Horse Elastin ELISA Kit | ELN elisa kit

Horse Elastin ELISA Kit

Cat. Num. AAA9432

• Gene Names: ELN; WS; WBS; SVAS
• Reactivity: Horse
• Synonyms: Elastin; Horse Elastin ELISA Kit; ELN elisa kit

• Reactivity: Horse
• Specificity: No significant cross-reactivity or interference between Horse ELN and analogues was observed.

• Samples: Serum, Plasma, Tissue Homogenate, Feces, Urine and Body Fluids
• Assay Type: Sandwich
• Detection Range: 25-800ng/ml.
• Sensitivity: 2.0ng/ml.
• Intended Uses: ELISA is a simple and highly sensitive method of analysis that allows for simultaneous and rapid quantification of a large number of samples. The assay is based on the specific recognition of the target compound (analyte/antigen) by antibodies which bind to the compound. The antigen-antibody complex is detected and measured with the aid of an enzyme-labeled antibody or antigen. Upon addition of a non-colored reagent, the enzyme produces a color reaction where the color intensity is directly or inversely proportional to the concentration of the analyte in the sample. This quantitative Sandwich ELISA kit is in tended to determinate ELN concentrations in Horse serum, plasma, tissue homogenates, feces, urine and body fluids, and it is only for research, not for drug, household, therapeutic applications
• Intra-assay Precision: Intra-assay CV (%) is less than 15%.
• Inter-assay Precision: Inter-assay CV (%) is less than 15%. [CV(%) = SD/mean x100]
• Preparation and Storage: Store all reagents at 2-8 degree C

Typical Testing Data/Standard Curve (for reference only)

Related Product Information for ELN elisa kit

Introduction: ELISA is a simple and highly sensitive method of analysis that allows for simultaneous and rapid quantification of a large number of samples. The assay is based on the specific recognition of the target compound (analyte/antigen) by antibodies which bind to the compound. The antigen-antibody complex is detected and measured with the aid of an enzyme-labeled antibody or antigen. Upon addition of a non-colored reagent, the enzyme produces a color reaction where the color intensity is directly or inversely proportional to the concentration of the analyte in the sample. This quantitative Sandwich ELISA kit is in tended to determinate ELN concentrations in Horse serum, plasma, tissue homogenates, feces, urine and body fluids, and it is only for research!

NCBI and Uniprot Product Information

• NCBI GI #: 525313599
• NCBI GeneID: 2006
• NCBI Accession #: NP_001265868.1
• NCBI GenBank Nucleotide #: NM_001278939.1
• UniProt Accession #: P15502; O15336; O15337; Q14233; Q14234; Q14235; Q14238; Q6P0L4; Q6ZWJ6; Q75MU5; Q7Z316; B3KTS6
• Molecular Weight: 68,469 Da
• NCBI Official Full Name: elastin isoform m
• NCBI Official Synonym Full Names: elastin
• NCBI Official Symbol: ELN
• NCBI Official Synonym Symbols: WS; WBS; SVAS
• NCBI Protein Information: elastin; tropoelastin
• UniProt Protein Name: Elastin
• Protein Family: Elastin
• UniProt Gene Name: ELN
• UniProt Entry Name: ELN_HUMAN

NCBI Description

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. [provided by RefSeq, Jul 2008]

Uniprot Description

elastin: Major structural protein of tissues such as aorta and nuchal ligament, which must expand rapidly and recover completely. Molecular determinant of the late arterial morphogenesis, stabilizing arterial structure by regulating proliferation and organization of vascular smooth muscle. Defects in ELN are the cause of cutis laxa, autosomal dominant, type 1 (ADCL1). A connective tissue disorder characterized by loose, hyperextensible skin with decreased resilience and elasticity leading to a premature aged appearance. Face, hands, feet, joints, and torso may be differentially affected. Additional variable clinical features are gastrointestinal diverticula, hernia, and genital prolapse. Rare manifestations are pulmonary artery stenosis, aortic aneurysm, bronchiectasis, and emphysema. Defects in ELN are the cause of supravalvular aortic stenosis (SVAS). SVAS is a congenital narrowing of the ascending aorta which can occur sporadically, as an autosomal dominant condition, or as one component of Williams-Beuren syndrome. ELN is located in the Williams-Beuren syndrome (WBS) critical region. WBS results from a hemizygous deletion of several genes on chromosome 7q11.23, thought to arise as a consequence of unequal crossing over between highly homologous low-copy repeat sequences flanking the deleted region. Haploinsufficiency of ELN may be the cause of certain cardiovascular and musculo-skeletal abnormalities observed in the disease. Belongs to the elastin family. 13 isoforms of the human protein are produced by alternative splicing.

Protein type: Extracellular matrix; Secreted; Secreted, signal peptide

Chromosomal Location of Human Ortholog: 7q11.23

Cellular Component: proteinaceous extracellular matrix; extracellular region

Molecular Function: protein binding; extracellular matrix structural constituent

Biological Process: cell proliferation; extracellular matrix disassembly; organ morphogenesis; extracellular matrix organization and biogenesis; blood circulation; respiratory gaseous exchange

Disease: Cutis Laxa, Autosomal Dominant 1; Williams-beuren Syndrome; Supravalvular Aortic Stenosis