profiles, including the GEDI LAI products, are not been fully validated. This study conducted a quantitative retrieval and validation of the LAI profiles using terrestrial and airborne laser scanning (TLS and ALS) and spaceborne GEDI data over a deciduous needleleaf forest site in northern China. The vertical LAI profile was estimated in the field using an upward digital hemispherical photography (DHP) attached to a portable measurement system in 2020 and 2021. A suite of new LiDAR indices combining both LiDAR return number and return intensity was explored for the LAI profile estimation. All LAI profiles obtained from the DHP, TLS, ALS, and GEDI during the leaf-on season and leaf-off season were compared. The DHP shows a good agreement with the TLS LAI profiles (R<sup>2</sup> = 0.97). The LAI profile derived from the ALS data using the combined light penetration index (LPI<sub>RI</sub>) agrees well (R<sup>2</sup> ≥0.86) with the DHP, TLS, and GEDI estimates. In general, the LPI<sub>RI</sub> is advantageous for regional LAI profile mapping from ALS. The GEDI cumulative LAI corresponds well with the DHP during the leaf-on season (R<sup>2</sup> = 0.90, RMSE = 0.23), but underestimates during the leaf-off season (R<sup>2</sup> = 0.70, RMSE = 0.14, bias=−0.13). The underestimation is attributed to the higher canopy and ground reflectance ratio (ρ<sub>v</sub>/ρ<sub>g</sub>) assigned in the algorithm and the height discrepancy between the GEDI and field measurements. For the GEDI LAI profile product, further validation and improvement are necessary for other biome types and landscape conditions, especially during the leaf-off season.
DOI: 10.6084/m9.figshare.7951724
title: Enhanced hydrogen evolution from CuOx-C/TiO2 with multiple electron transport pathways

description: The manuscript was accepted by journal "PLoS ONE" under the title of "Enhanced hydrogen evolution from CuOx-C/TiO2 with multiple electron transport pathways", with a doi of 10.1371/journal.pone.0215339. The compressed file "submited to Figshare.rar" included some excel files, which were the primary dataset of the figures, respectively.
DOI: 10.6084/m9.figshare.9524591
title: Hypoxia-induced shedding of MICA and HIF1A-mediated immune escape of pancreatic cancer cells from NK cells: role of circ_0000977/miR-153 axis

description: One key to malignant progression of pancreatic cancer (PC) is the acquired ability of tumour cells to escape immune-mediated lysis. Hypoxic microenvironment plays a causal role in PC metastasis. According to previous studies, hypoxia could induce the upregulation of HIF1A, ADAM10 and sMICA, leading to decreased NKG2D in NK cells and tumour cells escape from immune surveillance and NK cell-mediated lysis. In the present study, in NK cells derived from high-HIF1A expression patients, the levels of internalization of MICA/B and NKG2D were obviously higher than those in low-HIF1A expression group; hypoxia dramatically upregulated the levels of sMICA culture supernatant of Panc-1 cells. Regarding the molecular mechanism, dysregulated circRNAs and miRNAs that might modulate HIF1A-mediated immune escape were selected and examined for detailed functions. The expression of circ_0000977 could be induced by hypoxia, and circ_0000977 knockdown enhanced the killing effect of NK cells on PC cells under hypoxia through HIF1A and ADAM10. HIF1 and ADAM10 were direct downstream targets of miR-153; circ_0000977 served as a sponge for miR-153 to counteract miR-153-mediated repression of HIF1 and ADAM10 mRNA through direct targeting in both 293T cells and Panc-1 cells. miR-153 inhibition exerted an opposing effect on HIF1A-mediated immune escape of PC cells to circ_0000977 knockdown; the effect of circ_0000977 knockdown were partially attenuated by miR-153 inhibition. In summary, circ_0000977/miR-153 axis modulates HIF1A-mediated immune escape of PC cells through miR-153 downstream targets HIF1A and ADAM10. We provided a novel mechanism of HIF1A-mediated immune escape of PC cells from the perspective of circRNAs-miRNA-mRNA axis. <b>Abbreviations:</b> Pancreatic cancer (PC); peripheral blood lymphocytes (PBLs); A Disintegrin and Metalloproteinase Domain 10 (ADAM10); MHC class I-related molecule A (MICA); soluble MICA (sMICA); membrane MICA (mMICA); Hypoxia-inducible factor 1-alpha (HI1FA); long non-coding RNAs (lncRNAs); non-coding RNAs (ncRNAs); natural killer (NK); Haematoxylin and eosin (H&E); Immunohistochemistry (IHC); natural killer group 2 member D (NKG2D);
DOI: 10.6084/m9.figshare.9524591.v1
title: Hypoxia-induced shedding of MICA and HIF1A-mediated immune escape of pancreatic cancer cells from NK cells: role of circ_0000977/miR-153 axis

description: One key to malignant progression of pancreatic cancer (PC) is the acquired ability of tumour cells to escape immune-mediated lysis. Hypoxic microenvironment plays a causal role in PC metastasis. According to previous studies, hypoxia could induce the upregulation of HIF1A, ADAM10 and sMICA, leading to decreased NKG2D in NK cells and tumour cells escape from immune surveillance and NK cell-mediated lysis. In the present study, in NK cells derived from high-HIF1A expression patients, the levels of internalization of MICA/B and NKG2D were obviously higher than those in low-HIF1A expression group; hypoxia dramatically upregulated the levels of sMICA culture supernatant of Panc-1 cells. Regarding the molecular mechanism, dysregulated circRNAs and miRNAs that might modulate HIF1A-mediated immune escape were selected and examined for detailed functions. The expression of circ_0000977 could be induced by hypoxia, and circ_0000977 knockdown enhanced the killing effect of NK cells on PC cells under hypoxia through HIF1A and ADAM10. HIF1 and ADAM10 were direct downstream targets of miR-153; circ_0000977 served as a sponge for miR-153 to counteract miR-153-mediated repression of HIF1 and ADAM10 mRNA through direct targeting in both 293T cells and Panc-1 cells. miR-153 inhibition exerted an opposing effect on HIF1A-mediated immune escape of PC cells to circ_0000977 knockdown; the effect of circ_0000977 knockdown were partially attenuated by miR-153 inhibition. In summary, circ_0000977/miR-153 axis modulates HIF1A-mediated immune escape of PC cells through miR-153 downstream targets HIF1A and ADAM10. We provided a novel mechanism of HIF1A-mediated immune escape of PC cells from the perspective of circRNAs-miRNA-mRNA axis. <b>Abbreviations:</b> Pancreatic cancer (PC); peripheral blood lymphocytes (PBLs); A Disintegrin and Metalloproteinase Domain 10 (ADAM10); MHC class I-related molecule A (MICA); soluble MICA (sMICA); membrane MICA (mMICA); Hypoxia-inducible factor 1-alpha (HI1FA); long non-coding RNAs (lncRNAs); non-coding RNAs (ncRNAs); natural killer (NK); Haematoxylin and eosin (H&E); Immunohistochemistry (IHC); natural killer group 2 member D (NKG2D);
DOI: 10.6084/m9.figshare.22624939
title: Additional file 3 of circMMD reduction following tumor treating fields inhibits glioblastoma progression through FUBP1/FIR/DVL1 and miR-15b-5p/FZD6 signaling

description: Additional file 3: Table S2. Clinical information of glioma array.
DOI: 10.6084/m9.figshare.22622767
title: Additional file 1 of The arabinose transporter MtLat-1 is involved in hemicellulase repression as a pentose transceptor in Myceliophthora thermophila

description: Additional file 1. Table S1: List of PCR primers used in this study. Table S2: Profiles of RNA-Seq reads mapped to the genome of M. thermophila. Table S3: Transcriptomic profiles of 26 sugar transporters with robust expression levels (RPKM &gt; 20) in at least one tested condition. Table S4: Genes showing significantly different transcriptional levels in strain ∆Mtlat-1 compared with the WT when grown on 1 × VMM with 2% arabinan for 4 days. Table S5: Transcriptomic profiles of genes encoding major hemicellulases from RNA-Seq data when grown on 1 × VMM with 2% arabinan. Table S6: Gene ontology (GO) analysis of up-regulated genes in strain ΔMtlat-1 compared with the WT when grown on 1 × VMM with 2% arabinan for 4 days. Table S7: Transcriptomic profiles of transcription factor genes with significantly upregulated expression levels in WT M. thermophila grown on l-arabinose, d-xylose, or d-glucose, compared with that under no carbon. Table S8: Genes showing significantly different transcriptional levels in strain ∆Mtara-1 compared with the WT strain when grown on 2% arabinan for the induction of 4 h.
DOI: 10.6084/m9.figshare.22624943.v1
title: Additional file 1 of Mitochondrial metabolism of the facultative parasite Chilodonella uncinata (Alveolata, Ciliophora)

description: Additional file 1: Table S1. Primers used in this study. Table S2. COG annotation results. Table S3. Annotation results of mitochondria metabolism.
DOI: 10.25345/c53n20r2k
title: MassIVE MSV000094041 - Regulation of Glycogen Synthase kinase 3beta by phosphorylation and O-beta-linked N-acetylglucosaminylation: implications on tau protein phosphorylation
title: Glycogen synthase kinase 3 (GSK3) plays a pivotal role in signaling pathways related to insulin metabolism and in the pathogenesis of Alzheimer s disease (AD) and other neurodegenerative disorders. More particularly, the GSK3beta isoform is involved in AD-associated tau pathology as one of the major kinases involved in the hyperphosphorylation of the microtubule-associated tau protein, one of the neuropathological hallmarks of AD. As a constitutively active serine/threonine proline-directed kinase, GSK3 is inactivated by Akt/PKB-mediated phosphorylation of Ser9 at the N-terminal disordered domain. Furthermore, GSK3 activity requires for most of its substrates a priming (pre-phosphorylation) by another kinase that allows binding of the substrate in a phosphate-specific pocket near to the active site. It has been shown that GSK3 is also post-translationally modified by O-linked beta-N-acetylglucosaminylation (O-GlcNAcylation) with still unknown functional implications. We have found that binding of the phosphorylated, active form of Akt inhibits GSK3beta kinase activity on both primed and unprimed tau substrates, and Akt-mediated Ser9 phosphorylation restores the GSK3beta kinase activity on primed tau only. Therefore, Ser9 phosphorylation only inactivates GSK3 kinase activity on an unprimed substrate. Additionally, we have shown that GSK3beta is O-GlcNAcylated at multiple sites in both its disordered N- and C-terminal domains including Ser9, but O-GlcNAcylation does not alter kinase activity nor the Akt-mediated regulation of GSK3.
DOI: 10.6084/m9.figshare.22625030.v1
title: Additional file 5 of Comparison of long-term outcomes of stereotactic body radiotherapy (SBRT) via Helical tomotherapy for early-stage lung cancer with or without pathological proof

description: Additional file 5: Table S2. Cause of death.
DOI: 10.6084/m9.figshare.13194738
title: Gastrodin promotes CNS myelination via a lncRNA Gm7237/miR-142a/MRF pathway

description: Treatment of central nervous system (CNS) demyelination is greatly hindered by lack of the knowledge regarding to underlying molecular mechanisms as well as therapeutic agents. Here, we report a novel small molecule agent, gastrodin (GAS), which can significantly promote CNS myelination in <i>in vivo</i> mice models. By using high-throughput sequencing analysis, we discover a key long non-coding RNA Gm7237 that can enhance CNS myelination and is up-regulated by GAS. Through using bioinformatic analysis and experimental validations, we further unravel that microRNA-142a (miR-142a) and its target myelin gene regulatory factor (MRF) is under the direct regulation by Gm7237. Finally, we demonstrate that Gm7237/miR-142a/MRF axis is the key pathway involved in CNS myelination mediated by GAS. Overall, our results provide not only a novel agent for therapeutic treatment of CNS demyelination but also a molecular basis responsible for GAS-promoted CNS myelination.
DOI: 10.6084/m9.figshare.10049012
title: MOESM1 of Accelerated evolution and diversifying selection drove the adaptation of cetacean bone microstructure

description: Additional file 1: Table S1-3. Datasets of rib, humerus and vertebrae compiled in the present study, respectively. Containing the list of species sampled, the collection number, the habitat, and the bone histological parameters measured for each species. Table S4. List of ‘root-to-tip’ dN/dS values of each species for 348 bone function-associated genes.
DOI: 10.6084/m9.figshare.10049012.v1
title: MOESM1 of Accelerated evolution and diversifying selection drove the adaptation of cetacean bone microstructure

description: Additional file 1: Table S1-3. Datasets of rib, humerus and vertebrae compiled in the present study, respectively. Containing the list of species sampled, the collection number, the habitat, and the bone histological parameters measured for each species. Table S4. List of ‘root-to-tip’ dN/dS values of each species for 348 bone function-associated genes.
DOI: 10.6084/m9.figshare.10049024
title: MOESM3 of Accelerated evolution and diversifying selection drove the adaptation of cetacean bone microstructure

description: Additional file 3:Â Table S6.Â List of positively selected genes (PSGs) and divergently selected genes (DSGs) in cetaceans identified from 348 bone function-associated genes. Table S7.Â List of divergently selected genes (DSGs) in cetaceans identified from 348 bone function-associated genes.
DOI: 10.6084/m9.figshare.10049024.v1
title: MOESM3 of Accelerated evolution and diversifying selection drove the adaptation of cetacean bone microstructure

description: Additional file 3:Â Table S6.Â List of positively selected genes (PSGs) and divergently selected genes (DSGs) in cetaceans identified from 348 bone function-associated genes. Table S7.Â List of divergently selected genes (DSGs) in cetaceans identified from 348 bone function-associated genes.
DOI: 10.6084/m9.figshare.10049030
title: MOESM4 of Accelerated evolution and diversifying selection drove the adaptation of cetacean bone microstructure

description: Additional file 4: Table 8-10. Result of regression analyses between ‘root-to-tip’ dN/dS and bone histological parameters for rib, humerus and vertebrae, respectively.
DOI: 10.6084/m9.figshare.10049030.v1
title: MOESM4 of Accelerated evolution and diversifying selection drove the adaptation of cetacean bone microstructure

description: Additional file 4: Table 8-10. Result of regression analyses between ‘root-to-tip’ dN/dS and bone histological parameters for rib, humerus and vertebrae, respectively.