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Timothy J Cole Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia
Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Monash Medical Centre, Clayton, Victoria, Australia

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Morag J Young Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Monash Medical Centre, Clayton, Victoria, Australia
Department of Molecular and Translational Research, Monash University, Melbourne, Victoria, Australia

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defect ( Bleich et al . 1999 ). The difficulty of maintaining these mice and their complicated systemic defects made them unsuitable for studies on the role of the MR in other tissue compartments or cell types. Development of the Cre recombinase-LoxP

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-17-0155
Volume/Issue:
Volume 234: Issue 1
Free access
Chirine Toufaily Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada

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Gauthier Schang Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada

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Xiang Zhou Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada

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Philipp Wartenberg Department of Experimental Pharmacology, Center for Molecular Signaling, Saarland University School of Medicine, Homburg, Germany

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Ulrich Boehm Department of Experimental Pharmacology, Center for Molecular Signaling, Saarland University School of Medicine, Homburg, Germany

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John P Lydon Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA

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Ferdinand Roelfsema Department of Internal Medicine, Section Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands

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Daniel J Bernard Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada

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and females (except on proestrus) is unlikely to derive from preservation of some PR function (i.e., incomplete recombination by Cre). Indeed, global Pgr -knockout mice similarly show normal LH and FSH production under most conditions ( Chappell et

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-19-0013
Volume/Issue:
Volume 244: Issue 1
Restricted access
Siân E Piret Academic Endocrine Unit, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Headington, Oxford OX3 7LJ, UK

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Rajesh V Thakker Academic Endocrine Unit, Oxford Centre for Diabetes, Endocrinology and Metabolism, Churchill Hospital, University of Oxford, Headington, Oxford OX3 7LJ, UK

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useful to generate tissue- (i.e. conditional knockout) or time-specific (i.e. inducible knockout) models. This is achieved by refining the gene trap and ‘conventional’ knockout strategies by the addition of LoxP or flippase (FLP) recombinase target (FRT

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0193
Volume/Issue:
Volume 211: Issue 3
Free access
Changjie Han Institute for Regenerative Medicine, Department of Human Anatomy and Embryology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA
Institute for Regenerative Medicine, Department of Human Anatomy and Embryology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA

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Yan Jiao Institute for Regenerative Medicine, Department of Human Anatomy and Embryology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA

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Qingguo Zhao Institute for Regenerative Medicine, Department of Human Anatomy and Embryology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA

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Baisong Lu Institute for Regenerative Medicine, Department of Human Anatomy and Embryology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157, USA

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. Synapsin 1 promoter-controlled cre expression significantly increases adiposity of tr/tr mice The gene trap vector in tr/tr mice contains two loxP sites, flanking the splicing acceptor (SA) sequences that disrupt normal Mex3c splicing ( Fig. 5 A). In

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0071
Volume/Issue:
Volume 221: Issue 3
Free access
Claes Ohlsson Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Petra Henning Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Karin H Nilsson Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Jianyao Wu Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Karin L Gustafsson Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Klara Sjögren Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Anna Törnqvist Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Antti Koskela Department of Anatomy and Cell Biology, Institute of Cancer Research and Translational Medicine, Faculty of Medicine, University of Oulu, Oulu, Finland

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Fu-Ping Zhang Research Centre for Integrative Physiology and Pharmacology, Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Turku, Finland

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Marie K Lagerquist Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Matti Poutanen Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden
Research Centre for Integrative Physiology and Pharmacology, Turku Center for Disease Modeling, Institute of Biomedicine, University of Turku, Turku, Finland

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Juha Tuukkanen Department of Anatomy and Cell Biology, Institute of Cancer Research and Translational Medicine, Faculty of Medicine, University of Oulu, Oulu, Finland

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Ulf H Lerner Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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Sofia Movérare-Skrtic Centre for Bone and Arthritis Research, Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, Gothenburg, Sweden

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16 activity than the previous cell-specific mouse models that we have used for detailed mechanistic studies of the effect of WNT16 on cortical bone. In these previous studies, we used Runx2-Cre and Dmp1-Cre mouse models to demonstrate that

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-18-0020
Volume/Issue:
Volume 237: Issue 2
Open access
Therese Standal St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia
St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia

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Rachelle W Johnson St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia

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Narelle E McGregor St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia

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Ingrid J Poulton St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia

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Patricia W M Ho St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia

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T John Martin St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia
St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia

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Natalie A Sims St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia
St.Vincent's Institute of Medical Research, Department of Medicine at St. Vincent's Hospital Melbourne, Department of Cancer Research and Molecular Medicine, 9 Princes St, Fitzroy, Victoria 3065, Australia

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obtained from Rodger McEver (Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Betz et al . 1998 ). Mice hemizygous for the Cre transgene were crossed with the gp130 flox mouse in which the transmembrane domain (exon 15) was flanked by loxP

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-14-0424
Volume/Issue:
Volume 223: Issue 2
Free access
Anyonya R Guntur The Musculoskeletal Laboratory, Maine Medical Center Research Institute, Center for Clinical and Translational Research, 81 Research Drive, Scarborough, Maine 04074, USA

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Clifford J Rosen The Musculoskeletal Laboratory, Maine Medical Center Research Institute, Center for Clinical and Translational Research, 81 Research Drive, Scarborough, Maine 04074, USA

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been shown in these cells. Table 1 Summarizes all the different knockouts and promoter Cre lines utilized to delete Pten and its downstream targets in different skeletal lineages along with some of the key observations Conditional knockouts of Pten

Article Type:
Research Article
DOI:
https://doi.org/10.1530/JOE-11-0175
Volume/Issue:
Volume 211: Issue 2
Free access
Samuel M Lee Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Jose Muratalla Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Marta Sierra-Cruz Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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Jose Cordoba-Chacon Department of Medicine, Division of Endocrinology, Diabetes and Metabolism, University of Illinois at Chicago, Chicago, Illinois, USA

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the phenotype obtained in the knockout mouse model and the understanding of the physiological relevance of the gene studied. Therefore, it should be necessary to assess the tissue-specific effects of PPARs with several Cre-LoxP-based methods (i

Article Type:
Review Article
DOI:
https://doi.org/10.1530/JOE-22-0155
Volume/Issue:
Volume 257: Issue 1
Free access
P Froment Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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M Vigier Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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D Nègre Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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I Fontaine Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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J Beghelli Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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F L Cosset Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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M Holzenberger Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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P Durand Institut de Génomique Fonctionnelle de Lyon, Université de Lyon, Lyon F-69003, France
INRA, CNRS, Université Lyon 1, Ecole Normale Supérieure, Lyon F-69364, France
INSERM U418, Lyon, France
Université de Lyon, (UCB-Lyon1), IFR128, Lyon F-69007, France
INSERM, U758, Lyon F-69007, France
Ecole Normale Supérieure de Lyon, Lyon F-69007, France
UMR 6175, INRA, CNRS, Université de Tours, Haras Nationaux, Physiologie de la Reproduction et des Comportements, 37380 Nouzilly, France
INSERM U515, Hôpital Saint-Antoine, 75571 Paris 12, France

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if for some of these factors produced by, and acting on, testicular cells, knockout models or spontaneous genetic defects have allowed us to understand their role on the early steps of spermatogenesis (e.g. stem cell factor (SCF), Besmer et al

Article Type:
Research Article
DOI:
https://doi.org/10.1677/JOE-07-0258
Volume/Issue:
Volume 194: Issue 3
Free access
Eun Jig Lee Endocrinology, Metabolism, and Molecular Medicine, Northwestern University, Feinberg School of Medicine, Chicago, Illinois 60611, USA

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J Larry Jameson Endocrinology, Metabolism, and Molecular Medicine, Northwestern University, Feinberg School of Medicine, Chicago, Illinois 60611, USA

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Cre-mediated recombination to activate repressed promoters in a cell-specific manner. Examples of each of these strategies are described below as pre-clinical models of pituitary tumor gene therapy. In addition to selective expression in the pituitary

Article Type:
Other
DOI:
https://doi.org/10.1677/joe.1.06023
Volume/Issue:
Volume 185: Issue 3
Free access