X
Forgot Password

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

APC/Cyanine7 anti-mouse Ly-6G/Ly-6C (Gr-1) antibody

RRID:AB_2137486

Antibody ID

AB_2137486

Target Antigen

Ly-6G/Ly-6C (Gr-1) mouse

Proper Citation

(BioLegend Cat# 108423, RRID:AB_2137486)

Clonality

monoclonal antibody

Comments

Applications: FC

Clone ID

Clone RB6-8C5

Host Organism

rat

Vendor

BioLegend Go To Vendor

Cat Num

108423

Publications that use this research resource

Cooperative Epigenetic Remodeling by TET2 Loss and NRAS Mutation Drives Myeloid Transformation and MEK Inhibitor Sensitivity.

  • Kunimoto H
  • Cancer Cell
  • 2018 Jan 8

Literature context:


Abstract:

Mutations in epigenetic modifiers and signaling factors often co-occur in myeloid malignancies, including TET2 and NRAS mutations. Concurrent Tet2 loss and NrasG12D expression in hematopoietic cells induced myeloid transformation, with a fully penetrant, lethal chronic myelomonocytic leukemia (CMML), which was serially transplantable. Tet2 loss and Nras mutation cooperatively led to decrease in negative regulators of mitogen-activated protein kinase (MAPK) activation, including Spry2, thereby causing synergistic activation of MAPK signaling by epigenetic silencing. Tet2/Nras double-mutant leukemia showed preferential sensitivity to MAPK kinase (MEK) inhibition in both mouse model and patient samples. These data provide insights into how epigenetic and signaling mutations cooperate in myeloid transformation and provide a rationale for mechanism-based therapy in CMML patients with these high-risk genetic lesions.

Funding information:
  • NCI NIH HHS - K08 CA169055()
  • NCI NIH HHS - K08 CA181507()
  • NCI NIH HHS - P30 CA008748()
  • NCI NIH HHS - R01 CA173636()
  • NCI NIH HHS - R01 CA198089()
  • NCI NIH HHS - R35 CA197594()
  • NCI NIH HHS - T32 CA009156(United States)
  • NIH HHS - U54 OD020355()

Bone Marrow Myeloid Cells Regulate Myeloid-Biased Hematopoietic Stem Cells via a Histamine-Dependent Feedback Loop.

  • Chen X
  • Cell Stem Cell
  • 2017 Dec 7

Literature context:


Abstract:

Myeloid-biased hematopoietic stem cells (MB-HSCs) play critical roles in recovery from injury, butĀ little is known about how they are regulated within the bone marrow niche. Here we describe an auto-/paracrine physiologic circuit that controls quiescence of MB-HSCs and hematopoietic progenitors marked by histidine decarboxylase (Hdc). Committed Hdc+ myeloid cells lie in close anatomical proximity to MB-HSCs and produce histamine, which activates the H2 receptor on MB-HSCs to promote their quiescence and self-renewal. Depleting histamine-producing cells enforces cell cycle entry, induces loss of serial transplant capacity, and sensitizes animals to chemotherapeutic injury. Increasing demand for myeloid cells via lipopolysaccharide (LPS) treatment specifically recruits MB-HSCs and progenitors into the cell cycle; cycling MB-HSCs fail to revert into quiescence in the absence of histamine feedback, leading to their depletion, while an H2 agonist protects MB-HSCs from depletion after sepsis. Thus, histamine couples lineage-specific physiological demands to intrinsically primed MB-HSCs to enforce homeostasis.

Funding information:
  • NCI NIH HHS - P30 CA013696()
  • NCI NIH HHS - R35 CA197745()
  • NCRR NIH HHS - S10 RR027050()
  • NHLBI NIH HHS - R01 HL115145()
  • NIDDK NIH HHS - R01 DK048077()
  • NIGMS NIH HHS - GM087476(United States)
  • NIH HHS - S10 OD012351()
  • NIH HHS - S10 OD020056()
  • NIH HHS - S10 OD021764()