Rabbit Anti-Human SAFB (a.a. 551-650) Polyclonal antibody

Scaffold attachment factor B1 (SAFB1) and SAFB2 are large, multifunctional proteins that have been implicated in numerous cellular processes including chromatin organization, transcriptional regulation, RNA splicing, and stress response. While the two homologous proteins show high similarity, and functional domains are highly conserved, evidence suggests that they also have unique properties. For example, SAFB2 can be found in both the nucleus and cytoplasm, whereas SAFB1 seems to be mainly localized in the nucleus. In breast cancer cells, SAFBs function as estrogen receptor corepressors and growth inhibitors. SAFB protein expression is lost in approximately 20% of breast cancers. Interestingly, the two genes reside in close proximity, oriented head-to-head, on chromosome 19p13, a locus which is frequently lost in clinical breast cancer specimens. Furthermore, SAFB1 mutations have been identified in breast tumors that were not present in adjacent normal tissue. The possibility that SAFB1 and SAFB2 are novel breast tumor suppressor genes, and how they might function in this role, are discussed. (C) 2003 Wiley-Liss, Inc.

Scaffold attachment factors SAFB1 and SAFB2 are multifunctional proteins that share >70% sequence similarity. SAFB1-knockout (SAFB1(-/-)) mice display a high degree of lethality, severe growth retardation, and infertility in male mice. To assess the in vivo role of SAFB2, and to identify unique functions of the two paralogs, we generated SAFB2(-/-) mice. In stark contrast to SAFB1(-/-), SAFB2(-/-) offspring were born at expected Mendelian ratios and did not show any obvious defects in growth or fertility. Generation of paralog-specific antibodies allowed extensive expression analysis of SAFB1 and SAFB2 in mouse tissues, showing high expression of both SAFB1 and SAFB2 in the immune system, and in hormonally controlled tissues, with especially high expression of SAFB2 in the male reproductive tract. 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. Thus, despite a high degree of sequence similarity, SAFB1(-/-) and SAFB2(-/-) mice do not totally phenocopy each other. SAFB2(-/-) mice are viable, and do not show any major defects, and our data suggest a role for SAFB2 in the differentiation and activity of Sertoli cells that deserves further study.