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  The progressive ankylosis protein ANK facilitates clathrin- and adaptor-mediated membrane traffic at the trans-Golgi network-to-endosome interface

Seifert, W., Posor, Y., Schu, P., Stenbeck, G., Mundlos, S., Klaassen, S., et al. (2016). The progressive ankylosis protein ANK facilitates clathrin- and adaptor-mediated membrane traffic at the trans-Golgi network-to-endosome interface. Human Molecular Genetics, 25(17), 3836-3848. doi:10.1093/hmg/ddw230.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-002D-E1D6-5 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-002D-E1D7-3
Genre: Journal Article

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Seifert, W., Author
Posor, Y., Author
Schu, P., Author
Stenbeck, G., Author
Mundlos, S.1, Author              
Klaassen, S., Author
Nurnberg, P., Author
Haucke, V., Author
Kornak, U.1, Author              
Kühnisch, J.1, Author
Affiliations:
1Research Group Development & Disease (Head: Stefan Mundlos), Max Planck Institute for Molecular Genetics, Max Planck Society, ou_1433557              

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 Abstract: Dominant or recessive mutations in the progressive ankylosis gene ANKH have been linked to familial chondrocalcinosis (CCAL2), craniometaphyseal dysplasia (CMD), mental retardation, deafness and ankylosis syndrome (MRDA). The function of the encoded membrane protein ANK in cellular compartments other than the plasma membrane is unknown. Here, we show that ANK localizes to the trans-Golgi network (TGN), clathrin-coated vesicles and the plasma membrane. ANK functionally interacts with clathrin and clathrin associated adaptor protein (AP) complexes as loss of either protein causes ANK dispersion from the TGN to cytoplasmic endosome-like puncta. Consistent with its subcellular localization, loss of ANK results in reduced formation of tubular membrane carriers from the TGN, perinuclear accumulation of early endosomes and impaired transferrin endocytosis. Our data indicate that clathrin/AP-mediated cycling of ANK between the TGN, endosomes, and the cell surface regulates membrane traffic at the TGN/endosomal interface. These findings suggest that dysfunction of Golgi-endosomal membrane traffic may contribute to ANKH-associated pathologies.

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Language(s): eng - English
 Dates: 2016-07-272016-09-01
 Publication Status: Published in print
 Pages: 13
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 Rev. Method: -
 Identifiers: DOI: 10.1093/hmg/ddw230
ISSN: 1460-2083 (Electronic)0964-6906 (Print)
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Title: Human Molecular Genetics
Source Genre: Journal
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Publ. Info: Oxford, England : IRL Press
Pages: - Volume / Issue: 25 (17) Sequence Number: - Start / End Page: 3836 - 3848 Identifier: ISSN: 0964-6906
CoNE: /journals/resource/954925581153