cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.6084/m9.figshare.22293379.v1
title: Dataset of Ophiocordyceps kuchinaraiensis

description: <em>Stromata</em> single or double on <em>Coleoptera</em> larvae, brown, dark brown to black, cylindrical, slightly curved to curved, emerging from the fallen off feet pairs of the larvae, 5.5–10 cm long and 2–3 mm broad, enlarging abruptly at the fertile head. <em>Fertile head</em> terminal, brown to dark brown, ovoid, limoniform, with ostioles slightly protruding on the surface of the fertile stroma, 5–7 mm long and 3–4 mm broad. <em>Perithecia</em> semi-immersed, obclavate, (630–)669.4–790.6(–820) × (210–)222.3–282.1(–300) μm. <em>Asci</em> cylindrical, (305–)364.8–485(–525) × (4.5–)4.8–5.1(–5.5) μm. <em>Asci-caps </em>convex 3–4× 5–5.5 μm. <em>Ascospores</em> filiform, multi-septate and breaking into 64 part-spores, (430–)480.8–569.3(–615) × 1–2 μm. <em>Part-spores</em> cylindrical with truncated apices, (5–)5.5–10.8(–20) × 1–2 μm.
DOI: 10.6084/m9.figshare.8247806.v3
title: Chromosomal instability suppresses the growth of K-Ras-induced lung adenomas

description: Chromosomal instability (CIN) is defined as a high rate of whole chromosome loss or gain and is a hallmark of many aneuploid solid tumors. CIN positively correlates with poor patient prognosis and chemotherapeutic resistance. Despite this clinical importance, the role of CIN in tumor initiation, growth and/or progression remains poorly understood. To date, the only strategies developed to determine how CIN contributes to tumorigenesis have relied on transgenic mouse models that deliberately increase the rate of chromosomal mis-segregation. Here we develop a strain of transgenic mice that is designed to strategically decrease the rate of chromosome mis-segregation and suppress CIN. These animals modestly overexpress the kinesin-13 microtubule depolymerase Kif2b, a strategy proven successful in restoring faithful chromosome segregation to human cancer cells in culture. Using the LA2 K-Ras G12D-induced model for lung cancer, we show that Kif2b expression reduces the number of chromosome segregation defects but does not change the incidence of lung tumor lesions. However, pulmonary tumors were significantly larger in animals expressing Kif2b and those tumors exhibited elevated rates of Ki-67 positive cells relative to controls. Thus, in lung cancers driven by mutations in K-Ras, CIN has little impact on tumor initiation but suppresses tumor growth. These data support a model in which CIN imposes a burden on tumor cells, and that enhancement of mitotic fidelity results in accelerated tumor growth.
DOI: 10.6084/m9.figshare.8247806
title: Chromosomal instability suppresses the growth of K-Ras-induced lung adenomas

description: Chromosomal instability (CIN) is defined as a high rate of whole chromosome loss or gain and is a hallmark of many aneuploid solid tumors. CIN positively correlates with poor patient prognosis and chemotherapeutic resistance. Despite this clinical importance, the role of CIN in tumor initiation, growth and/or progression remains poorly understood. To date, the only strategies developed to determine how CIN contributes to tumorigenesis have relied on transgenic mouse models that deliberately increase the rate of chromosomal mis-segregation. Here we develop a strain of transgenic mice that is designed to strategically decrease the rate of chromosome mis-segregation and suppress CIN. These animals modestly overexpress the kinesin-13 microtubule depolymerase Kif2b, a strategy proven successful in restoring faithful chromosome segregation to human cancer cells in culture. Using the LA2 K-Ras G12D-induced model for lung cancer, we show that Kif2b expression reduces the number of chromosome segregation defects but does not change the incidence of lung tumor lesions. However, pulmonary tumors were significantly larger in animals expressing Kif2b and those tumors exhibited elevated rates of Ki-67 positive cells relative to controls. Thus, in lung cancers driven by mutations in K-Ras, CIN has little impact on tumor initiation but suppresses tumor growth. These data support a model in which CIN imposes a burden on tumor cells, and that enhancement of mitotic fidelity results in accelerated tumor growth.
DOI: 10.6084/m9.figshare.8247806.v2
title: Chromosomal instability suppresses the growth of K-Ras-induced lung adenomas

description: Chromosomal instability (CIN) is defined as a high rate of whole chromosome loss or gain and is a hallmark of many aneuploid solid tumors. CIN positively correlates with poor patient prognosis and chemotherapeutic resistance. Despite this clinical importance, the role of CIN in tumor initiation, growth and/or progression remains poorly understood. To date, the only strategies developed to determine how CIN contributes to tumorigenesis have relied on transgenic mouse models that deliberately increase the rate of chromosomal mis-segregation. Here we develop a strain of transgenic mice that is designed to strategically decrease the rate of chromosome mis-segregation and suppress CIN. These animals modestly overexpress the kinesin-13 microtubule depolymerase Kif2b, a strategy proven successful in restoring faithful chromosome segregation to human cancer cells in culture. Using the LA2 K-Ras G12D-induced model for lung cancer, we show that Kif2b expression reduces the number of chromosome segregation defects but does not change the incidence of lung tumor lesions. However, pulmonary tumors were significantly larger in animals expressing Kif2b and those tumors exhibited elevated rates of Ki-67 positive cells relative to controls. Thus, in lung cancers driven by mutations in K-Ras, CIN has little impact on tumor initiation but suppresses tumor growth. These data support a model in which CIN imposes a burden on tumor cells, and that enhancement of mitotic fidelity results in accelerated tumor growth.
DOI: 10.6084/m9.figshare.9761792
title: Loss of CENPF leads to developmental failure in mouse embryos

description: Aneuploidy caused by abnormal chromosome segregation during early embryo development leads to embryonic death or congenital malformation. Centromere protein F (CENPF) is a member of centromere protein family that regulates chromosome segregation during mitosis. However, its necessity in early embryo development has not been fully investigated. In this study, expression and function of CENPF was investigated in mouse early embryogenesis. Detection of CENPF expression and localization revealed a cytoplasm, spindle and nuclear membrane related dynamic pattern throughout mitotic progression. Farnesyltransferase inhibitor (FTI) was employed to inhibit CENPF farnesylation in zygotes. The results showed that CENPF degradation was inhibited and its specific localization on nuclear membranes in morula and blastocyst vanished after FTI treatment. Also, CAAX motif mutation leads to failure of CENPF-C630 localization in morula and blastocyst. These results indicate that farnesylation plays a key role during CENPF degradation and localization in early embryos. To further assess CENPF function in parthenogenetic or fertilized embryos development, morpholino (MO) and Trim-Away were used to disturb CENPF function. CENPF knockdown in Metaphase II (MII) oocytes, zygotes or embryos with MO approach resulted in failure to develop into morulae and blastocysts, revealing its indispensable role in both parthenogenetic and fertilized embryos. Disturbing of CENPF with Trim-Away approach in zygotes resulted in impaired development of 2-cell and 4-cell, but did not affect the morula and blastocyst formation because of the recovered expression of CENPF. Taken together, our data suggest CENPF plays an important role during early embryonic development in mice. <b>Abbreviation</b>: CENPF: centromere protein F; MO: morpholino; FTI: Farnesyltransferase inhibitor; CENPE: centromere protein E; IVF: <i>in vitro</i> fertilization; MII: metaphase II; SAC: spindle assembly checkpoint; Mad1: mitotic arrest deficient 1; BUB1: budding uninhibited by benzimidazole 1; BUBR1: BUB1 mitotic checkpoint serine/threonine kinase B; Cdc20: cell division cycle 20
DOI: 10.6084/m9.figshare.9746003
title: Regulation of Cyclin E by transcription factors of the naïve pluripotency network in mouse embryonic stem cells

description: Continuous, non-cell cycle-dependent expression of cyclin E is a characteristic feature of mouse embryonic stem cells (mESCs). We studied the 5′ regulatory region of <i>Cyclin E</i>, also known as <i>Ccne1</i>, and identified binding sites for transcription factors of the naïve pluripotency network, including Esrrb, Klf4, and Tfcp2l1 within 1 kilobase upstream of the transcription start site. Luciferase assay and chromatin immunoprecipitation-quantitative polymerase chain reaction (ChiP–qPCR) study highlighted one binding site for Esrrb that is essential to transcriptional activity of the promoter region, and three binding sites for Klf4 and Tfcp2l1. Knockdown of Esrrb, Klf4, and Tfcp2l1 reduced <i>Cyclin E</i> expression whereas overexpression of Esrrb and Klf4 increased it, indicating a strong correlation between the expression level of these factors and that of cyclin E. We observed that cyclin E overexpression delays differentiation induced by Esrrb depletion, suggesting that cyclin E is an important target of Esrrb for differentiation blockade. We observed that mESCs express a low level of miR-15a and that transfection of a miR-15a mimic decreases <i>Cyclin E</i> mRNA level. These results lead to the conclusion that the high expression level of <i>Cyclin E</i> in mESCs can be attributed to transcriptional activation by Esrrb as well as to the absence of its negative regulator, miR-15a.
DOI: 10.6084/m9.figshare.9746003.v1
title: Regulation of Cyclin E by transcription factors of the naïve pluripotency network in mouse embryonic stem cells

description: Continuous, non-cell cycle-dependent expression of cyclin E is a characteristic feature of mouse embryonic stem cells (mESCs). We studied the 5′ regulatory region of <i>Cyclin E</i>, also known as <i>Ccne1</i>, and identified binding sites for transcription factors of the naïve pluripotency network, including Esrrb, Klf4, and Tfcp2l1 within 1 kilobase upstream of the transcription start site. Luciferase assay and chromatin immunoprecipitation-quantitative polymerase chain reaction (ChiP–qPCR) study highlighted one binding site for Esrrb that is essential to transcriptional activity of the promoter region, and three binding sites for Klf4 and Tfcp2l1. Knockdown of Esrrb, Klf4, and Tfcp2l1 reduced <i>Cyclin E</i> expression whereas overexpression of Esrrb and Klf4 increased it, indicating a strong correlation between the expression level of these factors and that of cyclin E. We observed that cyclin E overexpression delays differentiation induced by Esrrb depletion, suggesting that cyclin E is an important target of Esrrb for differentiation blockade. We observed that mESCs express a low level of miR-15a and that transfection of a miR-15a mimic decreases <i>Cyclin E</i> mRNA level. These results lead to the conclusion that the high expression level of <i>Cyclin E</i> in mESCs can be attributed to transcriptional activation by Esrrb as well as to the absence of its negative regulator, miR-15a.
DOI: 10.6084/m9.figshare.9730547.v1
title: Mild replication stress causes aneuploidy by deregulating microtubule dynamics in mitosis

description: Chromosomal instability (CIN) causes structural and numerical chromosome aberrations and represents a hallmark of cancer. Replication stress (RS) has emerged as a driver for structural chromosome aberrations while mitotic defects can cause whole chromosome missegregation and aneuploidy. Recently, first evidence indicated that RS can also influence chromosome segregation in cancer cells exhibiting CIN, but the underlying mechanisms remain unknown. Here, we show that chromosomally unstable cancer cells suffer from very mild RS, which allows efficient proliferation and which can be mimicked by treatment with very low concentrations of aphidicolin. Both, endogenous RS and aphidicolin-induced very mild RS cause chromosome missegregation during mitosis leading to the induction of aneuploidy. Moreover, RS triggers an increase in microtubule plus end growth rates in mitosis, an abnormality previously identified to cause chromosome missegregation in cancer cells. In fact, RS-induced chromosome missegregation is mediated by increased mitotic microtubule growth rates and is suppressed after restoration of proper microtubule growth rates and upon rescue of replication stress. Hence, very mild and cancer-relevant RS triggers aneuploidy by deregulating microtubule dynamics in mitosis.
DOI: 10.6084/m9.figshare.9730547
title: Mild replication stress causes aneuploidy by deregulating microtubule dynamics in mitosis

description: Chromosomal instability (CIN) causes structural and numerical chromosome aberrations and represents a hallmark of cancer. Replication stress (RS) has emerged as a driver for structural chromosome aberrations while mitotic defects can cause whole chromosome missegregation and aneuploidy. Recently, first evidence indicated that RS can also influence chromosome segregation in cancer cells exhibiting CIN, but the underlying mechanisms remain unknown. Here, we show that chromosomally unstable cancer cells suffer from very mild RS, which allows efficient proliferation and which can be mimicked by treatment with very low concentrations of aphidicolin. Both, endogenous RS and aphidicolin-induced very mild RS cause chromosome missegregation during mitosis leading to the induction of aneuploidy. Moreover, RS triggers an increase in microtubule plus end growth rates in mitosis, an abnormality previously identified to cause chromosome missegregation in cancer cells. In fact, RS-induced chromosome missegregation is mediated by increased mitotic microtubule growth rates and is suppressed after restoration of proper microtubule growth rates and upon rescue of replication stress. Hence, very mild and cancer-relevant RS triggers aneuploidy by deregulating microtubule dynamics in mitosis.
DOI: 10.5517/ccdc.csd.cc2dzv4d
title: CCDC 2234174: Experimental Crystal Structure Determination

description: Related Article: Chaowei Yin, Hanwei Lu, Hebo Ye, Zelin Feng, Hanxun Zou, Meilan Zhang, Lei You|2023|Org.Lett.|25|1470|doi:10.1021/acs.orglett.3c00205
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2dzv5f
title: CCDC 2234175: Experimental Crystal Structure Determination

description: Related Article: Chaowei Yin, Hanwei Lu, Hebo Ye, Zelin Feng, Hanxun Zou, Meilan Zhang, Lei You|2023|Org.Lett.|25|1470|doi:10.1021/acs.orglett.3c00205
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2dzv6g
title: CCDC 2234176: Experimental Crystal Structure Determination

description: Related Article: Chaowei Yin, Hanwei Lu, Hebo Ye, Zelin Feng, Hanxun Zou, Meilan Zhang, Lei You|2023|Org.Lett.|25|1470|doi:10.1021/acs.orglett.3c00205
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2dzv7h
title: CCDC 2234177: Experimental Crystal Structure Determination

description: Related Article: Chaowei Yin, Hanwei Lu, Hebo Ye, Zelin Feng, Hanxun Zou, Meilan Zhang, Lei You|2023|Org.Lett.|25|1470|doi:10.1021/acs.orglett.3c00205
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2dzv8j
title: CCDC 2234178: Experimental Crystal Structure Determination

description: Related Article: Chaowei Yin, Hanwei Lu, Hebo Ye, Zelin Feng, Hanxun Zou, Meilan Zhang, Lei You|2023|Org.Lett.|25|1470|doi:10.1021/acs.orglett.3c00205
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5517/ccdc.csd.cc2f3ddc
title: CCDC 2237592: Experimental Crystal Structure Determination

description: Related Article: Luo-Yu Wang, Jiapei Miao, Yu Zhao, Bin-Miao Yang|2023|Org.Lett.|25|1553|doi:10.1021/acs.orglett.3c00237
description: An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
DOI: 10.5519/qd.nh5cv9ea
title: Query on the Natural History Museum Data Portal (data.nhm.ac.uk) (1 records)
DOI: 10.5281/zenodo.7723277
title: Supplementary data and code to "Known allosteric proteins have central roles in genetic disease" by G. Abrusan, D. Ascher and M. Inouye, PLOS Computational Biology 18(2):e1009806.

description: Scripts and data to reproduce the figures and supplementary figures of "G. Abrusan, D. Ascher and M. Inouye (2022) Known allosteric proteins have central roles in genetic disease." PLOS Computational Biology 18(2):e1009806. https://doi.org/10.1371/journal.pcbi.1009806.
DOI: 10.5281/zenodo.7723276
title: Supplementary data and code to "Known allosteric proteins have central roles in genetic disease" by G. Abrusan, D. Ascher and M. Inouye, PLOS Computational Biology 18(2):e1009806.

description: Scripts and data to reproduce the figures and supplementary figures of "G. Abrusan, D. Ascher and M. Inouye (2022) Known allosteric proteins have central roles in genetic disease." PLOS Computational Biology 18(2):e1009806. https://doi.org/10.1371/journal.pcbi.1009806.
DOI: 10.5281/zenodo.7741635
title: Sample of 100 place names from 'special maps' by Charles Perthées (1:225,000, 1783-1804)

description: The dataset contains a sample of 100 place names from ‘special maps’ by Charles Perthées (1:225,000, 1783-1804). Place names are supplemented with possible matches from the “National Register of Geographical Names” (NRGM) or the "Historical Atlas of Poland (HAP). There are 19 266 matches for 100 place names. 85 of them have 'certain' or 'uncertain' matches and 15 remained unmatched and, therefore, not geocoded.
description: {"references": ["https://perthees.ihpan.edu.pl/?page_id=593&lang=en"]}
DOI: 10.5281/zenodo.7594901
title: Sample of 100 place names from 'special maps' by Charles Perthées (1:225,000, 1783-1804)

description: The dataset contains a sample of 100 place names from ‘special maps’ by Charles Perthées (1:225,000, 1783-1804). Place names are supplemented with possible matches from the “National Register of Geographical Names” (NRGM) or the "Historical Atlas of Poland (HAP). There are 19 266 matches for 100 place names. 85 of them have 'certain' or 'uncertain' matches and 15 remained unmatched and, therefore, not geocoded.
description: {"references": ["https://perthees.ihpan.edu.pl/?page_id=593&lang=en"]}
DOI: 10.5281/zenodo.7736203
title: Transcripciones de entrevistas de incidentes críticos de mujeres latinoamericanas migrantes en Alemania

description: Las siguientes transcripciones corresponden a un corpus de nueve entrevistas en las que mujeres latinoamericanas migrantes en Alemania fueron preguntas por incidentes críticos. El cuestionario utilizado para la investigación también se encuentra disponible junto con las transcripcciones. The following transcripts are part of a corpus of nine interviews in which migrant Latin American women in Germany were questioned about critical incidents. The questionnaire used for the investigation is also available along with the transcripts.
DOI: 10.5281/zenodo.7736202
title: Transcripciones de entrevistas de incidentes críticos de mujeres latinoamericanas migrantes en Alemania

description: Las siguientes transcripciones corresponden a un corpus de nueve entrevistas en las que mujeres latinoamericanas migrantes en Alemania fueron preguntas por incidentes críticos. El cuestionario utilizado para la investigación también se encuentra disponible junto con las transcripcciones. The following transcripts are part of a corpus of nine interviews in which migrant Latin American women in Germany were questioned about critical incidents. The questionnaire used for the investigation is also available along with the transcripts.
DOI: 10.5281/zenodo.6604707
title: AIO INDEX: Early Kadamba inscriptions

description: <strong>AIO INDEX</strong>: Early Kadamba inscriptions, with hyperlinks to texts and object data.
description: Epigraphic data in AIO is organised into individual Communities, with each community focusing on a specific site, region, language, dynasty or theme. The data in each community is curated by the contributors; indexes are prepared when the entries are sufficiently developed to benefit from an indexing guide.
DOI: 10.5281/zenodo.6604708
title: AIO INDEX: Early Kadamba inscriptions

description: <strong>AIO INDEX</strong>: Early Kadamba inscriptions, with hyperlinks to texts and object data.
description: Epigraphic data in AIO is organised into individual Communities, with each community focusing on a specific site, region, language, dynasty or theme. The data in each community is curated by the contributors; indexes are prepared when the entries are sufficiently developed to benefit from an indexing guide.
DOI: 10.5281/zenodo.7744505
title: AKM Dataset: Textureless Space Target Dataset

description: AKM dataset.<br> <br> The target in this dataset is the AKM motor (similar to the STAR 24 motor), a radially symmetric and textureless space object. The motor dimensions include a diameter of 24.5 inches (0.62 m) and a length of 42.0 (1.0668 m). The dataset is generated using Blender with lighting conditions similar to the orbital environment. The dataset contains 10000 images with an image size of 1024 x 1024 pixels, rendered with a pin-hole camera model having a field of view of 55 degrees. The target positions are obtained from a uniform random distribution between 1m and 10 m, and orientations are obtained from a uniform random distribution.<br> <pre><code>@inproceedings{rathinam2022pose, title={Pose Estimation of a Known Texture-Less Space Target using Convolutional Neural Networks}, author={Rathinam, Arunkumar and Gaudilliere, Vincent and Pauly, Leo and Aouada, Djamila}, booktitle={73rd International Astronautical Congress, Paris 18-22 September 2022}, year={2022} }</code></pre>