cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.1461685.v4
title: Evaluation of sterol transport from the endoplasmic reticulum to mitochondria using mitochondrially targeted bacterial sterol acyltransferase in <i>Saccharomyces cerevisiae</i>

description: To elucidate the mechanism of interorganelle sterol transport, a system to evaluate sterol transport from the endoplasmic reticulum (ER) to the mitochondria was constructed. A bacterial glycerophospholipid: cholesterol acyltransferase fused with a mitochondria-targeting sequence and a membrane-spanning domain of the mitochondrial inner membrane protein Pet100 and enhanced green fluorescent protein was expressed in a <i>Saccharomyces cerevisiae</i> mutant deleted for <i>ARE1</i> and <i>ARE2</i> encoding acyl-CoA:sterol acyltransferases. Microscopic observation and subcellular fractionation suggested that this fusion protein, which was named mito-SatA-EGFP, was localized in the mitochondria. Steryl esters were synthesized in the mutant expressing mito-SatA-EGFP. This system will be applicable for evaluations of sterol transport from the ER to the mitochondria in yeast by examining sterol esterification in the mitochondria.
DOI: 10.6084/m9.figshare.1461648
title: fMRI - Lecture 6

description: A lecture about Bayesian inference for fMRI.
DOI: 10.6084/m9.figshare.1461649.v1
title: fMRI - Lecture 7

description: A lecture about fMRI and brain connectivity.
DOI: 10.6084/m9.figshare.1461685.v3
title: Evaluation of sterol transport from the endoplasmic reticulum to mitochondria using mitochondrially targeted bacterial sterol acyltransferase in <i>Saccharomyces cerevisiae</i>

description: To elucidate the mechanism of interorganelle sterol transport, a system to evaluate sterol transport from the endoplasmic reticulum (ER) to the mitochondria was constructed. A bacterial glycerophospholipid: cholesterol acyltransferase fused with a mitochondria-targeting sequence and a membrane-spanning domain of the mitochondrial inner membrane protein Pet100 and enhanced green fluorescent protein was expressed in a <i>Saccharomyces cerevisiae</i> mutant deleted for <i>ARE1</i> and <i>ARE2</i> encoding acyl-CoA:sterol acyltransferases. Microscopic observation and subcellular fractionation suggested that this fusion protein, which was named mito-SatA-EGFP, was localized in the mitochondria. Steryl esters were synthesized in the mutant expressing mito-SatA-EGFP. This system will be applicable for evaluations of sterol transport from the ER to the mitochondria in yeast by examining sterol esterification in the mitochondria.
DOI: 10.6084/m9.figshare.1461647
title: fMRI - Lecture 5

description: A lecture about group analysis for fMRI.
DOI: 10.6084/m9.figshare.1461648.v1
title: fMRI - Lecture 6

description: A lecture about Bayesian inference for fMRI.
DOI: 10.6084/m9.figshare.1461645
title: fMRI - Lecture 4

description: A lecture about single subject analysis in fMRI.
DOI: 10.6084/m9.figshare.1461647.v1
title: fMRI - Lecture 5

description: A lecture about group analysis for fMRI.
DOI: 10.6084/m9.figshare.1461658.v4
title: Dataset for MOC and proxy at 26N

description: Matlab data file containing time series of the MOC and components at 26N (structure variable: mocgrid) and proxies (structure variable: recon). See README for more information.
DOI: 10.6084/m9.figshare.1461645.v1
title: fMRI - Lecture 4

description: A lecture about single subject analysis in fMRI.
DOI: 10.6084/m9.figshare.1461642
title: fMRI - Lecture 1

description: An introductory lecture to fMRI.
DOI: 10.6084/m9.figshare.1461643
title: fMRI - Lecture 2

description: A lecture about the basics of MRI and fMRI.
DOI: 10.6084/m9.figshare.1461644
title: fMRI - Lecture 3

description: A lecture about preprocessing of fMRI data.
DOI: 10.6084/m9.figshare.1461658.v5
title: Dataset for MOC and proxy at 26N

description: Matlab data file containing time series of the MOC and components at 26N (structure variable: mocgrid) and proxies (structure variable: recon). See README for more information.
DOI: 10.6084/m9.figshare.1461643.v1
title: fMRI - Lecture 2

description: A lecture about the basics of MRI and fMRI.
DOI: 10.6084/m9.figshare.1461644.v1
title: fMRI - Lecture 3

description: A lecture about preprocessing of fMRI data.
DOI: 10.6084/m9.figshare.1461642.v1
title: fMRI - Lecture 1

description: An introductory lecture to fMRI.
DOI: 10.6084/m9.figshare.1461658.v6
title: Dataset for MOC and proxy at 26N

description: Matlab data file containing time series of the MOC and components at 26N (structure variable: mocgrid) and proxies (structure variable: recon). See README for more information.
DOI: 10.6084/m9.figshare.1461658.v7
title: Blank

description: Matlab data file containing time series of the MOC and components at 26N (structure variable: mocgrid) and proxies (structure variable: recon). See README for more information.
DOI: 10.6084/m9.figshare.1461579
title: aSAH resting-state fMRI data

description: resting-state functional imaging data for patients with sub-arachnoid hemorrhage (SAH), along with matched controls. See README for more detail
DOI: 10.6084/m9.figshare.1461579.v2
title: aSAH resting-state fMRI data

description: resting-state functional imaging data for patients with sub-arachnoid hemorrhage (SAH), along with matched controls. See README for more detail
DOI: 10.17632/2h87h4r5w2.1
title: Twitter Candidate Rhetoric Database_Political Communication Corresponding Data

description: These data correspond to the manuscript titled "When ‘Following’ the Leader Inspires Action: Individuals’ Receptivity to Discursive Frame Elements on Social Media" that has been accepted for publication at Political Communication. Data and Do File to reproduce the main findings of the article are included here, updated as of September 3, 2020. The author reserves the right to update the data and do file. Please contact the author at kait.cassell@gmail.com with questions or concerns. See also the author's webpage describing aspects of the data at www.kaitlencassell.com
DOI: 10.6084/m9.figshare.1460872
title: Data of the PLOS Biology article: "Shifts of gamma phase across primary visual cortical sites reflect dynamic stimulus-modulated information transfer"

description: MATLAB data files containing the data to reproduce figures of the paper. All files are in the MATLAB .mat format, see README.txt for details.
DOI: 10.6084/m9.figshare.1461579.v1
title: new fileset

description: resting-state functional imaging data for patients with sub-arachnoid hemorrhage (SAH), along with matched controls. See README for more detail
DOI: 10.6084/m9.figshare.1460864
title: Wrong data - don't use

description: These data are visualized in an article in PLOS One on the networked relationships among Nobel Laureates in Physiology or Medicine. Figure 3 combined the laureates and non-laureates in a single graph to examine the extent to which they connect to once another.
DOI: 10.6084/m9.figshare.1460872.v1
title: Data of the PLOS Biology article: "Shifts of gamma phase across primary visual cortical sites reflect dynamic stimulus-modulated information transfer"

description: MATLAB data files containing the data to reproduce figures of the paper. All files are in the MATLAB .mat format, see README.txt for details.
DOI: 10.6084/m9.figshare.1460861
title: Inhibition of Janus kinases by tyrosine phosphorylation inhibitor, Tyrphostin AG-490

description: Janus kinases (JAKs) belong to a crucial family of tyrosine kinases, implicated in the patho-physiology of multiple cancer types, and serve as striking therapeutic targets. To date, many potent, either ATP-competitive (PTK domain) or non-ATP-competitive JAK inhibitors have been identified. Among them, Tyrphostin AG-490 (2-cyano-3-(3,4-dihydroxyphenyl)-N-(phenylmethyl)-2-propenamide) is a well-known ATP-competitive inhibitor. However, its mode of action, details of interacting residues, and induced conformational changes in JAK-specific binding sites remain elusive. Here, through comparative structure analysis, molecular docking, and molecular dynamics simulation assays, we explored comparative binding patterns of AG-490 against JAK1, JAK2, and JAK3. Our results entail noteworthy observations about the binding affinity of AG-490 by illustrating distinctive amino acid residues lying at the conserved ATP-binding domains of JAK family members. By subsequent assessment of their structural homology and conserved structural folds, we highlight intriguing prospects to design more specific and potent inhibitors for selective targeting of JAK family members. Our comparative study provides a platform for the rational design of precise and potent inhibitor for selective targeting of JAK family members.
DOI: 10.6084/m9.figshare.1460864.v2
title: Wrong data - don't use

description: These data are visualized in an article in PLOS One on the networked relationships among Nobel Laureates in Physiology or Medicine. Figure 3 combined the laureates and non-laureates in a single graph to examine the extent to which they connect to once another.
DOI: 10.6084/m9.figshare.1460860
title: Analysis of secondary structural and physicochemical changes in protein–protein complexes

description: Conformation switching in protein–protein complexes is considered important for the molecular recognition process. Overall analysis of 123 protein–protein complexes in a benchmark data-set showed that 6.8% of residues switched over their secondary structure conformation upon complex formation. Amino acid residue-wise preference for conformation change has been analyzed in binding and non-binding site residues separately. In this analysis, residues such as Ser, Leu, Glu, and Lys had higher frequency of secondary structural conformation change. The change of helix to coil and sheet to coil conformation and vice versa has been observed frequently, whereas the conformation change of helix to extended sheet occurred rarely in the studied complexes. Influence of conformation change toward the N and C terminal on either side of the binding site residues has been analyzed. Further, analysis on <i>φ</i> and <i>ψ</i> angle variation, conservation, stability, and solvent accessibility have been performed on binding site residues. Knowledge obtained from the present study could be effectively employed in the protein–protein modeling and docking studies.
DOI: 10.6084/m9.figshare.1460864.v1
title: Data for Figure 3_Nobel plus Non-Nobel

description: These data are visualized in an article in PLOS One on the networked relationships among Nobel Laureates in Physiology or Medicine. Figure 3 combined the laureates and non-laureates in a single graph to examine the extent to which they connect to once another.
DOI: 10.6084/m9.figshare.1460858
title: NiV Spillover Paper

description: 3 Figures and R code for NiV spillover paper in the journal, Transactions of the Royal Society of Tropical Medicine and Hygiene
DOI: 10.6084/m9.figshare.1460860.v1
title: Analysis of secondary structural and physicochemical changes in protein–protein complexes

description: Conformation switching in protein–protein complexes is considered important for the molecular recognition process. Overall analysis of 123 protein–protein complexes in a benchmark data-set showed that 6.8% of residues switched over their secondary structure conformation upon complex formation. Amino acid residue-wise preference for conformation change has been analyzed in binding and non-binding site residues separately. In this analysis, residues such as Ser, Leu, Glu, and Lys had higher frequency of secondary structural conformation change. The change of helix to coil and sheet to coil conformation and vice versa has been observed frequently, whereas the conformation change of helix to extended sheet occurred rarely in the studied complexes. Influence of conformation change toward the N and C terminal on either side of the binding site residues has been analyzed. Further, analysis on <i>φ</i> and <i>ψ</i> angle variation, conservation, stability, and solvent accessibility have been performed on binding site residues. Knowledge obtained from the present study could be effectively employed in the protein–protein modeling and docking studies.
DOI: 10.6084/m9.figshare.1460861.v2
title: Inhibition of Janus kinases by tyrosine phosphorylation inhibitor, Tyrphostin AG-490

description: Janus kinases (JAKs) belong to a crucial family of tyrosine kinases, implicated in the patho-physiology of multiple cancer types, and serve as striking therapeutic targets. To date, many potent, either ATP-competitive (PTK domain) or non-ATP-competitive JAK inhibitors have been identified. Among them, Tyrphostin AG-490 (2-cyano-3-(3,4-dihydroxyphenyl)-N-(phenylmethyl)-2-propenamide) is a well-known ATP-competitive inhibitor. However, its mode of action, details of interacting residues, and induced conformational changes in JAK-specific binding sites remain elusive. Here, through comparative structure analysis, molecular docking, and molecular dynamics simulation assays, we explored comparative binding patterns of AG-490 against JAK1, JAK2, and JAK3. Our results entail noteworthy observations about the binding affinity of AG-490 by illustrating distinctive amino acid residues lying at the conserved ATP-binding domains of JAK family members. By subsequent assessment of their structural homology and conserved structural folds, we highlight intriguing prospects to design more specific and potent inhibitors for selective targeting of JAK family members. Our comparative study provides a platform for the rational design of precise and potent inhibitor for selective targeting of JAK family members.
DOI: 10.6084/m9.figshare.1460861.v1
title: Inhibition of Janus kinases by tyrosine phosphorylation inhibitor, Tyrphostin AG-490

description: Janus kinases (JAKs) belong to a crucial family of tyrosine kinases, implicated in the patho-physiology of multiple cancer types, and serve as striking therapeutic targets. To date, many potent, either ATP-competitive (PTK domain) or non-ATP-competitive JAK inhibitors have been identified. Among them, Tyrphostin AG-490 (2-cyano-3-(3,4-dihydroxyphenyl)-N-(phenylmethyl)-2-propenamide) is a well-known ATP-competitive inhibitor. However, its mode of action, details of interacting residues, and induced conformational changes in JAK-specific binding sites remain elusive. Here, through comparative structure analysis, molecular docking, and molecular dynamics simulation assays, we explored comparative binding patterns of AG-490 against JAK1, JAK2, and JAK3. Our results entail noteworthy observations about the binding affinity of AG-490 by illustrating distinctive amino acid residues lying at the conserved ATP-binding domains of JAK family members. By subsequent assessment of their structural homology and conserved structural folds, we highlight intriguing prospects to design more specific and potent inhibitors for selective targeting of JAK family members. Our comparative study provides a platform for the rational design of precise and potent inhibitor for selective targeting of JAK family members.
DOI: 10.6084/m9.figshare.1460858.v2
title: NiV Spillover Paper

description: 3 Figures and R code for NiV spillover paper in the journal, Transactions of the Royal Society of Tropical Medicine and Hygiene
DOI: 10.6084/m9.figshare.1460859.v1
title: Intramembrane protease PARL defines a negative regulator of PINK1- and PARK2/Parkin-dependent mitophagy

description: SummaryMutations in PINK1 and PARK2/Parkin are a main risk factor for familial Parkinson disease. While the physiological mechanism of their activation is unclear, these proteins have been shown in tissue culture cells to serve as a key trigger for autophagy of depolarized mitochondria. Here we show that ablation of the mitochondrial rhomboid protease PARL leads to retrograde translocation of an intermembrane space-bridging PINK1 import intermediate. Subsequently, it is rerouted to the outer membrane in order to recruit PARK2, which phenocopies mitophagy induction by uncoupling agents. Consistent with a role of this retrograde translocation mechanism in neurodegenerative disease, we show that pathogenic PINK1 mutants which are not cleaved by PARL affect PINK1 kinase activity and the ability to induce PARK2-mediated mitophagy. Altogether we suggest that PARL is an important intrinsic player in mitochondrial quality control, a system substantially impaired in Parkinson disease as indicated by reduced removal of damaged mitochondria in affected patients.
DOI: 10.6084/m9.figshare.1460858.v1
title: NiV Spillover Paper

description: 3 Figures and R code for NiV spillover paper in the journal, Transactions of the Royal Society of Tropical Medicine and Hygiene
DOI: 10.6084/m9.figshare.1460859.v2
title: Intramembrane protease PARL defines a negative regulator of PINK1- and PARK2/Parkin-dependent mitophagy

description: Mutations in PINK1 and PARK2/Parkin are a main risk factor for familial Parkinson disease. While the physiological mechanism of their activation is unclear, these proteins have been shown in tissue culture cells to serve as a key trigger for autophagy of depolarized mitochondria. Here we show that ablation of the mitochondrial rhomboid protease PARL leads to retrograde translocation of an intermembrane space-bridging PINK1 import intermediate. Subsequently, it is rerouted to the outer membrane in order to recruit PARK2, which phenocopies mitophagy induction by uncoupling agents. Consistent with a role of this retrograde translocation mechanism in neurodegenerative disease, we show that pathogenic PINK1 mutants which are not cleaved by PARL affect PINK1 kinase activity and the ability to induce PARK2-mediated mitophagy. Altogether we suggest that PARL is an important intrinsic player in mitochondrial quality control, a system substantially impaired in Parkinson disease as indicated by reduced removal of damaged mitochondria in affected patients.
DOI: 10.6084/m9.figshare.1460846
title: Evolutionary trends and functional anatomy of the human expanded autophagy network

description: All eukaryotic cells utilize autophagy for protein and organelle turnover, thus assuring subcellular quality control, homeostasis, and survival. In order to address recent advances in identification of human autophagy associated genes, and to describe autophagy on a system-wide level, we established an autophagy-centered gene interaction network by merging various primary data sets and by retrieving respective interaction data. The resulting network (‘AXAN’) was analyzed with respect to subnetworks, e.g. the prime gene subnetwork (including the core machinery, signaling pathways and autophagy receptors) and the transcription subnetwork. To describe aspects of evolution within this network, we assessed the presence of protein orthologs across 99 eukaryotic model organisms. We visualized evolutionary trends for prime gene categories and evolutionary tracks for selected AXAN genes. This analysis confirms the eukaryotic origin of autophagy core genes while it points to a diverse evolutionary history of autophagy receptors. Next, we used module identification to describe the functional anatomy of the network at the level of pathway modules. In addition to obvious pathways (e.g., lysosomal degradation, insulin signaling) our data unveil the existence of context-related modules such as Rho GTPase signaling. Last, we used a tripartite, image-based RNAi – screen to test candidate genes predicted to play a role in regulation of autophagy. We verified the Rho GTPase, <i>CDC42</i>, as a novel regulator of autophagy-related signaling. This study emphasizes the applicability of system-wide approaches to gain novel insights into a complex biological process and to describe the human autophagy pathway at a hitherto unprecedented level of detail.
DOI: 10.6084/m9.figshare.1460844
title: The interactome of soybean GmWRKY53 using yeast 2-hybrid library screening to saturation

description: Soybean GmWRKY53 functions in both biotic and abiotic stress signaling. Using GmWRKY53 as a bait yeast 2-hybrid library screening to saturation isolated multiple independent fragments for many interacting proteins, enabling delineation of minimal interacting domains and computation of a confidence score. Multiple independent clones coding for the LATE ELONGATED HYPOCOTYL clock protein GmLCL2 (MYB114) were isolated and the binding site for GmWRKY53 was mapped to 90 amino acids separate from the MYB domain. This suggests a direct input from the clock on GmWRKY53 activity. The GmWRKY53-interacting proteins also included 3 water stress-inducible AP2/ERF transcription factors. One of these (Glyma03g26310) is one of the most strongly water stress induced genes in soybean roots, suggesting that GmWRKY53/ERF complexes regulate water stress responses.
DOI: 10.6084/m9.figshare.1460859.v3
title: Intramembrane protease PARL defines a negative regulator of PINK1- and PARK2/Parkin-dependent mitophagy

description: Mutations in PINK1 and PARK2/Parkin are a main risk factor for familial Parkinson disease. While the physiological mechanism of their activation is unclear, these proteins have been shown in tissue culture cells to serve as a key trigger for autophagy of depolarized mitochondria. Here we show that ablation of the mitochondrial rhomboid protease PARL leads to retrograde translocation of an intermembrane space-bridging PINK1 import intermediate. Subsequently, it is rerouted to the outer membrane in order to recruit PARK2, which phenocopies mitophagy induction by uncoupling agents. Consistent with a role of this retrograde translocation mechanism in neurodegenerative disease, we show that pathogenic PINK1 mutants which are not cleaved by PARL affect PINK1 kinase activity and the ability to induce PARK2-mediated mitophagy. Altogether we suggest that PARL is an important intrinsic player in mitochondrial quality control, a system substantially impaired in Parkinson disease as indicated by reduced removal of damaged mitochondria in affected patients.
DOI: 10.6084/m9.figshare.1460845.v1
title: Repetitive Stimulation of Autophagy-Lysosome Machinery by Intermittent Fasting Preconditions the Myocardium to Ischemia-Reperfusion Injury

description: ABSTRACTAutophagy, a lysosomal degradative pathway is potently stimulated in the myocardium by fasting and is essential for maintaining cardiac function during prolonged starvation. We tested the hypothesis that intermittent fasting protects against myocardial ischemia-reperfusion injury via transcriptional stimulation of the autophagy-lysosome machinery. Adult C57BL/6 mice subjected to 24-h periods of fasting, every other day, for 6 weeks were protected from in-vivo ischemia-reperfusion injury on a fed day, with marked reduction in infarct size in both sexes as compared with nonfasted controls. This protection was lost in mice heterozygous null for <i>Lamp2</i> (coding for lysosomal-associated membrane protein 2), which demonstrate impaired autophagy in response to fasting with accumulation of autophagosomes and SQSTM1, an autophagy substrate, in the heart. In <i>lamp2</i> null mice, intermittent fasting provoked progressive left ventricular dilation, systolic dysfunction and hypertrophy; worsening cardiomyocyte autophagosome accumulation and lack of protection to ischemia-reperfusion injury, suggesting that intact autophagy-lysosome machinery is essential for myocardial homeostasis during intermittent fasting; and consequent ischemic cardioprotection. Fasting and refeeding cycles resulted in transcriptional induction followed by downregulation of autophagy-lysosome genes in the myocardium. This was coupled with fasting-induced nuclear translocation of TFEB (transcription factor EB), a master regulator of autophagy-lysosome machinery; followed by rapid decline in nuclear TFEB levels with refeeding. Endogenous TFEB was essential for attenuation of hypoxia-reoxygenation-induced cell death by repetitive starvation, in neonatal rat cardiomyocytes, in-vitro. Taken together, these data suggest that TFEB-mediated transcriptional priming of the autophagy-lysosome machinery mediates the beneficial effects of fasting-induced autophagy in myocardial ischemia-reperfusion injury.