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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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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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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 (show FBN1 Antibodies) 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.
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
B-Myb (show MYBL2 Antibodies) represses SMC (show DYM Antibodies) elastin gene expression and cyclin A (show CCNA2 Antibodies) plays a role in the developmental regulation of elastin gene expression in the aorta
self-association and oxidation by lysyl oxidase (show LOX Antibodies) 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
exogenous growth factors enhance the expression of cola1 (show COL1A1 Antibodies), cola3, and Elastin, which is probably regulated via activating MAPK (show MAPK1 Antibodies) signaling pathway.
In conclusion, our results support the view that lysyl oxidase (LOX (show LOX Antibodies)) and tropoelastin are present on the cell surface and suggests the possibility that lysine oxidation by LOX (show LOX Antibodies) precedes tropoelastin deposition onto microfibrils.
Elastin degradation was correlated with age in COPD (show ARCN1 Antibodies) patients, smoker controls, and non-smoker controls. The correlation was weaker in the smoker control group compared with the never-smoker control or COPD (show ARCN1 Antibodies) 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 (show CDKN1C Antibodies))patient with emphysema where the diagnosis of WBS (show CDKN1C Antibodies) was established subsequent to the discovery of severe bullous emphysema. Haploinsufficiency of ELN likely contributed to this pulmonary manifestation of WBS (show CDKN1C Antibodies).
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
These results indicate that elastin neoepitopes generated by the same proteases but at different amino acid sites provide different tissue-related information depending on the disease in question.
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 (show AGTRAP Antibodies)-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 (show LOXL1 Antibodies) were co-associated with liver cirrhosis, while selective inhibition of LOXL1 (show LOXL1 Antibodies) arrested disease progression by reducing crosslinking of elastin.
Elastin-Derived Peptides Promote Abdominal Aortic Aneurysm Formation by Modulating M1/M2 Macrophage Polarization
mTOR (show FRAP1 Antibodies)-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 (show HMGB1 Antibodies) 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 (show FBLN1 Antibodies), fibulin-2 (show FBLN2 Antibodies) and fibulin-4 (show FBLN4 Antibodies) 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.
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)