Forgot Password

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

Anti-Mouse Ly-6G (Gr-1) Purified 500 ug antibody


Antibody ID


Target Antigen

Mouse Ly-6G (Gr-1) Purified 500 ug mouse

Proper Citation

(Thermo Fisher Scientific Cat# 14-5931-85, RRID:AB_467731)


monoclonal antibody


Applications: IP (Assay-Dependent), IHC (P) (10 µg/mL), WB (Assay-Dependent), IHC (F) (10 µg/mL), Flow (0.5 µg/test), FN (Assay-Dependent)

Clone ID

Clone RB6-8C5

Host Organism



Thermo Fisher Scientific Go To Vendor

Cat Num


Publications that use this research resource

Transformation of Accessible Chromatin and 3D Nucleome Underlies Lineage Commitment of Early T Cells.

  • Hu G
  • Immunity
  • 2018 Feb 20

Literature context:


How chromatin reorganization coordinates differentiation and lineage commitment from hematopoietic stem and progenitor cells (HSPCs) to mature immune cells has not been well understood. Here, we carried out an integrative analysis of chromatin accessibility, topologically associating domains, AB compartments, and gene expression from HSPCs to CD4+CD8+ T cells. We found that abrupt genome-wide changes at all three levels of chromatin organization occur during the transition from double-negative stage 2 (DN2) to DN3, accompanying the T lineage commitment. The transcription factor BCL11B, a critical regulator of T cell commitment, is associated with increased chromatin interaction, and Bcl11b deletion compromised chromatin interaction at its target genes. We propose that these large-scale and concerted changes in chromatin organization present an energy barrier to prevent the cell from reversing its fate to earlier stages or redirecting to alternatives and thus lock the cell fate into the T lineages.

Funding information:
  • Intramural NIH HHS - Z01 HL005801-05()
  • NIAID NIH HHS - R01 AI083514()
  • NIGMS NIH HHS - R01GM073943(United States)

Alternative RNA splicing in the endothelium mediated in part by Rbfox2 regulates the arterial response to low flow.

  • Murphy PA
  • Elife
  • 2018 Jan 2

Literature context:


Low and disturbed blood flow drives the progression of arterial diseases including atherosclerosis and aneurysms. The endothelial response to flow and its interactions with recruited platelets and leukocytes determine disease progression. Here, we report widespread changes in alternative splicing of pre-mRNA in the flow-activated murine arterial endothelium in vivo. Alternative splicing was suppressed by depletion of platelets and macrophages recruited to the arterial endothelium under low and disturbed flow. Binding motifs for the Rbfox-family are enriched adjacent to many of the regulated exons. Endothelial deletion of Rbfox2, the only family member expressed in arterial endothelium, suppresses a subset of the changes in transcription and RNA splicing induced by low flow. Our data reveal an alternative splicing program activated by Rbfox2 in the endothelium on recruitment of platelets and macrophages and demonstrate its relevance in transcriptional responses during flow-driven vascular inflammation.

Funding information:
  • Howard Hughes Medical Institute - F32 HL110484()
  • NCI NIH HHS - R00 HL125727()
  • NHLBI NIH HHS - P01 HL066105()
  • NHLBI NIH HHS - P30 CA014051()
  • NHLBI NIH HHS - R01 GM034277()
  • Wellcome Trust - MC_PC_12009(United Kingdom)