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In both patient and knockout cell lines reduced localisation of BLM (显示 BLM 抗体) to ultra fine DNA bridges and FANCD2 (显示 FANCD2 抗体) at foci linking bridges are observed. Overall, loss of RMI2 produces a partially active BLM (显示 BLM 抗体) complex with mild features of Bloom syndrome.
The results show that Topo IIIalpha stimulates DNA unwinding by BLM (显示 BLM 抗体) in a manner that is potentiated by RMI1 (显示 RMI1 抗体)-RMI2, and that the processivity of resection is reliant on the Topo IIIalpha-RMI1 (显示 RMI1 抗体)-RMI2 complex.
two proteins that interact with BLM (显示 BLM 抗体), RMI1 (显示 RMI1 抗体) and RMI2, are phosphorylated upon SAC (显示 ADCY10 抗体) activation, and, like BLM (显示 BLM 抗体), RMI1 (显示 RMI1 抗体), and RMI2, are phosphorylated in an MPS1 (显示 IDUA 抗体)-dependent manner.
Crystal structures of RMI1 (显示 RMI1 抗体) and RMI2, two OB-fold regulatory subunits of the BLM (显示 BLM 抗体) complex
RMI2 is a component of the BLM (RECQL3\; MIM 604610) complex, which plays a role in homologous recombination-dependent DNA repair and is essential for genome stability (Xu et al., 2008
BLM-associated protein of 18 kDa
, RMI2, RecQ mediated genome instability 2, homolog
, RecQ-mediated genome instability 2, S. cerevisiae, homolog of
, recQ-mediated genome instability protein 2