CoChat
Sign Up
Cited by 88

The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Systematic Proteomic Analysis Identifies β-Site Amyloid Precursor Protein Cleaving Enzyme 2 and 1 (BACE2 and BACE1) Substrates in Pancreatic β-Cells

Stützer, Ina, Selevsek, Nathalie, Esterházy, Daria, Schmidt, Alexander, Aebersold, Ruedi, Stoffel, Markus·2013·Journal of Biological Chemistry
DOI 10.1074/jbc.m112.444703
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1074/jbc.m112.444703

Cites

5 of 5 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

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?

  • The 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 [17]

    The Discussion (page unavailable) reports that the SEZ6 family had been shown to be cleaved by BACE1 in primary neurons. But this paper does not identify all three named proteins as candidate BACE1 substrates: it investigates SEZ6L and SEZ6L2 and validates them as BACE2-specific substrates in pancreatic islet β-cells. It also does not establish the claim that the BACE1 candidates had not been validated in detail. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • SEZ6L2 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 [17]

    The validation results identify BACE2, rather than BACE1, as the rate-limiting protease for SEZ6L2 shedding in pancreatic islets. The Discussion describes SEZ6L2 as a BACE2-specific substrate in pancreatic islets but notes that cleavage of the seizure 6 protein family can differ by tissue. The unqualified claim extends beyond the pancreatic-cell setting studied here. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • After initial BACE1 cleavage, the resulting C-terminal, membrane-bound protein fragments of several membrane proteins, including APP and SEZ6L, are further processed within their transmembrane domains by γ-secretase, in a process referred to as regulated intramembrane proteolysis.

    “After initial BACE1 cleavage, the resulting C-terminal, membrane-bound protein fragments of several membrane proteins, including APP and SEZ6L [17], are further processed within their transmembrane domains by γ-secretase, in a process referred to as regulated intramembrane proteolysis [41]”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [17]

    The Discussion identifies APP as a BACE1 substrate, but identifies SEZ6L as a BACE2-specific substrate in pancreatic islets; it also reports BACE1 cleavage of the Seizure 6 family in primary neurons. Thus the paper does not support unqualified BACE1 cleavage of SEZ6L in the studied cells. The later γ-secretase statement is attached to a different citation [41]. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

  • Another proteomic study using pancreatic cells and tissue failed to confirm SEZ6L as a BACE1 substrate and demonstrated that SEZ6L is cleaved by BACE2 in pancreas.

    “However, the proteomic data for SEZ6L have not been validated by other methods and another proteomic study using pancreatic cells and tissue failed to confirm SEZ6L as a BACE1 substrate. Instead, that study demonstrated that SEZ6L is cleaved by the BACE1-homolog BACE2 in pancreas [17].”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [17]

  • In pancreatic cells, SEZ6L is predominantly cleaved by BACE2, but not by BACE1.

    “A previous study reported that in pancreatic cells SEZ6L is predominantly cleaved by BACE2, but not by BACE1 [17].”

    From Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons (2016) · cites this paper as [17]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 59

  1. Bouwens, 2005, Regulation of pancreatic beta-cell mass, Physiol. Rev., 85, 1255, 10.1152/physrev.00025.2004 · DOI · Paper page
  2. Kahn, 2006, Mechanisms linking obesity to insulin resistance and type 2 diabetes, Nature, 444, 840, 10.1038/nature05482 · DOI · Paper page
  3. Eberhard, 2009, The pancreatic beta-cell in the islet and organ community, Curr. Opin. Genet. Dev., 19, 469, 10.1016/j.gde.2009.07.003 · DOI
  4. Stützer, 2012, The pancreatic beta cell surface proteome, Diabetologia, 55, 1877, 10.1007/s00125-012-2531-3 · DOI
  5. Buteau, 2003, Glucagon-like peptide 1 induces pancreatic beta-cell proliferation via transactivation of the epidermal growth factor receptor, Diabetes, 52, 124, 10.2337/diabetes.52.1.124 · DOI · Paper page
  6. Trajkovski, 2004, Nuclear translocation of an ICA512 cytosolic fragment couples granule exocytosis and insulin expression in {beta}-cells, J. Cell Biol., 167, 1063, 10.1083/jcb.200408172 · DOI
  7. Esterházy, 2011, Bace2 is a beta cell-enriched protease that regulates pancreatic beta cell function and mass, Cell Metabolism, 14, 365, 10.1016/j.cmet.2011.06.018 · DOI · Paper page
  8. Danzer, 2012, Comprehensive description of the N-glycoproteome of mouse pancreatic beta-cells and human islets, J. Proteome Res., 11, 1598, 10.1021/pr2007895 · DOI
  9. Arribas, 2003, Shedding of plasma membrane proteins, Current Topics in Dev. Biol., 54, 125, 10.1016/S0070-2153(03)54007-8 · DOI
  10. Lichtenthaler, 2007, Sheddases and intramembrane-cleaving proteases: RIPpers of the membrane. Symposium on regulated intramembrane proteolysis, EMBO Rep., 8, 537, 10.1038/sj.embor.7400978 · DOI
  11. Figueroa, 2001, Abetapp secretases are co-expressed with Abetapp in the pancreatic islets, J. Alzheimer's Disease : JAD, 3, 393, 10.3233/JAD-2001-3405 · DOI
  12. Makridakis, 2010, Secretome proteomics for discovery of cancer biomarkers, J. Proteomics, 73, 2291, 10.1016/j.jprot.2010.07.001 · DOI
  13. Akpinar, 2005, Tmem27: a cleaved and shed plasma membrane protein that stimulates pancreatic beta cell proliferation, Cell Metabolism, 2, 385, 10.1016/j.cmet.2005.11.001 · DOI
  14. Schmidt, 2011, Absolute quantification of microbial proteomes at different states by directed mass spectrometry, Mol. Systems Biol., 7, 510, 10.1038/msb.2011.37 · DOI
  15. Yates, 1995, Method to correlate tandem mass spectra of modified peptides to amino acid sequences in the protein database, Anal. Chem., 67, 1426, 10.1021/ac00104a020 · DOI
  16. Keller, 2002, Empirical statistical model to estimate the accuracy of peptide identifications made by MS/MS and database search, Anal. Chem., 74, 5383, 10.1021/ac025747h · DOI
  17. Nesvizhskii, 2003, A statistical model for identifying proteins by tandem mass spectrometry, Anal. Chem., 75, 4646, 10.1021/ac0341261 · DOI
  18. Mueller, 2007, SuperHirn - a novel tool for high resolution LC-MS-based peptide/protein profiling, Proteomics, 7, 3470, 10.1002/pmic.200700057 · DOI
  19. Picotti, 2010, High-throughput generation of selected reaction-monitoring assays for proteins and proteomes, Nature Methods, 7, 43, 10.1038/nmeth.1408 · DOI
  20. Käll, 2004, A combined transmembrane topology and signal peptide prediction method, J. Mol. Biol., 338, 1027, 10.1016/j.jmb.2004.03.016 · DOI
  21. Selevsek, 2011, Systematic quantification of peptides/proteins in urine using selected reaction monitoring, Proteomics, 11, 1135, 10.1002/pmic.201000599 · DOI
  22. MacLean, 2010, Skyline: an open source document editor for creating and analyzing targeted proteomics experiments, Bioinformatics, 26, 966, 10.1093/bioinformatics/btq054 · DOI · Paper page
  23. Chang, 2012, Protein significance analysis in selected reaction monitoring (SRM) measurements, Mol. Cell Proteomics, 11, 10.1074/mcp.M111.014662 · DOI
  24. Schiess, 2009, Analysis of cell surface proteome changes via label-free, quantitative mass spectrometry, Mol. Cell. Proteomics, 8, 624, 10.1074/mcp.M800172-MCP200 · DOI
  25. Zhang, 2003, Identification and quantification of N-linked glycoproteins using hydrazide chemistry, stable isotope labeling and mass spectrometry, Nature Biotechnol., 21, 660, 10.1038/nbt827 · DOI
  26. Huang da, 2009, Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources, Nature Protocols, 4, 44, 10.1038/nprot.2008.211 · DOI · Paper page
  27. Overall, 2007, In search of partners: linking extracellular proteases to substrates, Nat. Rev. Mol. Cell Biol., 8, 245, 10.1038/nrm2120 · DOI
  28. McDermott, 1999, Germline mutations in the extracellular domains of the 55 kDa TNF receptor, TNFR1, define a family of dominantly inherited autoinflammatory syndromes, Cell, 97, 133, 10.1016/S0092-8674(00)80721-7 · DOI
  29. Peiretti, 2005, Proteasome inhibition activates the transport and the ectodomain shedding of TNF-α receptors in human endothelial cells, J. Cell Science, 118, 1061, 10.1242/jcs.01696 · DOI
  30. Dowling, 2011, Conditioned media from cell lines: a complementary model to clinical specimens for the discovery of disease-specific biomarkers, Proteomics, 11, 794, 10.1002/pmic.201000530 · DOI
  31. Butler, 2009, Proteomic identification of multitasking proteins in unexpected locations complicates drug targeting, Nat. Rev. Drug Discov., 8, 935, 10.1038/nrd2945 · DOI
  32. Dowling, 2008, Proteomic analysis of conditioned media from glucose responsive and glucose non-responsive phenotypes reveals a panel of secreted proteins associated with beta cell dysfunction, Electrophoresis, 29, 4141, 10.1002/elps.200800152 · DOI
  33. Kahn, 1990, Evidence of cosecretion of islet amyloid polypeptide and insulin by beta-cells, Diabetes, 39, 634, 10.2337/diab.39.5.634 · DOI · Paper page
  34. Whim, 2011, Pancreatic beta cells synthesize neuropeptide Y and can rapidly release peptide co-transmitters, PloS one, 6, e19478, 10.1371/journal.pone.0019478 · DOI
  35. Thomas, 2003, PANTHER: a browsable database of gene products organized by biological function, using curated protein family and subfamily classification, Nucleic Acids Res., 31, 334, 10.1093/nar/gkg115 · DOI
  36. Kuhn, 2012, Secretome protein enrichment identifies physiological BACE1 protease substrates in neurons, EMBO J, 31, 3157, 10.1038/emboj.2012.173 · DOI · Paper page
  37. Zhou, 2012, The neural cell adhesion molecules L1 and CHL1 are cleaved by BACE1 protease in vivo, J. Biol. Chem., 287, 25927, 10.1074/jbc.M112.377465 · DOI · Paper page
  38. Hemming, 2009, Identification of beta-secretase (BACE1) substrates using quantitative proteomics, PloS one, 4, e8477, 10.1371/journal.pone.0008477 · DOI
  39. Butler, 2007, Proteomic validation of protease drug targets: pharmacoproteomics of matrix metalloproteinase inhibitor drugs using isotope-coded affinity tag labelling and tandem mass spectrometry, Curr. Pharm. Des., 13, 263, 10.2174/138161207779313524 · DOI
  40. Hald, 2012, Pancreatic islet and progenitor cell surface markers with cell sorting potential, Diabetologia, 55, 154, 10.1007/s00125-011-2295-1 · DOI
  41. Schroeter, 1998, Notch-1 signalling requires ligand-induced proteolytic release of intracellular domain, Nature, 393, 382, 10.1038/30756 · DOI
  42. Rawson, 1997, Complementation cloning of S2P, a gene encoding a putative metalloprotease required for intramembrane cleavage of SREBPs, Mol. Cell, 1, 47, 10.1016/S1097-2765(00)80006-4 · DOI · Paper page
  43. Gunnersen, 2007, Sez-6 proteins affect dendritic arborization patterns and excitability of cortical pyramidal neurons, Neuron, 56, 621, 10.1016/j.neuron.2007.09.018 · DOI · Paper page
  44. Ghosh, 2003, Mannose 6-phosphate receptors: new twists in the tale, Nature Reviews. Mol. Cell Biol., 4, 202, 10.1038/nrm1050 · DOI
  45. Brown, 2009, Interactions of IGF-II with the IGF2R/cation-independent mannose-6-phosphate receptor mechanism and biological outcomes, Vitam. Horm., 80, 699, 10.1016/S0083-6729(08)00625-0 · DOI
  46. Hill, 1998, Growth factors and the regulation of fetal growth, Diabetes Care, 21, B60
  47. Zhang, 1997, Insulin-like growth factor II signaling through the insulin-like growth factor II/mannose-6-phosphate receptor promotes exocytosis in insulin-secreting cells, Proc. Natl. Acad. Sci. U. S.A., 94, 6232, 10.1073/pnas.94.12.6232 · DOI
  48. Zaina, 1998, The soluble type 2 insulin-like growth factor (IGF-II) receptor reduces organ size by IGF-II-mediated and IGF-II-independent mechanisms, J. Biol. Chem., 273, 28610, 10.1074/jbc.273.44.28610 · DOI
  49. Willnow, 2008, VPS10P-domain receptors-regulators of neuronal viability and function, Nature Reviews. Neuroscience, 9, 899, 10.1038/nrn2516 · DOI
  50. Dolais-Kitabgi, 1979, Effect of neurotensin on insulin, glucagon, and somatostatin release from isolated pancreatic islets, Endocrinology, 105, 256, 10.1210/endo-105-1-256 · DOI
  51. Beraud-Dufour, 2010, Neurotensin is a regulator of insulin secretion in pancreatic beta-cells, Int. J. Biochem. Cell Biol., 42, 1681, 10.1016/j.biocel.2010.06.018 · DOI
  52. Evans, 2011, Neuronal brain-derived neurotrophic factor is synthesized in excess, with levels regulated by sortilin-mediated trafficking and lysosomal degradation, J. Biol. Chem., 286, 29556, 10.1074/jbc.M111.219675 · DOI · Paper page
  53. Casas, 2010, BACE2 plays a role in the insulin receptor trafficking in pancreatic ss-cells, Amer. J. Physiol. Endocrinol. Metab., 299, E1087, 10.1152/ajpendo.00420.2010 · DOI
  54. In't Veld, 2010, Microscopic anatomy of the human islet of Langerhans, Adv. Exp. Med. Biol., 654, 1, 10.1007/978-90-481-3271-3_1 · DOI
  55. Mziaut, 2006, Synergy of glucose and growth hormone signalling in islet cells through ICA512 and STAT5, Nature Cell Biol., 8, 435, 10.1038/ncb1395 · DOI
  56. Torii, 2009, Gene silencing of phogrin unveils its essential role in glucose-responsive pancreatic beta-cell growth, Diabetes, 58, 682, 10.2337/db08-0970 · DOI
  57. Fukumoto, 2002, Beta-secretase protein and activity are increased in the neocortex in Alzheimer disease, Arch. Neurol., 59, 1381, 10.1001/archneur.59.9.1381 · DOI · Paper page
  58. Holsinger, 2002, Increased expression of the amyloid precursor beta-secretase in Alzheimer's disease, Annals Neurol., 51, 783, 10.1002/ana.10208 · DOI · Paper page
  59. Miyazaki, 1990, Establishment of a pancreatic beta cell line that retains glucose-inducible insulin secretion: special reference to expression of glucose transporter isoforms, Endocrinology, 127, 126, 10.1210/endo-127-1-126 · DOI

Cited by

Sorted by citations

Metadata

Authors
Stützer, I., Selevsek, N., Esterházy, D., Schmidt, A., Aebersold, R., & Stoffel, M.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2013-04
Volume
288
Issue
15
Pages
10536-10547
ISSN
0021-9258
DOI
10.1074/jbc.m112.444703
Cited by
88
References
5
Language
en
Licence

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.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review