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BrdU Antibody


Antibody ID


Target Antigen

BrdU all species, amoeba/protozoa, bacteria/archaea, bovine, sheep, mouse, non-human primate, plant, rat, virus, canine, feline, reptile, c elegans/worm, chemical, drosophila/arthropod, hamster, human, xenopus/amphibian, zebrafish/fish, chicken/bird, guinea pig, other invertebrate, other mammalian, donkey, goat, horse, mollusc, rabbit, porcine, yeast/fungi

Proper Citation

(Novus Cat# NB500-169, RRID:AB_10002608)


monoclonal antibody


validation status unknown, reseller suggested use: IgG2a; IgG2a Flow Cytometry, Immunofluorescence, Immunocytochemistry, Immunohistochemistry-Paraffin; Flow Cytometry; Immunohistochemistry; Immunohistochemistry - fixed; Immunofluorescence; Immunocytochemistry

Host Organism




Cat Num


Publications that use this research resource

Reversible De-differentiation of Mature White Adipocytes into Preadipocyte-like Precursors during Lactation.

  • Wang QA
  • Cell Metab.
  • 2018 Jun 8

Literature context:


Adipose tissue in the mammary gland undergoes dramatic remodeling during reproduction. Adipocytes are replaced by mammary alveolar structures during pregnancy and lactation, then reappear upon weaning. The fate of the original adipocytes during lactation and the developmental origin of the re-appearing adipocyte post involution are unclear. Here, we reveal that adipocytes in the mammary gland de-differentiate into Pdgfrα+ preadipocyte- and fibroblast-like cells during pregnancy and remain de-differentiated during lactation. Upon weaning, de-differentiated fibroblasts proliferate and re-differentiate into adipocytes. This cycle occurs over multiple pregnancies. These observations reveal the potential of terminally differentiated adipocytes to undergo repeated cycles of de-differentiation and re-differentiation in a physiological setting.

Funding information:
  • NIDDK NIH HHS - P30DK079333(United States)

p53 orchestrates DNA replication restart homeostasis by suppressing mutagenic RAD52 and POLθ pathways.

  • Roy S
  • Elife
  • 2018 Jan 15

Literature context:


Classically, p53 tumor suppressor acts in transcription, apoptosis, and cell cycle arrest. Yet, replication-mediated genomic instability is integral to oncogenesis, and p53 mutations promote tumor progression and drug-resistance. By delineating human and murine separation-of-function p53 alleles, we find that p53 null and gain-of-function (GOF) mutations exhibit defects in restart of stalled or damaged DNA replication forks that drive genomic instability, which isgenetically separable from transcription activation. By assaying protein-DNA fork interactions in single cells, we unveil a p53-MLL3-enabled recruitment of MRE11 DNA replication restart nuclease. Importantly, p53 defects or depletion unexpectedly allow mutagenic RAD52 and POLθ pathways to hijack stalled forks, which we find reflected in p53 defective breast-cancer patient COSMIC mutational signatures. These data uncover p53 as a keystone regulator of replication homeostasis within a DNA restart network. Mechanistically, this has important implications for development of resistance in cancer therapy. Combined, these results define an unexpected role for p53-mediated suppression of replication genome instability.

Funding information:
  • NIAID NIH HHS - R01 AI038382(United States)

Pseudotemporal Ordering of Single Cells Reveals Metabolic Control of Postnatal β Cell Proliferation.

  • Zeng C
  • Cell Metab.
  • 2017 May 2

Literature context:


Pancreatic β cell mass for appropriate blood glucose control is established during early postnatal life. β cell proliferative capacity declines postnatally, but the extrinsic cues and intracellular signals that cause this decline remain unknown. To obtain a high-resolution map of β cell transcriptome dynamics after birth, we generated single-cell RNA-seq data of β cells from multiple postnatal time points and ordered cells based on transcriptional similarity using a new analytical tool. This analysis captured signatures of immature, proliferative β cells and established high expression of amino acid metabolic, mitochondrial, and Srf/Jun/Fos transcription factor genes as their hallmark feature. Experimental validation revealed high metabolic activity in immature β cells and a role for reactive oxygen species and Srf/Jun/Fos transcription factors in driving postnatal β cell proliferation and mass expansion. Our work provides the first high-resolution molecular characterization of state changes in postnatal β cells and paves the way for the identification of novel therapeutic targets to stimulate β cell regeneration.

Funding information:
  • NIDDK NIH HHS - P30 DK063491()
  • NIDDK NIH HHS - R01 DK064391()
  • NIDDK NIH HHS - R01 DK068471()
  • NIDDK NIH HHS - R01 DK078803()

Hippocampal neurogenesis enhancers promote forgetting of remote fear memory after hippocampal reactivation by retrieval.

  • Ishikawa R
  • Elife
  • 2016 Sep 26

Literature context:


Forgetting of recent fear memory is promoted by treatment with memantine (MEM), which increases hippocampal neurogenesis. The approaches for treatment of post-traumatic stress disorder (PTSD) using rodent models have focused on the extinction and reconsolidation of recent, but not remote, memories. Here we show that, following prolonged re-exposure to the conditioning context, enhancers of hippocampal neurogenesis, including MEM, promote forgetting of remote contextual fear memory. However, these interventions are ineffective following shorter re-exposures. Importantly, we find that long, but not short re-exposures activate gene expression in the hippocampus and induce hippocampus-dependent reconsolidation of remote contextual fear memory. Furthermore, remote memory retrieval becomes hippocampus-dependent after the long-time recall, suggesting that remote fear memory returns to a hippocampus dependent state after the long-time recall, thereby allowing enhanced forgetting by increased hippocampal neurogenesis. Forgetting of traumatic memory may contribute to the development of PTSD treatment.