cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.25573/data.10042616.v4
title: Fortuna, Tower_Solar Radiation, Pyranometer

description: Fortuna station (Centro de Investigaciones Jorge L. Arauz)<br>Tower<br>Location: 8° 43.340'N, 82° 14.241'W<br>Solar Radiation, Pyranometer, Interval max/min/avg<br><br>Located in the highlands of the Chiriqui Province, in western Panama.There are three sensor locations: north clearing, south clearing, and a 15m tower.<br>
DOI: 10.5517/ccdc.csd.cc252bm7
title: CCDC 1998248: Experimental Crystal Structure Determination

description: Related Article: Alicia M. W. Dufter-Münster, Alexander G. Harter, Thomas M. Klapötke, Elena Reinhardt, Julia Römer, Jörg Stierstorfer|2022|Eur.J.Inorg.Chem.|2022|e202101048|doi:10.1002/ejic.202101048
DOI: 10.5517/ccdc.csd.cc25vp0r
title: CCDC 2021634: Experimental Crystal Structure Determination

description: Related Article: Alicia M. W. Dufter-Münster, Alexander G. Harter, Thomas M. Klapötke, Elena Reinhardt, Julia Römer, Jörg Stierstorfer|2022|Eur.J.Inorg.Chem.|2022|e202101048|doi:10.1002/ejic.202101048
DOI: 10.5517/ccdc.csd.cc25vp1s
title: CCDC 2021635: Experimental Crystal Structure Determination

description: Related Article: Alicia M. W. Dufter-Münster, Alexander G. Harter, Thomas M. Klapötke, Elena Reinhardt, Julia Römer, Jörg Stierstorfer|2022|Eur.J.Inorg.Chem.|2022|e202101048|doi:10.1002/ejic.202101048
DOI: 10.5517/ccdc.csd.cc25vp2t
title: CCDC 2021636: Experimental Crystal Structure Determination

description: Related Article: Alicia M. W. Dufter-Münster, Alexander G. Harter, Thomas M. Klapötke, Elena Reinhardt, Julia Römer, Jörg Stierstorfer|2022|Eur.J.Inorg.Chem.|2022|e202101048|doi:10.1002/ejic.202101048
DOI: 10.5517/ccdc.csd.cc25vp3v
title: CCDC 2021637: Experimental Crystal Structure Determination

description: Related Article: Alicia M. W. Dufter-Münster, Alexander G. Harter, Thomas M. Klapötke, Elena Reinhardt, Julia Römer, Jörg Stierstorfer|2022|Eur.J.Inorg.Chem.|2022|e202101048|doi:10.1002/ejic.202101048
DOI: 10.5517/ccdc.csd.cc27yd0m
title: CCDC 2083820: Experimental Crystal Structure Determination

description: Related Article: Florian Goerigk, Nicholas Birchall, Christoph M. Feil, Martin Nieger, Dietrich Gudat|2022|Eur.J.Inorg.Chem.|2022|e202101026|doi:10.1002/ejic.202101026
DOI: 10.5517/ccdc.csd.cc27yd1n
title: CCDC 2083821: Experimental Crystal Structure Determination

description: Related Article: Florian Goerigk, Nicholas Birchall, Christoph M. Feil, Martin Nieger, Dietrich Gudat|2022|Eur.J.Inorg.Chem.|2022|e202101026|doi:10.1002/ejic.202101026
DOI: 10.5517/ccdc.csd.cc27yd2p
title: CCDC 2083822: Experimental Crystal Structure Determination

description: Related Article: Florian Goerigk, Nicholas Birchall, Christoph M. Feil, Martin Nieger, Dietrich Gudat|2022|Eur.J.Inorg.Chem.|2022|e202101026|doi:10.1002/ejic.202101026
DOI: 10.5517/ccdc.csd.cc27yd4r
title: CCDC 2083824: Experimental Crystal Structure Determination

description: Related Article: Florian Goerigk, Nicholas Birchall, Christoph M. Feil, Martin Nieger, Dietrich Gudat|2022|Eur.J.Inorg.Chem.|2022|e202101026|doi:10.1002/ejic.202101026
DOI: 10.5517/ccdc.csd.cc28j713
title: CCDC 2100964: Experimental Crystal Structure Determination

description: Related Article: Sanjit Das, Dinesh Nugegoda, Wenzhi Yao, Fengrui Qu, Matthew T. Figgins, Robert W. Lamb, Charles Edwin Webster, Jared H. Delcamp, Elizabeth T. Papish|2022|Eur.J.Inorg.Chem.|2022|e202101016|doi:10.1002/ejic.202101016
DOI: 10.5517/ccdc.csd.cc28j724
title: CCDC 2100965: Experimental Crystal Structure Determination

description: Related Article: Sanjit Das, Dinesh Nugegoda, Wenzhi Yao, Fengrui Qu, Matthew T. Figgins, Robert W. Lamb, Charles Edwin Webster, Jared H. Delcamp, Elizabeth T. Papish|2022|Eur.J.Inorg.Chem.|2022|e202101016|doi:10.1002/ejic.202101016
DOI: 10.5517/ccdc.csd.cc28j735
title: CCDC 2100966: Experimental Crystal Structure Determination

description: Related Article: Sanjit Das, Dinesh Nugegoda, Wenzhi Yao, Fengrui Qu, Matthew T. Figgins, Robert W. Lamb, Charles Edwin Webster, Jared H. Delcamp, Elizabeth T. Papish|2022|Eur.J.Inorg.Chem.|2022|e202101016|doi:10.1002/ejic.202101016
DOI: 10.5517/ccdc.csd.cc28j746
title: CCDC 2100967: Experimental Crystal Structure Determination

description: Related Article: Sanjit Das, Dinesh Nugegoda, Wenzhi Yao, Fengrui Qu, Matthew T. Figgins, Robert W. Lamb, Charles Edwin Webster, Jared H. Delcamp, Elizabeth T. Papish|2022|Eur.J.Inorg.Chem.|2022|e202101016|doi:10.1002/ejic.202101016
DOI: 10.5517/ccdc.csd.cc28j757
title: CCDC 2100968: Experimental Crystal Structure Determination

description: Related Article: Sanjit Das, Dinesh Nugegoda, Wenzhi Yao, Fengrui Qu, Matthew T. Figgins, Robert W. Lamb, Charles Edwin Webster, Jared H. Delcamp, Elizabeth T. Papish|2022|Eur.J.Inorg.Chem.|2022|e202101016|doi:10.1002/ejic.202101016
DOI: 10.5517/ccdc.csd.cc28j768
title: CCDC 2100969: Experimental Crystal Structure Determination

description: Related Article: Sanjit Das, Dinesh Nugegoda, Wenzhi Yao, Fengrui Qu, Matthew T. Figgins, Robert W. Lamb, Charles Edwin Webster, Jared H. Delcamp, Elizabeth T. Papish|2022|Eur.J.Inorg.Chem.|2022|e202101016|doi:10.1002/ejic.202101016
DOI: 10.5517/ccdc.csd.cc28zxw2
title: CCDC 2115095: Experimental Crystal Structure Determination

description: Related Article: Zhou Lu, Alfredo Burini, Roy N. McDougald, Simone Ricci, Lorenzo Luciani, Vladimir N. Nesterov, Abdel-Monem M. Rawashdeh, Mohammad A. Omary, Rossana Galassi|2022|Eur.J.Inorg.Chem.|2022|e202101056|doi:10.1002/ejic.202101056
DOI: 10.5517/ccdc.csd.cc29b2wm
title: CCDC 2124860: Experimental Crystal Structure Determination

description: Related Article: Nabin Sarkar, Rajata Kumar Sahoo, Sayantan Mukhopadhyay, Sharanappa Nembenna|2022|Eur.J.Inorg.Chem.|2022|e202101030|doi:10.1002/ejic.202101030
DOI: 10.5517/ccdc.csd.cc29b2xn
title: CCDC 2124861: Experimental Crystal Structure Determination

description: Related Article: Nabin Sarkar, Rajata Kumar Sahoo, Sayantan Mukhopadhyay, Sharanappa Nembenna|2022|Eur.J.Inorg.Chem.|2022|e202101030|doi:10.1002/ejic.202101030
DOI: 10.5517/ccdc.csd.cc29bdsv
title: CCDC 2125167: Experimental Crystal Structure Determination

description: Related Article: Julien Egly, Weighang Chen, Aline Maisse-François, Stéphane Bellemin-Laponnaz, Thierry Achard|2022|Eur.J.Inorg.Chem.|2022|e202101033|doi:10.1002/ejic.202101033
DOI: 10.5517/ccdc.csd.cc29cvdy
title: CCDC 2126550: Experimental Crystal Structure Determination

description: Related Article: Julia Mahrholdt, Eduard Kovalski, Tobias Rüffer, Valerije Vrček, Heinrich Lang|2022|Eur.J.Inorg.Chem.|2022|e202101059|doi:10.1002/ejic.202101059
DOI: 10.25573/data.10042634
title: Fortuna, Tower_Wind Speed

description: Fortuna station (Centro de Investigaciones Jorge L. Arauz)<br>Tower<br>Location: 8° 43.340'N, 82° 14.241'W<br>Wind Speed, Interval max/min/avg<br><br>Located in the highlands of the Chiriqui Province, in western Panama.There are three sensor locations: north clearing, south clearing, and a 15m tower.<br>
DOI: 10.25573/data.10042634.v5
title: Fortuna, Tower_Wind Speed

description: Fortuna station (Centro de Investigaciones Jorge L. Arauz)<br>Tower<br>Location: 8° 43.340'N, 82° 14.241'W<br>Wind Speed, Interval max/min/avg<br><br>Located in the highlands of the Chiriqui Province, in western Panama.There are three sensor locations: north clearing, south clearing, and a 15m tower.<br>
DOI: 10.25573/data.10042634.v4
title: Fortuna, Tower_Wind Speed

description: Fortuna station (Centro de Investigaciones Jorge L. Arauz)<br>Tower<br>Location: 8° 43.340'N, 82° 14.241'W<br>Wind Speed, Interval max/min/avg<br><br>Located in the highlands of the Chiriqui Province, in western Panama.There are three sensor locations: north clearing, south clearing, and a 15m tower.<br>
DOI: 10.6084/m9.figshare.13256741
title: F4. watersheds

description: Watersheds geodatabase<br><br><br>Versioning Note<br>Version 2 includes an updated watersheds.gdb.zip with the following changes:1. the projection, WGS_1984_Web_Mercator_Auxiliary_Sphere has been changed to GCS_WGS_19842. NULL values in the 'dd' field have been replaced with '0'<br>
DOI: 10.6084/m9.figshare.13256741.v2
title: F4. watersheds

description: Watersheds geodatabase<br><br><br>Versioning Note<br>Version 2 includes an updated watersheds.gdb.zip with the following changes:1. the projection, WGS_1984_Web_Mercator_Auxiliary_Sphere has been changed to GCS_WGS_19842. NULL values in the 'dd' field have been replaced with '0'<br>
DOI: 10.6084/m9.figshare.13256741.v1
title: F4. watersheds

description: Watersheds geodatabase
DOI: 10.5281/zenodo.6359971
title: Characterizing and explaining impact of disease-associated mutations in proteins without known structures or structural homologues

description: AlphaFold and RoseTTAFold models of domains of disease associated human proteins without structures/known homologues. Tables containing the model quality, model region, sequence alignment statistics, matched FunFam, associated GO terms for the FunFam, ddG of mutation, pathogenicity of mutation, if mutation is near a predicted functional site (conserved residue/ligand binding site/protein-protein interface)
DOI: 10.5281/zenodo.5708831
title: Characterizing and explaining impact of disease-associated mutations in proteins without known structures or structural homologues

description: AlphaFold and RoseTTAFold models of domains of disease associated human proteins without structures/known homologues. Tables containing the model quality, model region, sequence alignment statistics, matched FunFam, associated GO terms for the FunFam, ddG of mutation, pathogenicity of mutation, if mutation is near a predicted functional site (conserved residue/ligand binding site/protein-protein interface)
DOI: 10.6084/m9.figshare.14750852.v1
title: Enhanced autophagy in <i>Becn1<sup>F121A/F121A</sup></i> knockin mice counteracts aging-related neural stem cell exhaustion and dysfunction

description: Macroautophagy/autophagy is emerging as a major pathway that regulates both aging and stem cell function. Previous studies have demonstrated a positive correlation of autophagy with longevity; however, these studies did not directly address the consequence of altered autophagy in stem cells during aging. In this study, we used <i>Becn1<sup>F121A/F121A</sup></i> knockin mice (designated as <i>Becn1</i> KI mice) with the F121A allele in the autophagy gene <i>Becn1</i> to investigate the consequences of enhanced autophagy in postnatal neural stem cells (NSCs) during aging. We found that increased autophagy protected NSCs from exhaustion and promoted neurogenesis in old (≥18-months-old) mice compared with age-matched wild-type (WT) mice, although it did not affect NSCs in young (3-months-old) mice. After pharmacologically-induced elimination of proliferative cells in the subventricular zone (SVZ), there was enhanced re-activation of quiescent NSCs in old <i>Becn</i><i>1</i> KI mice as compared to those in WT mice, with more efficient exit from quiescent status to generate proliferative cells and neuroblasts. Moreover, there was also improved maintenance and increased neuronal differentiation of NSCs isolated from the SVZ of old <i>Becn1</i> KI mice in <i>in vitro</i> assays. Lastly, the increased neurogenesis in <i>Becn1</i> KI mice was associated with better olfactory function in aged animals. Together, our results suggest a protective role of increased autophagy in aging NSCs, which may help the development of novel strategies to treat age-related neurodegeneration. <b>Abbreviations:</b> ATG: autophagy related; Baf A<sub>1</sub>: bafilomycin A<sub>1</sub>; <i>Becn1</i>: beclin 1; BrdU: bromodeoxyuridine/5-bromo-2ʹ-deoxyuridine; DCX: doublecortin; GFAP: glial fibrillary acidic protein; GFP: green fluorescent protein; H&E: hematoxylin and eosin; HSCs: hematopoietic stem cells; KI: knockin; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; mo: month; NSCs: neural stem cells; OB: olfactory bulb; RB1CC1: RB1-inducible coiled-coil 1; ROS: reactive oxygen species; SOX2: SRY (sex determining region Y)-box 2; SGZ: subgranular zone; SVZ: subventricular zone; TMZ: temozolomide; WT: wild type.
DOI: 10.6084/m9.figshare.14750852
title: Enhanced autophagy in <i>Becn1<sup>F121A/F121A</sup></i> knockin mice counteracts aging-related neural stem cell exhaustion and dysfunction

description: Macroautophagy/autophagy is emerging as a major pathway that regulates both aging and stem cell function. Previous studies have demonstrated a positive correlation of autophagy with longevity; however, these studies did not directly address the consequence of altered autophagy in stem cells during aging. In this study, we used <i>Becn1<sup>F121A/F121A</sup></i> knockin mice (designated as <i>Becn1</i> KI mice) with the F121A allele in the autophagy gene <i>Becn1</i> to investigate the consequences of enhanced autophagy in postnatal neural stem cells (NSCs) during aging. We found that increased autophagy protected NSCs from exhaustion and promoted neurogenesis in old (≥18-months-old) mice compared with age-matched wild-type (WT) mice, although it did not affect NSCs in young (3-months-old) mice. After pharmacologically-induced elimination of proliferative cells in the subventricular zone (SVZ), there was enhanced re-activation of quiescent NSCs in old <i>Becn</i><i>1</i> KI mice as compared to those in WT mice, with more efficient exit from quiescent status to generate proliferative cells and neuroblasts. Moreover, there was also improved maintenance and increased neuronal differentiation of NSCs isolated from the SVZ of old <i>Becn1</i> KI mice in <i>in vitro</i> assays. Lastly, the increased neurogenesis in <i>Becn1</i> KI mice was associated with better olfactory function in aged animals. Together, our results suggest a protective role of increased autophagy in aging NSCs, which may help the development of novel strategies to treat age-related neurodegeneration. <b>Abbreviations:</b> ATG: autophagy related; Baf A<sub>1</sub>: bafilomycin A<sub>1</sub>; <i>Becn1</i>: beclin 1; BrdU: bromodeoxyuridine/5-bromo-2ʹ-deoxyuridine; DCX: doublecortin; GFAP: glial fibrillary acidic protein; GFP: green fluorescent protein; H&E: hematoxylin and eosin; HSCs: hematopoietic stem cells; KI: knockin; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; mo: month; NSCs: neural stem cells; OB: olfactory bulb; RB1CC1: RB1-inducible coiled-coil 1; ROS: reactive oxygen species; SOX2: SRY (sex determining region Y)-box 2; SGZ: subgranular zone; SVZ: subventricular zone; TMZ: temozolomide; WT: wild type.
DOI: 10.6084/m9.figshare.14714906
title: Epigenetic reader BRD4 supports mycobacterial pathogenesis by co-modulating host lipophagy and angiogenesis

description: <i>Mycobacterium tuberculosis</i> (Mtb)-driven lipid accumulation is intricately associated with the progression of tuberculosis (TB) disease. Although several studies elucidating the mechanisms for lipid droplet (LD) biosynthesis exist, we provide evidence for the significance of their regulated turnover via macroautophagy/autophagy during Mtb infection. We demonstrate that Mtb utilizes EGFR (epidermal growth factor receptor) signaling to induce the expression of the histone acetylation reader, BRD4 (bromodomain containing 4). The EGFR-BRD4 axis suppresses lipid-specific autophagy, and hence favors cellular lipid accumulation. Specifically, we found that pharmacological inhibition or knockdown of <i>Egfr</i> or <i>Brd4</i> enhances autophagic flux and concomitantly decreases cellular LDs that is otherwise maintained at a significant level in chloroquine-treated or <i>Atg5</i> knocked down autophagy-compromised host cells. In line with the enhanced lipophagy, we found that loss of EGFR or BRD4 function restricts mycobacterial burden that is rescued by external replenishment with oleic acid. We also report that the EGFR-BRD4 axis exerts additional effects by modulating pro-angiogenic gene expression and consequently aberrant angiogenesis during mycobacterial infection. This is important in the context of systemic Mtb dissemination as well as for the efficient delivery of anti-mycobacterial therapeutics to the Mtb-rich core of TB granuloma. Finally, utilizing an <i>in vivo</i> mouse model of TB, we show that pharmacological inhibition of EGFR and BRD4 compromises LD buildup via enhanced lipophagy and normalizes angiogenesis, thereby restricting Mtb burden and rescuing mice from severe TB-like pathology. These findings shed light on the novel roles of BRD4 during Mtb infection, and its possible implication in potentiating anti-TB responses. <b>Abbreviations</b>: ATG5: autophagy related 5; BRDs: bromodomain containing; COL18A1: collagen type XVIII alpha 1 chain; EGFR: epidermal growth factor receptor; EP300: E1A binding protein p300; KDR: kinase insert domain receptor; KLF5: Kruppel like factor 5; LDs: lipid droplets; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; Mtb: <i>Mycobacterium tuberculosis</i>; PECAM1: platelet and endothelial cell adhesion molecule 1; SQSTM1/p62: sequestosome 1; TB: tuberculosis; THBS1: thrombospondin 1; VEGF: vascular endothelial growth factor
DOI: 10.6084/m9.figshare.15028702
title: Imbalanced autophagy causes synaptic deficits in a human model for neurodevelopmental disorders

description: Macroautophagy (hereafter referred to as autophagy) is a finely tuned process of programmed degradation and recycling of proteins and cellular components, which is crucial in neuronal function and synaptic integrity. Mounting evidence implicates chromatin remodeling in fine-tuning autophagy pathways. However, this epigenetic regulation is poorly understood in neurons. Here, we investigate the role in autophagy of KANSL1, a member of the nonspecific lethal complex, which acetylates histone H4 on lysine 16 (H4K16ac) to facilitate transcriptional activation. Loss-of-function of KANSL1 is strongly associated with the neurodevelopmental disorder Koolen-de Vries Syndrome (KdVS). Starting from KANSL1-deficient human induced-pluripotent stem cells, both from KdVS patients and genome-edited lines, we identified SOD1 (superoxide dismutase 1), an antioxidant enzyme, to be significantly decreased, leading to a subsequent increase in oxidative stress and autophagosome accumulation. In KANSL1-deficient neurons, autophagosome accumulation at excitatory synapses resulted in reduced synaptic density, reduced GRIA/AMPA receptor-mediated transmission and impaired neuronal network activity. Furthermore, we found that increased oxidative stress-mediated autophagosome accumulation leads to increased MTOR activation and decreased lysosome function, further preventing the clearing of autophagosomes. Finally, by pharmacologically reducing oxidative stress, we could rescue the aberrant autophagosome formation as well as synaptic and neuronal network activity in KANSL1-deficient neurons. Our findings thus point toward an important relation between oxidative stress-induced autophagy and synapse function, and demonstrate the importance of H4K16ac-mediated changes in chromatin structure to balance reactive oxygen species- and MTOR-dependent autophagy. <b>Abbreviations</b>: APO: apocynin; ATG: autophagy related; BAF: bafilomycin A<sub>1</sub>; BSO: buthionine sulfoximine; CV: coefficient of variation; DIV: days in vitro; H4K16ac: histone 4 lysine 16 acetylation; iPSC: induced-pluripotent stem cell; KANSL1: KAT8 regulatory NSL complex subunit 1; KdVS: Koolen-de Vries Syndrome; LAMP1: lysosomal associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MEA: micro-electrode array; MTOR: mechanistic target of rapamycin kinase; NSL complex: nonspecific lethal complex; 8-oxo-dG: 8-hydroxydesoxyguanosine; RAP: rapamycin; ROS: reactive oxygen species; sEPSCs: spontaneous excitatory postsynaptic currents; SOD1: superoxide dismutase 1; SQSTM1/p62: sequestosome 1; SYN: synapsin; WRT: wortmannin.
DOI: 10.6084/m9.figshare.15028702.v2
title: Imbalanced autophagy causes synaptic deficits in a human model for neurodevelopmental disorders

description: Macroautophagy (hereafter referred to as autophagy) is a finely tuned process of programmed degradation and recycling of proteins and cellular components, which is crucial in neuronal function and synaptic integrity. Mounting evidence implicates chromatin remodeling in fine-tuning autophagy pathways. However, this epigenetic regulation is poorly understood in neurons. Here, we investigate the role in autophagy of KANSL1, a member of the nonspecific lethal complex, which acetylates histone H4 on lysine 16 (H4K16ac) to facilitate transcriptional activation. Loss-of-function of KANSL1 is strongly associated with the neurodevelopmental disorder Koolen-de Vries Syndrome (KdVS). Starting from KANSL1-deficient human induced-pluripotent stem cells, both from KdVS patients and genome-edited lines, we identified SOD1 (superoxide dismutase 1), an antioxidant enzyme, to be significantly decreased, leading to a subsequent increase in oxidative stress and autophagosome accumulation. In KANSL1-deficient neurons, autophagosome accumulation at excitatory synapses resulted in reduced synaptic density, reduced GRIA/AMPA receptor-mediated transmission and impaired neuronal network activity. Furthermore, we found that increased oxidative stress-mediated autophagosome accumulation leads to increased MTOR activation and decreased lysosome function, further preventing the clearing of autophagosomes. Finally, by pharmacologically reducing oxidative stress, we could rescue the aberrant autophagosome formation as well as synaptic and neuronal network activity in KANSL1-deficient neurons. Our findings thus point toward an important relation between oxidative stress-induced autophagy and synapse function, and demonstrate the importance of H4K16ac-mediated changes in chromatin structure to balance reactive oxygen species- and MTOR-dependent autophagy. <b>Abbreviations</b>: APO: apocynin; ATG: autophagy related; BAF: bafilomycin A<sub>1</sub>; BSO: buthionine sulfoximine; CV: coefficient of variation; DIV: days in vitro; H4K16ac: histone 4 lysine 16 acetylation; iPSC: induced-pluripotent stem cell; KANSL1: KAT8 regulatory NSL complex subunit 1; KdVS: Koolen-de Vries Syndrome; LAMP1: lysosomal associated membrane protein 1; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MEA: micro-electrode array; MTOR: mechanistic target of rapamycin kinase; NSL complex: nonspecific lethal complex; 8-oxo-dG: 8-hydroxydesoxyguanosine; RAP: rapamycin; ROS: reactive oxygen species; sEPSCs: spontaneous excitatory postsynaptic currents; SOD1: superoxide dismutase 1; SQSTM1/p62: sequestosome 1; SYN: synapsin; WRT: wortmannin.