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The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Loss of sorting nexin 27 contributes to excitatory synaptic dysfunction by modulating glutamate receptor recycling in Down’s syndrome

Wang, Xin, Zhao, Yingjun, Zhang, Xiaofei, Badie, Hedieh, Zhou, Ying, Mu, Yangling, Loo, Li Shen, Cai, Lei, Thompson, Robert C, Yang, Bo, Chen, Yaomin, Johnson, Peter F, Wu, Chengbiao, Bu, Guojun, Mobley, William C, Zhang, Dongxian, Gage, Fred H, Ranscht, Barbara, Zhang, Yun-wu, Lipton, Stuart A, Hong, Wanjin, Xu, Huaxi·2013·Nature Medicine
DOI 10.1038/nm.3117PMC PMC3911880
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Crossref · 10.1038/nm.3117

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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 Wang et al., 2013

    The Results show that SNX27 affects glutamate-receptor recycling, including in primary neurons. But the Discussion says whether this recycling depends on retromer remains to be investigated; it also does not establish the broader claim that much of what is known about neuronal endocytic recycling comes from studies of that pathway. No page numbers are available in our copy. (LLM, conf=0.87)

    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 Wang et al., 2013

    The Results report that SNX27 promotes AMPAR recycling to the cell surface and that LTP is reduced in Snx27+/− mice. But the Discussion says whether AMPAR recycling depends on retromer remains to be investigated, and the paper does not show recycled receptors being added to synapses during LTP. It therefore does not establish the claimed instructive mechanism. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • SNX27 dysfunction is implicated in neurodegeneration and Down's syndrome, which greatly increases the risk for developing Alzheimer's disease.

    “Importantly, SNX27 dysfunction is implicated in neurodegeneration and Down's syndrome, which greatly increases the risk for developing Alzheimer's disease [63][64][65].”

    From Global identification of neuronal and astrocytic integral membrane proteins that require Retromer for their endosomal recycling (2026) · cites this paper as [65]

    The Discussion section on the miR-155–C/EBPβ–SNX27 pathway says that loss of SNX27 may help explain synaptic dysfunction, memory difficulties and neurodegeneration in Down syndrome. Our copy does not state that Down syndrome greatly increases the risk of developing Alzheimer’s disease, so that part of the sentence is unsupported by this source. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

  • Knockout of SNX27 in mice leads to severe neuronal death and early lethality.

    “Indeed, knockout of SNX27 in mice leads to severe neuronal death and early lethality [65] and SNX27 mutations in humans have been linked to epileptic seizures [63,64].”

    From Global identification of neuronal and astrocytic integral membrane proteins that require Retromer for their endosomal recycling (2026) · cites this paper as [65]

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Citations

Cites

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Research works printed but not linked: 39

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  2. Kajii, Y. et al. A developmentally regulated and psychostimulant-inducible novel rat gene mrt1 encoding PDZ-PX proteins isolated in the neocortex. Mol. Psychiatry 8, 434–444 (2003). · DOI
  3. 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
  4. 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
  5. Lunn, M.L. et al. A unique sorting nexin regulates trafficking of potassium channels via a PDZ domain interaction. Nat. Neurosci. 10, 1249–1259 (2007). · DOI · Paper page
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  7. Cai, L., Loo, L.S., Atlashkin, V., Hanson, B.J. & Hong, W. Deficiency of sorting nexin 27 (SNX27) leads to growth retardation and elevated levels of N-methyl-D-aspartate receptor 2C (NR2C). Mol. Cell Biol. 31, 1734–1747 (2011). · DOI
  8. Shepherd, J.D. & Huganir, R.L. The cell biology of synaptic plasticity: AMPA receptor trafficking. Annu. Rev. Cell Dev. Biol. 23, 613–643 (2007). · DOI · Paper page
  9. Malinow, R. New developments on the role of NMDA receptors in Alzheimer's disease. Curr. Opin. Neurobiol. 22, 559–563 (2012). · DOI · Paper page
  10. Weitzdoerfer, R., Dierssen, M., Fountoulakis, M. & Lubec, G. Fetal life in Down syndrome starts with normal neuronal density but impaired dendritic spines and synaptosomal structure. J. Neural Transm. Suppl. 61, 59–70 (2001).
  11. Petit, T.L., LeBoutillier, J.C., Alfano, D.P. & Becker, L.E. Synaptic development in the human fetus: a morphometric analysis of normal and Down's syndrome neocortex. Exp. Neurol. 83, 13–23 (1984). · DOI · Paper page
  12. Schmidt-Sidor, B., Wisniewski, K.E., Shepard, T.H. & Sersen, E.A. Brain growth in Down syndrome subjects 15 to 22 weeks of gestational age and birth to 60 months. Clin. Neuropathol. 9, 181–190 (1990).
  13. Reynolds, G.P. & Warner, C.E. Amino acid neurotransmitter deficits in adult Down's syndrome brain tissue. Neurosci. Lett. 94, 224–227 (1988). · DOI
  14. Risser, D., Lubec, G., Cairns, N. & Herrera-Marschitz, M. Excitatory amino acids and monoamines in parahippocampal gyrus and frontal cortical pole of adults with Down syndrome. Life Sci. 60, 1231–1237 (1997). · DOI
  15. Galdzicki, Z., Siarey, R., Pearce, R., Stoll, J. & Rapoport, S.I. On the cause of mental retardation in Down syndrome: extrapolation from full and segmental trisomy 16 mouse models. Brain Res. Brain Res. Rev. 35, 115–145 (2001). · DOI
  16. Bach, M.E., Hawkins, R.D., Osman, M., Kandel, E.R. & Mayford, M. Impairment of spatial but not contextual memory in CaMKII mutant mice with a selective loss of hippocampal LTP in the range of the theta frequency. Cell 81, 905–915 (1995). · DOI
  17. Elton, T.S., Sansom, S.E. & Martin, M.M. Trisomy-21 gene dosage over-expression of miRNAs results in the haploinsufficiency of specific target proteins. RNA Biol. 7, 540–547 (2010). · DOI
  18. Keck-Wherley, J. et al. Abnormal microRNA expression in Ts65Dn hippocampus and whole blood: contributions to Down syndrome phenotypes. Dev. Neurosci. 33, 451–467 (2011). · DOI
  19. He, M., Xu, Z., Ding, T., Kuang, D.M. & Zheng, L. MicroRNA-155 regulates inflammatory cytokine production in tumor-associated macrophages via targeting C/EBPβ. Cell Mol. Immunol. 6, 343–352 (2009). · DOI
  20. Fernandez, F. et al. Pharmacotherapy for cognitive impairment in a mouse model of Down syndrome. Nat. Neurosci. 10, 411–413 (2007). · DOI
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Metadata

Authors
Wang, X., Zhao, Y., Zhang, X., Badie, H., Zhou, Y., Mu, Y., Loo, L. S., Cai, L., Thompson, R. C., Yang, B., Chen, Y., Johnson, P. F., Wu, C., Bu, G., Mobley, W. C., Zhang, D., Gage, F. H., Ranscht, B., Zhang, Y.-W., Lipton, S. A., Hong, W., & Xu, H.
Venue
Nature Medicine
Publisher
Springer Science and Business Media LLC
Published
2013-03-24
Volume
19
Issue
4
Pages
473-480
ISSN
  • 1078-8956
  • 1546-170X
DOI
10.1038/nm.3117
PMC
PMC3911880
Cited by
220
References
6
Language
en
Licence
www.springer.com/tdm (tdm)

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