X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

Rat Anti-Mouse Ly-6A / E Monoclonal Antibody, PE-Cy7 Conjugated, Clone D7

RRID:AB_647253

Antibody ID

AB_647253

Target Antigen

Ly-6A / E mouse

Proper Citation

(BD Biosciences Cat# 558162, RRID:AB_647253)

Clonality

monoclonal antibody

Comments

Flow cytometry

Clone ID

D7

Host Organism

rat

Vendor

BD Biosciences Go To Vendor

Cat Num

558162

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)

Spred1 Safeguards Hematopoietic Homeostasis against Diet-Induced Systemic Stress.

  • Tadokoro Y
  • Cell Stem Cell
  • 2018 May 3

Literature context:


Abstract:

Stem cell self-renewal is critical for tissue homeostasis, and its dysregulation can lead to organ failure or tumorigenesis. While obesity can induce varied abnormalities in bone marrow components, it is unclear how diet might affect hematopoietic stem cell (HSC) self-renewal. Here, we show that Spred1, a negative regulator of RAS-MAPK signaling, safeguards HSC homeostasis in animals fed a high-fat diet (HFD). Under steady-state conditions, Spred1 negatively regulates HSC self-renewal and fitness, in part through Rho kinase activity. Spred1 deficiency mitigates HSC failure induced by infection mimetics and prolongs HSC lifespan, but it does not initiate leukemogenesis due to compensatory upregulation of Spred2. In contrast, HFD induces ERK hyperactivation and aberrant self-renewal in Spred1-deficient HSCs, resulting in functional HSC failure, severe anemia, and myeloproliferative neoplasm-like disease. HFD-induced hematopoietic abnormalities are mediated partly through alterations to the gut microbiota. Together, these findings reveal that diet-induced stress disrupts fine-tuning of Spred1-mediated signals to govern HSC homeostasis.

Funding information:
  • Arthritis Research UK - 17522(United Kingdom)

Nutritional Support from the Intestinal Microbiota Improves Hematopoietic Reconstitution after Bone Marrow Transplantation in Mice.

  • Staffas A
  • Cell Host Microbe
  • 2018 Apr 11

Literature context:


Abstract:

Bone marrow transplantation (BMT) offers curative potential for patients with high-risk hematologic malignancies, but the post-transplantation period is characterized by profound immunodeficiency. Recent studies indicate that the intestinal microbiota not only regulates mucosal immunity, but can also contribute to systemic immunity and hematopoiesis. Using antibiotic-mediated microbiota depletion in a syngeneic BMT mouse model, here we describe a role for the intestinal flora in hematopoietic recovery after BMT. Depletion of the intestinal microbiota resulted in impaired recovery of lymphocyte and neutrophil counts, while recovery of the hematopoietic stem and progenitor compartments and the erythroid lineage were largely unaffected. Depletion of the intestinal microbiota also reduced dietary energy uptake and visceral fat stores. Caloric supplementation through sucrose in the drinking water improved post-BMT hematopoietic recovery in mice with a depleted intestinal flora. Taken together, we show that the intestinal microbiota contribute to post-BMT hematopoietic reconstitution in mice through improved dietary energy uptake.

Funding information:
  • NCI NIH HHS - P01 CA023766()
  • NCI NIH HHS - P30 CA008748()
  • NCI NIH HHS - P30 CA016672()
  • NCRR NIH HHS - P30 RR031152(United States)
  • NHLBI NIH HHS - R01 HL069929()
  • NHLBI NIH HHS - R01 HL124112()
  • NIAID NIH HHS - R01 AI080455()
  • NIAID NIH HHS - R01 AI100288()
  • NIAID NIH HHS - R01 AI101406()
  • NIDDK NIH HHS - R01 DK048873()
  • NIDDK NIH HHS - R01 DK056626()
  • NIDDK NIH HHS - R01 DK103046()
  • NIDDK NIH HHS - R29 DK048873()
  • NIDDK NIH HHS - R37 DK048873()

Role of Macrophages and Plasminogen Activator Inhibitor-1 in Delayed Bone Repair in Diabetic Female Mice.

  • Shimoide T
  • Endocrinology
  • 2018 Apr 1

Literature context:


Abstract:

Delayed fracture healing is a clinical problem in diabetic patients. However, the mechanisms of diabetic delayed bone repair remain unknown. Here, we investigate the role of macrophages in diabetic delayed bone repair after femoral bone injury in streptozotocin (STZ)-treated and plasminogen activator inhibitor-1 (PAI-1)-deficient female mice. STZ treatment significantly decreased the numbers of F4/80-positive cells (macrophages) but not granulocyte-differentiation antigen-1-positive cells (neutrophils) at the damaged site on day 2 after femoral bone injury in mice. It significantly decreased the messenger RNA (mRNA) levels of macrophage colony-stimulating factor, inducible nitric oxide synthase (iNOS), interleukin (IL)-6, and CD206 at the damaged site on day 2 after bone injury. Moreover, STZ treatment attenuated a decrease in the number of hematopoietic stem cells in bone marrow induced by bone injury. On the other hand, PAI-1 deficiency significantly attenuated a decrease in the number of F4/80-positive cells induced by STZ treatment at the damaged site on day 2 after bone injury in mice. PAI-1 deficiency did not affect the mRNA levels of iNOS and IL-6 in F4/80- and CD11b-double-positive cells from the bone marrow of the damaged femurs decreased by diabetes in mice. PAI-1 deficiency significantly attenuated the phagocytosis of macrophages at the damaged site suppressed by diabetes. In conclusion, we demonstrated that type 1 diabetes decreases accumulation and phagocytosis of macrophages at the damaged site during early bone repair after femoral bone injury through PAI-1 in female mice.

Funding information:
  • Intramural NIH HHS - (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()