R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
Phospho-TACC3 (Ser558) (D8H10) XP® Rabbit mAb #8842
Filter:
- WB
- IF
Supporting Data
REACTIVITY | H |
SENSITIVITY | Endogenous |
MW (kDa) | 140 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunofluorescence (Immunocytochemistry) | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
Phospho-TACC3 (Ser558) (D8H10) XP® Rabbit mAb recognizes endogenous levels of TACC3 protein only when phosphorylated at Ser558.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Ser558 of human TACC3 protein.
Background
Transforming acid coiled-coil (TACC) proteins are a family of proteins characterized by a common coiled-coil motif of approximately 200 amino acids at the carboxy-terminal end (1). Three family members have been identified in humans: TACC1, TACC2, and TACC3. These proteins are thought to be involved in centrosomal microtubule assembly and have been mapped to chromosomal regions that are disrupted in some cancers (reviewed in 2). TACC3 has been shown to be upregulated in many cancer cell lines (3). When phosphorylated at Ser558 by Aurora A, mammalian TACC3 is localized to mitotic spindles and increases microtubule stability (4,5). For this reason, it has been suggested that monitoring the localization of phosphorylated TACC3 would be an effective way to determine the efficacy of Aurora A inhibitors that show promise as anti-cancer drugs (6,7). In addition, studies have shown that TACC3 could be useful as a prognostic marker for non-small cell lung cancer (8).
- Gergely, F. et al. (2000) Proc Natl Acad Sci USA 97, 14352-7.
- Peset, I. and Vernos, I. (2008) Trends Cell Biol 18, 379-88.
- Still, I.H. et al. (1999) Genomics 58, 165-70.
- Kinoshita, K. et al. (2005) J Cell Biol 170, 1047-55.
- Schneider, L. et al. (2007) J Biol Chem 282, 29273-83.
- LeRoy, P.J. et al. (2007) Cancer Res 67, 5362-70.
- Tyler, R.K. et al. (2007) Cell Cycle 6, 2846-54.
- Jung, C.K. et al. (2006) Pathol Int 56, 503-9.
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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