Partial duplication in the Lepr db-Pas mutation is a result of unequal crossing over

Partial duplication in the Lepr db-Pas mutation is a result of unequal crossing over Mammalian Genome 9, 780–781 (1998). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1998 db-Pas Partial duplication in the Lepr mutation is a result of unequal crossing over Shun Mei Liu, Rudolph L. Leibel, Streamson C. Chua, Jr. Division of Molecular Genetics, Department of Pediatrics, Columbia University College of Physicians and Surgeons, Russ Berrie Medical Sciences Pavilion, 1150 St. Nicholas Avenue, Box 110, New York, New York 10032, USA Received: 2 March 1998 / Accepted: 15 May 1998 The leptin receptor gene (Lepr) has multiple splice variants, com- sizes (2 kbp) were amplified from both types of mice. The frag- prising at least five isoforms that have different signal transduction ment amplified from a wild-type DW/Pas mouse was sequenced and putative binding/transport capabilities (Lee et al. 1996; Tarta- with primer NewR1. A portion of this fragment showed perfect glia et al. 1995; Chua et al. 1997). A molecular analysis of the homology to the segment 38 of coding exon 6 of the Ex5L fi Ex4L functions of the various Lepr isoforms will require information fragment from the db-Pas mice. This indicates that the segment regarding the molecular nature of various spontaneous mutations that interrupts coding exon 6 in the http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Mammalian Genome Springer Journals

Partial duplication in the Lepr db-Pas mutation is a result of unequal crossing over

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Publisher
Springer-Verlag
Copyright
Copyright © 1998 by Springer-Verlag New York Inc.
Subject
Life Sciences; Cell Biology; Animal Genetics and Genomics; Human Genetics
ISSN
0938-8990
eISSN
1432-1777
D.O.I.
10.1007/s003359900865
Publisher site
See Article on Publisher Site

Abstract

Mammalian Genome 9, 780–781 (1998). Incorporating Mouse Genome © Springer-Verlag New York Inc. 1998 db-Pas Partial duplication in the Lepr mutation is a result of unequal crossing over Shun Mei Liu, Rudolph L. Leibel, Streamson C. Chua, Jr. Division of Molecular Genetics, Department of Pediatrics, Columbia University College of Physicians and Surgeons, Russ Berrie Medical Sciences Pavilion, 1150 St. Nicholas Avenue, Box 110, New York, New York 10032, USA Received: 2 March 1998 / Accepted: 15 May 1998 The leptin receptor gene (Lepr) has multiple splice variants, com- sizes (2 kbp) were amplified from both types of mice. The frag- prising at least five isoforms that have different signal transduction ment amplified from a wild-type DW/Pas mouse was sequenced and putative binding/transport capabilities (Lee et al. 1996; Tarta- with primer NewR1. A portion of this fragment showed perfect glia et al. 1995; Chua et al. 1997). A molecular analysis of the homology to the segment 38 of coding exon 6 of the Ex5L fi Ex4L functions of the various Lepr isoforms will require information fragment from the db-Pas mice. This indicates that the segment regarding the molecular nature of various spontaneous mutations that interrupts coding exon 6 in the

Journal

Mammalian GenomeSpringer Journals

Published: Sep 1, 1998

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