Anti-FLT3L polyclonal antibody [Biotin]

Name: Anti-FLT3L polyclonal antibody [Biotin]
SKU: DPABY-556
Rating: 5 (1 reviews)

Goat Anti-Human FLT3L polyclonal antibody for WB, ELISA(Det)

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Human

Immunogen

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

Conjugate

Biotin

Applications

Application Notes

Western Blot: 0.1 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

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Customer Reviews

References

Promoter profiling and coexpression data analysis identifies 24 novel genes that are coregulated with AMPA receptor genes, GRIAs

GENOMICS

Authors: Chong, Allen; Zhang, Zhuo; Choi, Kwok Pui; Choudhary, Vidhu; Djamgoz, Mustafa B. A.; Zhang, Guanglan; Bajic, Vladimir B.

Abstract

We identified a set of transcriptional elements that are conserved and overrepresented within the promoters of human, mouse, and rat GRIAs by comparing these promoters against a collection of 10,741 gene promoters. Cells regulate functional groups of genes by coordinating the transcriptional and/or posttranscriptional mRNA levels of interacting genes. As such, it is expected that functional groups of genes share the same transcriptional features within their promoters. We found 47 genes whose promoters contain the same combination of transcriptional elements that are overrepresented within the promoters of the GRIA gene family. Coexpressed genes may be transcriptionally coregulated, which in turn suggests that these genes may play complementary roles within a particular functional context. Using microarray expression data, we found 24 (of the 47) genes that share not only a similar promoter profile with GRIAs but also a well-correlated gene expression profile and, thus, we believe these to be coregulated with GRIAs. (c) 2006 Elsevier Inc. All rights reserved.

Sjogren Syndrome-associated lymphomas: an update on pathogenesis and management

BRITISH JOURNAL OF HAEMATOLOGY

Authors: Nocturne, Gaetane; Mariette, Xavier

Abstract

Primary Sjogren Syndrome (pSS) is an autoimmune disease associated with an increased risk of lymphoma. Lymphomas complicating pSS are mostly low-grade B cell non-Hodgkin lymphomas, predominantly of marginal zone histological type. Mucosal localization is predominant, notably mucosa-associated lymphoid tissue lymphomas. Lymphomas often develop in organs where pSS is active, such as salivary glands. Germinal centre (GC)-like structures, high TNFSF13B (BAFF) and Flt3-ligand (FLT3LG) levels and genetic impairment of TNFAIP3 are new predictors of lymphoma development. These new findings allow a better understanding of the pathogenic mechanisms leading to lymphoma. We propose the following scenario: auto-immune B cells with rheumatoid factor (RF) activity are continuously stimulated by immune complexes containing antibodies against more specific auto-antigens, such as SSA/Ro, SSB/La or others. Germline abnormality of TNFAIP3 leads to a decreased control of the NF-kB pathway and thus promotes survival of B cells and oncogenic mutations especially in GC structure. Moreover, B cells are stimulated by a positive loop of activation induced by BAFF secretion. Thus, lymphomagenesis associated with pSS exemplifies the development of antigen-driven B-cell lymphoma. The control of disease activity by a well-targeted immunosuppressor is the primary objective of the management of the patient in order to repress chronic B cell stimulation.