GLI2 (R770) Antibody #2585
Filter:
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Transfected Only |
| MW (kDa) | 220 |
| SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
GLI2 (R770) Antibody detects transfected levels of human GLI2 protein.
Species Reactivity:
Human
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg770 of human GLI2. Antibodies are purified by peptide affinity chromatography.
Background
GLI was first identified as a gene amplified in a malignant glioma (1) capable of transforming primary cells in cooperation with adenovirus E1A (2). GLI belongs to the Krüppel family of zinc finger proteins that includes three mammalian GLI proteins: GLI1, GLI2, and GLI3 (3). These GLI proteins are similar to the Drosophila homolog Cubitus interruptus (Ci) and function as transcription factors activated by the Hedgehog signaling pathway. Hedgehog signaling plays an important role in animal development, and research studies have shown that this pathway is aberrantly activated in many types of cancers (4,5).
GLI2 contains both transcription repression and activation domains (6) and several isoforms of GLI2 have been reported that may have different activities (7-9). Overexpression of GLI2 in skin causes basal cell carcinoma in mice (10), while loss-of-function of GLI2 is associated with pituitary anomalies (11).
GLI2 contains both transcription repression and activation domains (6) and several isoforms of GLI2 have been reported that may have different activities (7-9). Overexpression of GLI2 in skin causes basal cell carcinoma in mice (10), while loss-of-function of GLI2 is associated with pituitary anomalies (11).
- Kinzler, K.W. et al. (1987) Science 236, 70-3.
- Ruppert, J.M. et al. (1991) Mol Cell Biol 11, 1724-8.
- Kinzler, K.W. et al. (1988) Nature 332, 371-4.
- Ingham, P.W. and McMahon, A.P. (2001) Genes Dev 15, 3059-87.
- McMahon, A.P. et al. (2003) Curr Top Dev Biol 53, 1-114.
- Sasaki, H. et al. (1999) Development 126, 3915-24.
- Tanimura, A. et al. (1998) J Virol 72, 3958-64.
- Tojo, M. et al. (2003) Br J Dermatol 148, 892-7.
- Speek, M. et al. (2006) BMC Mol Biol 7, 13.
- Grachtchouk, M. et al. (2000) Nat Genet 24, 216-7.
- Roessler, E. et al. (2003) Proc Natl Acad Sci USA 100, 13424-9.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意，否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件，除非书 CST 的合法授书代表以书面形式书独接受， 否书均被拒书，并且无效。
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For Research Use Only. Not For Use In Diagnostic Procedures.
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