Anti-FLT3L monoclonal antibody, clone 50527

Name: Anti-FLT3L monoclonal antibody, clone 50527
SKU: DCABY-4034
Rating: 5 (1 reviews)

Mouse Anti-Human FLT3L monoclonal antibody for WB, ELISA(Cap), Neut

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG1

Clone

50527

Species Reactivity

Human

Immunogen

S. frugiperda insect ovarian cell line Sf 21-derived recombinant human Flt-3 Ligand. Thr27-Pro185 Accession Number AAA17999

Conjugate

Unconjugated

Applications

Application Notes

Western Blot: 1 μg/mL; ELISA Capture: 2-8 μg/mL; ELISA Detection: 0.1-0.4 μg/mL
We recommend the following for sandwich ELISA (Capture - Detection):
DCABY-4034 - DPABY-556

Target

Alternative Names

FLT3LG; fms-related tyrosine kinase 3 ligand; FL; FLT3L; flt3 ligand;

Entrez Gene ID

2323

UniProt ID

B7ZLY4

Product Background

Antigen Description

Flt-3 Ligand, also known as FL, is an alpha-helical cytokine that promotes the differentiation of multiple hematopoietic cell lineages. Mature human Flt-3 Ligand consists of a 158 amino acid (aa) extracellular domain (ECD) with a cytokine-like domain and a juxtamembrane tether region, a 21 aa transmembrane segment, and a 30 aa cytoplasmic tail. Within the ECD, human Flt-3 Ligand shares 71% and 65% aa sequence identity with mouse and rat Flt-3 Ligand, respectively. Human and mouse Flt-3 Ligand show cross-species activity. Flt-3 Ligand is expressed as a noncovalently-linked dimer by T cells and bone marrow and thymic fibroblasts. Each 36 kDa chain carries approximately 12 kDa of N- and O-linked carbohydrates. Alternate splicing and proteolytic cleavage of the transmembrane form can generate a soluble 30 kDa fragment that includes the cytokine domain. Alternate splicing of human Flt-3 Ligand also generates membrane-associated isoforms that contain either a truncated cytoplasmic tail or an 85 aa substitution following the cytokine domain. Both transmembrane and soluble Flt-3 Ligand signal through the tyrosine kinase receptor Flt-3/Flk-2. Flt-3 Ligand induces the expansion of monocytes and immature dendritic cells as well as early B cell lineage differentiation. It synergizes with IL-3, GM-CSF, and SCF to promote the mobilization and myeloid differentiation of hematopoietic stem cells. It cooperates with IL-2, -6, -7, and -15 to induce NK cell development and with IL-3, -7, and -11 to induce terminal B cell maturation. Animal studies also show Flt-3 Ligand to reduce the severity of experimentally induced allergic inflammation.

Pathway

Cytokine-cytokine receptor interaction; Hematopoietic cell lineage; Pathways in cancer;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

A natural killer-dendritic cell axis defines checkpoint therapy-responsive tumor microenvironments

NATURE MEDICINE

Authors: Barry, Kevin C.; Hsu, Joy; Broz, Miranda L.; Cueto, Francisco J.; Binnewies, Mikhail; Combes, Alexis J.; Nelson, Amanda E.; Loo, Kimberly; Kumar, Raj; Rosenblum, Michael D.; Alvarado, Michael D.; Wolf, Denise M.; Bogunovic, Dusan; Bhardwaj, Nina; Daud, Adil, I; Ha, Patrick K.; Ryan, William R.; Pollack, Joshua L.; Samad, Bushra; Asthana, Saurabh; Chan, Vincent; Krummel, Matthew F.

Abstract

Intratumoral stimulatory dendritic cells (SDCs) play an important role in stimulating cytotoxic T cells and driving immune responses against cancer. Understanding the mechanisms that regulate their abundance in the tumor microenvironment (TME) could unveil new therapeutic opportunities. We find that in human melanoma, SDC abundance is associated with intratumoral expression of the gene encoding the cytokine FLT3LG. FLT3LG is predominantly produced by lymphocytes, notably natural killer (NK) cells in mouse and human tumors. NK cells stably form conjugates with SDCs in the mouse TME, and genetic and cellular ablation of NK cells in mice demonstrates their importance in positively regulating SDC abundance in tumor through production of FLT3L. Although anti-PD-1 'checkpoint' immunotherapy for cancer largely targets T cells, we find that NK cell frequency correlates with protective SDCs in human cancers, with patient responsiveness to anti-PD-1 immunotherapy, and with increased overall survival. Our studies reveal that innate immune SDCs and NK cells cluster together as an excellent prognostic tool for T cell-directed immunotherapy and that these innate cells are necessary for enhanced T cell tumor responses, suggesting this axis as a target for new therapies.

Comparison of Gene Expression in Human Embryonic Stem Cells, hESC-Derived Mesenchymal Stem Cells and Human Mesenchymal Stem Cells

STEM CELLS INTERNATIONAL

Authors: Barbet, Romain; Peiffer, Isabelle; Hatzfeld, Antoinette; Charbord, Pierre; Hatzfeld, Jacques A.

Abstract

We present a strategy to identify developmental/differentiation and plasma membrane marker genes of the most primitive human Mesenchymal Stem Cells (hMSCs). Using sensitive and quantitative TaqMan Low Density Arrays (TLDA) methodology, we compared the expression of 381 genes in human Embryonic Stem Cells (hESCs), hESC-derived MSCs (hES-MSCs), and hMSCs. Analysis of differentiation genes indicated that hES-MSCs express the sarcomeric muscle lineage in addition to the classical mesenchymal lineages, suggesting they are more primitive than hMSCs. Transcript analysis of membrane antigens suggests that IL1R1(low), BMPR1B(low), FLT4(low), LRRC32(low), and CD34 may be good candidates for the detection and isolation of the most primitive hMSCs. The expression in hMSCs of cytokine genes, such as IL6, IL8, or FLT3LG, without expression of the corresponding receptor, suggests a role for these cytokines in the paracrine control of stem cell niches. Our database may be shared with other laboratories in order to explore the considerable clinical potential of hES-MSCs, which appear to represent an intermediate developmental stage between hESCs and hMSCs.