A disease causing ATLASTIN 3 mutation affects multiple endoplasmic reticulum-related pathways
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Title
A disease causing ATLASTIN 3 mutation affects multiple endoplasmic reticulum-related pathways
Authors
Keywords
Atlastin, Hereditary spastic paraplegia, Endoplasmic reticulum, Secretory transport
Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume -, Issue -, Pages -
Publisher
Springer Nature
Online
2019-01-21
DOI
10.1007/s00018-019-03010-x
References
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Note: Only part of the references are listed.- Sensory-Neuropathy-Causing Mutations in ATL3 Cause Aberrant ER Membrane Tethering
- (2018) Michiel Krols et al. Cell Reports
- Atlastins remodel the endoplasmic reticulum for selective autophagy
- (2018) Jin Rui Liang et al. JOURNAL OF CELL BIOLOGY
- Sensory neuropathy-causing mutations in ATL3 affect ER–mitochondria contact sites and impair axonal mitochondrial distribution
- (2018) Michiel Krols et al. HUMAN MOLECULAR GENETICS
- Molecular mechanisms of atlastin-mediated ER membrane fusion revealed by a FRET-based single-vesicle fusion assay
- (2017) Kyung Tae Kim et al. Scientific Reports
- Efficient protein targeting to the inner nuclear membrane requires Atlastin-dependent maintenance of ER topology
- (2017) Sumit Pawar et al. eLife
- Mammalian knock out cells reveal prominent roles for atlastin GTPases in ER network morphology
- (2016) Guohua Zhao et al. EXPERIMENTAL CELL RESEARCH
- Inhibition of cargo export at ER exit sites and the trans-Golgi network by the secretion inhibitor FLI-06
- (2016) Yoji Yonemura et al. JOURNAL OF CELL SCIENCE
- Increased spatiotemporal resolution reveals highly dynamic dense tubular matrices in the peripheral ER
- (2016) J. Nixon-Abell et al. SCIENCE
- Fusion of the endoplasmic reticulum by membrane-bound GTPases
- (2016) Junjie Hu et al. SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY
- Cooperation of the ER-shaping proteins atlastin, lunapark, and reticulons to generate a tubular membrane network
- (2016) Songyu Wang et al. eLife
- Structures of the yeast dynamin-like GTPase Sey1p provide insight into homotypic ER fusion
- (2015) Liming Yan et al. JOURNAL OF CELL BIOLOGY
- ERES: sites for autophagosome biogenesis and maturation?
- (2015) J. Sanchez-Wandelmer et al. JOURNAL OF CELL SCIENCE
- ER network formation and membrane fusion by atlastin1/SPG3A disease variants
- (2015) Idil Ulengin et al. MOLECULAR BIOLOGY OF THE CELL
- The Ubiquitin Ligase CBLC Maintains the Network Organization of the Golgi Apparatus
- (2015) Wan Yin Lee et al. PLoS One
- Golgi Fragmentation in ALS Motor Neurons. New Mechanisms Targeting Microtubules, Tethers, and Transport Vesicles
- (2015) Georg Haase et al. Frontiers in Neuroscience
- Stain-free detection as loading control alternative to Ponceau and housekeeping protein immunodetection in Western blotting
- (2014) B. Rivero-Gutiérrez et al. ANALYTICAL BIOCHEMISTRY
- A novel missense mutation confirms ATL3 as a gene for hereditary sensory neuropathy type 1
- (2014) Dirk Fischer et al. BRAIN
- Membrane-shaping disorders: a common pathway in axon degeneration
- (2014) Christian A. Hübner et al. BRAIN
- Sensory neuropathy with bone destruction due to a mutation in the membrane-shaping atlastin GTPase 3
- (2014) Uwe Kornak et al. BRAIN
- Dynamic association of the ULK1 complex with omegasomes during autophagy induction
- (2013) E. Karanasios et al. JOURNAL OF CELL SCIENCE
- ER exit sites are physical and functional core autophagosome biogenesis components
- (2013) Martin Graef et al. MOLECULAR BIOLOGY OF THE CELL
- A Conserved Role for Atlastin GTPases in Regulating Lipid Droplet Size
- (2013) Robin W. Klemm et al. Cell Reports
- Cellular Pathways of Hereditary Spastic Paraplegia
- (2012) Craig Blackstone Annual Review of Neuroscience
- Guidelines for the use and interpretation of assays for monitoring autophagy
- (2012) Daniel J. Klionsky et al. Autophagy
- Overlapping molecular pathological themes link Charcot–Marie–Tooth neuropathies and hereditary spastic paraplegias
- (2012) Vincent Timmerman et al. EXPERIMENTAL NEUROLOGY
- High-curvature domains of the ER are important for the organization of ER exit sites in Saccharomyces cerevisiae
- (2012) M. Okamoto et al. JOURNAL OF CELL SCIENCE
- Hereditary spastic paraplegia-causing mutations in atlastin-1 interfere with BMPRII trafficking
- (2012) Jiali Zhao et al. MOLECULAR AND CELLULAR NEUROSCIENCE
- Mechanisms of disease in hereditary sensory and autonomic neuropathies
- (2012) Annelies Rotthier et al. Nature Reviews Neurology
- Polar Transmembrane-based Amino Acids in Presenilin 1 Are Involved in Endoplasmic Reticulum Localization, Pen2 Protein Binding, and γ-Secretase Complex Stabilization
- (2011) Matthias Fassler et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- COPII and the regulation of protein sorting in mammals
- (2011) Giulia Zanetti et al. NATURE CELL BIOLOGY
- Entry and Exit Mechanisms at the cis-Face of the Golgi Complex
- (2011) A. Lorente-Rodriguez et al. Cold Spring Harbor Perspectives in Biology
- Targeted High-Throughput Sequencing Identifies Mutations in atlastin-1 as a Cause of Hereditary Sensory Neuropathy Type I
- (2010) Christian Guelly et al. AMERICAN JOURNAL OF HUMAN GENETICS
- Autophagosome Formation Depends on the Small GTPase Rab1 and Functional ER Exit Sites
- (2010) Felipe Carlos Martín Zoppino et al. TRAFFIC
- A Class of Dynamin-like GTPases Involved in the Generation of the Tubular ER Network
- (2009) Junjie Hu et al. CELL
- Homotypic fusion of ER membranes requires the dynamin-like GTPase Atlastin
- (2009) Genny Orso et al. NATURE
- Atlastin GTPases are required for Golgi apparatus and ER morphogenesis
- (2008) Neggy Rismanchi et al. HUMAN MOLECULAR GENETICS
- Golgi apparatus and neurodegenerative diseases
- (2008) Jie Fan et al. INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE
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