Cited by 195

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Protein Region Important for Regulation of Lipid Metabolism in Angiopoietin-like 3 (ANGPTL3)

Ono, Mitsuru, Shimizugawa, Tetsuya, Shimamura, Mitsuru, Yoshida, Kenichi, Noji-Sakikawa, Chisa, Ando, Yosuke, Koishi, Ryuta, Furukawa, Hidehiko·2003·Journal of Biological Chemistry

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Integrity signals

Registry

Crossref · 10.1074/jbc.m302861200

Cites

1 of 1 references verified0 citation errors · 0 not checkable

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  • Most studies showing ANGPTL3-mediated LPL inhibition in vitro required supraphysiological concentrations of ANGPTL3 to achieve significant inhibition.

    “and most of the studies showing that ANGPTL3-mediated LPL inhibition in vitro required supraphysiological concentrations of ANGPTL3 to achieve significant inhibition (60, 105, 107, 115).”
  • In vitro studies of the effect of cleavage on ANGPTL3-mediated inhibition have reported increased inhibition, decreased inhibition, and no effect on inhibition.

    “In vitro studies of the effect of cleavage on ANGPTL3-mediated inhibition have reported increased inhibition, decreased inhibition, and no effect on inhibition (107, 115, 124).”
  • ANGPTL3 contains a protease cleavage site and in vivo can be cleaved into two domains both intracellularly by PCSK3 and extracellularly by PACE4.

    “ANGPTL3 contains a protease cleavage site, and in vivo can be cleaved into two domains both intracellularly by PCSK3 and extracellularly by PACE4 (107, 124, 131, 132).”
  • The N-terminal cleavage product of ANGPTL3 is necessary and sufficient for lipase inhibition.

    “Several studies have identified the N-terminal cleavage product to be necessary and sufficient for lipase inhibition (107, 123, 124).”
  • Overexpression or injection of ANGPTL3 into mice increases plasma triglycerides.

    “Overexpression or injection of ANGPTL3 into mice increases plasma triglycerides (15, 107).”

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Citations

Cites

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Research works printed but not linked: 19

  1. Maisonpierre, 1997, Science, 277, 55, 10.1126/science.277.5322.55 · DOI · Paper page
  2. Davis, 1996, Cell, 87, 1161, 10.1016/S0092-8674(00)81812-7 · DOI · Paper page
  3. Valenzuela, 1999, Proc. Natl. Acad. Sci. U. S. A., 96, 1904, 10.1073/pnas.96.5.1904 · DOI
  4. Procopio, 1999, J. Biol. Chem., 274, 30196, 10.1074/jbc.274.42.30196 · DOI
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  6. Shiraki, 1993, Diabetes Frontier, 4, 641
  7. Koishi, 2002, Nat. Genet., 30, 151, 10.1038/ng814 · DOI
  8. Rossetti, 2002, Nat. Med., 8, 112, 10.1038/nm0202-112 · DOI
  9. Naoumova, 2002, Lancet, 359, 2215, 10.1016/S0140-6736(02)09315-7 · DOI
  10. Shimizugawa, 2002, J. Biol. Chem., 277, 33742, 10.1074/jbc.M203215200 · DOI · Paper page
  11. Miyake, 1996, Proc. Natl. Acad. Sci. U. S. A., 93, 1320, 10.1073/pnas.93.3.1320 · DOI
  12. Kanegae, 1994, Jpn. J. Med. Sci. Biol., 47, 157, 10.7883/yoken1952.47.157 · DOI
  13. Cardin, 1989, Arteriosclerosis, 9, 21, 10.1161/01.ATV.9.1.21 · DOI
  14. Lithell, 1977, Scand. J. Clin. Lab. Investig., 37, 551, 10.3109/00365517709101845 · DOI
  15. Yoshida, 2002, J. Lipid Res., 43, 1770, 10.1194/jlr.C200010-JLR200 · DOI
  16. Taipale, 1997, FASEB J., 11, 51, 10.1096/fasebj.11.1.9034166 · DOI · Paper page
  17. Hooper, 1997, Biochem. J., 321, 265, 10.1042/bj3210265 · DOI
  18. Fowlkes, 2002, Cytokine Growth Factor Rev., 13, 277, 10.1016/S1359-6101(02)00005-9 · DOI
  19. Shimamura, 2003, Biochem. Biophys Res. Comm., 301, 604, 10.1016/S0006-291X(02)03058-9 · DOI

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Metadata

Authors
Ono, M., Shimizugawa, T., Shimamura, M., Yoshida, K., Noji-Sakikawa, C., Ando, Y., Koishi, R., & Furukawa, H.
Venue
Journal of Biological Chemistry
Publisher
Elsevier BV
Published
2003-10
Volume
278
Issue
43
Pages
41804-41809
ISSN
0021-9258
Cited by
195
References
1
Language
en

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