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Armenian Hamster Anti-Mouse Lineage Cocktail (CD3e / CD11b / CD45R(B220) / Erythroid Cells / Ly-6G / Ly-6C) Monoclonal Antibody, APC Conjugated, Clone M1/70

RRID:AB_1645213

Antibody ID

AB_1645213

Target Antigen

Mouse Lineage Cocktail (CD3e / CD11b / CD45R(B220) / Erythroid Cells / Ly-6G / Ly-6C) mouse

Proper Citation

(BD Biosciences Cat# 558074, RRID:AB_1645213)

Clonality

monoclonal antibody

Comments

Flow cytometry

Clone ID

Clone M1/70

Host Organism

armenian hamster

Vendor

BD Biosciences Go To Vendor

Cat Num

558074

Publications that use this research resource

Mapping Active Gene-Regulatory Regions in Human Repopulating Long-Term HSCs.

  • Wünsche P
  • Cell Stem Cell
  • 2018 Jul 5

Literature context:


Abstract:

Genes that regulate hematopoietic stem cell (HSC) self-renewal, proliferation, and differentiation are tightly controlled by regulatory regions. However, mapping such regions relies on surface markers and immunophenotypic definition of HSCs. Here, we use γ-retroviral integration sites (γRV ISs) from a gene therapy trial for 10 patients with Wiskott-Aldrich syndrome to mark active enhancers and promoters in functionally defined long-term repopulating HSCs. Integration site clusters showed the highest ATAC-seq signals at HSC-specific peaks and strongly correlated with hematopoietic risk variants. Tagged genes were significantly enriched for HSC gene sets. We were able to map over 3,000 HSC regulatory regions in late-contributing HSCs, and we used these data to identify miR-10a and miR-335 as two miRNAs regulating early hematopoiesis. In this study, we show that viral insertion sites can be used as molecular tags to assess chromatin conformation on functionally defined cell populations, thereby providing a genome-wide resource for regulatory regions in human repopulating long-term HSCs.

Funding information:
  • NCI NIH HHS - K08 CA120060-04(United States)

A polymorphism in the tumor suppressor p53 affects aging and longevity in mouse models.

  • Zhao Y
  • Elife
  • 2018 Mar 20

Literature context:


Abstract:

Tumor suppressor p53 prevents early death due to cancer development. However, the role of p53 in aging process and longevity has not been well-established. In humans, single nucleotide polymorphism (SNP) with either arginine (R72) or proline (P72) at codon 72 influences p53 activity; the P72 allele has a weaker p53 activity and function in tumor suppression. Here, employing a mouse model with knock-in of human TP53 gene carrying codon 72 SNP, we found that despite increased cancer risk, P72 mice that escape tumor development display a longer lifespan than R72 mice. Further, P72 mice have a delayed development of aging-associated phenotypes compared with R72 mice. Mechanistically, P72 mice can better retain the self-renewal function of stem/progenitor cells compared with R72 mice during aging. This study provides direct genetic evidence demonstrating that p53 codon 72 SNP directly impacts aging and longevity, which supports a role of p53 in regulation of longevity.

Funding information:
  • Lawrence Ellison Foundation - New Investigate Award AG-NS-0781-11()
  • National Institutes of Health - 1R01CA160558()
  • National Institutes of Health - 1R01CA203965()
  • National Institutes of Health - 1R01CA227912()
  • National Institutes of Health - F99CA222734()
  • NCI NIH HHS - F99 CA222734()
  • New Jersey Commission on Cancer Research - Postdoctoral Fellowship Award()
  • NICHD NIH HHS - R37HD033082(United States)
  • U.S. Department of Defense - W81XWH-16-1-0358()