cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.25402/cer.18618929
title: cer-2021-0216_Supplementary tables

description: - Statistical
Analysis Plan

 

- Supplementary
Figure 1. PRISMA flow chart of the systematic literature review.

- Supplementary
Figure 2. Evidence networks in Type 1 and Types 2/3 SMA.

- Supplementary
Figure 3. Histogram of re-scaled weights in the ENDEAR-matched FIREFISH
population (total N=58).

- Supplementary
Figure 4. Overall survival in patients with Type 1 SMA treated with nusinersen,
risdiplam and BSC.

- Supplementary
Figure 5. Histograms of re-scaled weights in the CHERISH-matched SUNFISH
population.

- Supplementary
Figure 6. Matching of SUNFISH and CHERISH placebo groups for RULM and HFMSE.

 

- Supplementary
Table 1. PICOS framework and additional search criteria for the SLR.

- Supplementary
Table 2. List of data sources used in the SLR.

- Supplementary
Table 3. Key deviations from statistical
analysis plan and justification.

- Supplementary
Table 4. Clinical trials excluded from the SLR.

- Supplementary
Table 5. Availability of endpoints of interest in Type 1 SMA.

- Supplementary
Table 6. Baseline characteristics of FIREFISH pre- and post‑matching
with STR1VE‑US (MAIC analysis).

- Supplementary
Table 7. STC model fit statistics of FIREFISH versus STR1VE-US.

- Supplementary
Table 8. BSID-III covariate estimates (STC FIREFISH vs STR1VE-US).

- Supplementary
Table 9. CHOP-INTEND covariate estimates (STC FIREFISH vs STR1VE-US).

- Supplementary
Table 10. Availability of endpoints of interest in Types 2 and 3 SMA.

- Supplementary
Table 11. Analyses of HFMSE outcomes in SUNFISH and CHERISH at Month 12.<br>
DOI: 10.6084/m9.figshare.12851759.v1
title: Overexpression of a B-type cytokinin response regulator (<i>OsORR2</i>) reduces plant height in rice

description: Cytokinin plays crucial roles in regulating plant growth and development, with the signal transduction mediated by type-A and type-B response regulators (RRs).While much genetic knowledge about RRs on regulating plant height remains unclear. Here, we found that overexpressing an <i>OsORR2</i> gene (a type-B RR) could reduce plant height in rice compared with the wild type (WT). Using quantitative real time (RT-qPCR) assay, <i>OsORR2</i>was expressed widely in most tissues such as root, culm, sheath, leaf, and panicle. Strong signals were detected in leaf mesophyll cells and anther by in situ hybridization assays (ISH). The subcellular localization of OsORR2 was in cell nucleus. In addition, we found that the transcriptional expression levels of type-A RR genes such as <i>OsRR9, OsRR10, OsRR12</i>, and <i>OsRR13</i> were significantly up-regulated in the overexpression transgenic plants (OE) plants. Taken together, our data suggested that <i>OsORR2</i>was involved in the development of plant height in rice and provided a foundation for future deep molecular research of the type-B RRs.
DOI: 10.25402/cer.18618929.v1
title: cer-2021-0216_Supplementary tables

description: - Statistical
Analysis Plan

 

- Supplementary
Figure 1. PRISMA flow chart of the systematic literature review.

- Supplementary
Figure 2. Evidence networks in Type 1 and Types 2/3 SMA.

- Supplementary
Figure 3. Histogram of re-scaled weights in the ENDEAR-matched FIREFISH
population (total N=58).

- Supplementary
Figure 4. Overall survival in patients with Type 1 SMA treated with nusinersen,
risdiplam and BSC.

- Supplementary
Figure 5. Histograms of re-scaled weights in the CHERISH-matched SUNFISH
population.

- Supplementary
Figure 6. Matching of SUNFISH and CHERISH placebo groups for RULM and HFMSE.

 

- Supplementary
Table 1. PICOS framework and additional search criteria for the SLR.

- Supplementary
Table 2. List of data sources used in the SLR.

- Supplementary
Table 3. Key deviations from statistical
analysis plan and justification.

- Supplementary
Table 4. Clinical trials excluded from the SLR.

- Supplementary
Table 5. Availability of endpoints of interest in Type 1 SMA.

- Supplementary
Table 6. Baseline characteristics of FIREFISH pre- and post‑matching
with STR1VE‑US (MAIC analysis).

- Supplementary
Table 7. STC model fit statistics of FIREFISH versus STR1VE-US.

- Supplementary
Table 8. BSID-III covariate estimates (STC FIREFISH vs STR1VE-US).

- Supplementary
Table 9. CHOP-INTEND covariate estimates (STC FIREFISH vs STR1VE-US).

- Supplementary
Table 10. Availability of endpoints of interest in Types 2 and 3 SMA.

- Supplementary
Table 11. Analyses of HFMSE outcomes in SUNFISH and CHERISH at Month 12.<br>
DOI: 10.6084/m9.figshare.12851774
title: Different strategies of strigolactone and karrikin signals in regulating the resistance of <i>Arabidopsis thaliana</i> to water-deficit stress

description: Strigolactone and karrikin receptors, DWARF14 (D14) and KARRIKIN INSENSITIVE 2 (KAI2), respectively, have been shown to positively regulate drought resistance in <i>Arabidopsis thaliana</i> by modulating abscisic acid responsiveness, anthocyanin accumulation, stomatal closure, cell membrane integrity and cuticle formation. Here, we aim to identify genes specifically or commonly regulated by D14 and KAI2 under water scarcity, using comparative analysis of the transcriptome data of the <i>A. thaliana d14-1</i> and <i>kai2-2</i> mutants under dehydration conditions. In comparison with wild-type, under dehydration conditions, the expression levels of genes related to photosynthesis and the metabolism of glucosinolates and trehalose were significantly changed in both <i>d14-1</i> and <i>kai2-2</i> mutant plants, whereas the transcript levels of genes related to the metabolism of cytokinins and brassinosteroids were significantly altered in the <i>d14-1</i> mutant plants only. These results suggest that cytokinin and brassinosteroid metabolism might be specifically regulated by the D14 pathway, whereas photosynthesis and metabolism of glucosinolates and trehalose are potentially regulated by both D14 and KAI2 pathways in plant response to water scarcity.
DOI: 10.6084/m9.figshare.12851774.v1
title: Different strategies of strigolactone and karrikin signals in regulating the resistance of <i>Arabidopsis thaliana</i> to water-deficit stress

description: Strigolactone and karrikin receptors, DWARF14 (D14) and KARRIKIN INSENSITIVE 2 (KAI2), respectively, have been shown to positively regulate drought resistance in <i>Arabidopsis thaliana</i> by modulating abscisic acid responsiveness, anthocyanin accumulation, stomatal closure, cell membrane integrity and cuticle formation. Here, we aim to identify genes specifically or commonly regulated by D14 and KAI2 under water scarcity, using comparative analysis of the transcriptome data of the <i>A. thaliana d14-1</i> and <i>kai2-2</i> mutants under dehydration conditions. In comparison with wild-type, under dehydration conditions, the expression levels of genes related to photosynthesis and the metabolism of glucosinolates and trehalose were significantly changed in both <i>d14-1</i> and <i>kai2-2</i> mutant plants, whereas the transcript levels of genes related to the metabolism of cytokinins and brassinosteroids were significantly altered in the <i>d14-1</i> mutant plants only. These results suggest that cytokinin and brassinosteroid metabolism might be specifically regulated by the D14 pathway, whereas photosynthesis and metabolism of glucosinolates and trehalose are potentially regulated by both D14 and KAI2 pathways in plant response to water scarcity.
DOI: 10.6084/m9.figshare.12851792
title: Genome-wide identification and expression analysis of <i>SABATH</i> methyltransferases in tea plant (<i>Camellia sinensis</i>): insights into their roles in plant defense responses

description: SABATH methyltransferases convent plant small-molecule metabolites into volatile methyl esters, which play important roles in many biological processes and defense reactions in plants. In this study, a total of 32 <i>SABATH</i> genes were identified in the <i>Camellia sinensis</i> var. <i>sinensis</i> (CSS) genome, which were renamed CsSABATH1 to CsSABATH32. Genome location annotation suggested that tandem duplication was responsible for the expansion of <i>SABATH</i> genes in tea plant. Multiple sequence alignment and phylogenetic analysis showed that the CsSABATHs could be classified into three groups (I, II and III), which were also supported by gene structures and conserved motifs analysis. Group II contained only two CsSABATH proteins, which were closely related to PtIAMT, AtIAMT and OsIAMT. The group III SABATH genes of tea plant exhibited expansion on the CSS genome compared with <i>Camellia sinensis</i> var. <i>assamica</i> (CSA) genome. Based on RNA-seq data, the <i>CsSABATHs</i> exhibited tissue-specific expression patterns, and the members with high expression in buds and young leaves were also obviously upregulated after MeJA treatment. The expression of many transcription factors was significantly correlated with that of different members of the <i>CsSABATH</i> gene family, suggesting a potential regulatory relationship between them. Quantitative real-time PCR (qPCR) expression analysis showed that <i>CsSABATHs</i> could respond to exogenous JA, SA and MeSA treatments in tea plants. RNA-seq data analysis and qPCR validation suggested that <i>CsSABATH8</i>, 11, 16, 25, 29 and 32 might play a special role in plant defense against insect herbivory. These results provide references for evolutionary studies of the plant <i>SABATH</i> family and the exploration of the potential roles of <i>CsSABATHs</i> in tea plant defense responses.
DOI: 10.6084/m9.figshare.12851792.v1
title: Genome-wide identification and expression analysis of <i>SABATH</i> methyltransferases in tea plant (<i>Camellia sinensis</i>): insights into their roles in plant defense responses

description: SABATH methyltransferases convent plant small-molecule metabolites into volatile methyl esters, which play important roles in many biological processes and defense reactions in plants. In this study, a total of 32 <i>SABATH</i> genes were identified in the <i>Camellia sinensis</i> var. <i>sinensis</i> (CSS) genome, which were renamed CsSABATH1 to CsSABATH32. Genome location annotation suggested that tandem duplication was responsible for the expansion of <i>SABATH</i> genes in tea plant. Multiple sequence alignment and phylogenetic analysis showed that the CsSABATHs could be classified into three groups (I, II and III), which were also supported by gene structures and conserved motifs analysis. Group II contained only two CsSABATH proteins, which were closely related to PtIAMT, AtIAMT and OsIAMT. The group III SABATH genes of tea plant exhibited expansion on the CSS genome compared with <i>Camellia sinensis</i> var. <i>assamica</i> (CSA) genome. Based on RNA-seq data, the <i>CsSABATHs</i> exhibited tissue-specific expression patterns, and the members with high expression in buds and young leaves were also obviously upregulated after MeJA treatment. The expression of many transcription factors was significantly correlated with that of different members of the <i>CsSABATH</i> gene family, suggesting a potential regulatory relationship between them. Quantitative real-time PCR (qPCR) expression analysis showed that <i>CsSABATHs</i> could respond to exogenous JA, SA and MeSA treatments in tea plants. RNA-seq data analysis and qPCR validation suggested that <i>CsSABATH8</i>, 11, 16, 25, 29 and 32 might play a special role in plant defense against insect herbivory. These results provide references for evolutionary studies of the plant <i>SABATH</i> family and the exploration of the potential roles of <i>CsSABATHs</i> in tea plant defense responses.
DOI: 10.6084/m9.figshare.12851810
title: TRA2A-induced upregulation of LINC00662 regulates blood-brain barrier permeability by affecting ELK4 mRNA stability in Alzheimer’s microenvironment

description: The blood-brain barrier (BBB) plays a pivotal role in the maintenance and regulation of the neural microenvironment. The BBB breakdown is a pathological change in early Alzheimer’s disease (AD). RNA-binding proteins (RBPs) and long non-coding RNAs (lncRNAs) are involved in the regulation of BBB permeability. Our study demonstrates the role of TRA2A/LINC00662/ELK4 axis in regulating BBB permeability in AD microenvironment. In Aβ<sub>1-42</sub>-incubated microvascular endothelial cells (ECs) of the BBB model <i>in vitro</i>, TRA2A and LINC00662 were enriched. TRA2A increased the stability of LINC00662 by binding with it. The knockdown of either TRA2A or LINC00662 decreased BBB permeability due to increased expression of tight junction-related proteins. ELK4 was less expressed in the BBB model in AD microenvironment <i>in vitro</i>. LINC00662 mediated the degradation of ELK4 mRNA by SMD pathway. Downregulation of ELK4 increased BBB permeability by increasing the tight junction-related protein expression.TRA2A/LINC00662/ELK4 axis plays a crucial role in the regulation of BBB permeability in AD microenvironment, which may provide a novel target for the therapy of AD.
DOI: 10.6084/m9.figshare.12851810.v1
title: TRA2A-induced upregulation of LINC00662 regulates blood-brain barrier permeability by affecting ELK4 mRNA stability in Alzheimer’s microenvironment

description: The blood-brain barrier (BBB) plays a pivotal role in the maintenance and regulation of the neural microenvironment. The BBB breakdown is a pathological change in early Alzheimer’s disease (AD). RNA-binding proteins (RBPs) and long non-coding RNAs (lncRNAs) are involved in the regulation of BBB permeability. Our study demonstrates the role of TRA2A/LINC00662/ELK4 axis in regulating BBB permeability in AD microenvironment. In Aβ<sub>1-42</sub>-incubated microvascular endothelial cells (ECs) of the BBB model <i>in vitro</i>, TRA2A and LINC00662 were enriched. TRA2A increased the stability of LINC00662 by binding with it. The knockdown of either TRA2A or LINC00662 decreased BBB permeability due to increased expression of tight junction-related proteins. ELK4 was less expressed in the BBB model in AD microenvironment <i>in vitro</i>. LINC00662 mediated the degradation of ELK4 mRNA by SMD pathway. Downregulation of ELK4 increased BBB permeability by increasing the tight junction-related protein expression.TRA2A/LINC00662/ELK4 axis plays a crucial role in the regulation of BBB permeability in AD microenvironment, which may provide a novel target for the therapy of AD.
DOI: 10.6084/m9.figshare.12851816
title: LINC01198 facilitates gliomagenesis through activating PI3K/AKT pathway

description: Glioma is the most malignant primary brain cancer which frequently occurred in adults. In recent years, long-non coding RNAs (lncRNAs) have been demonstrated to play pivotal roles in human cancers. However, the role of most lncRNAs in gliomagenesis has not been probed. Presently, through TCGA, a novel lncRNA LINC01198 was found to be up-regulated and associated with clinical outcomes in glioblastoma multiforme (GBM). In our study, LINC01198 was proved to be up-regulated in glioma cell lines, and silenced LINC01198 curbed glioma cell proliferation and accelerated cell apoptosis. Importantly, we corroborated that LINC01198 activated the PI3 K/AKT pathway to aggravate glioma progression by targeting PIK3 CA and PTEN. Subsequently, LINC01198 was validated to localize in both cytoplasm and nucleus of glioma cells. Through mechanistic exploration, we illustrated that LINC01198 increased PIK3CA expression by sponging miR-129-5p in the cytoplasm. Furthermore, PTEN was transcriptionally repressed by REST/RCOR1/HDAC2 complex. More importantly, LINC01198 accelerated the assembly of REST/RCOR1/HDAC2 complex and recruited such complex to PTEN promoter so as to impair PTEN expression in glioma. Finally, we further verified that LINC01198 hindered glioma tumour growth in vivo through AKT-dependent manner. Jointly, LINC01198 activates PI3 K/AKT signalling to exert oncogenic function in gliomagenesis by regulating PIK3CA and PTEN, which highlights a new approach for glioma treatment.
DOI: 10.6084/m9.figshare.12851816.v1
title: LINC01198 facilitates gliomagenesis through activating PI3K/AKT pathway

description: Glioma is the most malignant primary brain cancer which frequently occurred in adults. In recent years, long-non coding RNAs (lncRNAs) have been demonstrated to play pivotal roles in human cancers. However, the role of most lncRNAs in gliomagenesis has not been probed. Presently, through TCGA, a novel lncRNA LINC01198 was found to be up-regulated and associated with clinical outcomes in glioblastoma multiforme (GBM). In our study, LINC01198 was proved to be up-regulated in glioma cell lines, and silenced LINC01198 curbed glioma cell proliferation and accelerated cell apoptosis. Importantly, we corroborated that LINC01198 activated the PI3 K/AKT pathway to aggravate glioma progression by targeting PIK3 CA and PTEN. Subsequently, LINC01198 was validated to localize in both cytoplasm and nucleus of glioma cells. Through mechanistic exploration, we illustrated that LINC01198 increased PIK3CA expression by sponging miR-129-5p in the cytoplasm. Furthermore, PTEN was transcriptionally repressed by REST/RCOR1/HDAC2 complex. More importantly, LINC01198 accelerated the assembly of REST/RCOR1/HDAC2 complex and recruited such complex to PTEN promoter so as to impair PTEN expression in glioma. Finally, we further verified that LINC01198 hindered glioma tumour growth in vivo through AKT-dependent manner. Jointly, LINC01198 activates PI3 K/AKT signalling to exert oncogenic function in gliomagenesis by regulating PIK3CA and PTEN, which highlights a new approach for glioma treatment.
DOI: 10.6084/m9.figshare.12851825
title: miR-34 regulates larval growth and wing morphogenesis by directly modulating ecdysone signalling and cuticle protein in <i>Bombyx mori</i>

description: microRNAs (miRNA) are small non-coding RNAs that modulate the myriad biological activities by targeting genes, and many studies showed that miRNAs played a pivotal role in insect development. Here, we find that Bm-miRNA (miR-34) controls larval growth and wing morphology by targeting <i>BmE74</i> and <i>BmCPG4</i>. Overexpression of miR-34 in the whole body caused a smaller body size, partially displays deformed wings and venation defects in adults. Ablation of miR-34 by transgenic CRISPR/Cas9 technology resulted in a severe developmental delay during the larval stage. Moreover, we confirmed that miR-34 directly targeted <i>BmE74</i> and <i>BmCPG4</i> by using a dual luciferase reporter assay in HEK293T cells. Remarkably, loss-of-function of <i>BmCPG4</i> caused wing defects, which was similar to the phenotype of miR-34 overexpression in animals. In addition, our analysis revealed that ecdysone strongly inhibited miR-34 expression in <i>vivo</i>. Taken together, our study identifies miR-34 as a modulator that regulates larval growth and wing morphogenesis by directly modulating ecdysone signalling and cuticle protein in <i>Bombyx mori</i>.
DOI: 10.6084/m9.figshare.12851825.v1
title: miR-34 regulates larval growth and wing morphogenesis by directly modulating ecdysone signalling and cuticle protein in <i>Bombyx mori</i>

description: microRNAs (miRNA) are small non-coding RNAs that modulate the myriad biological activities by targeting genes, and many studies showed that miRNAs played a pivotal role in insect development. Here, we find that Bm-miRNA (miR-34) controls larval growth and wing morphology by targeting <i>BmE74</i> and <i>BmCPG4</i>. Overexpression of miR-34 in the whole body caused a smaller body size, partially displays deformed wings and venation defects in adults. Ablation of miR-34 by transgenic CRISPR/Cas9 technology resulted in a severe developmental delay during the larval stage. Moreover, we confirmed that miR-34 directly targeted <i>BmE74</i> and <i>BmCPG4</i> by using a dual luciferase reporter assay in HEK293T cells. Remarkably, loss-of-function of <i>BmCPG4</i> caused wing defects, which was similar to the phenotype of miR-34 overexpression in animals. In addition, our analysis revealed that ecdysone strongly inhibited miR-34 expression in <i>vivo</i>. Taken together, our study identifies miR-34 as a modulator that regulates larval growth and wing morphogenesis by directly modulating ecdysone signalling and cuticle protein in <i>Bombyx mori</i>.
DOI: 10.6084/m9.figshare.12851825.v3
title: miR-34 regulates larval growth and wing morphogenesis by directly modulating ecdysone signalling and cuticle protein in <i>Bombyx mori</i>

description: microRNAs (miRNA) are small non-coding RNAs that modulate the myriad biological activities by targeting genes, and many studies showed that miRNAs played a pivotal role in insect development. Here, we find that Bm-miRNA (miR-34) controls larval growth and wing morphology by targeting <i>BmE74</i> and <i>BmCPG4</i>. Overexpression of miR-34 in the whole body caused a smaller body size, partially displays deformed wings and venation defects in adults. Ablation of miR-34 by transgenic CRISPR/Cas9 technology resulted in a severe developmental delay during the larval stage. Moreover, we confirmed that miR-34 directly targeted <i>BmE74</i> and <i>BmCPG4</i> by using a dual luciferase reporter assay in HEK293T cells. Remarkably, loss-of-function of <i>BmCPG4</i> caused wing defects, which was similar to the phenotype of miR-34 overexpression in animals. In addition, our analysis revealed that ecdysone strongly inhibited miR-34 expression in <i>vivo</i>. Taken together, our study identifies miR-34 as a modulator that regulates larval growth and wing morphogenesis by directly modulating ecdysone signalling and cuticle protein in <i>Bombyx mori</i>.
DOI: 10.6084/m9.figshare.12851825.v2
title: miR-34 regulates larval growth and wing morphogenesis by directly modulating ecdysone signaling and cuticle protein in <i>Bombyx mori</i>

description: microRNAs (miRNA) are small non-coding RNAs that modulate the myriad biological activities by targeting genes, and many studies showed that miRNAs played a pivotal role in insect development. Here, we find that Bm-miRNA (miR-34) controls larval growth and wing morphology by targeting <i>BmE74</i> and <i>BmCPG4</i>. Overexpression of miR-34 in the whole body caused a smaller body size, partially displays deformed wings and venation defects in adults. Ablation of miR-34 by transgenic CRISPR/Cas9 technology resulted in a severe developmental delay during the larval stage. Moreover, we confirmed that miR-34 directly targeted <i>BmE74</i> and <i>BmCPG4</i> by using a dual luciferase reporter assay in HEK293T cells. Remarkably, loss-of-function of <i>BmCPG4</i> caused wing defects, which was similar to the phenotype of miR-34 overexpression in animals. In addition, our analysis revealed that ecdysone strongly inhibited miR-34 expression in <i>vivo</i>. Taken together, our study identifies miR-34 as a modulator that regulates larval growth and wing morphogenesis by directly modulating ecdysone signaling and cuticle protein in <i>Bombyx mori</i>.