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