Disease relevance of S100g

• We found that VDR-/- mice show mild hypocalcemia, clear rickets and osteomalacia on bone histomorphometry, lower cortical bone density on quantitative tomography, and reduced concentrations of calbindin-D9k (CaBP-D9k) in duodenal mucosa and kidney [1].
• We have produced transgenic mice expressing the simian virus 40 T antigen driven by the promoter of the Calbindin-D9K (CaBP9K) gene and either -1,000 or -117 bp of regulatory sequences so as to establish in vivo, uterine smooth muscle tumor models [2].

High impact information on S100g

• Peak steady-state mRNA levels of the vitamin D-dependent calbindin-D9K gene were induced by 1,25(OH)2D more rapidly in the DBP-/- mice [3].
• Ontogeny of calbindin-D28K and calbindin-D9K in the mouse kidney, duodenum, cerebellum and placenta [4].
• CaBP-D9K first appears in enterocytes of the duodenum on day E18, in trophoblastic giant cells (TGC) of the placenta on day E10, and in the metanephric duct on day E15 [4].
• Intestinal expression of the calbindin-D9K gene in transgenic mice. Requirement for a Cdx2-binding site in a distal activator region [5].
• The calbindin-D9K gene encodes a vitamin D-induced calcium-binding protein that is expressed as a marker of small intestine differentiation [5].

Biological context of S100g

• Novel progestogenic activity of environmental endocrine disruptors in the upregulation of calbindin-D9k in an immature mouse model [6].
• The amino acid sequence was identical with the deduced sequence reported for rat intestinal calbindin-D9k in 73 of 77 positions [7].
• The inserted glutamine was located at the site of an intron in the rat calbindin gene, suggesting the possibility that alternative splicing produced the two forms of calbindin-D9k [7].
• Differential regulation by 1,25-dihydroxyvitamin D3 of calbindin-D9k and calbindin-D28k gene expression in mouse kidney [8].
• One of the isolated clones was the cDNA for the calcium binding protein D-9k (Cabp9k), which is considered to regulate intracytoplasmic concentration and transport of free calcium ions [9].

Anatomical context of S100g

• We therefore isolated mouse genomic clones of the calbindin-D9K gene and analyzed their expression in the mouse uterus [10].
• Supplementation with 17beta-E2 increased duodenal gene expression of TRPV5 and TRPV6 but also calbindin-D9K and plasma membrane Ca2+-ATPase (PMCA1b) in ovariectomized rats [11].
• Transfer of embryos into the uterine cavity of pseudopregnant mice reduced the expression of Cabp9k mRNA in the glandular epithelium, suggesting that Cabp9k mRNA expression is also regulated by embryonal signal(s) [9].
• Initial RT-PCR analysis demonstrated that CaBP-d28k but not CaBP-d9k mRNA expression is detectable in the endometrium of both species [12].
• Probing DNA from human-rodent somatic cell hybrids mapped human calbindin-D9k to chromosome Xp [13].

Associations of S100g with chemical compounds

• In the uterus of oophorectomized mice, the calbindin-D9k gene was up-regulated by progesterone, but not by estrogen [10].
• Differential transcriptional and translational regulations of calbindin-D9k by steroid hormones and their receptors in the uterus of immature mice [14].
• Calbindin-D9k levels in the rat uterus are under the control of estrogen [10].
• In the present studies, calbindin-D9k was purified from the intestines of mice (270 animals per purification) by use of gel permeation chromatography and two preparative electrophoresis steps in the presence and absence of EDTA [7].
• The 9,000 Mr calcium-binding protein calbindin-D9k (CaBP9k) is markedly induced by 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] in mammalian intestine [15].

Regulatory relationships of S100g

• Vitamin D receptor is required for dietary calcium-induced repression of calbindin-D9k expression in mice [16].

Other interactions of S100g

• The skeletal response to pregnancy was comparable in wt and VDR-/- mice; duodenal CaBP-D9k concentrations increased during pregnancy in VDR-/- as in wt mice, but remained 40% lower than in wt mice [1].
• The developmental appearance of vitamin D-dependent calcium-binding protein (calbindin-D9k) and alkaline phosphatase was studied in oc mutant and normal mice from birth to weaning, as were serum concentrations of 25-hydroxyvitamin D3 (25OHD3), 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3], calcium, and phosphorus [17].
• ST-630 was more effective than 1, 25-dihydroxyvitamin D3 [1,25(OH)2D3] with respect to the induction of Cyp24 and calbindin-D9k mRNAs in the kidney and in the small intestine [18].

Analytical, diagnostic and therapeutic context of S100g

• Northern blot and in-situ hybridization analyses demonstrated that the Cabp9k mRNA was expressed in the endometrial epithelia, both luminal and glandular, in the uterus at the time of implantation [9].
• Molecular cloning and chromosomal assignment of human calbindin-D9k [13].

References