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The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Sorting Nexin 27 regulates basal and activity-dependent trafficking of AMPARs

Hussain, Natasha K., Diering, Graham H., Sole, Jonathan, Anggono, Victor, Huganir, Richard L.·2014·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1412415111
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Abstract

Significance: AMPA-type glutamate receptors (AMPARs) are principal regulators of synaptic signaling in the brain. Modulation of AMPA receptor activity, whether through changes in surface expression or conductance, contributes significantly to the dynamic nature of neuronal networks. AMPA receptor mediated-synaptic plasticity is thought to underlie learning and memory, as aberrant AMPAR trafficking contributes to impaired plasticity and to memory deficits. We demonstrate that the membrane trafficking and sorting protein, SNX27, regulates basal and activity dependent targeting of AMPA receptors to the neuronal surface. Elucidating the mechanism of receptor sorting mediated by SNX27 will not only further our understanding AMPAR-mediated changes in synaptic plasticity, but may ultimately shed light on the molecular mechanisms that govern learning.

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Crossref · 10.1073/pnas.1412415111

Cites

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Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • SNX27 is required for LTP, and alterations in this pathway prevent cLTP by impairing the activity-dependent recruitment of surface AMPA receptors.

    “Similar to SNX17, SNX27 is also required for LTP. Alterations in this pathway prevent cLTP by impairing the activity-dependent recruitment of surface AMPA receptors”

    From PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity (2025) · cites this paper as Hussain et al., 2014

    The Results report that SNX27 depletion completely blocked the cLTP-induced increase in surface GluA1, supporting the claim about impaired activity-dependent AMPAR recruitment. The paper used chemical stimulation to mimic LTP and measured receptor surface expression; it does not show that SNX27 loss prevents LTP or cLTP itself. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Much of what is known about endocytic recycling in neurons has come from studies focused on the SNX27-Retromer pathway.

    “Much of what we know about endocytic recycling in neurons has come from studies focused on the SNX27-Retromer pathway”

    From PI(3)P coordinates SNX17- and SNX27-dependent protein recycling for long-term synaptic plasticity (2025) · cites this paper as Hussain et al., 2014

    The Discussion reports that SNX27 binds AMPA receptors and facilitates their trafficking to the neuronal surface, so this is a study of SNX27-related endocytic recycling. It does not establish that much of what is known about neuronal endocytic recycling comes from SNX27–Retromer studies, nor does it directly examine the combined pathway. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • Both SNX17 and SNX27 are predominantly localized to endosomes.

    “Moreover, both SNX17 and SNX27 are predominantly localized to endosomes, which is consistent with previous studies examining SNX27 distribution in neurons (Loo et al., 2014; Hussain et al., 2014).”

    From Dual endomembrane recycling pathways function in parallel to support synapse maintenance and plasticity (2025) · cites this paper as Hussain et al., 2014

    The citation is attached specifically to the statement about SNX27 distribution in neurons, not the finding about SNX17. The Results report that SNX27 partially colocalizes with an endosomal marker, but is also concentrated at synapses; they do not establish that it is predominantly localized to endosomes. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • SNX27 Retromer-dependent AMPAR recycling is essential for synaptic potentiation and plasticity.

    “SNX27 Retromer-dependent AMPAR recycling is essential for synaptic potentiation and plasticity”

    From Dual endomembrane recycling pathways function in parallel to support synapse maintenance and plasticity (2025) · cites this paper as Hussain et al., 2014

    The Discussion identifies SNX27 as an AMPAR recycling adaptor, and the Results show that SNX27 depletion blocks AMPAR surface recruitment during chemical LTP. The paper does not establish that this recycling is retromer-dependent or directly show that SNX27 is essential for synaptic potentiation itself; the Discussion presents that latter role as a possibility. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • SNX27-dependent recycling of AMPARs via Retromer adds new receptors to synapses during LTP, an instructive role.

    “As noted above, SNX27-dependent recycling of AMPARs via Retromer has been shown to add new receptors to synapses during LTP (Wang et al., 2013; Loo et al.,2014; Hussain et al., 2014; Temkin et al., 2017), a clear instructive role.”

    From Dual endomembrane recycling pathways function in parallel to support synapse maintenance and plasticity (2025) · cites this paper as Hussain et al., 2014

    The Results report that SNX27 depletion blocked the increase in surface AMPARs during chemical LTP, and the Discussion describes SNX27 as an AMPAR recycling adaptor. But the study measures recruitment to the neuronal surface rather than directly showing new receptors added to synapses, and our copy does not establish that this LTP-dependent recruitment occurs via Retromer. The paper uses a chemical protocol mimicking LTP. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Citations

Cites

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Metadata

Authors
Hussain, N. K., Diering, G. H., Sole, J., Anggono, V., & Huganir, R. L.
Affiliations
  • Solomon H. Snyder Department of Neuroscience,
  • Clem Jones Centre for Ageing Dementia Research, Queensland Brain Institute, The University of Queensland, Brisbane 4072, Queensland, Australia
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2014-07-28
Volume
111
Issue
32
Pages
11840-11845
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.1412415111
Cited by
87
References
2
Language
en

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