GNE sirna

GNE siRNA (Rat)

Cat. Num. AAA8228572

• Gene Names: Gne; Uae1
• Reactivity: Rat
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: GNE; GNE siRNA (Rat); GLCNE; Bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase; UDP-GlcNAc-2-epimerase/ManAc kinase; GNE sirna

• Host: Synthetic
• Reactivity: Rat
• Specificity: GNE siRNA (Rat) 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: 722

• Applicable Applications for GNE 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 rat GNE 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 GNE sirna

siRNA to inhibit GNE expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 16758602
• NCBI GeneID: 114711
• NCBI Accession #: NP_446217.1
• NCBI GenBank Nucleotide #: NM_053765.2
• UniProt Accession #: O35826
• Molecular Weight: 79,227 Da
• NCBI Official Full Name: bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase
• NCBI Official Synonym Full Names: glucosamine (UDP-N-acetyl)-2-epimerase/N-acetylmannosamine kinase
• NCBI Official Symbol: Gne
• NCBI Official Synonym Symbols: Uae1
• NCBI Protein Information: bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase
• UniProt Protein Name: Bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase
• Protein Family: Bifunctional UDP-N-acetylglucosamine 2-epimerase/N-acetylmannosamine kinase
• UniProt Gene Name: Gne
• UniProt Synonym Gene Names: Glcne
• UniProt Entry Name: GLCNE_RAT

NCBI Description

bifunctional enzyme, catalyzes the first two steps of biosynthesis of Neu5Ac (UDP-GlcNAc 2-epimerase and ManNAc kinase), precursor of sialic acids [RGD, Feb 2006]

Uniprot Description

GNE: Regulates and initiates biosynthesis of N- acetylneuraminic acid (NeuAc), a precursor of sialic acids. Plays an essential role in early development. Required for normal sialylation in hematopoietic cells. Sialylation is implicated in cell adhesion, signal transduction, tumorigenicity and metastatic behavior of malignant cells. Defects in GNE are a cause of sialuria (SIALURIA); also known as sialuria French type. In sialuria, free sialic acid accumulates in the cytoplasm and gram quantities of neuraminic acid are secreted in the urine. The metabolic defect involves lack of feedback inhibition of UDP-GlcNAc 2-epimerase by CMP-Neu5Ac, resulting in constitutive overproduction of free Neu5Ac. Clinical features include variable degrees of developmental delay, coarse facial features and hepatomegaly. Sialuria inheritance is autosomal dominant. Defects in GNE are the cause of inclusion body myopathy type 2 (IBM2). Hereditary inclusion body myopathies are a group of neuromuscular disorders characterized by adult onset, slowly progressive distal and proximal weakness and a typical muscle pathology including rimmed vacuoles and filamentous inclusions. IBM2 is an autosomal recessive disorder affecting mainly leg muscles, but with an unusual distribution that spares the quadriceps as also observed in Nonaka myopathy. Defects in GNE are the cause of Nonaka myopathy (NM); also known as distal myopathy with rimmed vacuoles (DMRV). NM is an autosomal recessive muscular disorder, allelic to inclusion body myopathy 2. It is characterized by weakness of the anterior compartment of the lower limbs with onset in early adulthood, and sparing of the quadriceps muscles. As the inclusion body myopathy, NM is histologically characterized by the presence of numerous rimmed vacuoles without inflammatory changes in muscle specimens. 5 isoforms of the human protein are produced by alternative splicing.

Protein type: Isomerase; Cytoskeletal; Cell adhesion; EC 2.7.1.60; Carbohydrate Metabolism - amino sugar and nucleotide sugar; Motility/polarity/chemotaxis; EC 3.2.1.183; Kinase, other

Cellular Component: cytosol

Molecular Function: protein binding; metal ion binding; UDP-N-acetylglucosamine 2-epimerase activity; ATP binding; N-acylmannosamine kinase activity; hydrolase activity, hydrolyzing O-glycosyl compounds

Biological Process: N-acetylglucosamine biosynthetic process; UDP-N-acetylglucosamine metabolic process; N-acetylneuraminate biosynthetic process; carbohydrate phosphorylation