Limits...
Scaffold attachment factor B2 (SAFB2)- mice reveal non-redundant functions of SAFB2 compared with its paralog, SAFB1.

Jiang S, Katz TA, Garee JP, DeMayo FJ, Lee AV, Oesterreich S - Dis Model Mech (2015)

Bottom Line: Scaffold attachment factors SAFB1 and SAFB2 are multifunctional proteins that share >70% sequence similarity.Further analysis showed a significantly increased testis weight in SAFB2(-/-) mice, which was associated with an increased number of Sertoli cells.Our data suggest that this is at least in part caused by alterations in androgen-receptor function and expression upon deletion of SAFB2.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

No MeSH data available.


Related in: MedlinePlus

Body weight and IGF-I levels in SAFB2−/− mice. (A) Body weight measurements in male (n=5) and female (n=6) SAFB2+/+ and SAFB2−/− mice, presented as mean±s.e.m. (B) Serum IGF-I levels (mean±s.e.m.) in SAFB2+/+ (n=10) and SAFB2−/− (n=10) mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4582101&req=5

DMM019885F2: Body weight and IGF-I levels in SAFB2−/− mice. (A) Body weight measurements in male (n=5) and female (n=6) SAFB2+/+ and SAFB2−/− mice, presented as mean±s.e.m. (B) Serum IGF-I levels (mean±s.e.m.) in SAFB2+/+ (n=10) and SAFB2−/− (n=10) mice.

Mentions: We have previously shown that SAFB1−/− mice display both prenatal and neonatal lethality, growth retardation (caused by defects in the IGF signaling system), infertility in male mice and reduced testis weight (Ivanova et al., 2005). To determine whether SAFB2−/− mice displayed similar defects, we first assessed if there was some degree of lethality by analyzing genotypes of litters from SAFB2+/− intercrosses. All three genotypes of SAFB2 (+/+, +/− and −/−) were produced at the expected Mendelian distribution (1:2:1 ratio), suggesting that SAFB2−/− did not affect viability (Table 1). There were also no significant differences in body weight (Fig. 2A) or levels of circulating IGF-1 (Fig. 2B) between SAFB2+/+ and SAFB2−/− mice.Table 1.


Scaffold attachment factor B2 (SAFB2)- mice reveal non-redundant functions of SAFB2 compared with its paralog, SAFB1.

Jiang S, Katz TA, Garee JP, DeMayo FJ, Lee AV, Oesterreich S - Dis Model Mech (2015)

Body weight and IGF-I levels in SAFB2−/− mice. (A) Body weight measurements in male (n=5) and female (n=6) SAFB2+/+ and SAFB2−/− mice, presented as mean±s.e.m. (B) Serum IGF-I levels (mean±s.e.m.) in SAFB2+/+ (n=10) and SAFB2−/− (n=10) mice.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4582101&req=5

DMM019885F2: Body weight and IGF-I levels in SAFB2−/− mice. (A) Body weight measurements in male (n=5) and female (n=6) SAFB2+/+ and SAFB2−/− mice, presented as mean±s.e.m. (B) Serum IGF-I levels (mean±s.e.m.) in SAFB2+/+ (n=10) and SAFB2−/− (n=10) mice.
Mentions: We have previously shown that SAFB1−/− mice display both prenatal and neonatal lethality, growth retardation (caused by defects in the IGF signaling system), infertility in male mice and reduced testis weight (Ivanova et al., 2005). To determine whether SAFB2−/− mice displayed similar defects, we first assessed if there was some degree of lethality by analyzing genotypes of litters from SAFB2+/− intercrosses. All three genotypes of SAFB2 (+/+, +/− and −/−) were produced at the expected Mendelian distribution (1:2:1 ratio), suggesting that SAFB2−/− did not affect viability (Table 1). There were also no significant differences in body weight (Fig. 2A) or levels of circulating IGF-1 (Fig. 2B) between SAFB2+/+ and SAFB2−/− mice.Table 1.

Bottom Line: Scaffold attachment factors SAFB1 and SAFB2 are multifunctional proteins that share >70% sequence similarity.Further analysis showed a significantly increased testis weight in SAFB2(-/-) mice, which was associated with an increased number of Sertoli cells.Our data suggest that this is at least in part caused by alterations in androgen-receptor function and expression upon deletion of SAFB2.

View Article: PubMed Central - PubMed

Affiliation: Department of Molecular and Cellular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA Lester and Sue Smith Breast Center, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.

No MeSH data available.


Related in: MedlinePlus