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Human Polyclonal ELN Primary Antibody for IF (p), IHC (p) - ABIN734003
Guo, Li, Dong, Chen, Deng, Wang, Ying: Piezoelectric PU/PVDF electrospun scaffolds for wound healing applications. in Colloids and surfaces. B, Biointerfaces 2012
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Dog (Canine) Monoclonal ELN Primary Antibody for IHC (p), IHC - ABIN250614
Wrenn, Griffin, Senior, Mecham: Characterization of biologically active domains on elastin: identification of a monoclonal antibody to a cell recognition site. in Biochemistry 1986
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Human Polyclonal ELN Primary Antibody for IHC, IHC (p) - ABIN4307718
Votteler, Berrio, Horke, Sabatier, Reinhardt, Nsair, Aikawa, Schenke-Layland: Elastogenesis at the onset of human cardiac valve development. in Development (Cambridge, England) 2013
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Cow (Bovine) Monoclonal ELN Primary Antibody for IHC (p) - ABIN533287
Uitto, Christiano, Kähäri, Bashir, Rosenbloom: Molecular biology and pathology of human elastin. in Biochemical Society transactions 1992
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Cat (Feline) Monoclonal ELN Primary Antibody for IHC (fro), IHC (p) - ABIN114749
Schenke-Layland, Madershahian, Riemann, Starcher, Halbhuber, König, Stock: Impact of cryopreservation on extracellular matrix structures of heart valve leaflets. in The Annals of thoracic surgery 2006
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we show on the molecular level that elastin formation involves random cross-linking of tropoelastin monomers resulting in an unordered network, an unexpected finding compared with previous assumptions of an overall beaded structure
Data suggest that cross-linking involving desmosine and isodesmosine residues in bovine elastin and human tropoelastin contributes to long-term stability of these proteins.
Immersing elastin in various glycerol-water mixtures, we observe at room temperature that the protein mobility is higher for lower glycerol fractions in the solvent and, thus, lower solvent viscosity.
domain 36 of tropoelastin contributes to the binding to fibrillin-1 and microfibril-associated glycoprotein through two cysteine residues and Lysine-Arginine-Lysine-Arginine sequence, resulting in the promotion of elastic fiber assembly.
Biaxial force-controlled experiments were used to quantify regional variations in the anisotropy and nonlinearity of elastin isolated from bovine aortic tissues proximal and distal to the heart.
the mechanism by which ONOO(-) prevents cell binding to TE is by introducing negatively charged sulfonic acid residues near the positively charged cluster.
In cases of vascular calcification, the decreased expression of tropoelastin may be partially responsible for decreased vascular elasticity and also for the decreased formation of new elastic fibers.
tropoelastin has domains that mediate elastin deposition in vitro and in vivo
TE can associate with elastic fiber components in the absence of live cells through a process that does not depend on crosslink formation
B-Myb represses SMC elastin gene expression and cyclin A plays a role in the developmental regulation of elastin gene expression in the aorta
self-association and oxidation by lysyl oxidase precedes tropoelastin deposition onto microfibrils; the entire molecule of tropoelastin is required for this following maturation process
analysis of functional inactivation of the tropoelastin carboxy-terminal domain in cross-linked elastin
A heterozygous c.1985delG mutation was identified in the ELN gene in patients with cutis laxa
The majority of familial SVAS patients appear to carry ELN mutations, which strongly indicates that elastin is the most important causative gene for SVAS. The frequency of intragenic deletions highlights the need for quantitative tests to analyze ELN for efficient genetic diagnosis of SVAS.
Results show that rare alteration of the elastin (ELN) gene produces disease by impacting protein dosage (supravalvar aortic stenosis, Williams Beuren syndrome and Williams Beuren region duplication syndrome) and protein function (autosomal dominant cutis laxa). [review]
Analysis of polymorphisms of elastin gene (rs7787362) did not show differences in allele distribution between women with and without SD.
High elastin expression is associated with lung cancer.
Three families with Midaortic Syndrome were found to have a likely causal mutation in ELN.
The functional role of PAX5-ELN as a potent oncoprotein in B-cell acute lymphoblastic leukemia development.
Elastin plays an important role in the growth of A. fumigatus and that it participates in the formation of thick biofilm.
Molecular model of human tropoelastin and implications of associated mutations
Study implies that the rs2856728 variant in elastin gene polymorphisms might play crucial roles in the development and pathogenesis of intracranial aneurysms in Korean population.
Degradation of tropoelastin and skin elastin by neprilysin
exogenous growth factors enhance the expression of cola1, cola3, and Elastin, which is probably regulated via activating MAPK signaling pathway.
In conclusion, our results support the view that lysyl oxidase (LOX) and tropoelastin are present on the cell surface and suggests the possibility that lysine oxidation by LOX precedes tropoelastin deposition onto microfibrils.
Elastin degradation was correlated with age in COPD patients, smoker controls, and non-smoker controls. The correlation was weaker in the smoker control group compared with the never-smoker control or COPD group.
The aim was to examine if the serum concentrations of elastin-related proteins correlate to signs of cardiovascular diseases in patients with Diabetes mellitus type 2.
There is evidence that the ELN variant INT20 1315T > C is implicated in the development of intracranial aneurysm.
Direct gene sequencing of ELN confirmed the diagnosis showing a previously undescribed c.2156del (p.Gly719Glufs*36) mutation in exon 30 of ELN gene. This mutation results in a shift of the reading frame.
Here we report a second adult Williams-Beuren syndrome (WBS)patient with emphysema where the diagnosis of WBS was established subsequent to the discovery of severe bullous emphysema. Haploinsufficiency of ELN likely contributed to this pulmonary manifestation of WBS.
the study contributes to a better understanding of the correlation between genotypic and elastin-related phenotypic features of Williams-Beuren syndrome patients
We herein report the case of a Japanese female patient presenting with multiple arteriopathy including moyamoya disease, a tortuosity of abdominal arteries and pulmonary hypertension due to peripheral pulmonary artery stenosis. This case suggests the possible progression of cerebral arteriopathy including moyamoya disease in patients with elastin mutations
Data (including data from studies in mutant mice and cells from such mice) suggest that elastin-derived peptides are involved in regulation of lipid storage in hepatocytes; thus, elastin-derived peptides may play role in development and progression of non-alcoholic fatty liver.
Elastin insufficiency triggers structural defects and abnormal remodeling of renal vascular signaling involving AT1R-mediated vascular mechanotransduction and renal hyperfiltration with increased blood pressure sensitivity to dietary sodium contributing to systolic hypertension.
findings strongly suggested that elastin crosslinking and LOXL1 were co-associated with liver cirrhosis, while selective inhibition of LOXL1 arrested disease progression by reducing crosslinking of elastin.
Elastin-Derived Peptides Promote Abdominal Aortic Aneurysm Formation by Modulating M1/M2 Macrophage Polarization
mTOR-sensitive perturbation of smooth muscle cell mechanosensing contributes to elastin aortopathy.
Deficient circumferential growth is the predominant mechanism for moderate obstructive aortic disease resulting from partial elastin deficiency in Williams syndrome.
Elevations of whole lung HMGB1 level were associated with impaired alveolar development and aberrant elastin production in 85% O2-exposed newborn lungs.
Eln was ubiquitously present, with enrichment in regions with cardiomyocyte differentiation, while there was an inverse correlation between ColI and cardiomyocyte differentiation.
Lung histology revealed aberrant elastin production and impaired lung septation in oxygen-exposed lungs, while tropoelastin, integrin alphav, fibulin-1, fibulin-2 and fibulin-4 gene expression were elevated.
Data suggest that expression of elastin in uterus, vagina, and bladder is down-regulated both in naturally aging mice and in mouse model of accelerated ovarian aging; such down-regulation may lead to pelvic floor disorders.
Data indicate significantly reduced volumetric density of elastin and collagen and thinner skin dermis were observed in Marfan mice.
These results suggest that elastin haploinsufficiency adversely impacts pulmonary angiogenesis.
The increased levels of elastin, type V collagen and tenascin C are probably the result of increased expression by fibroblastic cells; reversely, elastin influences myofibroblast differentiation.
Compared to control SMCs, the modulus of Eln-/- SMCs is reduced by 40%, but is unchanged in Fbln4-/- SMCs. The Eln-/- SMC modulus is rescued by soluble or alpha elastin treatment.
Elastin haploinsufficiency impedes the progression of arterial calcification in MGP-deficient mice.
Fstl1 is crucial for elastin expression and deposition in mesenchyme during lung alveologenesis
Eln insufficiency induced hypertension is due to increased sensitivity of the resistance vasculature to circulating ANG II and to impaired endothelium-dependent vasodilatation.
Two sides of MGP null arterial disease: chondrogenic lesions dependent on transglutaminase 2 and elastin fragmentation associated with induction of adipsin.
tested the hypothesis that adhesive strength varies with atherosclerotic plaque composition of collagen and elastin in apoE and MMP12 knock outs
Data show that tropoelastin staining was relatively weak in the ligamentum flavum from E15 through P0, P7 was the first stage that staining intensity was observed to be substantially stronger, intensity remained relatively high until P35.
The elastic fibers are under tension and impart an intrinsic compressive stress on the collagen.
A biomechanical model of the common carotid artery predicts that the majority of elastin is in-series with vascular smooth muscle (74 +/-8%), thus only about one-fourth of elastin acts in parallel to the vascular smooth muscle within the arterial wall.
This gene encodes a protein that is one of the two components of elastic fibers. The encoded protein is rich in hydrophobic amino acids such as glycine and proline, which form mobile hydrophobic regions bounded by crosslinks between lysine residues. Deletions and mutations in this gene are associated with supravalvular aortic stenosis (SVAS) and autosomal dominant cutis laxa. Multiple transcript variants encoding different isoforms have been found for this gene.
elastin (supravalvular aortic stenosis, Williams-Beuren syndrome)