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In both patient and knockout cell lines reduced localisation of BLM to ultra fine DNA bridges and FANCD2 at foci linking bridges are observed. Overall, loss of RMI2 produces a partially active BLM complex with mild features of Bloom syndrome.
The results show that Topo IIIalpha stimulates DNA unwinding by BLM in a manner that is potentiated by RMI1 (show RMI1 Proteins)-RMI2, and that the processivity of resection is reliant on the Topo IIIalpha-RMI1 (show RMI1 Proteins)-RMI2 complex.
two proteins that interact with BLM, RMI1 (show RMI1 Proteins) and RMI2, are phosphorylated upon SAC (show ADCY10 Proteins) activation, and, like BLM, RMI1 (show RMI1 Proteins), and RMI2, are phosphorylated in an MPS1 (show IDUA Proteins)-dependent manner.
Crystal structures of RMI1 and RMI2, two OB-fold regulatory subunits of the BLM 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