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J. Biol. Chem., Vol. 278, Issue 31, 28528-28532, August 1, 2003

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Identification of Small PDZK1-associated Protein, DD96/MAP17, as a Regulator of PDZK1 and Plasma High Density Lipoprotein Levels^*

David L. Silver  , Nan Wang  and Silke Vogel ¶

From the Department of Medicine, Division of Molecular Medicine, and the ^¶Division of Preventative Medicine, Columbia University College of Physicians and Surgeons, New York, New York 10032

Scavenger receptor class B, type I (SR-BI) is the high density lipoprotein (HDL) receptor essential for hepatic uptake of HDL cholesterol. SR-BI was shown to impact plasma HDL levels and be anti-atherogenic. Thus, the ability to regulate hepatic SR-BI may allow for the modulation of plasma HDL cholesterol and progression of atherosclerosis. However, regulation of SR-BI in liver is not well understood. Recently, the PDZ domain containing protein PDZK1 was shown to interact with SR-BI and may serve an essential role in SR-BI cell surface expression. Here we identify an in vivo PDZK1-interacting protein that we named small PDZK1-associated protein (SPAP; also known as DD96/MAP17). Unexpectedly, we found that hepatic overexpression of SPAP in mice resulted in liver deficiency of PDZK1. The absence of PDZK1 in SPAP transgenic mice resulted in a deficiency of SR-BI in liver and markedly increased plasma HDL. Metabolic labeling experiments showed that the proteasome plays a role in the turnover of newly synthesized PDZK1, but that SPAP overexpression in liver increased PDZK1 turnover in an alternate, proteasome-independent pathway. Thus, SPAP may be an endogenous regulator of cellular PDZK1 levels by regulating PDZK1 turnover.

Received for publication, April 18, 2003 , and in revised form, May 13, 2003.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EBI Data Bank with accession number(s) AK008253.

^* This work was supported by Grant AHA0130305N (to D. L. S.) from the American Heart Association and Pfizer International HDL Research Award CU516105. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Medicine, P&S Rm. 8-401, Columbia University College of Physicians and Surgeons, 630 W. 168 St., New York, NY 10032. E-mail: dls51{at}columbia.edu.

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