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Cited by 103

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

A role for sorting nexin 27 in AMPA receptor trafficking

Loo, Li Shen, Tang, Ning, Al-Haddawi, Muthafar, Stewart Dawe, Gavin, Hong, Wanjin·2014·Nature Communications
DOI 10.1038/ncomms4176PMC PMC3921469
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Crossref · 10.1038/ncomms4176

Cites

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  • 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 Loo et al., 2014

    The Discussion (page unavailable) says that several studies established SNX27’s importance in endosome-to-plasma-membrane trafficking, and the Results show that SNX27 loss impairs recycling in neurons. The paper mentions retromer cargoes, but it does not establish that much of what is known about neuronal endocytic recycling comes from studies focused on the SNX27–retromer pathway. (LLM, conf=0.82)

    Experimental — accuracy not yet measured

  • 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 Loo et al., 2014

    The Results section reports that SNX27 knockout abolished LTP in hippocampal slices and that glycine-induced stimulation barely increased surface GluA1 in knockout neurons. The paper does not directly show that chemical LTP itself was prevented: it measured receptor insertion after chemical stimulation, while the abolished LTP response was measured in slices using electrical stimulation. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • Knockdown of SNX27 blocks cLTP induction in cultured rat hippocampal neurons.

    “Similarly, knockdown of SNX27 also blocked cLTP (Figure 5E–G), again similar to earlier reports (Loo et al., 2014; Hussain et al., 2014; see also, Temkin et al., 2017).”

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

    In Results (“SNX27 important for AMPA receptor delivery and LTP”; page unavailable), glycine stimulation barely increased the GluA1 insertion signal in cultured neurons lacking SNX27. The paper used neurons from SNX27-knockout mice, not SNX27 knockdown in rat neurons; its direct measurement of abolished LTP was in mouse hippocampal slices, not the cultured neurons. (LLM, conf=0.88)

    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 Loo et al., 2014

    The Results and Discussion report that loss of SNX27 impairs GluA1 delivery during LTP and abolishes synaptic potentiation in brain slices. The paper mentions retromer cargoes, but does not establish that the AMPAR trafficking required for potentiation is retromer-dependent. (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 Loo et al., 2014

    The Discussion (page unavailable) reports that SNX27 is required for GluA1 delivery during synaptic potentiation and for LTP, supporting the claim that it helps add AMPARs to synapses. The paper describes recycling endosomes and a CaM/K-ras–SNX27 mechanism, but does not establish that this delivery occurs via Retromer. Its description of SNX27 as relaying plasticity stimuli supports the proposed instructive role. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 32

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  2. Wang, X. et al. Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down’s syndrome. Nat. Med. 19, 473–480 (2013). · DOI · Paper page
  3. Ghai, R. et al. Phox homology band 4.1/ezrin/radixin/moesin-like proteins function as molecular scaffolds that interact with cargo receptors and Ras GTPases. Proc. Natl Acad. Sci. USA 108, 7763–7768 (2011). · DOI · Paper page
  4. Zhu, J. J., Qin, Y., Zhao, M., Van Aelst, L. & Malinow, R. Ras and Rap control AMPA receptor trafficking during synaptic plasticity. Cell 110, 443–455 (2002). · DOI · Paper page
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  7. Di Cristo, G. et al. Requirement of ERK activation for visual cortical plasticity. Science 292, 2337–2340 (2001). · DOI
  8. Cai, L., Loo, L. S., Atlasin, V., Hanson, B. J. & Hong, W. Deficiency of Sorting Nexin 27 (SNX27) leads to growth retardation and elevated levels of N-methyl-D-aspartate (NMDA) receptor 2C (NR2C). Mol. Cell Biol. 31, 1734–1747 (2011). · DOI
  9. Lauffer, B. E. et al. SNX27 mediates PDZ-directed sorting from endosomes to the plasma membrane. J. Cell Biol. 190, 565–574 (2010). · DOI · Paper page
  10. Villalonga, P. et al. Calmodulin binds to K-Ras, but not to H- or N-Ras, and modulates its downstream signaling. Mol. Cell Biol. 21, 7345–7354 (2001). · DOI
  11. Wu, L. J., Xu, L. R., Liao, J. M., Chen, J. & Liang, Y. Both the C-terminal polylysine region and the farnesylation of K-RasB are important for its specific interaction with calmodulin. PLoS One 6, e21929 (2011). · DOI
  12. Hayashi, Y. et al. Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction. Science 287, 2262–2267 (2000). · DOI · Paper page
  13. Piccini, A. & Malinow, R. Critical postsynaptic density 95/disc large/zonula occludens-1 interactions by glutamate receptor 1 (GluR1) and GluR2 required at different subcellular sites. J. Neurosci. 22, 5387–5392 (2002). · DOI
  14. Steinberg, F. et al. A global analysis of SNX27-retromer assembly and cargo specificity reveals a function in glucose and metal ion transport. Nat. Cell Biol. 15, 461–471 (2013). · DOI · Paper page
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  16. Forcelini, C. M. et al. Down syndrome with congenital hydrocephalus: case report. Arq. Neuropsiquiatr. 64, 869–871 (2006). · DOI
  17. Fabia, J. & Drolette, M. Malformations and leukemia in children with Dowńs syndrome. Pediatrics 45, 60–70 (1970). · DOI
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  20. Joubert, L. et al. New sorting nexin (SNX27) and NHERF specifically interact with the 5-HT4a receptor splice variant: roles in receptor targeting. J. Cell Sci. 117, 5367–5379 (2004). · DOI
  21. Temkin, P. et al. SNX27 mediates retromer tubule entry and endosome-to-plasma membrane trafficking of signalling receptors. Nat. Cell Biol. 13, 715–721 (2011). · DOI · Paper page
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Metadata

Authors
Loo, L. S., Tang, N., Al-Haddawi, M., Stewart Dawe, G., & Hong, W.
Venue
Nature Communications
Publisher
Springer Science and Business Media LLC
Published
2014-01-24
Volume
5
Issue
1
ISSN
2041-1723
DOI
10.1038/ncomms4176
PMC
PMC3921469
Cited by
103
References
2
Language
en
Licence
creativecommons.org/licenses/by-nc-nd/3.0 (unspecified)

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