cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.20764282.v1
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764318
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764318.v1
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.25574/56501
title: Chandra X-ray Observatory ObsId 56501
DOI: 10.25574/56503
title: Chandra X-ray Observatory ObsId 56503
DOI: 10.25574/56506
title: Chandra X-ray Observatory ObsId 56506
DOI: 10.25574/56512
title: Chandra X-ray Observatory ObsId 56512
DOI: 10.25574/56523
title: Chandra X-ray Observatory ObsId 56523
DOI: 10.25574/56525
title: Chandra X-ray Observatory ObsId 56525
DOI: 10.25574/56529
title: Chandra X-ray Observatory ObsId 56529
DOI: 10.25574/56531
title: Chandra X-ray Observatory ObsId 56531
DOI: 10.25574/56534
title: Chandra X-ray Observatory ObsId 56534
DOI: 10.25574/56538
title: Chandra X-ray Observatory ObsId 56538
DOI: 10.25574/56540
title: Chandra X-ray Observatory ObsId 56540
DOI: 10.25574/56544
title: Chandra X-ray Observatory ObsId 56544
DOI: 10.25574/56546
title: Chandra X-ray Observatory ObsId 56546
DOI: 10.25574/56550
title: Chandra X-ray Observatory ObsId 56550
DOI: 10.25574/56552
title: Chandra X-ray Observatory ObsId 56552
DOI: 10.25574/56554
title: Chandra X-ray Observatory ObsId 56554
DOI: 10.25574/56556
title: Chandra X-ray Observatory ObsId 56556
DOI: 10.25574/56558
title: Chandra X-ray Observatory ObsId 56558
DOI: 10.25574/56560
title: Chandra X-ray Observatory ObsId 56560
DOI: 10.25574/56563
title: Chandra X-ray Observatory ObsId 56563
DOI: 10.25574/56568
title: Chandra X-ray Observatory ObsId 56568
DOI: 10.25574/56570
title: Chandra X-ray Observatory ObsId 56570
DOI: 10.25574/56575
title: Chandra X-ray Observatory ObsId 56575
DOI: 10.25574/56578
title: Chandra X-ray Observatory ObsId 56578
DOI: 10.25574/56580
title: Chandra X-ray Observatory ObsId 56580
DOI: 10.25574/56582
title: Chandra X-ray Observatory ObsId 56582
DOI: 10.25574/56585
title: Chandra X-ray Observatory ObsId 56585
DOI: 10.25574/56590
title: Chandra X-ray Observatory ObsId 56590
DOI: 10.25574/56594
title: Chandra X-ray Observatory ObsId 56594
DOI: 10.25574/56597
title: Chandra X-ray Observatory ObsId 56597
DOI: 10.25574/56601
title: Chandra X-ray Observatory ObsId 56601
DOI: 10.25574/56604
title: Chandra X-ray Observatory ObsId 56604
DOI: 10.25574/56608
title: Chandra X-ray Observatory ObsId 56608
DOI: 10.25574/56610
title: Chandra X-ray Observatory ObsId 56610
DOI: 10.25574/56614
title: Chandra X-ray Observatory ObsId 56614
DOI: 10.25574/56617
title: Chandra X-ray Observatory ObsId 56617
DOI: 10.25574/56622
title: Chandra X-ray Observatory ObsId 56622
DOI: 10.5281/zenodo.7031924
title: Datasets for 3D shape reconstruction from 2D microscopy images

description: Here we publish two single cell datasets for 3D shape reconstruction from 2D microscopy images with a detailed description.
DOI: 10.25574/56624
title: Chandra X-ray Observatory ObsId 56624
DOI: 10.5281/zenodo.7031923
title: Datasets for 3D shape reconstruction from 2D microscopy images

description: Here we publish two single cell datasets for 3D shape reconstruction from 2D microscopy images with a detailed description.
DOI: 10.25574/56630
title: Chandra X-ray Observatory ObsId 56630
DOI: 10.25574/56635
title: Chandra X-ray Observatory ObsId 56635
DOI: 10.25574/56642
title: Chandra X-ray Observatory ObsId 56642
DOI: 10.25574/56644
title: Chandra X-ray Observatory ObsId 56644
DOI: 10.25574/56648
title: Chandra X-ray Observatory ObsId 56648
DOI: 10.25574/56651
title: Chandra X-ray Observatory ObsId 56651
DOI: 10.25574/56654
title: Chandra X-ray Observatory ObsId 56654
DOI: 10.25574/56658
title: Chandra X-ray Observatory ObsId 56658
DOI: 10.25574/56662
title: Chandra X-ray Observatory ObsId 56662
DOI: 10.25574/56665
title: Chandra X-ray Observatory ObsId 56665
DOI: 10.25574/56670
title: Chandra X-ray Observatory ObsId 56670
DOI: 10.25574/56674
title: Chandra X-ray Observatory ObsId 56674
DOI: 10.25574/56678
title: Chandra X-ray Observatory ObsId 56678
DOI: 10.25574/56680
title: Chandra X-ray Observatory ObsId 56680
DOI: 10.25574/56685
title: Chandra X-ray Observatory ObsId 56685
DOI: 10.25574/56687
title: Chandra X-ray Observatory ObsId 56687
DOI: 10.25574/56692
title: Chandra X-ray Observatory ObsId 56692
DOI: 10.25574/56695
title: Chandra X-ray Observatory ObsId 56695
DOI: 10.25574/56699
title: Chandra X-ray Observatory ObsId 56699
DOI: 10.25574/56702
title: Chandra X-ray Observatory ObsId 56702
DOI: 10.25574/56707
title: Chandra X-ray Observatory ObsId 56707
DOI: 10.25574/56709
title: Chandra X-ray Observatory ObsId 56709
DOI: 10.25574/56711
title: Chandra X-ray Observatory ObsId 56711
DOI: 10.25574/56714
title: Chandra X-ray Observatory ObsId 56714
DOI: 10.25574/56716
title: Chandra X-ray Observatory ObsId 56716
DOI: 10.25574/56719
title: Chandra X-ray Observatory ObsId 56719
DOI: 10.25574/56723
title: Chandra X-ray Observatory ObsId 56723
DOI: 10.25574/56727
title: Chandra X-ray Observatory ObsId 56727
DOI: 10.25574/56730
title: Chandra X-ray Observatory ObsId 56730
DOI: 10.25574/56732
title: Chandra X-ray Observatory ObsId 56732
DOI: 10.25574/56736
title: Chandra X-ray Observatory ObsId 56736
DOI: 10.25574/56739
title: Chandra X-ray Observatory ObsId 56739
DOI: 10.25574/56742
title: Chandra X-ray Observatory ObsId 56742
DOI: 10.25574/56745
title: Chandra X-ray Observatory ObsId 56745
DOI: 10.25574/56748
title: Chandra X-ray Observatory ObsId 56748
DOI: 10.6084/m9.figshare.20764429
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764429.v1
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764456
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764456.v1
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764423
title: Synthetic velocity models of firn

description: Synthetic velocity models of firn with: - Varying accumulation rates - an ice slab placed at varying depths - an ice slab placed with varying thickness
DOI: 10.26302/sshade/experiment_pc_20220301_001
title: V K edge XAS HERFD of V reference compounds 10K
DOI: 10.6084/m9.figshare.20764522
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764522.v1
title: Supplementary Material for: Upregulation of miRNA-26a enhances the apoptosis of cerebral neurons by targeting EphA2 and inhibiting the MAPK pathway

description: Neural tube defects (NTDs) constitute the second most common congenital malformation of the central nervous system. The pathogenesis of NTDs is not entirely clear. In recent years, microRNAs have become a hot spot in genetic and developmental biology research. The present study aimed to explore the potential role of microRNA (miRNA)-26a in NTDs and the underlying pathogenesis thereof. First, we found significantly increased miRNA-26a expression in fetuses with NTDs (p&lt;0.0001), which significantly downregulated EphA2 and ERK1 mRNA and protein expression levels in fetuses with NTDs compared to normal controls (p&lt;0.01). In addition, dual-luciferase reporter assay showed that miR-26a negatively regulated EphA2 by directly binding with the 3'-untranslated region of EphA2. Second, upregulation of miRNA-26a expression increased caspase 3 and 9 protein expression levels (p&lt;0.01); and decreased EphA2 mRNA and protein expression levels (p&lt;0.01), as well as ERK1 and SRF protein expression levels (p&lt;0.01) in mouse neural stem cells (NE-4C) and human astroblastoma cells (U87MG). Furthermore, the upregulation of miRNA-26a inhibited cell proliferation and enhanced apoptosis of NE-4C and U87MG cells (p&lt;0.05). Similar results were observed with the MAPK inhibitor PD98059 (p&lt;0.01). These results suggest that miR-26a downregulates EphA2 to regulate SRF through the MAPK pathway, which affects nervous system development miR-26a targets EphA2, modulates phosphorylation of MAPK/ERK(MEK) pathway, regulates SRF, and participates in regulating nervous cell proliferation and apoptosis. Dysregulation of the aforementioned mechanism may be involved in the pathogenesis of NTDs.
DOI: 10.6084/m9.figshare.20764468
title: Supplementary Material.pdf

description: Supplementary Material
DOI: 10.6084/m9.figshare.20764468.v1
title: Supplementary Material.pdf

description: Supplementary Material
DOI: 10.6084/m9.figshare.20454867
title: pHlim source data

description: Changes in sub-cellular pH play a key role in metabolism, cell growth, membrane transport, and can also be exploited to control cargo release from therapeutic delivery systems. Most methods to measure pH rely on intensity changes of pH sensitive fluorophores, however these measurements are hampered by high uncertainty in the inferred pH and the need for multiple fluorophores. To address this, we have developed a method to accurately quantify sub-cellular pH in individual vesicles using fluorescent lifetime imaging microscopy (pHLIM). This project contains all the source data for the corresponding Nature Communications article.