1.Expression of deafness protein Tmie in postnatal developmental stages of C57BL/6J mice.
Sankarapandian KARUPPASAMY ; Yoonyi NAM ; Harry JUNG ; Jun Gyo SUH
Laboratory Animal Research 2012;28(2):147-150
Loss-of function mutations in the transmembrane inner ear expressed (Tmie/TMIE) gene have been shown to cause deafness in mice and humans (DFNB6). Previous studies report that the circling mouse can be an animal model for DFNB6. However, the expression pattern of Tmie protein in postnatal developmental stages has not been clearly revealed. In this study we tried to investigate the expression of Tmie protein in the liver, spleen, kidney, and lung, as well as in the cochlea. We examined various tissue samples from five different age groups of C57BL/6J animals. Using western blotting analysis, the expression of Tmie protein in these organs has been identified. The results show that Tmie protein expression in the cochlea has been increased in postnatal developmental stages, indicating that Tmie plays an important role in not only the development and also in the function of the cochlea. The expression pattern of Tmie in adult mouse organs such as the liver, spleen, kidney, and spleen significantly vary in adult rats. The order of Tmie expression level in mice (63 days after birth) was spleen, liver, lung, cochlea, and kidney, whereas in the adult rat it was liver, cochlea, lung, spleen, and kidney.
Adult
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Animals
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Blotting, Western
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Cochlea
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Deafness
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Ear, Inner
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Humans
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Kidney
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Liver
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Lung
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Mice
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Models, Animal
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Rats
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Spleen
2.Mapping of the Faded (fe) Gene to a Region between D10mit191 and D10mit44 on Mouse Chromosome 10.
Seung Hun OH ; Yoonyi NAM ; Jun Gyo SUH
Laboratory Animal Research 2011;27(1):41-46
The faded mouse is a coat color mutant that shows faded coat color and age-related loss of pigmentation. This mutation is transmitted by an autosomal recessive gene with 100% penetrance. In the present study, we carried out linkage analysis of the faded (fe) gene using intra-specific backcross panels. Affected faded mice were carefully confirmed by their faded coat color at about 4 weeks of age. In the intra-specific backcross between faded and CBA mice (n=198), the fe gene was mapped to a region 2.1 cM distal to D10mit191. Therefore, the gene order was defined as follows: centromere-D10mit51 (12.4+/-2.4 cM)-D10mit191 (2.1+/-1.0 cM)-fe-D10mit44 (13.3+/-2.4 cM)-D10mit42 (14.4+/-2.5 cM). This linkage map of the fe locus will provide a good entry point to isolate the fe gene. Since the faded mouse has pigmentary abnormalities, this mutant may be a useful model for studies of pigmentary abnormalities in humans.
Animals
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Chromosomes, Human, Pair 10
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Gene Order
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Genes, Recessive
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Humans
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Mice
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Mice, Inbred CBA
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Penetrance
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Pigmentation
3.New Splicing Variants of the Murine Damaged DNA Binding 2.
Jun Hong PARK ; YoonYi NAM ; Jungkee KWON ; Jun Gyo SUH
Laboratory Animal Research 2010;26(1):91-94
Damaged DNA binding (DDB) protein is an important gene in the repair of damaged DNA. DDB is a heterodimer (DDB1 and DDB2) protein, murine DDB2 has 10 exons about 1.5kb in size (Genbank Accession No. AY027937). Here we identified five DDB2 variants (M1-M5) from various mouse tissues that are generated by alternative splicing. We used reverse transcription-PCR (RT-PCR) to identify splicing variants and isolated PCR products using an agarose-gel PCR purification kit. All isolated PCR products were cloned and the structure of splicing variants was confirmed by sequencing. The first splicing variant M1 was generated by omission of exon 4. The second splicing variant M2, by omission of exons 4-5. The third variants M3 was generated by omission from the middle of exon 1 to exon 6 and was expressed in the heart. Fourth variants M4 was generated by omission of exon 2 and exons 4-7. M5, the last splicing variant was generated by omission of exons 4-7. M4 and M5 were expressed in the spleen. Analysis of tissue distribution by RT-PCR indicates that M1 is most highly expressed in the mouse brain. These results indicated that murine DDB2 has five splicing variants and splicing variants expression patterns were different depending on mouse tissue. Further functional studies of each splicing variants will provide more information about the molecular mechanism of DDB2 function and DDB2 gene expression regulation.
Alternative Splicing
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Animals
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Brain
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Clone Cells
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DNA
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Exons
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Gene Expression Regulation
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Heart
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Hydrocarbons, Chlorinated
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Mice
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Polymerase Chain Reaction
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Spleen
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Tissue Distribution
4.Anti-hyperlipidemic effect of soybean extract fermented by Bacillus subtilis MORI in db/db mice.
Yoonyi NAM ; Harry JUNG ; Sankarapandian KARUPPASAMY ; Jae Yeon LEE ; Kyung Don KANG ; Kyo Yeol HWANG ; Su Il SEONG ; Jun Gyo SUH
Laboratory Animal Research 2012;28(2):123-129
The purpose of this study was to investigate the anti-hyperlipidemic effect of soy bean extract solution fermented by Bacillus subtilis MORI (BTD-1E) in obese db/db mice. Eight-week-old male db/db mice were administered 33.3 mg/kg BTD-1E solution orally once a day for four weeks. The BTD-1E group showed significantly lower body weight compared with the db control group (P<0.05). The BTD-1E group showed significantly lower serum total cholesterol and LDL cholesterol levels compared with the db control group, respectively (P<0.05, P<0.01). The BTD-1E group showed significantly decreased liver weight relative to final body weight compared with the db control group (P<0.01). After four weeks of BTD-1E administration, lipid droplets in the liver were apparently decreased in the BTD-1E group compared to the db control group. In summary, our results suggest that BTD-1E has an anti-hyperlipidemic effect in the obese mouse model.
1-Deoxynojirimycin
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Animals
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Bacillus
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Bacillus subtilis
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Body Weight
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Cholesterol
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Cholesterol, LDL
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Humans
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Liver
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Male
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Mice
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Mice, Obese
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Soybeans