Targeted disruption of mouse fibroblast activation protein

被引：107

作者：

Niedermeyer, J

Kriz, M

Hilberg, F

Garin-Chesa, P

Bamberger, U

Lenter, MC

Park, J

Viertel, B

Püschner, H

Mauz, M

Rettig, WJ

Schnapp, A ^{[1
]}

机构：

[1] Boehringer Ingelheim Pharma KG, Dept Oncol Res, D-88397 Biberach, Germany

[2] Boehringer Ingelheim Pharma KG, Dept Nonclin Drug Safety, D-88397 Biberach, Germany

[3] Boehringer Ingelheim Austria, Dept Mol Biol, A-1121 Vienna, Austria

来源：

MOLECULAR AND CELLULAR BIOLOGY | 2000年 / 20卷 / 03期

关键词：

D O I：

10.1128/MCB.20.3.1089-1094.2000

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Human fibroblast activation protein (FAP), a member of the serine prolyl oligopeptidase family, is a type II cell surface glycoprotein selectively expressed by fibroblastic cells in areas of active tissue remodeling, such as the embryonic mesenchyme, areas of wound healing, the gravid uterus, and the reactive stroma of epithelial cancers. Homologues of FAP have been identified in the mouse and Xenopus laevis. FAP is a dual-specificity enzyme that acts as a dipeptidyl peptidase and collagenase in vitro. To explore the role of FAP in vivo, Fap(-/-) mice were generated by homologous recombination. RNase protection analysis and reverse transcription-PCR confirmed the absence of full-length Fap transcripts in mouse embryonic tissues. No FAP protein was detected in Fap(-/-) animals by immunohistochemistry, and no FAP-specific dipeptidyl peptidase activity was found. We report that Fap(-/-) mice are fertile, show no overt developmental defects, and have no general change in cancer susceptibility.

引用

页码：1089 / 1094

页数：6

共 21 条

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