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Titolo:
The triple threat to nascent apolipoprotein B - Evidence for multiple, distinct degradative pathways
Autore:
Fisher, EA; Pan, M; Chen, XL; Wu, XY; Wang, HX; Jamil, H; Sparks, JD; Williams, KJ;
Indirizzi:
Mt Sinai Sch Med, Zena & Michael A Wiener Cardiovasc Inst, Lab Lipoprot Res, New York, NY 10029 USA Mt Sinai Sch Med New York NY USA 10029 poprot Res, New York, NY 10029 USA Mt Sinai Sch Med, Dept Med, New York, NY 10029 USA Mt Sinai Sch Med New York NY USA 10029 , Dept Med, New York, NY 10029 USA Bristol Myers Squibb Co, Div Metab Dis, Princeton, NJ 08543 USA Bristol Myers Squibb Co Princeton NJ USA 08543 s, Princeton, NJ 08543 USA Univ Rochester, Sch Med, Dept Pathol & Lab Med, Rochester, NY 14642 USA Univ Rochester Rochester NY USA 14642 & Lab Med, Rochester, NY 14642 USA Thomas Jefferson Univ, Jefferson Med Coll, Dept Med,Dorrance H Hamilton Res Labs, Div Endocrinol Diabet & Metab Dis, Philadelphia, PA 19107 USA Thomas Jefferson Univ Philadelphia PA USA 19107 hiladelphia, PA 19107 USA
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 30, volume: 276, anno: 2001,
pagine: 27855 - 27863
SICI:
0021-9258(20010727)276:30<27855:TTTTNA>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; TRIGLYCERIDE TRANSFER PROTEIN; HEPARAN-SULFATE PROTEOGLYCANS; UBIQUITIN-PROTEASOME PATHWAY; PLACEBO-CONTROLLED TRIAL; N-3 FATTY-ACIDS; HEP G2 CELLS; INTRACELLULAR DEGRADATION; INSULIN-RESISTANCE; RAT HEPATOCYTES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
82
Recensione:
Indirizzi per estratti:
Indirizzo: Fisher, EA Mt Sinai Sch Med, Zena & Michael A Wiener Cardiovasc Inst, Lab Lipoprot Res, 1 Gustave Levy Pl,Box 1269, New York, NY 10029 USA Mt Sinai Sch Med 1 Gustave Levy Pl,Box 1269 New York NY USA 10029
Citazione:
E.A. Fisher et al., "The triple threat to nascent apolipoprotein B - Evidence for multiple, distinct degradative pathways", J BIOL CHEM, 276(30), 2001, pp. 27855-27863

Abstract

We previously showed that Omega -3 fatty acids reduce secretion of apolipoprotein B (apoB) from cultured hepatocytes by stimulating post-translational degradation. In this report, we now characterize this process, particularly in regard to the two known processes that degrade newly synthesized apoB, endoplasmic reticulum (ER)-associated degradation and re-uptake from the cell surface. First, we found that Omega -3-induced degradation preferentially reduces the secretion of large, assembled apoB-lipoprotein particles, and apoB polypeptide length is not a determinant. Second, based on several experimental approaches, ER-associated degradation is not involved. Third, re-uptake, the only process known to destroy fully assembled nascent lipoproteins, was clearly active in primary hepatocytes, but Omega -3-induced degradation of apoB continued even when re-uptake was blocked. Cell fractionation showed that Omega -3 fatty acids induced a striking loss of apoB(100) from the Golgi, while sparing apoB(100) in the ER, indicating a post-ER process. To determine the signaling involved, we used wortmannin, a phosphatidylinositol 3-kinase (PI3K) inhibitor, which blocked most, if not all, of the Omega -3 fatty acid effect. Therefore, nascent apoB is subject to ER-associated degradation, re-uptake, and a third distinct degradative pathway that appears to target lipoproteins after considerable assembly and involves a post-ER compartment and PI3K signaling. Physiologic, pathophysiologic, and pharmacologic regulation of net apoB secretion may involve alterations in any of these three degradative steps.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 16:53:47