FBLN5 sirna

FBLN5 siRNA (Human)

Cat. Num. AAA8222801

• Gene Names: FBLN5; EVEC; UP50; ADCL2; ARMD3; DANCE; ARCL1A; FIBL-5
• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: FBLN5; FBLN5 siRNA (Human); DANCE; Fibulin-5; FIBL-5; Developmental arteries and neural crest EGF-like protein; Dance; Urine p50 protein; UP50; FBLN5 sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: FBLN5 siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 448

• Applicable Applications for FBLN5 sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human FBLN5 gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for FBLN5 sirna

siRNA to inhibit FBLN5 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 19743803
• NCBI GeneID: 10516
• NCBI Accession #: NP_006320.2
• NCBI GenBank Nucleotide #: NM_006329.3
• UniProt Accession #: Q9UBX5; O75966; Q6IAL4; Q6UWA3
• Molecular Weight: 50,180 Da
• NCBI Official Full Name: fibulin-5
• NCBI Official Synonym Full Names: fibulin 5
• NCBI Official Symbol: FBLN5
• NCBI Official Synonym Symbols: EVEC; UP50; ADCL2; ARMD3; DANCE; ARCL1A; FIBL-5
• NCBI Protein Information: fibulin-5
• UniProt Protein Name: Fibulin-5
• Protein Family: Fibulin
• UniProt Gene Name: FBLN5
• UniProt Synonym Gene Names: DANCE; FIBL-5; Dance; UP50
• UniProt Entry Name: FBLN5_HUMAN

NCBI Description

The protein encoded by this gene is a secreted, extracellular matrix protein containing an Arg-Gly-Asp (RGD) motif and calcium-binding EGF-like domains. It promotes adhesion of endothelial cells through interaction of integrins and the RGD motif. It is prominently expressed in developing arteries but less so in adult vessels. However, its expression is reinduced in balloon-injured vessels and atherosclerotic lesions, notably in intimal vascular smooth muscle cells and endothelial cells. Therefore, the protein encoded by this gene may play a role in vascular development and remodeling. Defects in this gene are a cause of autosomal dominant cutis laxa, autosomal recessive cutis laxa type I (CL type I), and age-related macular degeneration type 3 (ARMD3). [provided by RefSeq, Jul 2008]

Uniprot Description

FBLN5: Promotes adhesion of endothelial cells through interaction of integrins and the RGD motif. Could be a vascular ligand for integrin receptors and may play a role in vascular development and remodeling. Defects in FBLN5 are the cause of cutis laxa, autosomal dominant, type 2 (ADCL2). 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 FBLN5 are a cause of cutis laxa, autosomal recessive, type 1A (ARCL1A). 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. The clinical spectrum of autosomal recessive cutis laxa is highly heterogeneous with respect to organ involvement and severity. Type I autosomal recessive cutis laxa is a specific, life-threatening disorder with organ involvement, lung atelectasis and emphysema, diverticula of the gastrointestinal and genitourinary systems, and vascular anomalies. Associated cranial anomalies, late closure of the fontanel, joint laxity, hip dislocation, and inguinal hernia have been observed but are uncommon. Defects in FBLN5 are the cause of age-related macular degeneration type 3 (ARMD3). ARMD is a multifactorial disease and the most common cause of irreversible vision loss in the developed world. In most patients, the disease is manifest as ophthalmoscopically visible yellowish accumulations of protein and lipid (known as drusen) that lie beneath the retinal pigment epithelium and within an elastin-containing structure known as Bruch membrane. Belongs to the fibulin family.

Protein type: Secreted; Secreted, signal peptide

Chromosomal Location of Human Ortholog: 14q32.1

Cellular Component: extracellular matrix; proteinaceous extracellular matrix; extracellular space; extracellular region

Molecular Function: protein C-terminus binding; integrin binding; protein binding; protein homodimerization activity; calcium ion binding

Biological Process: elastic fiber assembly; secretion; extracellular matrix organization and biogenesis; cell-matrix adhesion; regulation of cell growth

Disease: Cutis Laxa, Autosomal Dominant 2; Macular Degeneration, Age-related, 3; Cutis Laxa, Autosomal Recessive, Type Ia