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  1. Article: Eighth International Chorea–Acanthocytosis Symposium: Summary of Workshop Discussion and Action Points

    Haucke, Volker

    Tremor and other hyperkinetic movements, 7: 428

    2017  

    Abstract: Chorea-Acanthocytosis (ChAc) is a rare hereditary neurological disorder characterized by abnormal movements, red blood cell pathology, and progressive neurodegeneration. Little is understood of the pathogenesis of ChAc and related disorders (collectively ...

    Institution Leibniz-Forschungsinstitut für Molekulare Pharmakologie
    Abstract Chorea-Acanthocytosis (ChAc) is a rare hereditary neurological disorder characterized by abnormal movements, red blood cell pathology, and progressive neurodegeneration. Little is understood of the pathogenesis of ChAc and related disorders (collectively Neuroacanthocytosis). The Eighth International Chorea-Acanthocytosis Symposium was held in May 2016 in Ann Arbor, MI, USA, and focused on molecular mechanisms driving ChAc pathophysiology. Accompanying the meeting, members of the neuroacanthocytosis research community and other invited scientists met in a workshop to discuss the current understanding and next steps needed to better understand ChAc pathogenesis. These discussions identified several broad and critical needs for advancing ChAc research and patient care, and led to the definition of 18 specific action points related to functional and molecular studies, animal models, and clinical research. These action points, described below, represent tractable research goals to pursue for the next several years.
    Keywords Chorea Acanthocytosis ; Chorein ; Neuroacanthocytosis ; VPS13 ; VPS13A
    Language English
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  2. Article: Phosphatidylinositol 3-phosphates—at the interface between cell signalling and membrane traffic

    Haucke, Volker

    The EMBO journal, 35(6): 555 - 698

    2016  

    Abstract: Phosphoinositides (PIs) form a minor class of phospholipids with crucial functions in cell physiology, ranging from cell signalling and motility to a role as signposts of compartmental membrane identity. Phosphatidylinositol 3-phosphates are present at ... ...

    Institution Leibniz-Institut für Molekulare Pharmakologie
    Abstract Phosphoinositides (PIs) form a minor class of phospholipids with crucial functions in cell physiology, ranging from cell signalling and motility to a role as signposts of compartmental membrane identity. Phosphatidylinositol 3-phosphates are present at the plasma membrane and within the endolysosomal system, where they serve as key regulators of both cell signalling and of intracellular membrane traffic. Here, we provide an overview of the metabolic pathways that regulate cellular synthesis of PI 3-phosphates at distinct intracellular sites and discuss the mechanisms by which these lipids regulate cell signalling and membrane traffic. Finally, we provide a framework for how PI 3-phosphate metabolism is integrated into the cellular network.
    Keywords autophagy ; endolysosomal system ; membrane traffic ; signalling ; phosphatidylinositol 3-phosphate
    Language English
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  3. Article: Type II PI4-kinases control Weibel-Palade body biogenesis and von Willebrand factor structure in human endothelial cells

    Haucke, Volker

    Journal of cell science, 129(10): 2096-2105

    2016  

    Abstract: Weibel-Palade bodies (WPBs) are endothelial storage organelles that mediate the release of molecules involved in thrombosis, inflammation and angiogenesis, including the pro-thrombotic glycoprotein von Willebrand factor (VWF). Although many protein ... ...

    Institution Leibniz-Institut für Molekulare Pharmakologie
    Abstract Weibel-Palade bodies (WPBs) are endothelial storage organelles that mediate the release of molecules involved in thrombosis, inflammation and angiogenesis, including the pro-thrombotic glycoprotein von Willebrand factor (VWF). Although many protein components required for WPB formation and function have been identified, the role of lipids is almost unknown. We examined two key phosphatidylinositol kinases that control phosphatidylinositol 4-phosphate levels at the trans-Golgi network, the site of WPB biogenesis. RNA interference of the type II phosphatidylinositol 4-kinases PI4KIIα and PI4KIIβ in primary human endothelial cells leads to formation of an increased proportion of short WPB with perturbed packing of VWF, as exemplified by increased exposure of antibody-binding sites. When stimulated with histamine, these cells release normal levels of VWF yet, under flow, form very few platelet-catching VWF strings. In PI4KIIα-deficient mice, immuno-microscopy revealed that VWF packaging is also perturbed and these mice exhibit increased blood loss after tail cut compared to controls. This is the first demonstration that lipid kinases can control the biosynthesis of VWF and the formation of WPBs that are capable of full haemostatic function.
    Keywords Phosphatidylinositol 4-kinase alpha ; Phosphatidylinositol 4-kinase beta ; Weibel-Palade body ; Von Willebrand factor
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  4. Article: Gottfried Schatz (1936–2015)—mitochondrial pioneer and ambassador for science

    Haucke, Volker

    The EMBO journal, 34: 2725-2726

    2015  

    Institution Leibniz-Forschungsinstitut für Molekulare Pharmakologie
    Language English
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  5. Article: A grab to move on: ER–endosome contacts in membrane protrusion formation and neurite outgrowth

    Haucke, Volker

    The EMBO journal, 34(11): 1435-1600

    2015  

    Abstract: A key feature of many eukaryotic cells, most prominently seen in developing neurons, is their ability to form and extend membrane protrusions. How protrusion formation is linked to exocytic membrane trafficking is largely unclear. In a recent paper ... ...

    Institution Leibniz-Forschungsinstitut für Molekulare Pharmakologie
    Abstract A key feature of many eukaryotic cells, most prominently seen in developing neurons, is their ability to form and extend membrane protrusions. How protrusion formation is linked to exocytic membrane trafficking is largely unclear. In a recent paper published in Nature, Raiborg et al identify a crucial role in this process for dynamic membrane contact sites (MCSs) between the ER and endosomes. The MCSs are formed by endoplasmic reticulum (ER)‐localized protein protrudin and the late endosomal kinesin adaptor FYCO1 and the small GTPase Rab7.
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  6. Article: Lipids, GTPases, and their regulators in membrane dynamics: an intracellular ménage à trois

    Haucke, Volker

    Molecular biology of the cell, 26(6): 1012-1013

    2015  

    Abstract: Essentially all aspects of eukaryotic cell physiology depend on their compartmentalization and on membrane flux between these compartments mediated by small GTPases and their regulators, as well as by specific membrane lipids (Behnia and Munro, 2005). ... ...

    Institution Leibniz-Institut für Molekulare Pharmakologie
    Abstract Essentially all aspects of eukaryotic cell physiology depend on their compartmentalization and on membrane flux between these compartments mediated by small GTPases and their regulators, as well as by specific membrane lipids (Behnia and Munro, 2005). Talks at the Minisymposium on “Membrane Traffic: Dynamic and Regulation” featured how Rab-and Arf-family GTPases, together with diverse phospholipids, most notably phosphoinositides (Balla, 2013), control key cell functions ranging from plasma membrane compartmentalization to organelle contacts, endosomal fission, cell motility, intracellular signaling, and cell cycle progression.
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  7. Article: Simian Hemorrhagic Fever Virus Cell Entry Is Dependent on CD163 and Uses a Clathrin-Mediated Endocytosis-Like Pathway

    Haucke, Volker

    Journal of virology, 89(1): 844-856

    2014  

    Abstract: Simian hemorrhagic fever virus (SHFV) causes a severe and almost uniformly fatal viral hemorrhagic fever in Asian macaques but is thought to be nonpathogenic for humans. To date, the SHFV life cycle is almost completely uncharacterized on the molecular ... ...

    Institution Leibniz-Institut für Molekulare Pharmakologie
    Abstract Simian hemorrhagic fever virus (SHFV) causes a severe and almost uniformly fatal viral hemorrhagic fever in Asian macaques but is thought to be nonpathogenic for humans. To date, the SHFV life cycle is almost completely uncharacterized on the molecular level. Here, we describe the first steps of the SHFV life cycle. Our experiments indicate that SHFV enters target cells by low-pH-dependent endocytosis. Dynamin inhibitors, chlorpromazine, methyl-β-cyclodextrin, chloroquine, and concanamycin A dramatically reduced SHFV entry efficiency, whereas the macropinocytosis inhibitors EIPA, blebbistatin, and wortmannin and the caveolin-mediated endocytosis inhibitors nystatin and filipin III had no effect. Furthermore, overexpression and knockout study and electron microscopy results indicate that SHFV entry occurs by a dynamin-dependent clathrin-mediated endocytosis-like pathway. Experiments utilizing latrunculin B, cytochalasin B, and cytochalasin D indicate that SHFV does not hijack the actin polymerization pathway. Treatment of target cells with proteases (proteinase K, papain, α-chymotrypsin, and trypsin) abrogated entry, indicating that the SHFV cell surface receptor is a protein. Phospholipases A2 and D had no effect on SHFV entry. Finally, treatment of cells with antibodies targeting CD163, a cell surface molecule identified as an entry factor for the SHFV-related porcine reproductive and respiratory syndrome virus, diminished SHFV replication, identifying CD163 as an important SHFV entry component.
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  8. Article: PI3K Class II α Controls Spatially Restricted Endosomal PtdIns3P and Rab11 Activation to Promote Primary Cilium Function

    Haucke, Volker

    Developmental cell, 28(6): 647–658

    2014  

    Abstract: Multiple phosphatidylinositol (PtdIns) 3-kinases (PI3Ks) can produce PtdIns3P to control endocytic trafficking, but whether enzyme specialization occurs in defined subcellular locations is unclear. Here, we report that PI3K-C2α is enriched in the ... ...

    Institution Leibniz-Institut für Molekulare Pharmakologie
    Abstract Multiple phosphatidylinositol (PtdIns) 3-kinases (PI3Ks) can produce PtdIns3P to control endocytic trafficking, but whether enzyme specialization occurs in defined subcellular locations is unclear. Here, we report that PI3K-C2α is enriched in the pericentriolar recycling endocytic compartment (PRE) at the base of the primary cilium, where it regulates production of a specific pool of PtdIns3P. Loss of PI3K-C2α-derived PtdIns3P leads to mislocalization of PRE markers such as TfR and Rab11, reduces Rab11 activation, and blocks accumulation of Rab8 at the primary cilium. These changes in turn cause defects in primary cilium elongation, Smo ciliary translocation, and Sonic Hedgehog (Shh) signaling and ultimately impair embryonic development. Selective reconstitution of PtdIns3P levels in cells lacking PI3K-C2α rescues Rab11 activation, primary cilium length, and Shh pathway induction. Thus, PI3K-C2α regulates the formation of a PtdIns3P pool at the PRE required for Rab11 and Shh pathway activation.
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  9. Article: Clathrin Terminal Domain-Ligand Interactions Regulate Sorting of Mannose 6-Phosphate Receptors Mediated by AP-1 and GGA Adaptors

    Haucke, Volker

    The journal of biological chemistry, 289: 4906-4918

    2014  

    Abstract: Clathrin plays important roles in intracellular membrane traffic including endocytosis of plasma membrane proteins and receptors and protein sorting between the trans-Golgi network (TGN) and endosomes. Whether clathrin serves additional roles in receptor ...

    Institution Leibniz-Institut für Molekulare Pharmakologie
    Abstract Clathrin plays important roles in intracellular membrane traffic including endocytosis of plasma membrane proteins and receptors and protein sorting between the trans-Golgi network (TGN) and endosomes. Whether clathrin serves additional roles in receptor recycling, degradative sorting, or constitutive secretion has remained somewhat controversial. Here we have used acute pharmacological perturbation of clathrin terminal domain (TD) function to dissect the role of clathrin in intracellular membrane traffic. We report that internalization of major histocompatibility complex I (MHCI) is inhibited in cells depleted of clathrin or its major clathrin adaptor complex 2 (AP-2), a phenotype mimicked by application of Pitstop® inhibitors of clathrin TD function. Hence, MHCI endocytosis occurs via a clathrin/AP-2-dependent pathway. Acute perturbation of clathrin also impairs the dynamics of intracellular clathrin/adaptor complex 1 (AP-1)- or GGA (Golgi-localized, γ-ear-containing, Arf-binding protein)-coated structures at the TGN/endosomal interface, resulting in the peripheral dispersion of mannose 6-phosphate receptors. By contrast, secretory traffic of vesicular stomatitis virus G protein, recycling of internalized transferrin from endosomes, or degradation of EGF receptor proceeds unperturbed in cells with impaired clathrin TD function. These data indicate that clathrin is required for the function of AP-1- and GGA-coated carriers at the TGN but may be dispensable for outward traffic en route to the plasma membrane.
    Keywords Cell Biology ; Endosomes ; Lysosomes ; Molecular Cell Biology ; Membrane Trafficking ; Protein Sorting
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  10. Article: A dual role of SNAP‐25 as carrier and guardian of synaptic transmission

    Haucke, Volker

    EMBO reports, 14(7): 579-580

    2013  

    Institution Leibniz-Forschungsinstitut für Molekulare Pharmakologie
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