{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T13:04:54Z","timestamp":1791205494269,"version":"4.1.0"},"reference-count":37,"publisher":"National Academy of Sciences","issue":"19","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[1999,9,14]]},"abstract":"<jats:p>\n                    Peroxisome proliferator-activated receptor binding protein (PBP), a nuclear receptor coactivator, interacts with estrogen receptor \u03b1 (ER\u03b1) in the absence of estrogen. This interaction was enhanced in the presence of estrogen but was reduced in the presence of antiestrogen, tamoxifen. Transfection of PBP in CV-1 cells resulted in enhancement of estrogen-dependent transcription, indicating that PBP serves as a coactivator in ER signaling. To examine whether overexpression of PBP plays a role in breast cancer because of its coactivator function in ER signaling, we determined the levels of PBP expression in breast tumors. High levels of PBP expression were detected in \u224850% of primary breast cancers and breast cancer cell lines by ribonuclease protection analysis,\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization, and immunoperoxidase staining. Fluorescence\n                    <jats:italic>in situ<\/jats:italic>\n                    hybridization of human chromosomes revealed that the\n                    <jats:italic>PBP<\/jats:italic>\n                    gene is located on chromosome 17q12, a region that is amplified in some breast cancers. We found\n                    <jats:italic>PBP<\/jats:italic>\n                    gene amplification in \u224824% (6\/25) of breast tumors and \u224830% (2\/6) of breast cancer cell lines, implying that PBP gene overexpression can occur independent of gene amplification. This gene comprises 17 exons that, together, span &gt;37 kilobases. The 5\u2032-flanking region of 2.5 kilobase pairs inserted into a luciferase reporter vector revealed that the promoter activity in CV-1 cells increased by deletion of nucleotides from \u22122,500 to \u2212273. The \u2212273 to +1 region, which exhibited high promoter activity, contains a typical CCAT box and multiple cis-elements such as C\/EBP\u03b2, YY1, c-Ets-1, AP1, AP2, and NF\u03baB binding sites. These observations, in particular\n                    <jats:italic>PBP<\/jats:italic>\n                    gene amplification, suggest that PBP, by its ability to function as ER\u03b1 coactivator, might play a role in mammary epithelial differentiation and in breast carcinogenesis.\n                  <\/jats:p>","DOI":"10.1073\/pnas.96.19.10848","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:43:20Z","timestamp":1027680200000},"page":"10848-10853","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":149,"title":["Amplification and overexpression of peroxisome proliferatoractivated receptor binding protein (\n                    <i>PBP\/PPARBP<\/i>\n                    ) gene in breast cancer"],"prefix":"10.1073","volume":"96","author":[{"given":"Yijun","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Pathology, Northwestern University Medical School, Chicago, IL 60611-3008; Department of Medicine, University of Chicago Medical Center, Chicago, IL 60637-1470; and Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine and Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chao","family":"Qi","sequence":"additional","affiliation":[{"name":"Department of Pathology, Northwestern University Medical School, Chicago, IL 60611-3008; Department of Medicine, University of Chicago Medical Center, Chicago, IL 60637-1470; and Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine and Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjay","family":"Jain","sequence":"additional","affiliation":[{"name":"Department of Pathology, Northwestern University Medical School, Chicago, IL 60611-3008; Department of Medicine, University of Chicago Medical Center, Chicago, IL 60637-1470; and Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine and Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michelle M.","family":"Le Beau","sequence":"additional","affiliation":[{"name":"Department of Pathology, Northwestern University Medical School, Chicago, IL 60611-3008; Department of Medicine, University of Chicago Medical Center, Chicago, IL 60637-1470; and Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine and Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"III","given":"Rafael","family":"Espinosa","sequence":"additional","affiliation":[{"name":"Department of Pathology, Northwestern University Medical School, Chicago, IL 60611-3008; Department of Medicine, University of Chicago Medical Center, Chicago, IL 60637-1470; and Division of Endocrinology, Diabetes, and Metabolism, Departments of Medicine and Genetics, University of Pennsylvania School of Medicine, Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G. 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