LYVE1 Antibody [C2N8] | Primary Antibodies

Application: Reactivity: Mouse

Usage Information

Dilution
FCM1:10000

Application
IHC, IF, FCM

Reactivity
Mouse

Source
Rat Monoclonal Antibody

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Positive Control	Mouse intestine
Negative Control

Datasheet & SDS

Biological Description

Specificity
LYVE1 Antibody [C2N8] detects endogenous levels of total LYVE1 protein.

Clone
C2N8

Synonym(s)
cell surface retention sequence binding protein-1; Cell surface retention sequence-binding protein 1; CRSBP-1; extra cellular link domain-containing 1; LYVE-1; sLyve 1; sLyve1; soluble LYVE 1; soluble LYVE1; 1200012G08Rik; Crsbp-1; Crsbp1; Lyve-1; Lyve1; Xlkd1

Background
LYVE1 (Lymphatic Vessel Endothelial Hyaluronan Receptor 1) is a type I integral membrane glycoprotein and CD44 homolog predominantly expressed on lymphatic endothelial cells, featuring an N-terminal Link module hyaluronan-binding domain (HABD) that forms a deep, positively charged groove stabilized by three disulfide bridges (e.g., Cys84–Cys105) and β4/β5 loop residues Arg104 and Lys107, which clasp hyaluronan (HA) chains through a sliding mechanism. This domain is flanked by a heavily glycosylated stalk with N- and O-linked glycosylation sites regulating HABD accessibility, followed by a transmembrane helix and a short cytoplasmic tail that enables homodimerization via disulfide bonds at Cys201 and Cys204 for cooperative ligand binding. In its resting monomeric state, sialylated glycans sterically mask the HABD; however, inflammatory stimuli such as VEGF-C induce neuraminidase-mediated desialylation, exposing the binding groove for non-reducing end docking of immobilized HA polymers. These HA chains thread serially through adjacent LYVE1 receptors, each with a detachment force of ~40 pN, via a water-lubricated sliding interaction that supports reversible leukocyte haptotaxis and enables dendritic cells to roll along the lymphatic surface using their HA-rich glycocalyx, while soluble HA endocytosis by LYVE1 recycles the interstitial matrix to maintain fluid homeostasis without signal transduction due to the short cytoplasmic tail. This mechanosensitive adhesion mechanism underlies immune cell trafficking to lymph nodes and lymphangiogenesis, as well as clearance of tissue HA; notably, LYVE1 is upregulated in tumor-associated lymphatics, promoting metastasis by enhancing dendritic cell and tumor cell entry, especially when coexpressed with VEGFR3, while impaired LYVE1-mediated HA clearance contributes to lymphatic dysfunction in lymphedema.

Background

LYVE1 (Lymphatic Vessel Endothelial Hyaluronan Receptor 1) is a type I integral membrane glycoprotein and CD44 homolog predominantly expressed on lymphatic endothelial cells, featuring an N-terminal Link module hyaluronan-binding domain (HABD) that forms a deep, positively charged groove stabilized by three disulfide bridges (e.g., Cys84–Cys105) and β4/β5 loop residues Arg104 and Lys107, which clasp hyaluronan (HA) chains through a sliding mechanism. This domain is flanked by a heavily glycosylated stalk with N- and O-linked glycosylation sites regulating HABD accessibility, followed by a transmembrane helix and a short cytoplasmic tail that enables homodimerization via disulfide bonds at Cys201 and Cys204 for cooperative ligand binding. In its resting monomeric state, sialylated glycans sterically mask the HABD; however, inflammatory stimuli such as VEGF-C induce neuraminidase-mediated desialylation, exposing the binding groove for non-reducing end docking of immobilized HA polymers. These HA chains thread serially through adjacent LYVE1 receptors, each with a detachment force of ~40 pN, via a water-lubricated sliding interaction that supports reversible leukocyte haptotaxis and enables dendritic cells to roll along the lymphatic surface using their HA-rich glycocalyx, while soluble HA endocytosis by LYVE1 recycles the interstitial matrix to maintain fluid homeostasis without signal transduction due to the short cytoplasmic tail. This mechanosensitive adhesion mechanism underlies immune cell trafficking to lymph nodes and lymphangiogenesis, as well as clearance of tissue HA; notably, LYVE1 is upregulated in tumor-associated lymphatics, promoting metastasis by enhancing dendritic cell and tumor cell entry, especially when coexpressed with VEGFR3, while impaired LYVE1-mediated HA clearance contributes to lymphatic dysfunction in lymphedema.

References
https://pubmed.ncbi.nlm.nih.gov/40113779/ https://pubmed.ncbi.nlm.nih.gov/26823460/

Reference Table for Selecting PVDF Membrane Pore Size Specifications

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%