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Mouse Anti-Mcm7 Monoclonal Antibody, Unconjugated, Clone DCS-141

RRID:AB_260666

Antibody ID

AB_260666

Target Antigen

Mcm7 human, xenopus, human, xenopus

Proper Citation

(Sigma-Aldrich Cat# M7931, RRID:AB_260666)

Clonality

monoclonal antibody

Comments

Vendor recommendations: Immunocytochemistry; Immunoprecipitation; Western Blot; Immunoblotting, Immunocytochemistry, Immunoprecipitation

Clone ID

Clone DCS-141

Host Organism

mouse

Vendor

Sigma-Aldrich

Cat Num

M7931

Publications that use this research resource

RECQ5 Helicase Cooperates with MUS81 Endonuclease in Processing Stalled Replication Forks at Common Fragile Sites during Mitosis.

  • Di Marco S
  • Mol. Cell
  • 2017 Jun 1

Literature context:


Abstract:

The MUS81-EME1 endonuclease cleaves late replication intermediates at common fragile sites (CFSs) during early mitosis to trigger DNA-repair synthesis that ensures faithful chromosome segregation. Here, we show that these DNA transactions are promoted by RECQ5 DNA helicase in a manner dependent on its Ser727 phosphorylation by CDK1. Upon replication stress, RECQ5 associates with CFSs in early mitosis through its physical interaction with MUS81 and promotes MUS81-dependent mitotic DNA synthesis. RECQ5 depletion or mutational inactivation of its ATP-binding site, RAD51-interacting domain, or phosphorylation site causes excessive binding of RAD51 to CFS loci and impairs CFS expression. This leads to defective chromosome segregation and accumulation of CFS-associated DNA damage in G1 cells. Biochemically, RECQ5 alleviates the inhibitory effect of RAD51 on 3'-flap DNA cleavage by MUS81-EME1 through its RAD51 filament disruption activity. These data suggest that RECQ5 removes RAD51 filaments stabilizing stalled replication forks at CFSs and hence facilitates CFS cleavage by MUS81-EME1.

RhoD Inhibits RhoC-ROCK-Dependent Cell Contraction via PAK6.

  • Durkin CH
  • Dev. Cell
  • 2017 May 8

Literature context:


Abstract:

RhoA-mediated regulation of myosin-II activity in the actin cortex controls the ability of cells to contract and bleb during a variety of cellular processes, including cell migration and division. Cell contraction and blebbing also frequently occur as part of the cytopathic effect seen during many different viral infections. We now demonstrate that the vaccinia virus protein F11, which localizes to the plasma membrane, is required for ROCK-mediated cell contraction from 2 hr post infection. Curiously, F11-induced cell contraction is dependent on RhoC and not RhoA signaling to ROCK. Moreover, RhoC-driven cell contraction depends on the upstream inhibition of RhoD signaling by F11. This inhibition prevents RhoD from regulating its downstream effector Pak6, alleviating the suppression of RhoC by the kinase. Our observations with vaccinia have now demonstrated that RhoD recruits Pak6 to the plasma membrane to antagonize RhoC signaling during cell contraction and blebbing.