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BM28 antibody

RRID:AB_398024

Antibody ID

AB_398024

Target Antigen

BM28 canine, chicken/bird, mouse, rat, human, chicken, dog, human, mouse, rat

Proper Citation

(BD Biosciences Cat# 610701, RRID:AB_398024)

Clonality

monoclonal antibody

Comments

Immunofluorescence, Immunohistochemistry, Western blot

Host Organism

mouse

Vendor

BD Biosciences Go To Vendor

Cat Num

610701

Publications that use this research resource

Polε Instability Drives Replication Stress, Abnormal Development, and Tumorigenesis.

  • Bellelli R
  • Mol. Cell
  • 2018 May 17

Literature context:


Abstract:

DNA polymerase ε (POLE) is a four-subunit complex and the major leading strand polymerase in eukaryotes. Budding yeast orthologs of POLE3 and POLE4 promote Polε processivity in vitro but are dispensable for viability in vivo. Here, we report that POLE4 deficiency in mice destabilizes the entire Polε complex, leading to embryonic lethality in inbred strains and extensive developmental abnormalities, leukopenia, and tumor predisposition in outbred strains. Comparable phenotypes of growth retardation and immunodeficiency are also observed in human patients harboring destabilizing mutations in POLE1. In both Pole4-/- mouse and POLE1 mutant human cells, Polε hypomorphy is associated with replication stress and p53 activation, which we attribute to inefficient replication origin firing. Strikingly, removing p53 is sufficient to rescue embryonic lethality and all developmental abnormalities in Pole4 null mice. However, Pole4-/-p53+/- mice exhibit accelerated tumorigenesis, revealing an important role for controlled CMG and origin activation in normal development and tumor prevention.

Funding information:
  • NIAID NIH HHS - U01 AI070499(United States)

The High-Affinity Interaction between ORC and DNA that Is Required for Replication Licensing Is Inhibited by 2-Arylquinolin-4-Amines.

  • Gardner NJ
  • Cell Chem Biol
  • 2017 Aug 17

Literature context:


Abstract:

In late mitosis and G1, origins of DNA replication must be "licensed" for use in the upcoming S phase by being encircled by double hexamers of the minichromosome maintenance proteins MCM2-7. A "licensing checkpoint" delays cells in G1 until sufficient origins have been licensed, but this checkpoint is lost in cancer cells. Inhibition of licensing can therefore kill cancer cells while only delaying normal cells in G1. In a high-throughput cell-based screen for licensing inhibitors we identified a family of 2-arylquinolin-4-amines, the most potent of which we call RL5a. The binding of the origin recognition complex (ORC) to origin DNA is the first step of the licensing reaction. We show that RL5a prevents ORC forming a tight complex with DNA that is required for MCM2-7 loading. Formation of this ORC-DNA complex requires ATP, and we show that RL5a inhibits ORC allosterically to mimic a lack of ATP.