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PerCP/Cy5.5 Streptavidin antibody

RRID:AB_2716577

Antibody ID

AB_2716577

Target Antigen

Biotin human, mouse, rat

Proper Citation

(BioLegend Cat# 405214, RRID:AB_2716577)

Clonality

unknown

Comments

Discontinued; Application: FC, ICFC

Host Organism

n, a

Vendor

BioLegend

Cat Num

405214

Publications that use this research resource

CARM1 Is Essential for Myeloid Leukemogenesis but Dispensable for Normal Hematopoiesis.

  • Greenblatt SM
  • Cancer Cell
  • 2018 Jun 11

Literature context: 214, RRID:AB_2716577 PE-CD71 Biolegend 113808, RRID:


Abstract:

Chromatin-modifying enzymes, and specifically the protein arginine methyltransferases (PRMTs), have emerged as important targets in cancer. Here, we investigated the role of CARM1 in normal and malignant hematopoiesis. Using conditional knockout mice, we show that loss of CARM1 has little effect on normal hematopoiesis. Strikingly, knockout of Carm1 abrogates both the initiation and maintenance of acute myeloid leukemia (AML) driven by oncogenic transcription factors. We show that CARM1 knockdown impairs cell-cycle progression, promotes myeloid differentiation, and ultimately induces apoptosis. Finally, we utilize a selective, small-molecule inhibitor of CARM1 to validate the efficacy of CARM1 inhibition in leukemia cells in vitro and in vivo. Collectively, this work suggests that targeting CARM1 may be an effective therapeutic strategy for AML.

Funding information:
  • Wellcome Trust - A11961(United Kingdom)

CRIg, a tissue-resident macrophage specific immune checkpoint molecule, promotes immunological tolerance in NOD mice, via a dual role in effector and regulatory T cells.

  • Yuan X
  • Elife
  • 2017 Nov 24

Literature context: CP/Cy5.5-streptavidin BioLegend RRID:AB_2716577


Abstract:

How tissue-resident macrophages (TRM) impact adaptive immune responses remains poorly understood. We report novel mechanisms by which TRMs regulate T cell activities at tissue sites. These mechanisms are mediated by the complement receptor of immunoglobulin family (CRIg). Using animal models for autoimmune type 1 diabetes (T1D), we found that CRIg+ TRMs formed a protective barrier surrounding pancreatic islets. Genetic ablation of CRIg exacerbated islet inflammation and local T cell activation. CRIg exhibited a dual function of attenuating early T cell activation and promoting the differentiation of Foxp3+ regulatory (Treg) cells. More importantly, CRIg stabilized the expression of Foxp3 in Treg cells, by enhancing their responsiveness to interleukin-2. The expression of CRIg in TRMs was postnatally regulated by gut microbial signals and metabolites. Thus, environmental cues instruct TRMs to express CRIg, which functions as an immune checkpoint molecule to regulate adaptive immunity and promote immune tolerance.

Funding information:
  • NIGMS NIH HHS - T32 GM07270(United States)