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PCNA Monoclonal Antibody (PC10)


Antibody ID


Target Antigen

PCNA human

Proper Citation

(Thermo Fisher Scientific Cat# MA5-11358, RRID:AB_10982348)


monoclonal antibody


Applications: IF (1:50-1:100), ICC (1:50-1:100), Flow (1:2-1:4), IHC (P) (1:200-1:400), IP (1:25), WB (1:50)

Clone ID

Clone PC10

Host Organism



Thermo Fisher Scientific Go To Vendor

Cat Num


Publications that use this research resource

Movement maintains forebrain neurogenesis via peripheral neural feedback in larval zebrafish.

  • Hall ZJ
  • Elife
  • 2018 Mar 12

Literature context:


The postembryonic brain exhibits experience-dependent development, in which sensory experience guides normal brain growth. This neuroplasticity is thought to occur primarily through structural and functional changes in pre-existing neurons. Whether neurogenesis also mediates the effects of experience on brain growth is unclear. Here, we characterized the importance of motor experience on postembryonic neurogenesis in larval zebrafish. We found that movement maintains an expanded pool of forebrain neural precursors by promoting progenitor self-renewal over the production of neurons. Physical cues associated with swimming (bodily movement) increase neurogenesis and these cues appear to be conveyed by dorsal root ganglia (DRG) in the zebrafish body: DRG-deficient larvae exhibit attenuated neurogenic responses to movement and targeted photoactivation of DRG in immobilized larvae expands the pallial pool of proliferative cells. Our results demonstrate the importance of movement in neurogenic brain growth and reveal a fundamental sensorimotor association that may couple early motor and brain development.

Funding information:
  • Biotechnology and Biological Sciences Research Council - (United Kingdom)
  • Natural Sciences and Engineering Research Council of Canada - Discovery grant (RGPIN-2016-06325)()
  • Natural Sciences and Engineering Research Council of Canada - Post-doctoral fellowship (PDF 454019-2014)()

Restoration of Replication Fork Stability in BRCA1- and BRCA2-Deficient Cells by Inactivation of SNF2-Family Fork Remodelers.

  • Taglialatela A
  • Mol. Cell
  • 2017 Oct 19

Literature context:


To ensure the completion of DNA replication and maintenance of genome integrity, DNA repair factors protect stalled replication forks upon replication stress. Previous studies have identified a critical role for the tumor suppressors BRCA1 and BRCA2 in preventing the degradation of nascent DNA by the MRE11 nuclease after replication stress. Here we show that depletion of SMARCAL1, a SNF2-family DNA translocase that remodels stalled forks, restores replication fork stability and reduces the formation of replication stress-induced DNA breaks and chromosomal aberrations in BRCA1/2-deficient cells. In addition to SMARCAL1, other SNF2-family fork remodelers, including ZRANB3 and HLTF, cause nascent DNA degradation and genomic instability in BRCA1/2-deficient cells upon replication stress. Our observations indicate that nascent DNA degradation in BRCA1/2-deficient cells occurs as a consequence of MRE11-dependent nucleolytic processing of reversed forks generated by fork remodelers. These studies provide mechanistic insights into the processes that cause genome instability in BRCA1/2-deficient cells.

Funding information:
  • NCI NIH HHS - R01 CA197774()