ArticleDisease models & mechanisms2015
Scaffold attachment factor B2 (SAFB2)-null mice reveal non-redundant functions of SAFB2 compared with its paralog, SAFB1.
Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- A scaffold attachment factor PHM-2 regulates synaptic transmission through SLO-2 potassium channel in C. elegans.PLoS genetics · 2026Article
- A scaffold attachment factor PHM-2 regulates synaptic transmission through SLO-2 potassium channel inbioRxiv : the preprint server for biology · 2025Article
- Origin and evolution of acrocentric chromosomes in human and great apes.bioRxiv : the preprint server for biology · 2025Article
- Article
- SAFB associates with nascent RNAs and can promote gene expression in mouse embryonic stem cells.RNA (New York, N.Y.) · 2023Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
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.
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