cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.4039980.v1
title: Zrf1 Controls Mesoderm Lineage Genes and Cardiomyocyte Differentiation

description: In the present study we addressed the function of the transcriptional activator Zrf1 in the generation of the three germ layers during <i>in vitro</i> development. Currently, Zrf1 is rather regarded as a factor that drives the expression of neuronal genes. Here, we have employed mouse embryonic stem cells and P19 cells to understand the role of Zrf1 in the generation of mesoderm-derived tissues like adipocytes, cartilage and heart. Our data shows that Zrf1 is essential for the transcriptional activation of genes that give rise to mesoderm and in particular heart development. In both, the mESC and P19 systems, we provide evidence that Zrf1 contributes to the generation of functional cardiomyocytes. We further demonstrate that Zrf1 binds to the transcription start sites (TSSs) of heart tissue-specific genes from the first and second heart field where it drives their temporal expression during differentiation. Taken together, we have identified Zrf1 as a novel regulator of the mesodermal lineage that might facilitate spatiotemporal expression of genes.
DOI: 10.7910/dvn/v1rjpf/geqjz7
title: blc20170708_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039971
title: Fbxo28 promotes mitotic progression and regulates topoisomerase IIα-dependent DNA decatenation

description: Topoisomerase IIα is an essential enzyme that resolves topological constraints in genomic DNA. It functions in disentangling intertwined chromosomes during anaphase leading to chromosome segregation thus preserving genomic stability. Here we describe a previously unrecognized mechanism regulating topoisomerase IIα activity that is dependent on the F-box protein Fbxo28. We find that Fbxo28, an evolutionarily conserved protein, is required for proper mitotic progression. Interfering with Fbxo28 function leads to a delay in metaphase-to-anaphase progression resulting in mitotic defects as lagging chromosomes, multipolar spindles and multinucleation. Furthermore, we find that Fbxo28 interacts and colocalizes with topoisomerase IIα throughout the cell cycle. Depletion of Fbxo28 results in an increase in topoisomerase IIα−dependent DNA decatenation activity. Interestingly, blocking the interaction between Fbxo28 and topoisomerase IIα also results in multinucleated cells. Our findings suggest that Fbxo28 regulates topoisomerase IIα decatenation activity and plays an important role in maintaining genomic stability.
DOI: 10.7910/dvn/v1rjpf/926fw5
title: blc20171117_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039971.v2
title: Fbxo28 promotes mitotic progression and regulates topoisomerase IIα-dependent DNA decatenation

description: Topoisomerase IIα is an essential enzyme that resolves topological constraints in genomic DNA. It functions in disentangling intertwined chromosomes during anaphase leading to chromosome segregation thus preserving genomic stability. Here we describe a previously unrecognized mechanism regulating topoisomerase IIα activity that is dependent on the F-box protein Fbxo28. We find that Fbxo28, an evolutionarily conserved protein, is required for proper mitotic progression. Interfering with Fbxo28 function leads to a delay in metaphase-to-anaphase progression resulting in mitotic defects as lagging chromosomes, multipolar spindles and multinucleation. Furthermore, we find that Fbxo28 interacts and colocalizes with topoisomerase IIα throughout the cell cycle. Depletion of Fbxo28 results in an increase in topoisomerase IIα−dependent DNA decatenation activity. Interestingly, blocking the interaction between Fbxo28 and topoisomerase IIα also results in multinucleated cells. Our findings suggest that Fbxo28 regulates topoisomerase IIα decatenation activity and plays an important role in maintaining genomic stability.
DOI: 10.6084/m9.figshare.4039971.v1
title: Fbxo28 promotes Mitotic Progression and regulates Topoisomerase IIα-dependent DNA Decatenation

description: Topoisomerase IIα is an essential enzyme that resolves topological constraints in genomic DNA. It functions in disentangling intertwined chromosomes during anaphase leading to chromosome segregation thus preserving genomic stability. Here we describe a previously unrecognized mechanism regulating topoisomerase IIα activity that is dependent on the F-box protein Fbxo28. We find that Fbxo28, an evolutionarily conserved protein, is required for proper mitotic progression. Interfering with Fbxo28 function leads to a delay in metaphase-to-anaphase progression resulting in mitotic defects as lagging chromosomes, multipolar spindles and multinucleation. Furthermore, we find that Fbxo28 interacts and colocalizes with topoisomerase IIα throughout the cell cycle. Depletion of Fbxo28 results in an increase in topoisomerase IIα-dependent DNA decatenation activity. Interestingly, blocking the interaction between Fbxo28 and topoisomerase IIα also results in multinucleated cells. Our findings suggest that Fbxo28 regulates topoisomerase IIα decatenation activity and plays an important role in maintaining genomic stability.
DOI: 10.7910/dvn/v1rjpf/6hncdw
title: blc20170408_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039932
title: TRPV3 mutants causing <i>Olmsted Syndrome</i> induce impaired cell adhesion and nonfunctional lysosomes

description: TRPV3 is a non-selective cationic channel and is important for several physiological functions. It can be activated by physiological temperature and selective endogenous and exogenous compounds. TRPV3 is one of the key ion channel involved in Ca<sup>2+</sup>-signaling in keratinocyte and thus involved in skin-related functions. Recently, naturally occurring mutations in TRPV3, namely G573A, G573S, G573C and W692G have been detected which are linked with the development of pathophysiological conditions such as <i>Olmsted Syndrome</i> (OS) and other skin disorders. Our qualitative and quantitative data suggests that these naturally occurring TRPV3 mutants are mainly restricted in the ER. Expression of OS-mutants cause impaired vesicular trafficking resulting reduced surface localization of these mutants and other membrane proteins too. OS-mutants also cause reduced cell adhesion, altered distribution and less number of lysosomes. Our data confirms that TRPV3 is a lysosomal protein suggesting that <i>Olmsted Syndrome</i> is a lysosomal disorder. These findings may have a broad implication in the context of keratinocyte functions, skin-degeneration and in skin-cancer.
DOI: 10.7910/dvn/v1rjpf/afi1nj
title: blc20171208_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039932.v1
title: TRPV3 mutants causing <i>Olmsted Syndrome</i> induce impaired cell adhesion and nonfunctional lysosomes

description: TRPV3 is a non-selective cationic channel and is important for several physiological functions. It can be activated by physiological temperature and selective endogenous and exogenous compounds. TRPV3 is one of the key ion channel involved in Ca<sup>2+</sup>-signaling in keratinocyte and thus involved in skin-related functions. Recently, naturally occurring mutations in TRPV3, namely G573A, G573S, G573C and W692G have been detected which are linked with the development of pathophysiological conditions such as <i>Olmsted Syndrome</i> (OS) and other skin disorders. Our qualitative and quantitative data suggests that these naturally occurring TRPV3 mutants are mainly restricted in the ER. Expression of OS-mutants cause impaired vesicular trafficking resulting reduced surface localization of these mutants and other membrane proteins too. OS-mutants also cause reduced cell adhesion, altered distribution and less number of lysosomes. Our data confirms that TRPV3 is a lysosomal protein suggesting that <i>Olmsted Syndrome</i> is a lysosomal disorder. These findings may have a broad implication in the context of keratinocyte functions, skin-degeneration and in skin-cancer.
DOI: 10.7910/dvn/v1rjpf/obr8mm
title: blc20170624_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039917
title: Incongruity and Humor degrees

description: Incongruity and Humor degrees used in the parametric models<br>
DOI: 10.6084/m9.figshare.4039917.v2
title: Incongruity and Humor degrees

description: Incongruity and Humor degrees used in the parametric models<br>
DOI: 10.7910/dvn/v1rjpf/iibnak
title: blc20170711_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039917.v1
title: Incongruity and Humor degrees

description: Incongruity and Humor degrees used in the parametric models<br>
DOI: 10.6084/m9.figshare.4039899
title: 16_S10_L001_R2_001_run2.fastq.gz

description: This is the raw sequence file (R2 direction) of a second paired-end Illumina MiSeq sequencing run.
DOI: 10.7910/dvn/v1rjpf/9sy2v2
title: blc20171018_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039899.v1
title: 16_S10_L001_R2_001_run2.fastq.gz

description: This is the raw sequence file (R2 direction) of a second paired-end Illumina MiSeq sequencing run.
DOI: 10.6084/m9.figshare.4039893
title: 16_S10_L001_R1_001_run2.fastq.gz

description: This is the raw sequence file (R1 direction) of a second paired-end Illumina MiSeq sequencing run.
DOI: 10.7910/dvn/v1rjpf/hsnjdt
title: blc20170907_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039893.v1
title: 16_S10_L001_R1_001_run2.fastq.gz

description: This is the raw sequence file (R1 direction) of a second paired-end Illumina MiSeq sequencing run.
DOI: 10.7910/dvn/v1rjpf/upgd1h
title: blc20170414_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039860
title: 16_S10_L001_R2_001_run1.fastq.gz

description: This is the raw sequence file (R2 direction) of a paired-end Illumina MiSeq sequencing run.
DOI: 10.7910/dvn/v1rjpf/3a7rpv
title: blc20170115_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039821
title: 16_S10_L001_R1_001_run1.fastq.gz

description: This is the raw sequence file (R1 direction) of a paired-end Illumina MiSeq sequencing run.
DOI: 10.7910/dvn/v1rjpf/1zcvcf
title: blc20170601_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/eupldl
title: blc20170622_03.txt.gz

description: :unav
DOI: 10.5281/zenodo.4013716
title: Perl et al 2020 Substantial variability in morphological scaling among bumblebee colonies

description: Data and R code for the submitted manuscript Perl et al 2020 Substantial variability in morphological scaling among bumblebee colonies
DOI: 10.7910/dvn/v1rjpf/qvxqsv
title: blc20170225_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/kc91eq
title: blc20170603_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/etiukw
title: blc20170520_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039734
title: How to Use Endothelial Cells to Promote Increased Production of Hematopoietic Stem Cells Ex Vivo for Patient Therapy

description: This review article describes a method by which hematopoietic stem cells (HSCs) may be expanded ex vivo using autologous endothelial cells in place of stromal cells hitherto used as feeder cells in culture. The method proposed promises to boost expansion of HSCs to produce long-term repopulating cells that may be used for effective patient therapy.
DOI: 10.7910/dvn/v1rjpf/7y9fhe
title: blc20170201_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039734.v1
title: How to Use Endothelial Cells to Promote Increased Production of Hematopoietic Stem Cells Ex Vivo for Patient Therapy

description: This review article describes a method by which hematopoietic stem cells (HSCs) may be expanded ex vivo using autologous endothelial cells in place of stromal cells hitherto used as feeder cells in culture. The method proposed promises to boost expansion of HSCs to produce long-term repopulating cells that may be used for effective patient therapy.
DOI: 10.7910/dvn/v1rjpf/lt6pyj
title: blc20170529_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/kcmphp
title: blc20170710_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039719
title: FASTA Files of Influenza HA

description: FASTA files of influenza HAs<br>
DOI: 10.7910/dvn/v1rjpf/n1qixe
title: blc20170522_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039692
title: Coronary artery spasm: Is ST-elevation key for diagnosis?

description: Coronary vasospasm is uncommon during pregnancy and the postpartum period. We present a very rare case of an acute coronary vasospasm in a 36-year-old woman who was two weeks postpartum. The coronary arteriograms showed a coronary vasospasm in the distal left anterior descending and circumflex coronary arteries. Electrocardiogram (ECG) presentation was atypical, with T-wave inversions in leads I, aVL, and V2 to V6. To our knowledge, this is the first case with a well-documented coronary artery vasospasm in a postpartum woman without the classic ST elevation on ECG. Management should follow the usual principles of care for acute coronary vasospasm.
DOI: 10.7910/dvn/v1rjpf/li1cm5
title: blc20171101_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039692.v1
title: Coronary artery spasm: Is ST-elevation key for diagnosis?

description: Coronary vasospasm is uncommon during pregnancy and the postpartum period. We present a very rare case of an acute coronary vasospasm in a 36-year-old woman who was two weeks postpartum. The coronary arteriograms showed a coronary vasospasm in the distal left anterior descending and circumflex coronary arteries. Electrocardiogram (ECG) presentation was atypical, with T-wave inversions in leads I, aVL, and V2 to V6. To our knowledge, this is the first case with a well-documented coronary artery vasospasm in a postpartum woman without the classic ST elevation on ECG. Management should follow the usual principles of care for acute coronary vasospasm.
DOI: 10.7910/dvn/v1rjpf/kgulap
title: blc20170505_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039671
title: BEAST XML Files of Influenza HA Gene

description: 180 BEAST 1.8.4 XML files of influenza HA genes.<br>
DOI: 10.6084/m9.figshare.4039674
title: Extrinsic compression of left main coronary artery due to dilated pulmonary trunk resulting in ischaemic symptoms

description: Left coronary artery compression syndrome is an uncommon entity and characterized by compression of the LMCA in-between the aorta and an enlarged main pulmonary arterial trunk. It is usually associated with a congenital cardiac defect. Cardiac 64-slice MDCT provides a non-invasive and an accurate method for assessing the degree of dynamic LMCA compression throughout the cardiac cycle, its angulation relative to the left sinus of Valsalva and depiction of pulmonary pathology, making it a valuable tool in the workup of patients suspected of left coronary artery compression.
DOI: 10.6084/m9.figshare.4039674.v1
title: Extrinsic compression of left main coronary artery due to dilated pulmonary trunk resulting in ischaemic symptoms

description: Left coronary artery compression syndrome is an uncommon entity and characterized by compression of the LMCA in-between the aorta and an enlarged main pulmonary arterial trunk. It is usually associated with a congenital cardiac defect. Cardiac 64-slice MDCT provides a non-invasive and an accurate method for assessing the degree of dynamic LMCA compression throughout the cardiac cycle, its angulation relative to the left sinus of Valsalva and depiction of pulmonary pathology, making it a valuable tool in the workup of patients suspected of left coronary artery compression.
DOI: 10.7910/dvn/v1rjpf/oml00z
title: blc20170612_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/powwg8
title: blc20170718_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039671.v2
title: BEAST XML Files of Influenza HA Gene

description: 180 BEAST 1.8.4 XML files of influenza HA genes.<br>
DOI: 10.6084/m9.figshare.4039413
title: Influenza HA MCC Trees

description: 180 Influenza HA MCC trees from PLoS Comp Bio paper.<br>
DOI: 10.6084/m9.figshare.4039671.v1
title: BEAST XML Files of Influenza HA Gene

description: 108 BEAST 1.8.4 XML files of influenza HA genes.<br>
DOI: 10.7910/dvn/v1rjpf/ssk3nc
title: blc20170929_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/xdpphy
title: blc20170901_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4039413.v1
title: Influenza HA MCC Trees

description: 108 Influenza HA MCC trees from PLoS Comp Bio paper.<br>
DOI: 10.7910/dvn/v1rjpf/i3zqyn
title: blc20171228_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038831
title: p53 oligomerization status modulates cell fate decisions between growth, arrest and apoptosis

description: Mutations in the oligomerization domain of p53 are genetically linked to cancer susceptibility in Li-Fraumeni Syndrome. These mutations typically alter the oligomeric state of p53 and impair its transcriptional activity. Activation of p53 through tetramerization is required for its tumor suppressive function by inducing transcriptional programs that lead to cell fate decisions such as cell cycle arrest or apoptosis. How p53 chooses between these cell fate outcomes remains unclear. Here, we use 5 oligomeric variants of p53, including 2 novel p53 constructs, that yield either monomeric, dimeric or tetrameric forms of p53 and demonstrate that they induce distinct cellular activities and gene expression profiles that lead to different cell fate outcomes. We report that dimeric p53 variants are cytostatic and can arrest cell growth, but lack the ability to trigger apoptosis in p53-null cells. In contrast, p53 tetramers induce rapid apoptosis and cell growth arrest, while a monomeric variant is functionally inactive, supporting cell growth. In particular, the expression of pro-arrest <i>CDKN1A</i> and pro-apoptotic <i>P53AIP1</i> genes are important cell fate determinants that are differentially regulated by the oligomeric state of p53. This study suggests that the most abundant oligomeric species of p53 present in resting cells, namely p53 dimers, neither promote cell growth or cell death and that shifting the oligomeric state equilibrium of p53 in cells toward monomers or tetramers is a key parameter in p53-based cell fate decisions.
DOI: 10.7910/dvn/v1rjpf/xibleb
title: blc20171204_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038831.v1
title: p53 oligomerization status modulates cell fate decisions between growth, arrest and apoptosis

description: Mutations in the oligomerization domain of p53 are genetically linked to cancer susceptibility in Li-Fraumeni Syndrome. These mutations typically alter the oligomeric state of p53 and impair its transcriptional activity. Activation of p53 through tetramerization is required for its tumor suppressive function by inducing transcriptional programs that lead to cell fate decisions such as cell cycle arrest or apoptosis. How p53 chooses between these cell fate outcomes remains unclear. Here, we use 5 oligomeric variants of p53, including 2 novel p53 constructs, that yield either monomeric, dimeric or tetrameric forms of p53 and demonstrate that they induce distinct cellular activities and gene expression profiles that lead to different cell fate outcomes. We report that dimeric p53 variants are cytostatic and can arrest cell growth, but lack the ability to trigger apoptosis in p53-null cells. In contrast, p53 tetramers induce rapid apoptosis and cell growth arrest, while a monomeric variant is functionally inactive, supporting cell growth. In particular, the expression of pro-arrest <i>CDKN1A</i> and pro-apoptotic <i>P53AIP1</i> genes are important cell fate determinants that are differentially regulated by the oligomeric state of p53. This study suggests that the most abundant oligomeric species of p53 present in resting cells, namely p53 dimers, neither promote cell growth or cell death and that shifting the oligomeric state equilibrium of p53 in cells toward monomers or tetramers is a key parameter in p53-based cell fate decisions.
DOI: 10.6084/m9.figshare.4039413.v2
title: Influenza HA MCC Trees

description: 180 Influenza HA MCC trees from PLoS Comp Bio paper.<br>
DOI: 10.7910/dvn/v1rjpf/9zphel
title: blc20170314_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/64xbjk
title: blc20170319_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/fjc0ml
title: blc20170318_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/osivfa
title: blc20171209_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/1iggra
title: blc20170416_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/ownr4p
title: blc20171005_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/wca4fq
title: blc20170604_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/fft3o2
title: blc20170304_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/gtf1kv
title: blc20170202_03.txt.gz

description: :unav
DOI: 10.6084/m9.figshare.4038534
title: Analysis of Proportional Odds Models With Censoring and Errors-in-Covariates

description: We propose a consistent method for estimating both the finite- and infinite-dimensional parameters of the proportional odds model when a covariate is subject to measurement error and time-to-events are subject to right censoring. The proposed method does not rely on the distributional assumption of the true covariate, which is not observed in the data. In addition, the proposed estimator does not require the measurement error to be normally distributed or to have any other specific distribution, and we do not attempt to assess the error distribution. Instead, we construct martingale-based estimators through inversion, using only the moment properties of the error distribution, estimable from multiple erroneous measurements of the true covariate. The theoretical properties of the estimators are established and the finite sample performance is demonstrated via simulations. We illustrate the usefulness of the method by analyzing a dataset from a clinical study on AIDS. Supplementary materials for this article are available online.
DOI: 10.6084/m9.figshare.4038534.v1
title: Analysis of Proportional Odds Models With Censoring and Errors-in-Covariates

description: We propose a consistent method for estimating both the finite- and infinite-dimensional parameters of the proportional odds model when a covariate is subject to measurement error and time-to-events are subject to right censoring. The proposed method does not rely on the distributional assumption of the true covariate, which is not observed in the data. In addition, the proposed estimator does not require the measurement error to be normally distributed or to have any other specific distribution, and we do not attempt to assess the error distribution. Instead, we construct martingale-based estimators through inversion, using only the moment properties of the error distribution, estimable from multiple erroneous measurements of the true covariate. The theoretical properties of the estimators are established and the finite sample performance is demonstrated via simulations. We illustrate the usefulness of the method by analyzing a dataset from a clinical study on AIDS. Supplementary materials for this article are available online.
DOI: 10.7910/dvn/v1rjpf/f9fxqf
title: blc20170928_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/zqgt03
title: blc20171225_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/cdnbxk
title: blc20170207_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/rhzba1
title: blc20170910_03.txt.gz

description: :unav
DOI: 10.7910/dvn/v1rjpf/jctmri
title: blc20170818_03.txt.gz

description: :unav