cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.7910/dvn/0waeam/dfud9q
title: bellows_sierra_leone_groupparticipation_std_viol_exp_std.tab

description: :unav
DOI: 10.6084/m9.figshare.3573567
title: Numb is involved in the non-random segregation of subcellular vesicles in colorectal cancer stem cells

description: The balance between the symmetric and asymmetric division of stem cells governs tissue homeostasis, and the deregulation of this balance initiates tumor formation. Although many functions of Numb have been demonstrated in normal stem cells, the role of Numb in cancer stem cells is relatively unclear. We recently demonstrated that in colorectal cancer stem cells, Numb was suppressed by miR-146a-5p, which resulted in the activation of the Wnt signaling pathway and symmetric template DNA division. Here, we demonstrate that the PKH26-labeled subcellular foci are enriched for endosomal markers such as EEA1 and RAB11. In colorectal cancer stem cells, the PKH-26-labeled vesicles are segregated equally at the first mitotic division; in contrast, they are unequally segregated in parental cells or in cancer stem cells undergoing serum-induced differentiation. The PKH<sup>Bright</sup> progeny of colorectal cancer stem cells harbors a stem cell phenotype, whereas the PKH<sup>Dim</sup> progeny behaves as the differentiating cells. The miR-146a-5p-regulated Numb controls the distribution of PKH26 vesicles. Our results suggest a critical role of Numb in controlling the segregation of subcellular vesicles during division of colorectal cancer stem cells.
DOI: 10.7910/dvn/0waeam/nycccl
title: gneezy_israel_ultimaumA_viol_exp_dummy.tab

description: :unav
DOI: 10.6084/m9.figshare.3573567.v2
title: Numb is involved in the non-random segregation of subcellular vesicles in colorectal cancer stem cells

description: The balance between the symmetric and asymmetric division of stem cells governs tissue homeostasis, and the deregulation of this balance initiates tumor formation. Although many functions of Numb have been demonstrated in normal stem cells, the role of Numb in cancer stem cells is relatively unclear. We recently demonstrated that in colorectal cancer stem cells, Numb was suppressed by miR-146a-5p, which resulted in the activation of the Wnt signaling pathway and symmetric template DNA division. Here, we demonstrate that the PKH26-labeled subcellular foci are enriched for endosomal markers such as EEA1 and RAB11. In colorectal cancer stem cells, the PKH-26-labeled vesicles are segregated equally at the first mitotic division; in contrast, they are unequally segregated in parental cells or in cancer stem cells undergoing serum-induced differentiation. The PKH<sup>Bright</sup> progeny of colorectal cancer stem cells harbors a stem cell phenotype, whereas the PKH<sup>Dim</sup> progeny behaves as the differentiating cells. The miR-146a-5p-regulated Numb controls the distribution of PKH26 vesicles. Our results suggest a critical role of Numb in controlling the segregation of subcellular vesicles during division of colorectal cancer stem cells.
DOI: 10.7910/dvn/0waeam/bn5qju
title: bateson_asia_prosocial_index_no_trustA_viol_exp_std.tab

description: :unav
DOI: 10.6084/m9.figshare.3573567.v1
title: Numb is Involved in the Non-Random Segregation of Subcellular Vesicles in Colorectal Cancer Stem Cells

description: The balance between the symmetric and asymmetric division of stem cells governs tissue homeostasis, and the deregulation of this balance initiates tumor formation. Although many functions of Numb have been demonstrated in normal stem cells, the role of Numb in cancer stem cells is relatively unclear. We recently demonstrated that in colorectal cancer stem cells, Numb was suppressed by miR-146a-5p, which resulted in the activation of the Wnt signaling pathway and symmetric template DNA division. Here, we demonstrate that the PKH26-labeled subcellular foci are enriched for endosomal markers such as EEA1 and RAB11. In colorectal cancer stem cells, the PKH-26-labeled vesicles are segregated equally at the first mitotic division; in contrast, they are unequally segregated in parental cells or in cancer stem cells undergoing serum-induced differentiation. The PKH<sup>Bright</sup> progeny of colorectal cancer stem cells harbors a stem cell phenotype, whereas the PKH<sup>Dim</sup> progeny behaves as the differentiating cells. The miR-146a-5p-regulated Numb controls the distribution of PKH26 vesicles. Our results suggest a critical role of Numb in controlling the segregation of subcellular vesicles during division of colorectal cancer stem cells.
DOI: 10.7910/dvn/0waeam/oynia4
title: cassar_tajikistan_trust_game_return_std_viol_exp_std.tab

description: :unav
DOI: 10.7910/dvn/0waeam/lfpula
title: gneezy_israel_prosocial_indexA_viol_exp_std.tab

description: :unav
DOI: 10.7910/dvn/0waeam/x4osnm
title: annan_ugandafemales_prosocial_indexM_viol_exp_dummy.tab

description: :unav
DOI: 10.6084/m9.figshare.3573552
title: Mobile small RNAs and their role in regulating cytosine methylation of DNA

description: Small (s)RNAs of 21 to 24 nucleotides are associated with RNA silencing and methylation of DNA cytosine residues. All sizes can move from cell-to-cell and long distance in plants, directing RNA silencing in destination cells. Twenty-four nucleotide sRNAs are the predominant long-distance mobile species. Thousands move from shoot to root, where they target methylation of transposable elements both directly and indirectly. We derive several classes of interaction between small RNAs and methylation and use these to explore the mechanisms of methylation and gene expression that associate with mobile sRNA signaling.
DOI: 10.7910/dvn/0waeam/ehsfpb
title: gilligan_nepal_prosocial_indexM_viol_exp_community_std.tab

description: :unav
DOI: 10.7910/dvn/0waeam/ffhtit
title: standardized_forest_games_all_RE.R

description: :unav
DOI: 10.6084/m9.figshare.3573552.v1
title: Mobile small RNAs and their role in regulating cytosine methylation of DNA

description: Small (s)RNAs of 21 to 24 nucleotides are associated with RNA silencing and methylation of DNA cytosine residues. All sizes can move from cell-to-cell and long distance in plants, directing RNA silencing in destination cells. Twenty-four nucleotide sRNAs are the predominant long-distance mobile species. Thousands move from shoot to root, where they target methylation of transposable elements both directly and indirectly. We derive several classes of interaction between small RNAs and methylation and use these to explore the mechanisms of methylation and gene expression that associate with mobile sRNA signaling.
DOI: 10.6084/m9.figshare.3573537
title: Efficacy and epigenetic interactions of novel DNA hypomethylating agent guadecitabine (SGI-110) in preclinical models of hepatocellular carcinoma

description: Hepatocellular carcinoma (HCC) is a deadly malignancy characterized at the epigenetic level by global DNA hypomethylation and focal hypermethylation on the promoter of tumor suppressor genes. In most cases it develops on a background of liver steatohepatitis, fibrosis, and cirrhosis. Guadecitabine (SGI-110) is a second-generation hypomethylating agent, which inhibits DNA methyltransferases. Guadecitabine is formulated as a dinucleotide of decitabine and deoxyguanosine that is resistant to cytidine deaminase (CDA) degradation and results in prolonged <i>in vivo</i> exposure to decitabine following small volume subcutaneous administration of guadecitabine. Here we found that guadecitabine is an effective demethylating agent and is able to prevent HCC progression in pre-clinical models. In a xenograft HCC HepG2 model, guadecitabine impeded tumor growth and inhibited angiogenesis, while it could not prevent liver fibrosis and inflammation in a mouse model of steatohepatitis. Demethylating efficacy of guadecitabine on LINE-1 elements was found to be the highest 8 d post-infusion in blood samples of mice. Analysis of a panel of human HCC vs. normal tissue revealed a signature of hypermethylated tumor suppressor genes (<i>CDKN1A, CDKN2A, DLEC1, E2F1, GSTP1, OPCML, E2F1, RASSF1, RUNX3</i>, and <i>SOCS1</i>) as detected by methylation-specific PCR. A pronounced demethylating effect of guadecitabine was obtained also in the promoters of a subset of tumor suppressors genes (<i>CDKN2A, DLEC1</i>, and <i>RUNX3</i>) in HepG2 and Huh-7 HCC cells. Finally, we analyzed the role of macroH2A1, a variant of histone H2A, an oncogene upregulated in human cirrhosis/HCC that synergizes with DNA methylation in suppressing tumor suppressor genes, and it prevents the inhibition of cell growth triggered by decitabine in HCC cells. Guadecitabine, in contrast to decitabine, blocked growth in HCC cells overexpressing macroH2A1 histones and with high CDA levels, despite being unable to fully demethylate <i>CDKN2A, RUNX3</i>, and <i>DLEC1</i> promoters altered by macroH2A1. Collectively, our findings in human and mice models reveal novel epigenetic anti-HCC effects of guadecitabine, which might be effective specifically in advanced states of the disease.
DOI: 10.6084/m9.figshare.3573537.v1
title: Efficacy and epigenetic interactions of novel DNA hypomethylating agent guadecitabine (SGI-110) in preclinical models of hepatocellular carcinoma

description: Hepatocellular carcinoma (HCC) is a deadly malignancy characterized at the epigenetic level by global DNA hypomethylation and focal hypermethylation on the promoter of tumor suppressor genes. In most cases it develops on a background of liver steatohepatitis, fibrosis, and cirrhosis. Guadecitabine (SGI-110) is a second-generation hypomethylating agent, which inhibits DNA methyltransferases. Guadecitabine is formulated as a dinucleotide of decitabine and deoxyguanosine that is resistant to cytidine deaminase (CDA) degradation and results in prolonged <i>in vivo</i> exposure to decitabine following small volume subcutaneous administration of guadecitabine. Here we found that guadecitabine is an effective demethylating agent and is able to prevent HCC progression in pre-clinical models. In a xenograft HCC HepG2 model, guadecitabine impeded tumor growth and inhibited angiogenesis, while it could not prevent liver fibrosis and inflammation in a mouse model of steatohepatitis. Demethylating efficacy of guadecitabine on LINE-1 elements was found to be the highest 8 d post-infusion in blood samples of mice. Analysis of a panel of human HCC vs. normal tissue revealed a signature of hypermethylated tumor suppressor genes (<i>CDKN1A, CDKN2A, DLEC1, E2F1, GSTP1, OPCML, E2F1, RASSF1, RUNX3</i>, and <i>SOCS1</i>) as detected by methylation-specific PCR. A pronounced demethylating effect of guadecitabine was obtained also in the promoters of a subset of tumor suppressors genes (<i>CDKN2A, DLEC1</i>, and <i>RUNX3</i>) in HepG2 and Huh-7 HCC cells. Finally, we analyzed the role of macroH2A1, a variant of histone H2A, an oncogene upregulated in human cirrhosis/HCC that synergizes with DNA methylation in suppressing tumor suppressor genes, and it prevents the inhibition of cell growth triggered by decitabine in HCC cells. Guadecitabine, in contrast to decitabine, blocked growth in HCC cells overexpressing macroH2A1 histones and with high CDA levels, despite being unable to fully demethylate <i>CDKN2A, RUNX3</i>, and <i>DLEC1</i> promoters altered by macroH2A1. Collectively, our findings in human and mice models reveal novel epigenetic anti-HCC effects of guadecitabine, which might be effective specifically in advanced states of the disease.
DOI: 10.7910/dvn/0waeam/2dxdxf
title: forest_plot_trust_outgroup_RE.pdf

description: :unav
DOI: 10.7910/dvn/0waeam/gvmb2u
title: bauer_sierra_leone_egalitarian_std_viol_exp_personal_std.tab

description: :unav
DOI: 10.6084/m9.figshare.3573510
title: Synergistic effects of eIF4A and MEK inhibitors on proliferation of NRAS-mutant melanoma cell lines

description: Activating mutations of the NRAS (neuroblastoma rat sarcoma viral oncogene) protein kinase, present in many cancers, induce a constitutive activation of both the RAS-RAF-MEK-ERK mitogen-activated protein kinase (MAPK) signal transduction pathway and the PI(3)K-AKT-mTOR, pathway. This in turn regulates the formation of the eIF4F eukaryotic translation initiation complex, comprising the eIF4E cap-binding protein, the eIF4G scaffolding protein and the eIF4A RNA helicase, which binds to the 7-methylguanylate cap (m(7)G) at the 5′ end of messenger RNAs. Small molecules targeting MEK (MEKi: MEK inhibitors) have demonstrated activity in NRAS-mutant cell lines and tumors, but resistance sets in most cases within months of treatment. Using proximity ligation assays, that allows visualization of the binding of eIF4E to the scaffold protein eIF4G, generating the active eIF4F complex, we have found that resistance to MEKi is associated with the persistent formation of the eIF4F complex in MEKi-treated NRAS-mutant cell lines. Furthermore, inhibiting the eIF4A component of the eIF4F complex, with a small molecule of the flavagline/rocaglate family, synergizes with inhibiting MEK to kill NRAS-mutant cancer cell lines.
DOI: 10.7910/dvn/0waeam/1zdmov
title: annan_ugandafemales_communityparticipation_std_viol_exp_dummy.tab

description: :unav
DOI: 10.17632/yh7sbym5rn.1
title: Creating a Database for Health IT Events via a Hybrid Deep Learning Model

description: Column list: YEAR, MDR, GENERIC_NAME, BRAND_NAME, MANUFACTURER_NAME, REPORT
DOI: 10.7910/dvn/0waeam/rspxio
title: gilligan_nepal_knowledgepolitics_std_viol_exp_dummy.tab

description: :unav
DOI: 10.7910/dvn/0waeam/v5u7zs
title: bauer_sierra_leone_trustall_std_viol_exp_std.tab

description: :unav
DOI: 10.6084/m9.figshare.3573510.v3
title: Synergistic effects of eIF4A and MEK inhibitors on proliferation of NRAS-mutant melanoma cell lines

description: Activating mutations of the NRAS (neuroblastoma rat sarcoma viral oncogene) protein kinase, present in many cancers, induce a constitutive activation of both the RAS-RAF-MEK-ERK mitogen-activated protein kinase (MAPK) signal transduction pathway and the PI(3)K-AKT-mTOR, pathway. This in turn regulates the formation of the eIF4F eukaryotic translation initiation complex, comprising the eIF4E cap-binding protein, the eIF4G scaffolding protein and the eIF4A RNA helicase, which binds to the 7-methylguanylate cap (m(7)G) at the 5′ end of messenger RNAs. Small molecules targeting MEK (MEKi: MEK inhibitors) have demonstrated activity in NRAS-mutant cell lines and tumors, but resistance sets in most cases within months of treatment. Using proximity ligation assays, that allows visualization of the binding of eIF4E to the scaffold protein eIF4G, generating the active eIF4F complex, we have found that resistance to MEKi is associated with the persistent formation of the eIF4F complex in MEKi-treated NRAS-mutant cell lines. Furthermore, inhibiting the eIF4A component of the eIF4F complex, with a small molecule of the flavagline/rocaglate family, synergizes with inhibiting MEK to kill NRAS-mutant cancer cell lines.
DOI: 10.7910/dvn/0waeam/d13r2k
title: binary_forest_prosocial_indexM_FE.R

description: :unav
DOI: 10.7910/dvn/0waeam/bzrwyw
title: annan_ugandafemales_communityparticipation_std_viol_exp_std.tab

description: :unav
DOI: 10.6084/m9.figshare.3573510.v2
title: Synergistic effects of eIF4A and MEK inhibitors on proliferation of NRAS-mutant melanoma cell lines

description: Activating mutations of the NRAS (neuroblastoma rat sarcoma viral oncogene) protein kinase, present in many cancers, induce a constitutive activation of both the RAS-RAF-MEK-ERK mitogen-activated protein kinase (MAPK) signal transduction pathway and the PI(3)K-AKT-mTOR, pathway. This in turn regulates the formation of the eIF4F eukaryotic translation initiation complex, comprising the eIF4E cap-binding protein, the eIF4G scaffolding protein and the eIF4A RNA helicase, which binds to the 7-methylguanylate cap (m(7)G) at the 5′ end of messenger RNAs. Small molecules targeting MEK (MEKi: MEK inhibitors) have demonstrated activity in NRAS-mutant cell lines and tumors, but resistance sets in most cases within months of treatment. Using proximity ligation assays, that allows visualization of the binding of eIF4E to the scaffold protein eIF4G, generating the active eIF4F complex, we have found that resistance to MEKi is associated with the persistent formation of the eIF4F complex in MEKi-treated NRAS-mutant cell lines. Furthermore, inhibiting the eIF4A component of the eIF4F complex, with a small molecule of the flavagline/rocaglate family, synergizes with inhibiting MEK to kill NRAS-mutant cancer cell lines.
DOI: 10.7910/dvn/0waeam/oh6g75
title: forest_plot_games_outgroup_RE.pdf

description: :unav
DOI: 10.6084/m9.figshare.3573504
title: ATG3-dependent autophagy mediates mitochondrial homeostasis in pluripotency acquirement and maintenance

description: Pluripotent stem cells, including induced pluripotent and embryonic stem cells (ESCs), have less developed mitochondria than somatic cells and, therefore, rely more heavily on glycolysis for energy production.<sup>1-3</sup> However, how mitochondrial homeostasis matches the demands of nuclear reprogramming and regulates pluripotency in ESCs is largely unknown. Here, we identified ATG3-dependent autophagy as an executor for both mitochondrial remodeling during somatic cell reprogramming and mitochondrial homeostasis regulation in ESCs. Dysfunctional autophagy by <i>Atg3</i> deletion inhibited mitochondrial removal during pluripotency induction, resulting in decreased reprogramming efficiency and accumulation of abnormal mitochondria in established iPSCs. In <i>Atg3</i> null mouse ESCs, accumulation of aberrant mitochondria was accompanied by enhanced ROS generation, defective ATP production and attenuated pluripotency gene expression, leading to abnormal self-renewal and differentiation. These defects were rescued by reacquisition of wild-type but not lipidation-deficient <i>Atg3</i> expression. Taken together, our findings highlight a critical role of ATG3-dependent autophagy for mitochondrial homeostasis regulation in both pluripotency acquirement and maintenance.
DOI: 10.7910/dvn/0waeam/nizzsp
title: deluca_uganda_2015b_prosocial_indexA_viol_exp_community_std.tab

description: :unav
DOI: 10.6084/m9.figshare.3573504.v1
title: ATG3-dependent autophagy mediates mitochondrial homeostasis in pluripotency acquirement and maintenance

description: Pluripotent stem cells, including induced pluripotent and embryonic stem cells (ESCs), have less developed mitochondria than somatic cells and, therefore, rely more heavily on glycolysis for energy production.<sup>1-3</sup> However, how mitochondrial homeostasis matches the demands of nuclear reprogramming and regulates pluripotency in ESCs is largely unknown. Here, we identified ATG3-dependent autophagy as an executor for both mitochondrial remodeling during somatic cell reprogramming and mitochondrial homeostasis regulation in ESCs. Dysfunctional autophagy by <i>Atg3</i> deletion inhibited mitochondrial removal during pluripotency induction, resulting in decreased reprogramming efficiency and accumulation of abnormal mitochondria in established iPSCs. In <i>Atg3</i> null mouse ESCs, accumulation of aberrant mitochondria was accompanied by enhanced ROS generation, defective ATP production and attenuated pluripotency gene expression, leading to abnormal self-renewal and differentiation. These defects were rescued by reacquisition of wild-type but not lipidation-deficient <i>Atg3</i> expression. Taken together, our findings highlight a critical role of ATG3-dependent autophagy for mitochondrial homeostasis regulation in both pluripotency acquirement and maintenance.
DOI: 10.7910/dvn/0waeam/dzavz2
title: forest_plot_games_ingroup_RE.pdf

description: :unav
DOI: 10.7910/dvn/0waeam/bwtfm0
title: forest_plot_groups_FE.pdf

description: :unav
DOI: 10.7910/dvn/0waeam/mk4sac
title: bateson_us_canada_communityparticipation_std_viol_exp_std.tab

description: :unav
DOI: 10.7910/dvn/0waeam/enw9as
title: bateson_asia_prosocial_indexA_viol_exp_personal_std.tab

description: :unav
DOI: 10.7910/dvn/0waeam/qokhj5
title: bateson_us_canada_prosocial_indexA_viol_exp_dummy.tab

description: :unav
DOI: 10.7910/dvn/0waeam/kaconx
title: annan_ugandafemales_trustall_std_viol_exp_personal_std.tab

description: :unav
DOI: 10.7910/dvn/0waeam/7tvzsw
title: bateson_asia_trustingroup_std_viol_exp_dummy.tab

description: :unav
DOI: 10.7910/dvn/0waeam/fdlhke
title: forest_plot_games_outgroup_FE.pdf

description: :unav
DOI: 10.7910/dvn/0waeam/rsogq1
title: bateson_asia_prosocial_indexM_viol_exp_dummy.tab

description: :unav
DOI: 10.6084/m9.figshare.3573489
title: Spatial and temporal coordination of traction forces in one-dimensional cell migration

description: Migration of a fibroblast along a collagen fiber can be regarded as cell locomotion in one-dimension (1D). In this process, a cell protrudes forward, forms a new adhesion, produces traction forces, and releases its rear adhesion in order to advance itself along a path. However, how a cell coordinates its adhesion formation, traction forces, and rear release in 1D migration is unclear. Here, we studied fibroblasts migrating along a line of microposts. We found that when the front of a cell protruded onto a new micropost, the traction force produced at its front increased steadily, but did so without a temporal correlation in the force at its rear. Instead, the force at the front coordinated with a decrease in force at the micropost behind the front. A similar correlation in traction forces also occurred at the rear of a cell, where a decrease in force due to adhesion detachment corresponded to an increase in force at the micropost ahead of the rear. Analysis with a bio-chemo-mechanical model for traction forces and adhesion dynamics indicated that the observed relationship between traction forces at the front and back of a cell is possible only when cellular elasticity is lower than the elasticity of the cellular environment.
DOI: 10.7910/dvn/0waeam/bz2q47
title: deluca_uganda_2015b_prosocial_indexM_viol_exp_std.tab

description: :unav
DOI: 10.6084/m9.figshare.3573489.v2
title: Spatial and temporal coordination of traction forces in one-dimensional cell migration

description: Migration of a fibroblast along a collagen fiber can be regarded as cell locomotion in one-dimension (1D). In this process, a cell protrudes forward, forms a new adhesion, produces traction forces, and releases its rear adhesion in order to advance itself along a path. However, how a cell coordinates its adhesion formation, traction forces, and rear release in 1D migration is unclear. Here, we studied fibroblasts migrating along a line of microposts. We found that when the front of a cell protruded onto a new micropost, the traction force produced at its front increased steadily, but did so without a temporal correlation in the force at its rear. Instead, the force at the front coordinated with a decrease in force at the micropost behind the front. A similar correlation in traction forces also occurred at the rear of a cell, where a decrease in force due to adhesion detachment corresponded to an increase in force at the micropost ahead of the rear. Analysis with a bio-chemo-mechanical model for traction forces and adhesion dynamics indicated that the observed relationship between traction forces at the front and back of a cell is possible only when cellular elasticity is lower than the elasticity of the cellular environment.
DOI: 10.7910/dvn/0waeam/ftcl4l
title: standardized_community_forest_games_all_RE.R

description: :unav
DOI: 10.6084/m9.figshare.3573486
title: Additional File 23. PAML control file.

description: Additional File 23. PAML control file.<br>
DOI: 10.7910/dvn/0waeam/ce10jx
title: bellows_sierra_leone_knowledgepolitics_std_viol_exp_community_std.tab

description: :unav
DOI: 10.7910/dvn/0waeam/yeny0u
title: standardized_personal_forest_games_outgroup_FE.R

description: :unav
DOI: 10.6084/m9.figshare.3573486.v1
title: Additional File 23. PAML control file.

description: Additional File 23. PAML control file.<br>
DOI: 10.6084/m9.figshare.3573483
title: Additional File 22. nad5 codon alignment for PAML.

description: Additional File 22. nad5 codon alignment for PAML.