GLI Family Zinc Finger Protein 3 (GLI3) Recombinant Protein | GLI3 recombinant protein

Recombinant GLI Family Zinc Finger Protein 3 (GLI3)

Cat. Num. AAA2011171

• Gene Names: Gli3; Xt; Bph; Pdn; add; GLI3FL; AI854843; AU023367; GLI3-190
• Applications: SDS-Page, Western Blot, ELISA, Immunoprecipitation
• Purity: > 95%
• Synonyms: GLI Family Zinc Finger Protein 3 (GLI3); Recombinant GLI Family Zinc Finger Protein 3 (GLI3); GLI3 recombinant protein

• Host: E Coli
• Purity/Purification: > 95%
• Form/Format: Supplied as lyophilized form in PBS,pH7.4, containing 5% sucrose, 0.01% sarcosyl.
• Sequence: The target protein is fused with two N-terminal Tags, His-tag and T7-tag, its sequence is listed below.; MGSSHHHHHH SSGLVPRGSH MASMTGGQQM GRGSEF-SFDLQTMI RTSPNSLVTI LNNSRSSSSA SGSYGHLSAS AISPALSFTY PSAPVSLHMH QQILSRQQSL GSAFGHSPPL IHPAPTFPTQ RPIPGIPTVL NPVQVSSGPS ESSQSKPTSE SAVSSTGDPM HNKRSKIKPD EDLPSPGSRG QQEQPEGTTL VKEEADKDES KQEPEVIYET NCHWEGCTRE FDTQDQLVHH INNDHIHGEK KEFVCRWLDC SREQKPFKAQ YMLVVHMRRH TGEKPHKCTF EGCTKAYSRL E
• Sequence Length: 1583

• Applicable Applications for GLI3 recombinant protein: SDS-PAGE, Western Blot (WB), ELISA (EIA), Immunoprecipitation (IP)
• Organism: Mus musculus (Mouse)
• Expression System: Prokaryotic expression
• Residues: Ser303~Glu561 (Accession # Q61602) with two N-terminal Tags, His-tag and T7-tag
• Endotoxin Level: <1.0EU per 1ug (determined by the LAL method)
• Reconstitution: Reconstitute in sterile PBS, pH7.2-pH7.4.
• Preparation and Storage: Avoid repeated freeze/thaw cycles. Store at 2-8 degree C for one month. Aliquot and store at -80 degree C for 12 months.; Stability Test: The thermal stability is described by the loss rate of the targetprotein. The loss rate was determined by accelerated thermal degradation test,that is, incubate the protein at 37 degree C for 48h, and no obvious degradation andprecipitation were observed. (Referring from China Biological Products Standard,which was calculated by the Arrhenius equation.) The loss of this protein is lessthan 5% within the expiration date under appropriate storage condition.

SDS-Page

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: 32.5kDa
• 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; extra toes; brachyphalangy; polydactyly Nagoya; GLI3 form of 190 kDa; GLI3 full length protein; zinc finger protein GLI3; anterior digit pattern deformity
• 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: C2H2-type zinc finger protein; Transcription factor

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

Molecular Function: histone acetyltransferase binding; protein binding; DNA binding; nucleic acid binding; sequence-specific DNA binding; metal ion binding; histone deacetylase 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; heart development; positive regulation of transcription, DNA-dependent; T cell differentiation in the thymus; anterior/posterior pattern formation; regulation of apoptosis; embryonic digestive tract morphogenesis; oligodendrocyte differentiation; anatomical structure formation; pallium development; kidney development; inner ear development; embryonic gut development; lateral ganglionic eminence cell proliferation; 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; positive regulation of chondrocyte differentiation; camera-type eye morphogenesis; 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; tongue development; axon guidance; spinal cord dorsal/ventral patterning; forebrain dorsal/ventral pattern formation; palate development; negative regulation of transcription from RNA polymerase II promoter; negative regulation of cell proliferation; mammary gland development; regulation of transcription, DNA-dependent; 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; embryonic skeletal morphogenesis; odontogenesis of dentine-containing teeth; regulation of cell proliferation; positive regulation of osteoblast differentiation; telencephalon development; negative regulation of cell differentiation; 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; brain development; hindgut morphogenesis; positive regulation of alpha-beta T cell differentiation; lung development; negative regulation of alpha-beta T cell differentiation