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Human Polyclonal ELN Primary Antibody für 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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Human Polyclonal ELN Primary Antibody für 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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Dog (Canine) Monoclonal ELN Primary Antibody für 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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Cat (Feline) Monoclonal ELN Primary Antibody für 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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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.
Tropoelastin interacts with cells through cell surface receptors including integrins and glycosaminoglycans (GAGs); study mapped a cell-interactive sequence of tropoelastin to domain 17 and the first six amino acids of domain 18.
Tropoelastin acts through a PI3K (zeige PIK3CA Antikörper)-specific pathway that leads to the phosphorylation of eNOS (zeige NOS3 Antikörper) to enhance nitric oxide production in endothelial cells.
Deficient circumferential growth is the predominant mechanism for moderate obstructive aortic disease resulting from partial elastin deficiency in Williams syndrome.
In this report we describe a three-generation family suffering from supravalvular aortic stenosis, various other arterial stenoses, sudden death, and intracranial aneurysms. A frameshift mutation in exon 12 of the elastin gene, not described before, was detected in the affected family members.
Data show that skin aging is associated with the decomposition of elastin fibers, which is more pronounced in sun-exposed tissue.
Transcriptional and posttranscriptional mechanisms contribute to the dysregulation of elastin expression and elastogenesis in Schimke immuno-osseous dysplasia.
Neutrophil elastase (zeige ELANE Antikörper) degraded elastin fragments are increased in the serum of patients with idiopathic pulmonary fibrosis and lung cancer compared to controls.
Data suggest that MFAP4 (microfibrillar-associated protein 4 (zeige MFAP4 Antikörper)) binds tropoelastin, fibrillin-1 (zeige FBN1 Antikörper)/2, and elastin cross-linking amino acid desmosine; MFAP4 (zeige MFAP4 Antikörper) co-localizes with fibrillin-1 (zeige FBN1 Antikörper)-positive fibers; MFAP4 (zeige MFAP4 Antikörper) actively promotes tropoelastin self-assembly.
In asthma, MMP-1 (zeige MMP1 Antikörper) and MMP-2 (zeige MMP2 Antikörper) mediate IL-13 (zeige IL13 Antikörper)-induced suppression of ELN expression in airway fibroblasts.
Elastin-Derived Peptides Promote Abdominal Aortic Aneurysm Formation by Modulating M1/M2 Macrophage Polarization
mTOR (zeige FRAP1 Antikörper)-sensitive perturbation of smooth muscle cell mechanosensing contributes to elastin aortopathy.
Elevations of whole lung HMGB1 (zeige HMGB1 Antikörper) 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 (zeige FBLN1 Antikörper), fibulin-2 (zeige FBLN2 Antikörper) and fibulin-4 (zeige FBLN4 Antikörper) 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 (zeige COL5A1 Antikörper) and tenascin C (zeige TNC Antikörper) are probably the result of increased expression by fibroblastic cells; reversely, elastin influences myofibroblast differentiation.
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 (zeige FBN1 Antikörper) 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 (zeige MYBL2 Antikörper) represses SMC (zeige DYM Antikörper) elastin gene expression and cyclin A (zeige CCNA2 Antikörper) plays a role in the developmental regulation of elastin gene expression in the aorta
self-association and oxidation by lysyl oxidase (zeige LOX Antikörper) 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 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)