GLI3 sirna

GLI3 siRNA (Mouse)

Cat. Num. AAA8232178

• Gene Names: Gli3; Xt; Bph; Pdn; add; GLI3FL; AI854843; AU023367; GLI3-190
• Reactivity: Mouse
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: GLI3; GLI3 siRNA (Mouse); Transcriptional activator GLI3; GLI3 form of 190 kDa; GLI3-190; GLI3 full length protein; GLI3FL; GLI3 sirna

• Host: Synthetic
• Reactivity: Mouse
• Specificity: GLI3 siRNA (Mouse) 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: 1583

• Applicable Applications for GLI3 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 mouse GLI3 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 GLI3 sirna

siRNA to inhibit GLI3 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 120953173
• NCBI GeneID: 14634
• NCBI Accession #: NP_032156.2
• NCBI GenBank Nucleotide #: NM_008130.2
• UniProt Accession #: Q61602
• Molecular Weight: 171,655 Da
• NCBI Official Full Name: transcriptional activator GLI3
• NCBI Official Synonym Full Names: GLI-Kruppel family member GLI3
• NCBI Official Symbol: Gli3
• NCBI Official Synonym Symbols: Xt; Bph; Pdn; add; GLI3FL; AI854843; AU023367; GLI3-190
• NCBI Protein Information: transcriptional activator GLI3
• UniProt Protein Name: Transcriptional activator GLI3
• Protein Family: Zinc finger protein
• UniProt Gene Name: Gli3
• UniProt Synonym Gene Names: GLI3-190; GLI3FL; GLI3-83
• UniProt Entry Name: GLI3_MOUSE

Uniprot Description

GLI3: Has a dual function as a transcriptional activator and a repressor of the sonic hedgehog (Shh) pathway, and plays a role in limb development. The full-length GLI3 form (GLI3FL) after phosphorylation and nuclear translocation, acts as an activator (GLI3A) while GLI3R, its C-terminally truncated form, acts as a repressor. A proper balance between the GLI3 activator and the repressor GLI3R, rather than the repressor gradient itself or the activator/repressor ratio gradient, specifies limb digit number and identity. In concert with TRPS1, plays a role in regulating the size of the zone of distal chondrocytes, in restricting the zone of PTHLH expression in distal cells and in activating chondrocyte proliferation. Binds to the minimal GLI-consensus sequence 5'-GGGTGGTC-3'. Defects in GLI3 are the cause of Greig cephalo-poly- syndactyly syndrome (GCPS). GCPS is an autosomal dominant disorder affecting limb and craniofacial development. It is characterized by pre- and postaxial polydactyly, syndactyly of fingers and toes, macrocephaly and hypertelorism. Defects in GLI3 are a cause of Pallister-Hall syndrome (PHS). PHS is characterized by a wide range of clinical manifestations. It mainly associates central or postaxial polydactyly, syndactyly, and hypothalamic hamartoma. Malformations are frequent in the viscera, e.g. anal atresia, bifid uvula, congenital heart malformations, pulmonary or renal dysplasia. It is an autosomal dominant disorder. Defects in GLI3 are a cause of polydactyly postaxial type A1 (PAPA1). A trait characterized by an extra digit in the ulnar and/or fibular side of the upper and/or lower extremities. The extra digit is well formed and articulates with the fifth, or extra, metacarpal/metatarsal, and thus it is usually functional. Defects in GLI3 are a cause of polydactyly postaxial type B polydactyly (PAPB). A trait characterized by an extra digit in the ulnar and/or fibular side of the upper and/or lower extremities. The extra digit is not well formed and is frequently in the form of a skin. Defects in GLI3 are a cause of polydactyly preaxial type 4 (POP4). Polydactyly preaxial type 4 (i.e. polydactyly on the radial/tibial side of the hand/foot) covers a heterogeneous group of entities. In preaxial polydactyly type IV, the thumb shows only the mildest degree of duplication, and syndactyly of various degrees affects fingers 3 and 4. Belongs to the GLI C2H2-type zinc-finger protein family.

Protein type: Transcription factor; C2H2-type zinc finger protein

Cellular Component: cell projection; transcriptional repressor complex; cytoplasm; nuclear speck; Srb-mediator complex; cytosol; nucleus; cilium

Molecular Function: histone acetyltransferase binding; protein binding; nucleic acid binding; DNA binding; sequence-specific DNA binding; histone deacetylase binding; metal ion binding; beta-catenin binding; chromatin binding; transcription factor activity

Biological Process: neural tube development; developmental growth; radial glial cell differentiation in the forebrain; central nervous system development; anatomical structure development; positive regulation of transcription, DNA-dependent; heart development; T cell differentiation in the thymus; regulation of apoptosis; anterior/posterior pattern formation; embryonic digestive tract morphogenesis; anatomical structure formation; oligodendrocyte differentiation; pallium development; kidney development; embryonic gut development; lateral ganglionic eminence cell proliferation; inner ear development; embryonic limb morphogenesis; positive regulation of neuroblast proliferation; camera-type eye development; transcription, DNA-dependent; neuron fate commitment; subpallium development; optic nerve morphogenesis; negative thymic T cell selection; negative regulation of neuron differentiation; camera-type eye morphogenesis; positive regulation of chondrocyte differentiation; branching morphogenesis of a tube; regulation of gene expression; positive regulation of transcription from RNA polymerase II promoter; embryonic digit morphogenesis; negative regulation of transcription, DNA-dependent; tube development; metanephros development; smoothened signaling pathway involved in spinal cord motor neuron cell fate specification; negative regulation of apoptosis; limb development; axon guidance; tongue development; spinal cord dorsal/ventral patterning; forebrain dorsal/ventral pattern formation; negative regulation of transcription from RNA polymerase II promoter; palate development; negative regulation of cell proliferation; regulation of transcription, DNA-dependent; mammary gland development; regulation of cell differentiation; forebrain development; melanocyte differentiation; embryonic morphogenesis; smoothened signaling pathway involved in ventral spinal cord interneuron specification; proximal/distal pattern formation; smoothened signaling pathway; in utero embryonic development; hippocampus development; spinal cord motor neuron differentiation; pattern specification process; limb morphogenesis; regulation of cell proliferation; odontogenesis of dentine-containing teeth; embryonic skeletal morphogenesis; positive regulation of osteoblast differentiation; negative regulation of cell differentiation; telencephalon development; positive regulation of protein import into nucleus; dorsal/ventral pattern formation; cerebral cortex radial glia guided migration; ureteric bud branching; negative regulation of smoothened signaling pathway; protein processing; hindgut morphogenesis; brain development; positive regulation of alpha-beta T cell differentiation; lung development; negative regulation of alpha-beta T cell differentiation