Cited by 206

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

The Cell Adhesion Protein P-selectin Glycoprotein Ligand-1 Is a Substrate for the Aspartyl Protease BACE1

Lichtenthaler, Stefan F., Dominguez, Diana-ines, Westmeyer, Gil G., Reiss, Karina, Haass, Christian, Saftig, Paul, De Strooper, Bart, Seed, Brian·2003·Journal of Biological Chemistry

Abstract

The aspartyl protease BACE1 cleaves the amyloid precursor protein and the sialyltransferase ST6Gal I and is important in the pathogenesis of Alzheimer's disease. The normal function of BACE1 and additional physiological substrates have not been identified. Here we show that BACE1 acts on the P-selectin glycoprotein ligand 1 (PSGL-1), which mediates leukocyte adhesion in inflammatory reactions. In human monocytic U937 and human embryonic kidney 293 cells expressing endogenous or transfected BACE1, PSGL-1 was cleaved by BACE1 to generate a soluble ectodomain and a C-terminal transmembrane fragment. No evidence of the cleavage fragment was seen in primary cells derived from mice deficient in BACE1. By using deletion constructs and enzymatic deglycosylation of the C-terminal PSGL-1 fragments, the cleavage site in PSGL-1 was mapped to the juxtamembrane region within the ectodomain. In an in vitro assay BACE1 catalyzed the formation of the PSGL-1 products seen in vivo. The cleavage occurred at a Leu-Ser peptide bond as identified by mass spectrometry using a synthetic peptide. We conclude that PSGL-1 is an additional substrate for BACE1.

Overview

Integrity signals

Registry

Crossref · 10.1074/jbc.m303861200

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

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?

  • Sialyltransferase and PSGL-1, in addition to APP and its homologues APLP1 and 2, are the only other reported substrates of BACE.

    “Sialyltransferase and PSGL-1, in addition to APP and its homologues APLP1 and 2 are the only other reported substrates of BACE (6,43).”
  • PSGL-1 is a BACE1 substrate that plays an important role in immune defenses by recruiting white blood cells to the site of infection.

    “P‐selectin glycoprotein ligand‐1 (PSGL‐1) is a BACE1 substrate that plays an important role in immune defenses by recruiting white blood cells to the site of infection.”

    From BACE1: More than just a β‐secretase (2022) · cites this paper as [25]

  • 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 [25]

  • 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 [25]

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 38

  1. Selkoe, 2001, Physiol. Rev., 81, 741, 10.1152/physrev.2001.81.2.741 · DOI · Paper page
  2. Hooper, 1997, Biochem. J., 321, 265, 10.1042/bj3210265 · DOI
  3. Blobel, 2000, Curr. Opin. Cell Biol., 12, 606, 10.1016/S0955-0674(00)00139-3 · DOI
  4. Schlondorff, 1999, J. Cell Sci., 112, 3603, 10.1242/jcs.112.21.3603 · DOI
  5. Peschon, 1998, Science, 282, 1281, 10.1126/science.282.5392.1281 · DOI
  6. Yan, 1999, Nature, 402, 533, 10.1038/990107 · DOI · Paper page
  7. Sinha, 1999, Nature, 402, 537, 10.1038/990114 · DOI · Paper page
  8. Hussain, 1999, Mol. Cell. Neurosci., 14, 419, 10.1006/mcne.1999.0811 · DOI · Paper page
  9. Lin, 2000, Proc. Natl. Acad. Sci. U. S. A., 97, 1456, 10.1073/pnas.97.4.1456 · DOI
  10. Haass, 2002, Trends Cell Biol., 12, 556, 10.1016/S0962-8924(02)02394-2 · DOI
  11. Vassar, 2001, J. Mol. Neurosci., 17, 157, 10.1385/JMN:17:2:157 · DOI
  12. Citron, 2002, Nat. Neurosci., 5, 1055, 10.1038/nn940 · DOI
  13. Kitazume, 2001, Proc. Natl. Acad. Sci. U. S. A., 98, 13554, 10.1073/pnas.241509198 · DOI · Paper page
  14. McEver, 1997, J. Clin. Investig., 100, 485, 10.1172/JCI119556 · DOI
  15. Sastre, 2001, EMBO Rep., 2, 835, 10.1093/embo-reports/kve180 · DOI
  16. Pimentel-Muinos, 1999, Immunity, 11, 783, 10.1016/S1074-7613(00)80152-1 · DOI
  17. De Strooper, 1998, Nature, 391, 387, 10.1038/34910 · DOI · Paper page
  18. De Strooper, 1995, EMBO J., 14, 4932, 10.1002/j.1460-2075.1995.tb00176.x · DOI
  19. Steiner, 2002, J. Biol. Chem., 277, 39062, 10.1074/jbc.C200469200 · DOI
  20. Davenpeck, 2000, J. Immunol., 165, 2764, 10.4049/jimmunol.165.5.2764 · DOI
  21. Herman, 1998, J. Immunol., 160, 2478, 10.4049/jimmunol.160.5.2478 · DOI
  22. Bennett, 2000, J. Biol. Chem., 275, 37712, 10.1074/jbc.M005339200 · DOI
  23. Lammich, 1999, Proc. Natl. Acad. Sci. U. S. A., 96, 3922, 10.1073/pnas.96.7.3922 · DOI · Paper page
  24. Dovey, 2001, J. Neurochem., 76, 173, 10.1046/j.1471-4159.2001.00012.x · DOI
  25. Shearman, 2000, Biochemistry, 39, 8698, 10.1021/bi0005456 · DOI
  26. Capell, 2002, J. Biol. Chem., 277, 5637, 10.1074/jbc.M109119200 · DOI
  27. Pouyani, 1995, Cell, 83, 333, 10.1016/0092-8674(95)90174-4 · DOI
  28. Kitazume, 2002, J. Biol. Chem., 278, 14865, 10.1074/jbc.M206262200 · DOI
  29. Lefer, 2000, Annu. Rev. Pharmacol. Toxicol., 40, 283, 10.1146/annurev.pharmtox.40.1.283 · DOI
  30. Chamoun, 2000, Front. Biosci., 5, E103, 10.2741/chamoun · DOI
  31. Esler, 2001, Science, 293, 1449, 10.1126/science.1064638 · DOI · Paper page
  32. Sisodia, 1992, Proc. Natl. Acad. Sci. U. S. A., 89, 6075, 10.1073/pnas.89.13.6075 · DOI
  33. Citron, 1995, Neuron, 14, 661, 10.1016/0896-6273(95)90323-2 · DOI
  34. Gruninger-Leitch, 2002, J. Biol. Chem., 277, 4687, 10.1074/jbc.M109266200 · DOI · Paper page
  35. Turner, 2001, Biochemistry, 40, 10001, 10.1021/bi015546s · DOI
  36. Cai, 2001, Nat. Neurosci., 4, 233, 10.1038/85064 · DOI
  37. Luo, 2001, Nat. Neurosci., 4, 231, 10.1038/85059 · DOI · Paper page
  38. Roberds, 2001, Hum. Mol. Genet., 10, 1317, 10.1093/hmg/10.12.1317 · DOI · Paper page

Cited by

Sorted by citations

Metadata

Authors
Lichtenthaler, S. F., Dominguez, D.-I., Westmeyer, G. G., Reiss, K., Haass, C., Saftig, P., De Strooper, B., & Seed, B.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2003-12
Volume
278
Issue
49
Pages
48713-48719
ISSN
0021-9258
Cited by
206
References
2
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.

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