CLEC4M Antibody
- Known as:
- CLEC4M Antibody
- Catalog number:
- GWB-MP258F
- Product Quantity:
- 50ug
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- CLEC4M Antibody
Related genes to: CLEC4M Antibody
- Gene:
- CLEC4M NIH gene
- Name:
- C-type lectin domain family 4 member M
- Previous symbol:
- CD209L, CD299
- Synonyms:
- HP10347, DC-SIGNR, LSIGN, DCSIGNR, DC-SIGN2
- Chromosome:
- 19p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2000-09-19
- Date modifiied:
- 2016-10-05
Related products to: CLEC4M Antibody
Related articles to: CLEC4M Antibody
- Despite significant insights into factor VIII (FVIII) biosynthesis, the mechanisms involved in FVIII clearance remain poorly defined. To investigate genetic modifiers of FVIII clearance, we studied 106 SNPs across 43 different loci previously reported to influence plasma FVIII and/or von Willebrand (VWF) levels and reviewed their association with FVIII pharmacokinetic (PK) parameters in 52 patients with hemophilia A. Marked inter-individual variability in FVIII clearance was observed. Plasma VWF levels, ABO blood group and age all influenced FVIII PK parameters. Collectively however, linear regression analysis demonstrated that these explained less than 40% of the observed variance in FVIII clearance. Consistent with previous reports, SNPs mapped to the FVIII/VWF clearance receptors STAB2, ASGR2, and CLEC4M were associated with FVIII clearance. Importantly however, we identified four additional genetic signals marked by SNPs rs4904820 (TC2N), rs3124768 (ADAMTS13), rs12979891 (RASIP1/MAMSTR/FUT2) and rs6494314 (C2CD4B) that were also significantly associated with FVIII PK parameters. Of particular interest, the FUT2 gene on chromosome 19q13 determines Secretor blood group status and thus determines secretion of ABO(H) glycan determinants into plasma. In addition to the association between the rs12979891 SNP and FVIII clearance, we further observed an effect of Secretor genotype on FVIII PK parameters, with prolonged FVIII half-life in non-secretor individuals compared to homozygous secretors. Furthermore, plasma FVIII levels were significantly increased in Fut2 knockout mice. Cumulatively, these data identify novel modifiers of FVIII clearance in vivo. Given that plasma FVIII levels constitute a dose-dependent risk factor for cardiovascular disease, these findings are of direct clinical importance. - Source: PubMed
Publication date: 2026/08/24
Hulshof Anne-MarijeAntunes Heck LilianAtiq FerdowsLopes PatriciaByrne CiaraElsheikh EinasKelly ClaireLavin MichelleLarkin NiamhO'Connell Niamh MRyan KevinFallon Padraic GGormley JohnO'Mahony BrianDoyle Mairead MKeenan CatrionaPreston Roger J SGodfrey Andrew RobertWaters AllisonJohnsen Jill MTurecek Peter LDi Paola JorgeO'Donnell James S - Cholangiocarcinoma (CCA) has a complex tumor microenvironment (TME) and poor immunotherapy response. Understanding how the adaptive immune response (AIR) affects the TME and prognosis is critical. - Source: PubMed
Publication date: 2026/07/06
Jie WangJixiang ZhouYang BaoYanting WangLing Liu - Severe fever with thrombocytopenia syndrome virus (SFTSV), also known as Dabie bandavirus, is the pathogen causing severe fever with thrombocytopenia syndrome (SFTS). Human cell receptors are the first barriers to viral entry, proliferation, and host immune response. This study explored the association between single nucleotide polymorphisms (SNPs) in genes encoding receptors or related molecules that mediate SFTSV cell entry, such as dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), DC-SIGN-related protein (DC-SIGNR), and non-muscle myosin heavy chain IIA (NMMHC-IIA), and SFTSV infection susceptibility in the Chinese Han population, as well as the underlying potential biological mechanisms. From September 2020 to December 2022, 454 subjects from the First Affiliated Hospital with Nanjing Medical University were enrolled and divided into SFTSV-infected and uninfected groups based on SFTSV RNA and antibody test results. TaqMan SNP genotyping was performed on (rs7248637, rs4804800, and rs11465421), (rs2277998), and (rs2269529 and rs2269530). Logistic regression was used to assess the association between the candidate SNPs and SFTSV infection susceptibility, and the online bioinformatics tools were employed to explore potential biological functions of positive SNPs. Logistic regression analysis showed that individuals carrying the rs2277998 AA genotype were more susceptible to SFTSV infection, and bioinformatics analysis generated the hypothesis that this locus might be involved in influencing gene transcription and expression, which warrants further functional validation. rs2277998 is significantly associated with SFTSV infection susceptibility in the Chinese Han population. The exact regulatory mechanisms require further experimental validation.IMPORTANCESevere fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by severe fever with thrombocytopenia syndrome virus (SFTSV). Host genetic variation may modulate both disease susceptibility and severity by altering key functional proteins. Our study was the first to explore the association between single nucleotide polymorphisms (SNPs) in host genes encoding receptors or related molecules that mediate SFTSV cell entry, such as dendritic cell-specific intercellular adhesion molecule-3-grabbing non-integrin (DC-SIGN), DC-SIGN-related protein (DC-SIGNR), and non-muscle myosin heavy chain IIA (NMMHC-IIA), and SFTSV infection susceptibility in the Chinese Han population. The results showed that the homozygous mutation of rs2277998 AA genotype was associated with a significantly higher risk of SFTSV infection in the Chinese Han population, with predictions pointing to a potential, yet unverified, role in regulating the gene transcription and expression, which may provide a new scientific basis for SFTSV prevention and treatment. - Source: PubMed
Publication date: 2026/07/15
Wang MinRen ChengruiDeng GuoqiangShen YanCheng PengQian LiqinQi YongTan WeilongChai YinchuChen YutingZeng TianYin WenZhu ChuanlongYue Ming - Marburg virus (MARV), a highly pathogenic member of the Filoviridae family, causes severe hemorrhagic fever with a high case fatality rate and currently lacks effective therapeutics. The viral entry process, mediated by the interaction between the MARV glycoprotein (GP) and host receptor C-type lectin domain family 4 member M (CLEC4M) (L-SIGN), represents a critical target for early-stage intervention. The active compounds from BindingDB and the decoy from DUDE were used. The RDKit was used for feature engineering. Machine learning models were trained on an initial dataset consisting of 56 active chemicals and 1232 decoys. Among the tested algorithms, the Random Forest model demonstrated superior performance, achieving the highest discriminative ability (AUC = 0.93, MCC = 0.88) on the test set. Virtual screening of 11,032 phytochemicals resulted in 120 predicted actives, of which 42 compounds satisfied drug-likeness criteria. Subsequent molecular docking identified three lead compounds (PubChem IDs: 42608095, 5281601, and 11243993) with moderate-to-promising binding affinities (-6.3 to -6.5 kcal/mol) toward the CLEC4M binding site. ADMET analysis revealed favorable pharmacokinetic and toxicity profiles for the selected lead compounds. DFT calculations of the three compounds highlighted their electronic stability and reactive nature, indicating that PubChem IDs 42608095 and 5281601 possess particularly stable electronic properties conducive to favorable target interactions. Combining machine learning models with molecular docking and Molecular Dynamics (MD) simulations worked well in finding promising phytochemical inhibitors. The MM/GBSA binding free energy calculations further confirmed binding affinities, with values of -10.83 and -11.08 kcal/mol, respectively, suggesting favorable complex stability. These findings provide a pathway for developing new antiviral agents against MARV, pending further experimental validation and optimization. - Source: PubMed
Publication date: 2026/06/12
Almaghrabi MohammedAlturki Mansour S - Exposure to extreme stress within military contexts such as combat, captivity, survival training, or blast exposure triggers complex neurobiological responses that, in susceptible individuals, culminate in conditions such as Post-Traumatic Stress Disorder (PTSD). This inter-individual variability is rooted in profound genetic and epigenetic foundations. This manuscript reviews the critical relationship between chronic military stress and five key molecules: the glucocorticoid receptor (NR3C1), the FK506-binding protein 5 (FKBP5), brain-derived neurotrophic factor (BDNF), neuropeptide Y (NPY), and interleukin-6 (IL6). We examine how the dysregulation of this allostatic network predisposes individuals to PTSD and generates an altered systemic inflammatory and neuroendocrine microenvironment. Seeking an integrative biological perspective, this pathogenic model is linked to discoveries derived from extreme physical environments. Previous investigations by our group involving exposed to microgravity identified genes that are differentially inhibited under spaceflight-induced stress. Interactomic and evolutionary homology analyses revealed that five of these genes (LDHA, DNAJB5, ELOVL1, CLEC4M, SLC17A5) represent oncogenic vulnerabilities in human glandular epithelial tumors. Notably, network analysis demonstrates that and act as primary convergence nodes that interact directly with the allostatic stress network. We propose that the systemic attrition provoked by military stress acts as the physiological trigger that exploits these evolutionarily conserved epithelial vulnerabilities, thereby facilitating neoplastic progression. Understanding this translational convergence is fundamental for the development of predictive biomarkers and targeted therapies in high-risk populations. - Source: PubMed
Publication date: 2026/06/09
Laván DavidArgüelles NataliaRea RosaMorales JoséMontes SofiaHuaman DanielLluncor AlexisMoyano JuanPeña MiltonHerencia-Reyes VilmaGuerra AlcidesCalderón GabrielaVela-Ruiz José MGallo Aly