Related Experiment Video
Updated: Jul 7, 2026

Skeletal Phenotype Analysis of a Conditional Stat3 Deletion Mouse Model
Published on: July 3, 2020
The murine stanniocalcin 2 gene is a negative regulator of postnatal growth
Andy C-M Chang1, Jeff Hook, Frances A Lemckert
1Cancer Research Unit, The Children's Hospital, Westmead, New South Wales 2145, Australia.
Abstract:
Stanniocalcin (STC), a secreted glycoprotein, was first studied in fish as a classical hormone with a role in regulating serum calcium levels. There are two closely related proteins in mammals, STC1 and STC2, with functions that are currently unclear. Both proteins are expressed in numerous mammalian tissues rather than being secreted from a specific endocrine gland. No phenotype has been detected yet in Stc1-null mice, and to investigate whether Stc2 could have compensated for the loss of Stc1, we have now generated Stc2(-/-) and Stc1(-/-) Stc2(-/-) mice. Although Stc1 is expressed in the ovary and lactating mouse mammary glands, like the Stc1(-/-) mice, the Stc1(-/-) Stc2(-/-) mice had no detected decrease in fertility, fecundity, or weight gain up until weaning. Serum calcium and phosphate levels were normal in Stc1(-/-) Stc2(-/-) mice, indicating it is unlikely that the mammalian stanniocalcins have a major physiological role in mineral homeostasis. Mice with Stc2 deleted were 10-15% larger and grew at a faster rate than wild-type mice from 4 wk onward, and the Stc1(-/-) Stc2(-/-) mice had a similar growth phenotype. This effect was not mediated through the GH/IGF-I axis. The results are consistent with STC2 being a negative regulator of postnatal growth.
Insights
Mammalian stanniocalcin 2 (STC2) appears to regulate postnatal growth. Deleting STC2 in mice resulted in larger size and faster growth, suggesting STC2 acts as a growth inhibitor.
Area of Science:
- Endocrinology
- Molecular Biology
- Genetics
Background:
- Stanniocalcin (STC) was initially identified in fish as a hormone regulating calcium. Mammals possess two related proteins, STC1 and STC2, whose functions remain largely unknown.
- Unlike fish STC, mammalian STC1 and STC2 are expressed widely across tissues, not from a specific endocrine gland, and their physiological roles are unclear.
Purpose of the Study:
- To investigate the physiological roles of mammalian stanniocalcin 1 (STC1) and stanniocalcin 2 (STC2).
- To determine if STC2 compensates for the absence of STC1, and to elucidate the function of STC2 in postnatal growth and mineral homeostasis.
Main Methods:
- Generation and analysis of Stc1-null and Stc2-null mice, including double knockout (Stc1(-/-) Stc2(-/-)) models.
- Assessment of fertility, fecundity, weight gain, serum calcium, and phosphate levels in knockout mice.
- Evaluation of growth rates and potential mediation through the growth hormone/insulin-like growth factor I (GH/IGF-I) axis.
Main Results:
- Stc1(-/-) Stc2(-/-) mice exhibited normal fertility, fecundity, and mineral homeostasis, with no detected decrease compared to controls.
- Mice lacking STC2 (both Stc2(-/-) and Stc1(-/-) Stc2(-/-)) displayed significantly increased body size and accelerated growth rates from 4 weeks onward.
- The observed growth phenotype in STC2-deficient mice was independent of the GH/IGF-I axis.
Conclusions:
- Mammalian STC1 and STC2 do not appear to play a significant role in calcium and phosphate homeostasis.
- STC2 functions as a negative regulator of postnatal growth in mammals.
- Further research is warranted to fully understand the broader functions of STC1 and STC2.
Related Concept Videos
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Genomic Imprinting and Inheritance
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...
TGF - β Signaling Pathway
Hedgehog Signaling Pathway
Role Of Notch Signalling In Intestinal Stem Cell Renewal
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
PI3K/mTOR/AKT Signaling Pathway

