CLEC4M Antibody, HRP conjugated
Description
Antibody Overview
The CLEC4M Antibody, HRP conjugated, targets the middle region of the human CLEC4M protein. Key characteristics include:
Molecular and Functional Context
CLEC4M (C-type lectin domain family 4 member M) is a transmembrane receptor expressed in endothelial cells, liver sinusoids, and lymph nodes . It functions as a pathogen recognition receptor, binding carbohydrate ligands on microbes and endogenous cells . Key features include:
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Protein Structure:
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Biological Roles:
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Immune Recognition: Binds pathogens (e.g., HIV, HCV, Ebola virus) and modulates immune responses .
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Hepatocellular Carcinoma (HCC): Reduced expression in HCC tissues correlates with poor prognosis .
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Factor VIII Clearance: Mediates internalization of factor VIII (FVIII) via mannose-exposed glycans, influencing hemostasis .
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Applications in Research
The HRP-conjugated CLEC4M antibody is primarily used for detection and quantification of CLEC4M in experimental settings.
Western Blotting (WB)
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Protocol:
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Example: Used to confirm CLEC4M overexpression in HCC cell lines (e.g., Huh7, PLC/PRF/5) .
Immunohistochemistry (IHC)
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Protocol:
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Relevance: Identifies CLEC4M localization in sinusoidal endothelial cells of liver and lymphoid tissues .
ELISA
Role in Hemostasis
CLEC4M binds and internalizes factor VIII (FVIII) via mannose-exposed glycans, influencing its clearance. Studies using CLEC4M-Fc chimeras and anti-FVIII HRP antibodies demonstrated:
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Mechanism: Clathrin-coated pit-dependent endocytosis, leading to lysosomal degradation .
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Clinical Implications: Dysregulation may contribute to FVIII deficiency or hemophilia A .
Prognostic Biomarker in HCC
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Expression Patterns: Reduced CLEC4M expression in HCC tissues correlates with poor survival outcomes (OS, RFS, PFS) .
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Functional Impact: CLEC4M overexpression suppresses proliferation and enhances apoptosis in HCC cells, partly via the JAK1/STAT3 pathway .
Viral Pathogenesis
CLEC4M facilitates viral entry by binding envelope glycoproteins (e.g., HIV-1 gp120, HCV E2, Ebola GP) . While the HRP-conjugated antibody is not directly cited in these studies, its use in detecting CLEC4M in viral infection models is inferred.
Cross-Reactivity and Controls
Product Specs
Target Background
CLEC4M is a probable pathogen-recognition receptor involved in peripheral immune surveillance within the liver. It may mediate the endocytosis of pathogens, which are subsequently degraded in lysosomal compartments. It functions as a receptor for ICAM3, likely through binding to mannose-like carbohydrates. Furthermore, CLEC4M has been implicated in microbial infection as an attachment receptor for a range of viruses, including Ebolavirus, Hepatitis C virus, HIV-1, Human coronavirus 229E, Human cytomegalovirus (HHV-5), Influenzavirus, SARS-CoV, West Nile virus, Japanese encephalitis virus, and Marburg virus glycoprotein. Additionally, it may play a role in the recognition of M. bovis by dendritic cells.
Research indicates that CLEC4M plays a significant role in various biological processes and diseases:
- Heterozygous VNTR genotypes 57 and 67 of CLEC4M are significantly enriched in the Swedish type 1 von Willebrand disease population, suggesting a key role in the disease pathogenesis. (PMID: 29389944)
- DC-SIGNR (a related C-type lectin receptor) promotes gastric cancer liver metastasis through interactions with HNRNPKP2 (expression regulated by STAT5A), leading to decreased CXCR4 expression. This suggests potential therapeutic targets for gastric cancer liver metastasis. (PMID: 28403883)
- The neck domains of DC-SIGN and DC-SIGNR contribute to their functional differences by influencing the presentation of their sugar-binding sites. (PMID: 27859859)
- DC-SIGN and L-SIGN (another related receptor) act as attachment and entry receptors for human metapneumovirus infection. (PMID: 27334579)
- In contrast, DC-SIGNR and DC-SIGN VNTRs were not associated with pulmonary tuberculosis risk in an Iranian population. (PMID: 27309478)
- Variations in CD209L (another name for CLEC4M) may influence HIV-1 susceptibility, treatment response, and disease progression. (PMID: 25656622)
- Higher DC-SIGNR expression in HIV-1-infected patients, correlated with viral load and inversely with CD4+ T cell counts, suggests a potential role in HIV-1 infection. (PMID: 26313015)
- Lower serum DC-SIGNR levels in lung cancer patients, correlated with brain metastasis and serum NK cell percentage, highlight its potential significance in lung cancer. (PMID: 26150177)
- Genetic variations in STXBP5 and CLEC4M are associated with von Willebrand factor level variation in type 1, but not type 2, von Willebrand disease. (PMID: 25832887)
- Studies have investigated the association between CD209 and CD209L polymorphisms and tuberculosis development in a Brazilian population. (PMID: 24874302)
- DC-SIGN and DC-SIGNR are potential blood-based molecular markers for early-stage disease diagnosis. (PMID: 25504222)
- Japanese encephalitis virus utilizes DC-SIGN, DC-SIGNR, and LSECtin as entry receptors. (PMID: 24623090)
- L-SIGN neck region polymorphism influences HCV infection outcome, with the four-tandem repeat associated with HCV clearance. (PMID: 24283933)
- CLEC4M and CD81 remain crucial for hepatitis C virus entry into hepatocytes. (PMID: 24965233)
- The CLEC4M carbohydrate recognition domain rapidly and reversibly releases glycan ligands and Ca(2+) at reduced pH. (PMID: 24976257)
- Human DC-SIGN and L-SIGN mediate Junin virus entry, impacting infection and dissemination. (PMID: 24183720)
- HCV E2 upregulates the Raf-MEK-ERK pathway via L-SIGN, providing insights into L-SIGN signaling. (PMID: 23292357)
- DC-SIGNR neck region VNTR polymorphism is not directly associated with HIV-1 infection predisposition or route of infection. (PMID: 23602836)
- DC-SIGNR plays a role in the expression of lactic acid dehydrogenase and β2-microglobulin in non-Hodgkin lymphoma. (PMID: 23859015)
- Genetic polymorphism in DC-SIGNR is associated with HIV-1 infection. (PMID: 23354840)
- Variable number of tandem repeats (VNTRs) in CLEC4M are associated with type 1 von Willebrand disease. (PMID: 23529928)
- K3 and K5 proteins associate with DC-SIGN and DC-SIGNR, mediating their ubiquitylation and degradation. (PMID: 23460925)
- Polymorphisms in DC-SIGN and L-SIGN genes are associated with vertical HIV-1 transmission in a Northeastern Brazilian population. (PMID: 22902397)
- Studies suggest that cellular attachment factor expression, including DC-SIGNR, is not a significant contributor to the potency of neutralizing antibodies against flaviviruses. (PMID: 23312596)
- DC-SIGNR gene VNTR polymorphism moderately affects host susceptibility to HIV-1 infection, similar to CCR5 gene deletion. (PMID: 22957026)
- Evidence suggests that CLEC4M VNTR alleles did not arise from independent mutation events. (PMID: 22279577)
- RSV G interactions with DC/L-SIGN have immunomodulatory effects, diminishing DC activation and potentially limiting RSV-specific immunity. (PMID: 22090124)
- Multiple genotypes of the DC-SIGNR gene were observed in pregnant women infected with HBV. (PMID: 22338216)
- Upon ligand binding, DC-SIGNR undergoes a conformational change similar to DC-SIGN. (PMID: 21650186)
- Human C-type lectins (DC-SIGN and L-SIGN) mediate influenza virus attachment and entry independently of cell surface sialic acid. (PMID: 21191006)
- A 9/5 genotype distribution frequency of DC-SIGNR exon 4 is significantly higher in hepatitis C patients and may be associated with susceptibility to HCV infection. (PMID: 18171520)
- DC-SIGNR genotype variation affects the efficacy of HIV-1 trans-infection by influencing cell surface protein expression. (PMID: 20152818)
- No association was found between DC-SIGNR neck region polymorphism and longevity in a Han Chinese population. (PMID: 20003397)
- DC-SIGNR plays a crucial role in mother-to-child transmission (MTCT) of HIV-1, and impaired placental DC-SIGNR expression increases transmission risk. (PMID: 19809496)
- DC-SIGNR is primarily expressed in the membrane and cytoplasm of placental trophoblast cells. (PMID: 20108443)
- Studies have investigated the determinants in DC-SIGN required for HIV-1 transmission and the functional differences between DC-SIGN and L-SIGN affecting HIV-1 interactions. (PMID: 19833723)
- Structural studies reveal that DC-SIGNR selectively recognizes endogenous high-mannose oligosaccharides. (PMID: 11739956)
- DC-SIGNR mediates Ebola virus cellular entry. (PMID: 12050398)
- Research has investigated the restricted distribution of DC-SIGNR and its expression in relation to HIV entry receptors. (PMID: 12152166)
- Reviews have explored the interaction of DC-SIGN and DC-SIGNR with HIV and Ebola viruses, discussing the mechanism of DC-SIGN-mediated viral transmission. (PMID: 12223058)
- The influx and proliferation of DC-SIGN+ and L-SIGN+ cells are dynamically regulated. (PMID: 15111305)
- DC-SIGN and L-SIGN exhibit differences in their carbohydrate-binding profiles. (PMID: 15184372)
- L-SIGN is largely expressed on liver sinusoidal endothelial cells, facilitating efficient trans-infection of adjacent human liver cells by hepatitis C pseudoviruses captured by L-SIGN+ or DC-SIGN+ cells. (PMID: 15371595)
- DC-SIGNR can serve as an alternative receptor for SARS coronavirus. (PMID: 15496474)
- Structural studies reveal that DC-SIGNR CRDs are flexibly linked to the neck region, containing α-helical segments interspersed with non-helical regions. (PMID: 15509576)
- Structural studies have focused on the last repeat region of DC-SIGNR. (PMID: 15784257)
- DC-SIGNR, alongside DC-SIGN, is a cofactor in sexual HIV-1 transmission, with soluble isoforms potentially modulating transmission and dissemination efficiency. (PMID: 15812562)
- Variations in the number of DC-SIGNR repeats may influence its normal functions and binding capacity to pathogens. (PMID: 16061998)
- Individuals homozygous for CLEC4M tandem repeats show reduced susceptibility to SARS infection. (PMID: 16369534)
- CLEC4M recognizes pathogens and contributes to innate immunity. (PMID: 16386217)
