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Secretome protein enrichment identifies physiological BACE1 protease substrates in neurons
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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 [15]
The ‘Identification of neuronal BACE1 sheddome’ section reports 34 candidate membrane-protein substrates in mouse neurons, and the validation sections confirm L1 and CHL1 as physiological substrates. This paper alone does not establish a total of more than 40 substrate candidates across neuronal and CSF studies, or validate ENPP5 and PTPRN2. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe three members of the SEZ6 family (SEZ6, SEZ6L, SEZ6L2) have been identified as candidate BACE1 substrates in different studies, but have not yet been validated in detail.
“The three members of the seizure protein 6 (SEZ6) family, namely SEZ6, SEZ6-like (SEZ6L) and SEZ6-like 2 (SEZ6L2) have been identified as candidate BACE1 substrates in different studies [15, 17], but have not yet been validated in detail.”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
Table I and the Discussion identify SEZ6, SEZ6L1 and SEZ6L2 as BACE1 substrate candidates, with SEZ6L2 showing less dependence on BACE1 for shedding. However, the sections on validation in primary neurons and BACE1-deficient mouse brains report further validation of SEZ6. The claim that the family members had not yet been validated in detail therefore does not hold for SEZ6 in this source. (LLM, conf=0.87)
Experimental — accuracy not yet measuredRecent proteomic studies have identified more than 40 membrane proteins as potential BACE1 substrates.
“Recent proteomic studies have identified more than 40 membrane proteins as potential BACE1 substrates [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 [15]
The 'Identification of neuronal BACE1 sheddome' section reports 34 membrane proteins among 40 proteins whose shedding or secretion was reduced. It supports the identification of potential BACE1 substrates, but does not establish the citing sentence’s total of more than 40 membrane proteins; six of its 40 proteins were soluble. (LLM, conf=0.87)
Experimental — accuracy not yet measuredBACE1 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 [15]
The section “BACE1 inhibition increases cell surface levels of contactin-2” directly states that BACE1 negatively regulates contactin-2 at the neuronal plasma membrane. “Validation of BACE1 substrates in primary neurons” reports reduced CHL1 shedding and increased full-length protein in cell lysates after BACE1 inhibition, but does not establish reduced CHL1 surface levels or function. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe previously identified cleavage site in SEZ6L is not identical, but similar to SEZ6, as it also has a hydrophobic amino acid in the P1 and a negatively charged amino acid in the P1' position.
“The previously identified cleavage site in SEZ6L [15] is not identical, but similar to SEZ6, as it also has a hydrophobic amino acid in the P1 and a negatively charged amino acid in the P1’ position (Fig. 5a).”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
The Identification of neuronal BACE1 sheddome section reports a SEZ6L1 semi-tryptic peptide consistent with direct BACE1 cleavage. The Discussion proposes a leucine–aspartate cleavage site for SEZ6, but our copy does not give the amino acids flanking the SEZ6L1 site or establish the claimed similarity between the two sites. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Nearly 70 BACE1 substrates have been identified to date.
“through secretome enrichment experiments, nearly 70 BACE1 substrates have been identified to date.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [23]
The paper’s Abstract reports that secretome protein enrichment with click sugars (SPECS) identified 34 BACE1 substrates in primary neurons. This supports the identification method, but the paper does not substantiate the claim that nearly 70 substrates had been identified through secretome enrichment experiments to date. (LLM, conf=0.88)
Experimental — accuracy not yet measuredBACE-1 cleaves numerous substrates, conferring a wide spectrum of physiological and pathological activities.
“BACE-1 cleaves numerous substrates, which confers this enzyme a wide spectrum of physiological and pathological activities (Kuhn et al., 2012; Zhou et al., 2012; Vassar et al., 2014), but it is indisputably its ability to process APP that has attracted much attention, especially in relation to AD.”
From Emerging Alternative Proteinases in APP Metabolism and Alzheimer’s Disease Pathogenesis: A Focus on MT1-MMP and MT5-MMP (2019) · cites this paper as Kuhn et al., 2012
The Identification of neuronal BACE1 sheddome section reports 34 neuronal membrane proteins whose shedding depends on BACE1. The Introduction links APP cleavage to pathogenic amyloid production and neuregulin-1 cleavage to myelination. But the Discussion says the functional consequences of cleavage remain unknown for most substrates, so the claim that cleavage confers a wide spectrum of physiological and pathological activities is stronger than the paper establishes. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSEZ6L2 appeared to be mostly cleaved by proteases other than BACE1.
“The third family member, SEZ6L2, appeared to be mostly cleaved by proteases other than BACE1 [15, 17].”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
SEZ6 was shown to undergo reduced cleavage in BACE1-/- mouse brains.
“After the proteomic identification of SEZ6 as a BACE1 substrate candidate, SEZ6 was also shown to undergo reduced cleavage in BACE1-/- mouse brains [15].”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
In a previous proteomic study, several tryptic peptides of the secreted SEZ6 ectodomain were identified.
“In the previous proteomic study which identified SEZ6 as a BACE1 substrate candidate, several tryptic peptides of the secreted SEZ6 ectodomain were identified.”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
Substrates SEZ6, L1CAM, LRRN1, neurotrimin, and CHL1 are involved in neurite outgrowth.
“Substrates SEZ6, L1CAM, leucine rich repeat neuronal 1 (LRRN1), neurotrimin, and CHL1 are all involved in neurite outgrowth.”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [23]
SEZ6 and SEZ6L appeared to be almost exclusively cleaved by BACE1 in neurons.
“In contrast, the two type I membrane proteins SEZ6 and its homolog SEZ6L appeared to be almost exclusively cleaved by BACE1 in neurons [15], making them potential biomarkers for BACE activity in vivo.”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
Similar results were obtained for sSEZ6 and full-length SEZ6 both in C3-treated neurons and in BACE1 KO mouse brains.
“In agreement with our previous study on SEZ6 [15], similar results were obtained for sSEZ6 and full-length SEZ6 both in C3-treated neurons and in BACE1 KO mouse brains (Fig. 2b and c).”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
Several other previously identified BACE1 substrates, such as CHL1, L1, contactin-2, APP and its homolog APLP2, are not exclusively cleaved by BACE1, but also by other proteases, including ADAM10.
“Several other previously identified BACE1 substrates, such as CHL1, L1, contactin-2, APP and its homolog APLP2, are not exclusively cleaved by BACE1, but also by other proteases, including ADAM10 [15, 38].”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
The most C-terminal of the tryptic peptides of the secreted SEZ6 ectodomain encompassed amino acids 894 to 904 (AASLDGFYNGR) of murine SEZ6.
“The most C-terminal of these peptides encompassed amino acids 894 to 904 (AASLDGFYNGR) of murine SEZ6 (Fig. 5a).”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
Precedents for tissue-specific proteolytic cleavage are BACE1 substrates CHL1 and L1, which are mostly cleaved by BACE1 in the nervous system, but by ADAM proteases in non-neuronal cells.
“Precedents for such a tissue-specific proteolytic cleavage are the BACE1 substrates CHL1 and L1, which are mostly cleaved by BACE1 in the nervous system, but by ADAM proteases in non-neuronal cells [15, 37].”
From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [15]
APP is a poor substrate for BACE1.
“It is well acknowledged that APP is a poor substrate for BACE1”
From BACE1: More than just a β‐secretase (2022) · cites this paper as [23]
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Citations
Cites
Vassar, R., Bennett, B. D., Babu-Khan, S., Kahn, S., Mendiaz, E. A., Denis, P., Teplow, D. B., Ross, S., Amarante, P., Loeloff, R., et al. (1999) · Science · doi:10.1126/science.286.5440.735 · Cited by 3,876 · cited 6×
“…APP shedding was only mildly inhibited with C3, because inhibition of BACE1 cleavage of APP has been shown to be accompanied by an increase in the ADAM10-mediated cleavage, resulting in only a moderate inhibition of total APP shedding upon BACE1 inhibition (Vassar et al , 1999; May et al , 2011).”
InfluentialControl of Peripheral Nerve Myelination by the ß-Secretase BACE1
Willem, M., Garratt, A. N., Novak, B., Citron, M., Kaufmann, S., Rittger, A., DeStrooper, B., Saftig, P., Birchmeier, C., & Haass, C. (2006) · Science · doi:10.1126/science.1132341 · Cited by 703
Kuhn, P., Wang, H., Dislich, B., Colombo, A., Zeitschel, U., Ellwart, J. W., Kremmer, E., Roßner, S., & Lichtenthaler, S. F. (2010) · The EMBO Journal · doi:10.1038/emboj.2010.167 · Cited by 621 · cited 2×
“…provided by Peter Altevogt), pAb Sez6 (kindly provided by Jenny Gunnersen), PTPRF (Neuromab), mAb APP C-terminal antibody 2C11, mAb sAPP b BAWT (Kuhn et al , 2010), pAb 192wt (kindly provided by Dale Schenck), mAb 22C11 (kindly provided by Konrad Beyreuther), pAb EP2456Y clone TAU (Millipore),…”
InfluentialSelf-citationSavonenko, A. V., Melnikova, T., Laird, F. M., Stewart, K.-A., Price, D. L., & Wong, P. C. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0710373105 · Cited by 290
BACE1 Deficiency Causes Altered Neuronal Activity and Neurodegeneration
Hu, X., Zhou, X., He, W., Yang, J., Xiong, W., Wong, P., Wilson, C. G., & Yan, R. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.1334-10.2010 · Cited by 162
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Metadata
- Authors
- Kuhn, P., Koroniak, K., Hogl, S., Colombo, A., Zeitschel, U., Willem, M., Volbracht, C., Schepers, U., Imhof, A., Hoffmeister, A., Haass, C., Roßner, S., Bräse, S., & Lichtenthaler, S. F.
- Venue
- The EMBO Journal
- Published
- 2012-06-22
- Volume
- 31
- Issue
- 14
- Pages
- 3157-3168
- ISSN
- 0261-4189
- 1460-2075
- Cited by
- 301
- References
- 5
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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