cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.15468/dl.3musp4
title: Occurrence Download

description: A dataset containing 27140 species occurrences available in GBIF matching the query:
{
 "and" : [
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "OccurrenceStatus is Present",
 "TaxonKey is Carpobrotus edulis (L.) N.E.Br."
 ]
}

 The dataset includes 27140 records from 223 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0039044-231002084531237/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.h8a4hk
title: Occurrence Download

description: A dataset containing 103728 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Geometry POLYGON((-102.77069 18.81602,-100.93464 18.81602,-100.93464 20.1401,-102.77069 20.1401,-102.77069 18.81602))",
 "TaxonKey is Plantae"
 ]
}

 The dataset includes 103728 records from 232 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0055469-231002084531237/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.m8lvz1
title: Occurrence Download

description: A dataset containing 2395100 species occurrences available in GBIF matching the query:
{
 "and" : [
 "TaxonKey is Carex L.",
 "BasisOfRecord is Human Observation"
 ]
}

 The dataset includes 2395100 records from 423 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0006915-160623103540712/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.chg4uy
title: Occurrence Download

description: A dataset containing 615 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Colombia",
 "OccurrenceStatus is Present",
 "TaxonKey is Panthera onca (Linnaeus, 1758)",
 "Year 2018-2025"
 ]
}

 The dataset includes 615 records from 44 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003383-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.d6ehdu
title: Occurrence Download

description: A dataset containing 2223 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Goodea atripinnis Jordan, 1880"
 ]
}

 The dataset includes 2223 records from 39 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003384-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.8suzfu
title: Occurrence Download

description: A dataset containing 91 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is China",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "OccurrenceStatus is Present",
 "TaxonKey is Equisetum fluviatile L."
 ]
}

 The dataset includes 91 records from 5 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003385-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.z9c665
title: Occurrence Download

description: A dataset containing 223 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Calyptospadix cerulea Clarke, 1882"
 ]
}

 The dataset includes 223 records from 30 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003386-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.jwtyec
title: Occurrence Download

description: A dataset containing 819 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Girardinichthys multiradiatus (Meek, 1904)"
 ]
}

 The dataset includes 819 records from 35 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003387-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.fcqk2q
title: Occurrence Download

description: A dataset containing 248 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Skiffia lermae Meek, 1902"
 ]
}

 The dataset includes 248 records from 22 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003388-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.sqg373
title: Occurrence Download

description: A dataset containing 824 species occurrences available in GBIF matching the query:
{
 "TaxonKey" : [
 "is Xenotoca variata (Bean, 1887)"
 ]
}

 The dataset includes 824 records from 38 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003389-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.6084/m9.figshare.5102944.v3
title: Prdx1 (peroxiredoxin 1) deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux

description: Oxidative stress activates macroautophagy/autophagy and contributes to atherogenesis via lipophagic flux, a form of lipid removal by autophagy. However, it is not known exactly how endogenous antioxidant enzymes are involved in lipophagic flux. Here, we demonstrate that the antioxidant PRDX1 (peroxiredoxin 1) has a crucial role in the maintenance of lipophagic flux in macrophages. PRDX1 is more highly expressed than other antioxidant enzymes in monocytes and macrophages. We determined that <i>Prdx1</i> deficiency induced excessive oxidative stress and impaired maintenance of autophagic flux in macrophages. <i>Prdx1</i>-deficient macrophages had higher intracellular cholesterol mass and lower cholesterol efflux compared with wild type. This perturbation in cholesterol homeostasis was due to impaired lipophagic cholesterol hydrolysis caused by excessive oxidative stress, resulting in the inhibition of free cholesterol formation and the reduction of NR1H3 (nuclear receptor subfamily 1, group H, member 3) activity. Notably, impairment of both lipophagic flux and cholesterol efflux was restored by the 2-Cys PRDX-mimics ebselen and gliotoxin. Consistent with this observation, <i>apoe <sup>−/−</sup>
</i> mice transplanted with bone marrow from <i>prdx1<sup>−/−</sup>apoe<sup>−/−</sup>
</i> mice had increased plaque formation compared with <i>apoe<sup>−/−</sup>
</i> BM-transplanted recipients. This study reveals that PRDX1 is crucial to regulating lipophagic flux and maintaining macrophage cholesterol homeostasis against oxidative stress. We suggest that PRDX1-dependent control of oxidative stress may provide a strategy for treating atherosclerosis and autophagy-related human diseases.
DOI: 10.6084/m9.figshare.5962453
title: Antioxidant role of autophagy in maintaining the integrity of glomerular capillaries

description: Autophagy is a lysosomal degradation system by which cytosolic materials and damaged organelles are broken down into basic components. To explore the physiological role of autophagy in glomerular endothelial cells (GEnCs), we compared the autophagic flux among cells in the kidney under starvation. Inhibition of autophagy by chloroquine administration significantly increased the number of autophagosomes or autolysosomes in GEnCs and proximal tubular cells, but not in podocytes, suggesting that the GEnCs exhibit substantial autophagic activity. Next, we analyzed endothelial and hematopoietic cell-specific <i>atg5</i>-deficient mice (<i>atg5</i>-conditional KO [cKO] mice). Glomeruli of 4-wk-old <i>atg5</i>-cKO mice exhibited slightly distended capillary loops accompanied by an accumulation of reactive oxygen species (ROS). Glomeruli of 8-wk-old <i>atg5</i>-cKO mice showed a lobular pattern with thickening of the capillary loops and mesangial matrix expansion; however, the vasculature of other organs was preserved. The <i>atg5</i>-cKO mice died by 12 wk of age, presumably due to pancytopenia resulting from the defect in their hematopoietic lineages. Therefore, we subjected 4-wk <i>atg5</i>-cKO mice to irradiation followed by bone marrow transplantation from normal littermates. Transplanted mice recapitulated the glomerular phenotypes of the <i>atg5</i>-cKO mice with no obvious histological changes in other organs. Twelve-mo-old transplanted mice developed mesangiolysis and glomerulosclerosis with significant deterioration of kidney function. Administration of N-acetyl-l-cysteine, a ROS scavenger, to <i>atg5</i>-cKO mice rescued the glomerular phenotypes. These data suggest that endothelial autophagy protects glomeruli from oxidative stress and maintains the integrity of glomerular capillaries. Enhancing endothelial autophagy may provide a novel therapeutic approach to minimizing glomerular diseases.
DOI: 10.6084/m9.figshare.5102944
title: Prdx1 (peroxiredoxin 1) deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux

description: Oxidative stress activates macroautophagy/autophagy and contributes to atherogenesis via lipophagic flux, a form of lipid removal by autophagy. However, it is not known exactly how endogenous antioxidant enzymes are involved in lipophagic flux. Here, we demonstrate that the antioxidant PRDX1 (peroxiredoxin 1) has a crucial role in the maintenance of lipophagic flux in macrophages. PRDX1 is more highly expressed than other antioxidant enzymes in monocytes and macrophages. We determined that <i>Prdx1</i> deficiency induced excessive oxidative stress and impaired maintenance of autophagic flux in macrophages. <i>Prdx1</i>-deficient macrophages had higher intracellular cholesterol mass and lower cholesterol efflux compared with wild type. This perturbation in cholesterol homeostasis was due to impaired lipophagic cholesterol hydrolysis caused by excessive oxidative stress, resulting in the inhibition of free cholesterol formation and the reduction of NR1H3 (nuclear receptor subfamily 1, group H, member 3) activity. Notably, impairment of both lipophagic flux and cholesterol efflux was restored by the 2-Cys PRDX-mimics ebselen and gliotoxin. Consistent with this observation, <i>apoe <sup>−/−</sup>
</i> mice transplanted with bone marrow from <i>prdx1<sup>−/−</sup>apoe<sup>−/−</sup>
</i> mice had increased plaque formation compared with <i>apoe<sup>−/−</sup>
</i> BM-transplanted recipients. This study reveals that PRDX1 is crucial to regulating lipophagic flux and maintaining macrophage cholesterol homeostasis against oxidative stress. We suggest that PRDX1-dependent control of oxidative stress may provide a strategy for treating atherosclerosis and autophagy-related human diseases.
DOI: 10.6084/m9.figshare.5962453.v1
title: Antioxidant role of autophagy in maintaining the integrity of glomerular capillaries

description: Autophagy is a lysosomal degradation system by which cytosolic materials and damaged organelles are broken down into basic components. To explore the physiological role of autophagy in glomerular endothelial cells (GEnCs), we compared the autophagic flux among cells in the kidney under starvation. Inhibition of autophagy by chloroquine administration significantly increased the number of autophagosomes or autolysosomes in GEnCs and proximal tubular cells, but not in podocytes, suggesting that the GEnCs exhibit substantial autophagic activity. Next, we analyzed endothelial and hematopoietic cell-specific <i>atg5</i>-deficient mice (<i>atg5</i>-conditional KO [cKO] mice). Glomeruli of 4-wk-old <i>atg5</i>-cKO mice exhibited slightly distended capillary loops accompanied by an accumulation of reactive oxygen species (ROS). Glomeruli of 8-wk-old <i>atg5</i>-cKO mice showed a lobular pattern with thickening of the capillary loops and mesangial matrix expansion; however, the vasculature of other organs was preserved. The <i>atg5</i>-cKO mice died by 12 wk of age, presumably due to pancytopenia resulting from the defect in their hematopoietic lineages. Therefore, we subjected 4-wk <i>atg5</i>-cKO mice to irradiation followed by bone marrow transplantation from normal littermates. Transplanted mice recapitulated the glomerular phenotypes of the <i>atg5</i>-cKO mice with no obvious histological changes in other organs. Twelve-mo-old transplanted mice developed mesangiolysis and glomerulosclerosis with significant deterioration of kidney function. Administration of N-acetyl-l-cysteine, a ROS scavenger, to <i>atg5</i>-cKO mice rescued the glomerular phenotypes. These data suggest that endothelial autophagy protects glomeruli from oxidative stress and maintains the integrity of glomerular capillaries. Enhancing endothelial autophagy may provide a novel therapeutic approach to minimizing glomerular diseases.
DOI: 10.6084/m9.figshare.5102944.v2
title: Prdx1 (peroxiredoxin 1) deficiency reduces cholesterol efflux via impaired macrophage lipophagic flux

description: Oxidative stress activates macroautophagy/autophagy and contributes to atherogenesis via lipophagic flux, a form of lipid removal by autophagy. However, it is not known exactly how endogenous antioxidant enzymes are involved in lipophagic flux. Here, we demonstrate that the antioxidant PRDX1 (peroxiredoxin 1) has a crucial role in the maintenance of lipophagic flux in macrophages. PRDX1 is more highly expressed than other antioxidant enzymes in monocytes and macrophages. We determined that <i>Prdx1</i> deficiency induced excessive oxidative stress and impaired maintenance of autophagic flux in macrophages. <i>Prdx1</i>-deficient macrophages had higher intracellular cholesterol mass and lower cholesterol efflux compared with wild type. This perturbation in cholesterol homeostasis was due to impaired lipophagic cholesterol hydrolysis caused by excessive oxidative stress, resulting in the inhibition of free cholesterol formation and the reduction of NR1H3 (nuclear receptor subfamily 1, group H, member 3) activity. Notably, impairment of both lipophagic flux and cholesterol efflux was restored by the 2-Cys PRDX-mimics ebselen and gliotoxin. Consistent with this observation, <i>apoe <sup>−/−</sup></i> mice transplanted with bone marrow from <i>prdx1<sup>−/−</sup>apoe<sup>−/−</sup></i> mice had increased plaque formation compared with <i>apoe<sup>−/−</sup></i> BM-transplanted recipients. This study reveals that PRDX1 is crucial to regulating lipophagic flux and maintaining macrophage cholesterol homeostasis against oxidative stress. We suggest that PRDX1-dependent control of oxidative stress may provide a strategy for treating atherosclerosis and autophagy-related human diseases.
DOI: 10.6084/m9.figshare.5619739.v3
title: Regulation of BECN1-mediated autophagy by HSPB6: Insights from a human HSPB6<sup>S10F</sup> mutant

description: HSPB6/Hsp20 (heat shock protein family B [small] member 6) has emerged as a novel cardioprotector against stress-induced injury. We identified a human mutant of HSPB6 (HSPB6<sup>S10F</sup>) exclusively present in dilated cardiomyopathy (DCM) patients. Cardiac expression of this mutant in mouse hearts resulted in remodeling and dysfunction, which progressed to heart failure and early death. These detrimental effects were associated with reduced interaction of mutant HSPB6<sup>S10F</sup> with BECN1/Beclin 1, leading to BECN1 ubiquitination and its proteosomal degradation. As a result, autophagy flux was substantially inhibited and apoptosis was increased in HSPB6<sup>S10F</sup>-mutant hearts. In contrast, overexpression of wild-type HSPB6 (HSPB6 WT) not only increased BECN1 levels, but also competitively suppressed binding of BECN1 to BCL2, resulting in stimulated autophagy. Indeed, preinhibition of autophagy attenuated the cardioprotective effects of HSPB6 WT. Taken together, these findings reveal a new regulatory mechanism of HSPB6 in cell survival through its interaction with BECN1. Furthermore, Ser10 appears to be crucial for the protective effects of HSPB6 and transversion of this amino acid to Phe contributes to cardiomyopathy.
DOI: 10.6084/m9.figshare.5619739
title: Regulation of BECN1-mediated autophagy by HSPB6: Insights from a human HSPB6<sup>S10F</sup> mutant

description: HSPB6/Hsp20 (heat shock protein family B [small] member 6) has emerged as a novel cardioprotector against stress-induced injury. We identified a human mutant of HSPB6 (HSPB6<sup>S10F</sup>) exclusively present in dilated cardiomyopathy (DCM) patients. Cardiac expression of this mutant in mouse hearts resulted in remodeling and dysfunction, which progressed to heart failure and early death. These detrimental effects were associated with reduced interaction of mutant HSPB6<sup>S10F</sup> with BECN1/Beclin 1, leading to BECN1 ubiquitination and its proteosomal degradation. As a result, autophagy flux was substantially inhibited and apoptosis was increased in HSPB6<sup>S10F</sup>-mutant hearts. In contrast, overexpression of wild-type HSPB6 (HSPB6 WT) not only increased BECN1 levels, but also competitively suppressed binding of BECN1 to BCL2, resulting in stimulated autophagy. Indeed, preinhibition of autophagy attenuated the cardioprotective effects of HSPB6 WT. Taken together, these findings reveal a new regulatory mechanism of HSPB6 in cell survival through its interaction with BECN1. Furthermore, Ser10 appears to be crucial for the protective effects of HSPB6 and transversion of this amino acid to Phe contributes to cardiomyopathy.
DOI: 10.6084/m9.figshare.5619739.v2
title: Regulation of BECN1-mediated autophagy by HSPB6: Insights from a human HSPB6<sup>S10F</sup> mutant

description: HSPB6/Hsp20 (heat shock protein family B [small] member 6) has emerged as a novel cardioprotector against stress-induced injury. We identified a human mutant of HSPB6 (HSPB6<sup>S10F</sup>) exclusively present in dilated cardiomyopathy (DCM) patients. Cardiac expression of this mutant in mouse hearts resulted in remodeling and dysfunction, which progressed to heart failure and early death. These detrimental effects were associated with reduced interaction of mutant HSPB6<sup>S10F</sup> with BECN1/Beclin 1, leading to BECN1 ubiquitination and its proteosomal degradation. As a result, autophagy flux was substantially inhibited and apoptosis was increased in HSPB6<sup>S10F</sup>-mutant hearts. In contrast, overexpression of wild-type HSPB6 (HSPB6 WT) not only increased BECN1 levels, but also competitively suppressed binding of BECN1 to BCL2, resulting in stimulated autophagy. Indeed, preinhibition of autophagy attenuated the cardioprotective effects of HSPB6 WT. Taken together, these findings reveal a new regulatory mechanism of HSPB6 in cell survival through its interaction with BECN1. Furthermore, Ser10 appears to be crucial for the protective effects of HSPB6 and transversion of this amino acid to Phe contributes to cardiomyopathy.
DOI: 10.6084/m9.figshare.5962456
title: The Vici syndrome protein EPG5 regulates intracellular nucleic acid trafficking linking autophagy to innate and adaptive immunity

description: Vici syndrome is a human inherited multi-system disorder caused by recessive mutations in <i>EPG5</i>, encoding the EPG5 protein that mediates the fusion of autophagosomes with lysosomes. Immunodeficiency characterized by lack of memory B cells and increased susceptibility to infection is an integral part of the condition, but the role of EPG5 in the immune system remains unknown. Here we show that EPG5 is indispensable for the transport of the TLR9 ligand CpG to the late endosomal-lysosomal compartment, and for TLR9-initiated signaling, a step essential for the survival of human memory B cells and their ultimate differentiation into plasma cells. Moreover, the predicted structure of EPG5 includes a membrane remodeling domain and a karyopherin-like domain, thus explaining its function as a carrier between separate vesicular compartments. Our findings indicate that EPG5, by controlling nucleic acids intracellular trafficking, links macroautophagy/autophagy to innate and adaptive immunity.
DOI: 10.6084/m9.figshare.5962456.v1
title: The Vici syndrome protein EPG5 regulates intracellular nucleic acid trafficking linking autophagy to innate and adaptive immunity

description: Vici syndrome is a human inherited multi-system disorder caused by recessive mutations in <i>EPG5</i>, encoding the EPG5 protein that mediates the fusion of autophagosomes with lysosomes. Immunodeficiency characterized by lack of memory B cells and increased susceptibility to infection is an integral part of the condition, but the role of EPG5 in the immune system remains unknown. Here we show that EPG5 is indispensable for the transport of the TLR9 ligand CpG to the late endosomal-lysosomal compartment, and for TLR9-initiated signaling, a step essential for the survival of human memory B cells and their ultimate differentiation into plasma cells. Moreover, the predicted structure of EPG5 includes a membrane remodeling domain and a karyopherin-like domain, thus explaining its function as a carrier between separate vesicular compartments. Our findings indicate that EPG5, by controlling nucleic acids intracellular trafficking, links macroautophagy/autophagy to innate and adaptive immunity.
DOI: 10.15468/dl.wjzzuz
title: Occurrence Download

description: A dataset containing 370797 species occurrences available in GBIF matching the query:
{
 "and" : [
 "DatasetKey is iNaturalist Research-grade Observations",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "Country is one of (Canada, Mexico, United States of America)",
 "EventDate is greater than or equal to 2024-12-03",
 "EventDate is less than or equal to 2025-01-02",
 {
 "not" : {
 "Issue" : [
 "is one of (Basis of record invalid, Coordinate reprojection failed, Coordinate reprojection suspicious, Coordinate precision invalid, Coordinate uncertainty meters invalid, Country mismatch, Country invalid, Geodetic datum invalid, Presumed swapped coordinate, Presumed negated longitude, Presumed negated latitude, Country coordinate mismatch)"
 ]
 }
 }
 ]
}

 The dataset includes 370797 records from 1 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003381-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.b696j6
title: Occurrence Download

description: A dataset containing 2408 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Mexico",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "TaxonKey is Cynomys mexicanus Merriam, 1892"
 ]
}

 The dataset includes 2408 records from 20 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003390-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.me2s6k
title: Occurrence Download

description: A dataset containing 1215 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Mexico",
 "TaxonKey is Lepomis macrochirus Rafinesque, 1819"
 ]
}

 The dataset includes 1215 records from 41 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003392-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.
DOI: 10.15468/dl.drnxqp
title: Occurrence Download

description: A dataset containing 4772 species occurrences available in GBIF matching the query:
{
 "and" : [
 "Country is Mexico",
 "HasCoordinate is true",
 "HasGeospatialIssue is false",
 "TaxonKey is Procyon lotor (Linnaeus, 1758)"
 ]
}

 The dataset includes 4772 records from 94 constituent datasets; see https://api.gbif.org/v1/occurrence/download/0003393-250127130748423/datasets/export for details.
 
Data from some individual datasets included in this download may be licensed under less restrictive terms.