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The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.

Antagonistic Effects of BACE1 and APH1B-γ-Secretase Control Axonal Guidance by Regulating Growth Cone Collapse

Barão, Soraia, Gärtner, Annette, Leyva-Díaz, Eduardo, Demyanenko, Galina, Munck, Sebastian, Vanhoutvin, Tine, Zhou, Lujia, Schachner, Melitta, López-Bendito, Guillermina, Maness, Patricia F., De Strooper, Bart·2015·Cell Reports
DOI 10.1016/j.celrep.2015.07.059PMC PMC4820248
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Crossref · 10.1016/j.celrep.2015.07.059

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  • BACE1 also negatively regulates surface levels and/or function of two other substrates, contactin-2 and CHL1.

    “because BACE1 also negatively regulates surface levels and/or function of two other substrates, contactin-2 and CHL1 [12, 15, 53].”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [12]

    The Discussion (page unavailable) says BACE1 cleavage of CHL1 is necessary for Sema3A-induced growth cone collapse, and that the resulting CHL1 fragment transmits the signal. That is contrary to the claim that BACE1 negatively regulates CHL1 function. Our copy does not address contactin-2 or establish a reduction in surface levels. (LLM, conf=0.84)

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  • BACE1 is highly expressed in the nervous system and contributes to additional physiological processes besides its role in AD, e.g., through neuregulin-1 cleavage in myelination and CHL1 cleavage in axon targeting.

    “BACE1 is highly expressed in the nervous system and contributes to additional physiological processes besides its role in AD, e.g. through neuregulin-1 cleavage in myelination and CHL1 cleavage in axon targeting [7–12].”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [12]

    The Introduction (page unavailable) identifies neuregulin-1 type III as a BACE1 substrate implicated in myelination, and the Discussion reports that BACE1 cleavage of CHL1 is necessary for growth-cone collapse during axonal guidance. The copy does not establish that BACE1 is highly expressed in the nervous system. The Introduction also says the precise link between neuregulin-1 processing and its function is unknown, so the claim's cleavage-to-myelination mechanism is more definite than the source supports. (LLM, conf=0.87)

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  • More than 40 substrate candidates for BACE1 were identified in recent proteomic studies in murine neurons or CSF, but only a few have been validated with functional or in vitro assays, including L1, CHL1, ENPP5 and PTPRN2.

    “More than 40 substrate candidates for BACE1 were identified in recent proteomic studies in murine neurons or cerebrospinal fluid (CSF), but only a few of them have been validated to date with functional or in vitro assays, including L1, CHL1, ENPP5 and PTPRN2 [12, 14–16].”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [12]

    The Introduction (page unavailable) reports a long list of potential BACE1 substrates, and the paper investigates the functional consequences of BACE1 processing of CHL1. It does not give the figure of more than 40, specify proteomic studies of cerebrospinal fluid, or address validation of ENPP5 and PTPRN2. (LLM, conf=0.85)

    Experimental — accuracy not yet measured

  • The function of SEZ6 and SEZ6L may not only be exerted by the full-length proteins, but also by sSEZ6 and sSEZ6L or even by the C-terminal fragments resulting from BACE1 cleavage.

    “However, the function of SEZ6 and SEZ6L may not only be exerted by the full-length proteins, but also by sSEZ6 and sSEZ6L or even by the C-terminal fragments resulting from BACE1 cleavage, as recently found for the BACE1 substrate CHL1 [12].”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [12]

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Citations

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Research works printed but not linked: 33

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  2. Annaert, 2001, Interaction with telencephalin and the amyloid precursor protein predicts a ring structure for presenilins, Neuron, 32, 579, 10.1016/S0896-6273(01)00512-8 · DOI
  3. Bagnard, 2001, Axonal surface molecules act in combination with semaphorin 3a during the establishment of corticothalamic projections, Cereb. Cortex, 11, 278, 10.1093/cercor/11.3.278 · DOI
  4. Cao, 2012, The precision of axon targeting of mouse olfactory sensory neurons requires the BACE1 protease, Sci. Rep., 2, 231, 10.1038/srep00231 · DOI
  5. Cheret, 2013, Bace1 and Neuregulin-1 cooperate to control formation and maintenance of muscle spindles, EMBO J., 32, 2015, 10.1038/emboj.2013.146 · DOI · Paper page
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  8. Fazzari, 2014, Cell autonomous regulation of hippocampal circuitry via Aph1b-γ-secretase/neuregulin 1 signalling, eLife, 3, e02196, 10.7554/eLife.02196 · DOI
  9. Fournier, 2000, Semaphorin3A enhances endocytosis at sites of receptor-F-actin colocalization during growth cone collapse, J. Cell Biol., 149, 411, 10.1083/jcb.149.2.411 · DOI
  10. Harrison, 2003, BACE1 (beta-secretase) transgenic and knockout mice: identification of neurochemical deficits and behavioral changes, Mol. Cell. Neurosci., 24, 646, 10.1016/S1044-7431(03)00227-6 · DOI · Paper page
  11. Hitt, 2012, β-Site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1)-deficient mice exhibit a close homolog of L1 (CHL1) loss-of-function phenotype involving axon guidance defects, J. Biol. Chem., 287, 38408, 10.1074/jbc.M112.415505 · DOI · Paper page
  12. Hu, 2006, Bace1 modulates myelination in the central and peripheral nervous system, Nat. Neurosci., 9, 1520, 10.1038/nn1797 · DOI · Paper page
  13. Kuhn, 2012, Secretome protein enrichment identifies physiological BACE1 protease substrates in neurons, EMBO J., 31, 3157, 10.1038/emboj.2012.173 · DOI · Paper page
  14. Laird, 2005, BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions, J. Neurosci., 25, 11693, 10.1523/JNEUROSCI.2766-05.2005 · DOI · Paper page
  15. Leyva-Díaz, 2014, FLRT3 is a Robo1-interacting protein that determines Netrin-1 attraction in developing axons, Curr. Biol., 24, 494, 10.1016/j.cub.2014.01.042 · DOI
  16. Mintz, 2008, ERM proteins regulate growth cone responses to Sema3A, J. Comp. Neurol., 510, 351, 10.1002/cne.21799 · DOI
  17. Montag-Sallaz, 2002, Misguided axonal projections, neural cell adhesion molecule 180 mRNA upregulation, and altered behavior in mice deficient for the close homolog of L1, Mol. Cell Biol., 22, 7967, 10.1128/MCB.22.22.7967-7981.2002 · DOI
  18. Naus, 2004, Ectodomain shedding of the neural recognition molecule CHL1 by the metalloprotease-disintegrin ADAM8 promotes neurite outgrowth and suppresses neuronal cell death, J. Biol. Chem., 279, 16083, 10.1074/jbc.M400560200 · DOI
  19. Pozas, 2001, Age-dependent effects of secreted semaphorins 3A, 3F, and 3E on developing hippocampal axons: in vitro effects and phenotype of semaphorin 3A (−/−) mice, Mol. Cell. Neurosci., 18, 26, 10.1006/mcne.2001.0999 · DOI
  20. Pratte, 2003, Mice deficient for the close homologue of the neural adhesion cell L1 (CHL1) display alterations in emotional reactivity and motor coordination, Behav. Brain Res., 147, 31, 10.1016/S0166-4328(03)00114-1 · DOI
  21. Rajapaksha, 2011, The Alzheimer’s β-secretase enzyme BACE1 is required for accurate axon guidance of olfactory sensory neurons and normal glomerulus formation in the olfactory bulb, Mol. Neurodegener., 6, 88, 10.1186/1750-1326-6-88 · DOI
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Metadata

Authors
Barão, S., Gärtner, A., Leyva-Díaz, E., Demyanenko, G., Munck, S., Vanhoutvin, T., Zhou, L., Schachner, M., López-Bendito, G., Maness, P. F., & De Strooper, B.
Venue
Cell Reports
Publisher
Elsevier BV
Published
2015-09
Volume
12
Issue
9
Pages
1367-1376
ISSN
2211-1247
DOI
10.1016/j.celrep.2015.07.059
PMC
PMC4820248
Cited by
62
References
3
Language
en
Licence

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