Login Register
icon_bulk_orderBulk order Acrobiosystems for English
There is no goods in the shopping cart !
A B C D E F G H I J K L M N O P Q R S T U V W X Y Z 0-9
Your Position: Home > LILRA4


Brief Information

Name:Leukocyte immunoglobulin-like receptor subfamily A member 4
Target Synonym:ILT7,CD85g,Immunoglobulin-like transcript 7,Leukocyte Immunoglobulin Like Receptor A4,CD85 Antigen-Like Family Member G,Leucocyte Ig-Like Receptor A4,Leukocyte Immunoglobulin-Like Receptor Subfamily A Member 4,CD85g Antigen,ILT-7,LILRA4,Leukocyte Immunogl
Number of Launched Drugs:0
Number of Drugs in Clinical Trials:1
Lastest Research Phase:Phase 1 Clinical

Product ListCompare or Buy

By Product Status:
By Product Category:
By Species:
By Tag:
By Conjugate:
Cat. No. Species Product Description Structure Purity Feature
LI4-H52H5 Human Human LILRA4 / CD85g / ILT7 Protein, His Tag
LI4-H5243 Human Human LILRA4 / CD85g / ILT7 Protein, His Tag (MALS verified)
ACRO Quality

Part of Bioactivity data


Immobilized Human LILRA4, His Tag (Cat. No. LI4-H5243) at 2 μg/mL (100 μL/well) can bind Monoclonal Anti-LILRA4 Antibody, Human IgG1 with a linear range of 0.001-0.008 μg/mL (QC tested).

LILRA4 MALS images

The purity of Human LILRA4, His Tag (Cat. No. LI4-H5243) is more than 95% and the molecular weight of this protein is around 55-74 kDa verified by SEC-MALS.

Synonym Name



Leukocyte immunoglobulin-like receptor subfamily A member 4 (LILRA4/ILT7/CD85g) is a marker of plasmacytoid dendritic cells (pDCs), which are reported to be a major source of the abnormally high levels of IFNα associated with autoimmune diseases. Targeting LILRA4 with therapeutic antibodies to promote killing of these IFNα-producing pDCs is being investigated as a novel approach to alleviating the symptoms of autoimmune diseases. LILRA4 is an immunoglobulin-like protein preferentially expressed on the surface of human plasmacytoid dendritic cells (pDCs). It interacts with bone marrow stromal cell antigen 2 to control the Toll-like receptor (TLR) driven response by pDCs to viral infection. It may also be involved in modulating pDC-tumour interactions. pDCs are a source of the excess IFNα which drives autoimmune disease symptoms.

Clinical and Translational Updates

This web search service is supported by Google Inc.

Call us
Call us
North America:
+1 800-810-0816 (Toll Free)
Asia & Pacific:
+86 400-682-2521
+1 888-377-6111
1 Innovation Way, Newark, DE 19711, USA

Leave a message