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  1. Article ; Online: Release and targeting of polycystin-2-carrying ciliary extracellular vesicles.

    Wang, Juan / Nikonorova, Inna A / Gu, Amanda / Sternberg, Paul W / Barr, Maureen M

    Current biology : CB

    2020  Volume 30, Issue 13, Page(s) R755–R756

    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cilia/metabolism ; Extracellular Vesicles/metabolism ; Hermaphroditic Organisms/genetics ; Hermaphroditic Organisms/physiology ; Male ; Protein Transport ; Reproduction ; TRPP Cation Channels/genetics ; TRPP Cation Channels/metabolism
    Chemical Substances Caenorhabditis elegans Proteins ; PKD-2 protein, C elegans ; TRPP Cation Channels
    Language English
    Publishing date 2020-08-04
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural
    ZDB-ID 1071731-6
    ISSN 1879-0445 ; 0960-9822
    ISSN (online) 1879-0445
    ISSN 0960-9822
    DOI 10.1016/j.cub.2020.05.079
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3208: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: Managing bank accounts and foreign exchange transactions in China

    Gu, Amanda

    Business insights: China : practical advice on entry strategy and engagement , p. 115-123

    2008  , Page(s) 115–123

    Author's details Amanda Gu
    Language English
    Publisher Kogan Page
    Publishing place London [u.a.]
    Document type Article
    Database ECONomics Information System

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  3. Article ; Online: CCP1, a Tubulin Deglutamylase, Increases Survival of Rodent Spinal Cord Neurons following Glutamate-Induced Excitotoxicity.

    Ramadan, Yasmin H / Gu, Amanda / Ross, Nicole / McEwan, Sara A / Barr, Maureen M / Firestein, Bonnie L / O'Hagan, Robert

    eNeuro

    2021  Volume 8, Issue 2

    Abstract: Microtubules (MTs) are cytoskeletal elements that provide structural support and act as roadways for intracellular transport in cells. MTs are also needed for neurons to extend and maintain long axons and dendrites that establish connectivity to transmit ...

    Abstract Microtubules (MTs) are cytoskeletal elements that provide structural support and act as roadways for intracellular transport in cells. MTs are also needed for neurons to extend and maintain long axons and dendrites that establish connectivity to transmit information through the nervous system. Therefore, in neurons, the ability to independently regulate cytoskeletal stability and MT-based transport in different cellular compartments is essential. Posttranslational modification of MTs is one mechanism by which neurons regulate the cytoskeleton. The carboxypeptidase CCP1 negatively regulates posttranslational polyglutamylation of MTs. In mammals, loss of CCP1, and the resulting hyperglutamylation of MTs, causes neurodegeneration. It has also long been known that CCP1 expression is activated by neuronal injury; however, whether CCP1 plays a neuroprotective role after injury is unknown. Using shRNA-mediated knock-down of CCP1 in embryonic rat spinal cord cultures, we demonstrate that CCP1 protects spinal cord neurons from excitotoxic death. Unexpectedly, excitotoxic injury reduced CCP1 expression in our system. We previously demonstrated that the CCP1 homolog in
    MeSH term(s) Animals ; Carboxypeptidases ; Gene Knockdown Techniques ; Glutamic Acid ; Neurons ; Rats ; Rodentia ; Spinal Cord ; Spinal Cord Injuries ; Tubulin
    Chemical Substances Tubulin ; Glutamic Acid (3KX376GY7L) ; Carboxypeptidases (EC 3.4.-)
    Language English
    Publishing date 2021-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2800598-3
    ISSN 2373-2822 ; 2373-2822
    ISSN (online) 2373-2822
    ISSN 2373-2822
    DOI 10.1523/ENEURO.0431-20.2021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Sensory cilia act as a specialized venue for regulated extracellular vesicle biogenesis and signaling.

    Wang, Juan / Nikonorova, Inna A / Silva, Malan / Walsh, Jonathon D / Tilton, Peter E / Gu, Amanda / Akella, Jyothi S / Barr, Maureen M

    Current biology : CB

    2021  Volume 31, Issue 17, Page(s) 3943–3951.e3

    Abstract: Ciliary extracellular vesicle (EV) shedding is evolutionarily conserved. In Chlamydomonas and C. elegans, ciliary EVs act as signaling devices. ...

    Abstract Ciliary extracellular vesicle (EV) shedding is evolutionarily conserved. In Chlamydomonas and C. elegans, ciliary EVs act as signaling devices.
    MeSH term(s) Animals ; Caenorhabditis elegans/physiology ; Caenorhabditis elegans Proteins/genetics ; Caenorhabditis elegans Proteins/metabolism ; Cilia/metabolism ; Extracellular Vesicles/metabolism ; Male ; Mammals ; Protein Transport
    Chemical Substances Caenorhabditis elegans Proteins
    Language English
    Publishing date 2021-07-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1071731-6
    ISSN 1879-0445 ; 0960-9822
    ISSN (online) 1879-0445
    ISSN 0960-9822
    DOI 10.1016/j.cub.2021.06.040
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3208: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Mutation of NEKL-4/NEK10 and TTLL genes suppress neuronal ciliary degeneration caused by loss of CCPP-1 deglutamylase function.

    Power, Kade M / Akella, Jyothi S / Gu, Amanda / Walsh, Jonathon D / Bellotti, Sebastian / Morash, Margaret / Zhang, Winnie / Ramadan, Yasmin H / Ross, Nicole / Golden, Andy / Smith, Harold E / Barr, Maureen M / O'Hagan, Robert

    PLoS genetics

    2020  Volume 16, Issue 10, Page(s) e1009052

    Abstract: Ciliary microtubules are subject to post-translational modifications that act as a "Tubulin Code" to regulate motor traffic, binding proteins and stability. In humans, loss of CCP1, a cytosolic carboxypeptidase and tubulin deglutamylating enzyme, causes ... ...

    Abstract Ciliary microtubules are subject to post-translational modifications that act as a "Tubulin Code" to regulate motor traffic, binding proteins and stability. In humans, loss of CCP1, a cytosolic carboxypeptidase and tubulin deglutamylating enzyme, causes infantile-onset neurodegeneration. In C. elegans, mutations in ccpp-1, the homolog of CCP1, result in progressive degeneration of neuronal cilia and loss of neuronal function. To identify genes that regulate microtubule glutamylation and ciliary integrity, we performed a forward genetic screen for suppressors of ciliary degeneration in ccpp-1 mutants. We isolated the ttll-5(my38) suppressor, a mutation in a tubulin tyrosine ligase-like glutamylase gene. We show that mutation in the ttll-4, ttll-5, or ttll-11 gene suppressed the hyperglutamylation-induced loss of ciliary dye filling and kinesin-2 mislocalization in ccpp-1 cilia. We also identified the nekl-4(my31) suppressor, an allele affecting the NIMA (Never in Mitosis A)-related kinase NEKL-4/NEK10. In humans, NEK10 mutation causes bronchiectasis, an airway and mucociliary transport disorder caused by defective motile cilia. C. elegans NEKL-4 localizes to the ciliary base but does not localize to cilia, suggesting an indirect role in ciliary processes. This work defines a pathway in which glutamylation, a component of the Tubulin Code, is written by TTLL-4, TTLL-5, and TTLL-11; is erased by CCPP-1; is read by ciliary kinesins; and its downstream effects are modulated by NEKL-4 activity. Identification of regulators of microtubule glutamylation in diverse cellular contexts is important to the development of effective therapies for disorders characterized by changes in microtubule glutamylation. By identifying C. elegans genes important for neuronal and ciliary stability, our work may inform research into the roles of the tubulin code in human ciliopathies and neurodegenerative diseases.
    MeSH term(s) Animals ; Caenorhabditis elegans/genetics ; Caenorhabditis elegans/growth & development ; Caenorhabditis elegans Proteins/genetics ; Carboxypeptidases/genetics ; Carrier Proteins/genetics ; Cilia/genetics ; Cilia/metabolism ; Glutamic Acid/metabolism ; Humans ; Kinesins/genetics ; Microtubules/genetics ; Mutation/genetics ; NIMA-Related Kinases/genetics ; Nerve Degeneration/genetics ; Nerve Degeneration/pathology ; Neurons/metabolism ; Neurons/pathology ; Peptide Synthases/genetics ; Protein Processing, Post-Translational/genetics ; Tubulin/genetics
    Chemical Substances Caenorhabditis elegans Proteins ; Carrier Proteins ; Tubulin ; Glutamic Acid (3KX376GY7L) ; NIMA-Related Kinases (EC 2.7.11.1) ; Nek10 protein, human (EC 2.7.11.1) ; Carboxypeptidases (EC 3.4.-) ; tubulin deglutamylase, C elegans (EC 3.4.-) ; Kinesins (EC 3.6.4.4) ; Peptide Synthases (EC 6.3.2.-) ; TTLL-4 protein, C elegans (EC 6.3.2.-) ; tyrosyltubulin ligase (EC 6.3.2.-)
    Language English
    Publishing date 2020-10-16
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1009052
    Database MEDical Literature Analysis and Retrieval System OnLINE

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