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PCNA (F-2) antibody

RRID:AB_628109

Antibody ID

AB_628109

Target Antigen

PCNA (F-2) human, mouse, rat, mouse, rat, human

Proper Citation

(Santa Cruz Biotechnology Cat# sc-25280, RRID:AB_628109)

Clonality

monoclonal antibody

Comments

validation status unknown check with seller; recommendations: Immunohistochemistry; Immunoprecipitation; ELISA; Immunofluorescence; Immunocytochemistry; Western Blot; WB, IP, IF, IHC(P), ELISA

Host Organism

mouse

Vendor

Santa Cruz Biotechnology

Cat Num

sc-25280

Publications that use this research resource

Genome-wide Control of Heterochromatin Replication by the Telomere Capping Protein TRF2.

  • Mendez-Bermudez A
  • Mol. Cell
  • 2018 May 3

Literature context:


Abstract:

Hard-to-replicate regions of chromosomes (e.g., pericentromeres, centromeres, and telomeres) impede replication fork progression, eventually leading, in the event of replication stress, to chromosome fragility, aging, and cancer. Our knowledge of the mechanisms controlling the stability of these regions is essentially limited to telomeres, where fragility is counteracted by the shelterin proteins. Here we show that the shelterin subunit TRF2 ensures progression of the replication fork through pericentromeric heterochromatin, but not centromeric chromatin. In a process involving its N-terminal basic domain, TRF2 binds to pericentromeric Satellite III sequences during S phase, allowing the recruitment of the G-quadruplex-resolving helicase RTEL1 to facilitate fork progression. We also show that TRF2 is required for the stability of other heterochromatic regions localized throughout the genome, paving the way for future research on heterochromatic replication and its relationship with aging and cancer.

Funding information:
  • Medical Research Council - (United Kingdom)

Striatal oligodendrogliogenesis and neuroblast recruitment are increased in the R6/2 mouse model of Huntington's disease.

  • McCollum MH
  • Brain Res.
  • 2013 Jun 26

Literature context:


Abstract:

The subventricular zone (SVZ) is one of the two major neurogenic regions in the adult mammalian brain. Its close proximity to the striatum suggests that a cell-based therapeutic strategy for the treatment of Huntington's disease (HD) is possible. To achieve this, it is important to understand how adult cell production, migration and differentiation may be altered in the HD brain. In this study, we quantified the number of adult-born striatal cells and characterized their fate in the R6/2 transgenic mouse model of HD. We found that the number of new striatal cells was approximately two-fold greater in R6/2 vs. wild type mice, while SVZ cell proliferation was not affected. Using cell-type specific markers, we demonstrated that the majority of new striatal cells were mature oligodendrocytes or oligodendroglial precursors that were intrinsic to the striatum. We also detected a significant increase in the number of migrating neuroblasts that appeared to be recruited from the SVZ to the striatum. However, these neuroblasts did not mature into neurons and most were lost between 1 and 2 weeks of cell age. Crossing the R6/2 mice with mice the over-expressing brain-derived neurotrophic factor in the striatum increased the numbers of neuroblasts that survived to 2 weeks, but did not promote their differentiation. Together, our data indicate that the potential treatment of HD based on manipulating endogenous progenitor cells should take into consideration the apparent enhancement in striatal oligodendrogliogenesis and the limited ability of recruited SVZ neuroblasts to survive long-term and differentiate in the diseased striatum.

Funding information:
  • Canadian Institutes of Health Research - (Canada)