LYVE1 Antibody [P8K5] | Primary Antibodies

Application: Reactivity: Human

Usage Information

Dilution
WB1:1000 IP1:20 IHC1:20000

Application
WB, IP, IHC

Reactivity
Human

Source
Rabbit 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

Predicted MW Observed MW
35 kDa 50-70 kDa
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Positive Control	Human fetal lung tissue; Human liver tissue; Human lymph node tissue; Human tonsil tissue; Human fetal spleen tissue; Human colon tissue
Negative Control	Human brain tissue

Datasheet & SDS

Biological Description

Specificity
LYVE1 Antibody [P8K5] detects endogenous levels of total LYVE1 protein.

Clone
P8K5

Synonym(s)
CRSBP1; HAR; XLKD1; UNQ230/PRO263; LYVE1; Lymphatic vessel endothelial hyaluronic acid receptor 1; LYVE-1; Cell surface retention sequence-binding protein 1; Extracellular link domain-containing protein 1; Hyaluronic acid receptor; CRSBP-1

Background
LYVE1 is a type I transmembrane glycoprotein and member of the Link module superfamily of hyaluronan (HA)-binding proteins, closely related to CD44, and serves as a highly specific marker of lymphatic endothelial cells. The 322-amino-acid protein features an extracellular N-terminal domain (residues 21–233) containing the signature HA-binding Link module (residues 48–162). This module forms a deep binding groove comprised of β-sheets and loops that capture HA chain ends through critical interactions involving Arg104, Lys107, Tyr86, and Trp115. The protein also has a single-span transmembrane helix (residues 234–255) and a short cytoplasmic tail (residues 256–322) equipped with dileucine motifs that mediate endocytosis. Unlike CD44, which binds immobilized HA with high affinity, LYVE1 preferentially recognizes soluble or pericellular HA on leukocyte glycocalyces. This interaction relies on a shear-resistant, end-on threading mechanism, where the non-reducing end of HA threads into the LYVE1 groove, requiring conformational changes like Arg104 flip and Lys107 shift to unblock the β4/β5 clasp. LYVE1 is particularly enriched at lymphatic blind-end junctions, where it facilitates dendritic cell (DC) and leukocyte transmigration by relaxing VE-cadherin junctions via Rac1/PI3K signaling. Soluble HA engagement also triggers VEGFR3-independent PI3K/AKT activation, promoting lymphangiogenesis during inflammation. LYVE1 mediates the internalization and lysosomal degradation of HA through clathrin-independent endocytosis, helping to clear interstitial HA, maintain tissue fluid balance, and prevent edema. In the tumor microenvironment, upregulation of LYVE1 on new lymphatic vessels enables binding to HA-rich metastasis clusters, enhancing VEGF-C-driven lymphatic sprouting and facilitating tumor spread to sentinel lymph nodes. LYVE1 deficiency impairs DC migration and T-cell priming, leading to reduced immune responses against pathogens.

Background

LYVE1 is a type I transmembrane glycoprotein and member of the Link module superfamily of hyaluronan (HA)-binding proteins, closely related to CD44, and serves as a highly specific marker of lymphatic endothelial cells. The 322-amino-acid protein features an extracellular N-terminal domain (residues 21–233) containing the signature HA-binding Link module (residues 48–162). This module forms a deep binding groove comprised of β-sheets and loops that capture HA chain ends through critical interactions involving Arg104, Lys107, Tyr86, and Trp115. The protein also has a single-span transmembrane helix (residues 234–255) and a short cytoplasmic tail (residues 256–322) equipped with dileucine motifs that mediate endocytosis. Unlike CD44, which binds immobilized HA with high affinity, LYVE1 preferentially recognizes soluble or pericellular HA on leukocyte glycocalyces. This interaction relies on a shear-resistant, end-on threading mechanism, where the non-reducing end of HA threads into the LYVE1 groove, requiring conformational changes like Arg104 flip and Lys107 shift to unblock the β4/β5 clasp. LYVE1 is particularly enriched at lymphatic blind-end junctions, where it facilitates dendritic cell (DC) and leukocyte transmigration by relaxing VE-cadherin junctions via Rac1/PI3K signaling. Soluble HA engagement also triggers VEGFR3-independent PI3K/AKT activation, promoting lymphangiogenesis during inflammation. LYVE1 mediates the internalization and lysosomal degradation of HA through clathrin-independent endocytosis, helping to clear interstitial HA, maintain tissue fluid balance, and prevent edema. In the tumor microenvironment, upregulation of LYVE1 on new lymphatic vessels enables binding to HA-rich metastasis clusters, enhancing VEGF-C-driven lymphatic sprouting and facilitating tumor spread to sentinel lymph nodes. LYVE1 deficiency impairs DC migration and T-cell priming, leading to reduced immune responses against pathogens.

References
https://pubmed.ncbi.nlm.nih.gov/19887450/ https://pubmed.ncbi.nlm.nih.gov/40113779/

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%