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Article

The Overexpression of the<i>Insl3</i>in Female Mice Causes Descent of the Ovaries

1 Feb 2002

Abstract excerpt

Testicular descent in mice is dependent upon proper outgrowth of the gubernaculum primordia under the influence of the insulin-like 3 gene product (Insl3). Deletion of this gene prevents gubernaculum growth and causes bilateral cryptorchidism. In vitro experiments have led to the suggestion that Insl3 and androgens together induce outgrowth of the gubernacular primordia. The experiments reported here were...

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PMID: 11818498
DOI: 10.1210/mend.16.2.0772

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Related research

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Research trail→

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The Overexpression of the<i>Insl3</i>in Female Mice Causes Descent of the OvariesPMID 11818498Read ↗

Targeted disruption of the Insl3 gene causes bilateral cryptorchidism.Semantic proximity Read ↗

Cryptorchidism in mice mutant for Insl3.Semantic proximity Read ↗

GREAT/LGR8 is the only receptor for insulin-like 3 peptide.Semantic proximity Read ↗

Insulin‐like 3 signalling in testicular descentSemantic proximity Read ↗

Loss of Insl3: a potential predisposing factor for testicular torsion.Semantic proximity Read ↗

Leydig insulin-like hormone, gubernacular development and testicular descent.Semantic proximity Read ↗

Suppression of Insulin-Like3 Receptor Reveals the Role of β-Catenin and Notch Signaling in Gubernaculum DevelopmentSemantic proximity Read ↗

INSL3/RXFP2 Signaling in Testicular DescentSemantic proximity Read ↗

Insulin-Like 3 Signaling Is Important for Testicular Descent but Dispensable for Spermatogenesis and Germ Cell Survival in Adult Mice1Semantic proximity Read ↗

Transabdominal testicular descent is disrupted in mice with deletion of insulinlike factor 3 receptor.Semantic proximity Read ↗

Developmental Expression and Gene Regulation of Insulin-like 3 Receptor RXFP2 in Mouse Male Reproductive Organs1Semantic proximity Read ↗

GLI3 resides at the intersection of hedgehog and androgen action to promote male sex differentiation.Semantic proximity Read ↗

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