Growth enhancement in suppressor of cytokine signaling 2 (SOCS-2)-deficient mice is dependent on signal transducer and activator of transcription 5b (STAT5b)
- Author(s)
- Greenhalgh, CJ; Bertolino, P; Asa, SL; Metcalf, D; Corbin, JE; Adams, TE; Davey, HW; Nicola, NA; Hilton, DJ; Alexander, WS;
- Details
- Publication Year 2002-06,Volume 16,Issue #6,Page 1394-1406
- Journal Title
- MOLECULAR ENDOCRINOLOGY
- Publication Type
- Journal Article
- Abstract
- Mice lacking suppressor of cytokine signaling-2 (SOCS-2) exhibit accelerated postnatal growth resulting in adult mice that are 1.3 to 1.5 times the size of normal mice. In this study we examined the somatotrophic pathway to determine whether the production or actions of GH or IGF-I are altered in these mice. We demonstrated that SOCS-2(-/-) mice do not have elevated GH levels and suffer no major pituitary dysmorphogenesis, and that SOCS-2-deficient embryonic fibroblasts do not have altered IGF-I signaling. Primary hepatocytes from SOCS-2(-/-) mice, however, did have moderately prolonged signal transducer and activator of transcription 5 signaling in response to GH stimulation. Furthermore, the deletion of SOCS-2 from mice also lacking signal transducer and activator of transcription 5b had little effect on growth, suggesting that the action of SOCS-2 may be the regulation of the GH signaling pathway.
- Publisher
- ENDOCRINE SOC
- Keywords
- FACTOR-I RECEPTOR; INDUCIBLE SH2 PROTEIN; SOCS-3 MESSENGER-RNA; LACKING SUPPRESSOR; TRANSGENIC MICE; POSTNATAL-GROWTH; GENE-EXPRESSION; BODY GROWTH; HORMONE; INSULIN
- Publisher's Version
- https://doi.org/10.1210/me.16.6.1394
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2002-06-01 12:00:00