DC-SIGNR Protein (CD299 Protein)

Dendritic Cell-Specific Intercellular Adhesion Molecule-3 (ICAM-3)-Grabbing Non-integrin-Related protein (Cluster of Differentiation 299)

DC-SIGNR Products

DC-SIGNR Protein, Recombinant

Molecule	Species	Description	Cat. No
DC-SIGNR/CD299	Human	DC-SIGNR/CD299/Fc Protein, Recombinant	10559-H01H

DC-SIGNR cDNA Clone

Molecule	Species	Description	Cat. No
DC-SIGNR/CD299	Human	Homo sapiens DC-SIGNR/CD299 cDNA Clone(NM_014257.3)	HG10559-M

DC-SIGNR Alternative Names

DC-SIGNR, CD299, CD209L, DC-SIGN2, DCSIGNR, CLEC4M, HP10347, L-SIGN, LSIGN, MGC129964, MGC47866 [Homo sapiens]

DC-SIGNR Related Areas

Stem Cell>>Hematopoietic Stem Cell (HSC)>>Hemangioblast>>Endothelial Cell Marker>>DC-SIGNR/CD299

Immunology>>Adhesion Molecule>>Lectin>>DC-SIGNR/CD299

Immunology>>Cluster of Differentiation>>Dendritic Cell CD Antigen>>Dendritic Cell Pathogen Recognition/Uptake>>DC-SIGNR/CD299

DC-SIGNR Background

C-type lectin domain family 4, member M, also known as DC-SIGNR and CLEC4M, is a type II integral membrane protein that is 77% amino acid identical to DC-SIGN, an HIV gp120-binding protein. Though the encoded gene located in the same chromosome, DC-SIGN is expressed solely on dendritic cells, while DC-SIGNR is predominantly found in liver sinusoidal endothelial cells and lymph node, as well as placental endothelium. DC-SIGNR exists as a homotetramer, and the tandem repeat domain, also called neck domain, mediates oligermerization. DC-SIGNR is ragarded as a pathogen-recognition receptor involved in peripheral immune surveillance in liver, and probably mediate the endocytosis of pathogens which are subsequently degraded in lysosomal compartments. DC-SIGNR appears to selectively recognize and bind many viral surface glycoproteins containing high mannose N-linked oligosaccharides in a calcium-dependent manner, including HIV-1 gp120, HIV-2 gp120, SIV gp120, ebolavirus glycoproteins, HCV E2, and human SARS coronavirus protein S, as well as the cellular adhesion protein ICAM3. DC-SIGNR have been thought to play an important role in establishing HIV infection by enhancing trans-infection of CD4(+)T cells in the regional lymph nodes. It may affect susceptibility to HIV infection by a mechanism that is different in females and males. DC-SIGNR can bind to hepatitis C virus (HCV), and its polymorphism might affect HCV loads supporting the concept that DC-SIGNR contributes to HCV replication efficacy.

DC-SIGNR Related Studies

1. Nattermann J, et al. (2006) The tandem-repeat polymorphism of the DC-SIGNR gene in HCV infection. J Viral Hepat. 13(1): 42-6.
2. Wichukchinda N, et al. (2007) The polymorphisms in DC-SIGNR affect susceptibility to HIV type 1 infection. AIDS Res Hum Retroviruses. 23(5): 686-92.