LATS1 Antibody #9153
Filter:
- WB
Supporting Data
REACTIVITY | H Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 140 |
SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
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
LATS1 Antibody detects endogenous levels of total LATS1 protein.
Species Reactivity:
Human, Monkey
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to amino acids surrounding Ser177 of human LATS1. Antibodies are purified by protein A and peptide affinity chromatography.
Background
The Large tumor suppressor (LATS) proteins (LATS1, LATS2) are serine/threonine kinases that belong to the NDR family (1). The Drosophila homolog (warts) was first identified as a tumor suppressor protein that plays a role in the maintenance of ploidy. Human LATS1 was shown to localize to the centrosome and the mitotic spindle and control G2/M transition by negatively regulating cdc2 kinase activity (2,3). LATS1 is also reported to play a role in the G1 tetraploidy checkpoint, via control of p53 expression (4). LATS1 affects cytokinesis by regulating actin polymerization through negative modulation of LIMK1 (5). LATS1 also binds the phosphorylated form of zyxin, a regulator of actin filament assembly. This interaction promotes localization of zyxin to the mitotic spindle, suggesting a role for actin regulatory proteins during mitosis (6). Decreased expression of LATS1 is associated with breast tumor aggressiveness (7), and mutations perturbing LATS1 have been associated with human sarcomas and ovarian sarcomas (8,9). LATS1 knockout mice develop soft-tissue sarcomas, ovarian stromal cell tumor, and display a high sensitivity to carcinogenic treatments (10). LATS1 and LATS2 have also been identified as key members of the Hippo signaling pathway, a conserved kinase cascade that functions to regulate cell growth and apoptosis (11). Phosphorylation of LATS by Mammalian Sterile-20-like proteins (e.g., MST1) results in LATS-mediated phosphorylation of the transcriptional co-activators YAP and TAZ (12, 13). LATS-mediated phosphorylation of YAP and TAZ promotes their cytoplasmic sequestration and association with 14-3-3 proteins, and subsequent proteasomal degradation, leading to downregulation of YAP/TAZ target genes that promote cell growth (11, 14).
- Tao, W. et al. (1999) Nat Genet 21, 177-81.
- Yang, X. et al. (2001) Oncogene 20, 6516-23.
- Xia, H. et al. (2002) Oncogene 21, 1233-41.
- Iida, S. et al. (2004) Oncogene 23, 5266-74.
- Yang, X. et al. (2004) Nat Cell Biol 6, 609-17.
- Hirota, T. et al. (2000) J Cell Biol 149, 1073-86.
- Morinaga, N. et al. (2000) Int J Oncol 17, 1125-9.
- Hansen, L.L. et al. (2002) Cancer Genet Cytogenet 139, 1-8.
- Hisaoka, M. et al. (2002) Lab Invest 82, 1427-35.
- St John, M.A. et al. (1999) Nat Genet 21, 182-6.
- Guo, C. et al. (2007) Curr Biol 17, 700-5.
- Hergovich, A. et al. (2006) Biochem Biophys Res Commun 345, 50-8.
- Hirabayashi, S. et al. (2008) Oncogene 27, 4281-92.
- Zhao, B. et al. (2010) J Cell Sci 123, 4001-6.
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。
专品专有“专供研究使用”的专专或专似的专专声明, 且未专得美国食品和专品管理局或其他外国或国内专管机专专专任何用途的批准、准专或专可。客专不得将任何专品用于任何专断或治专目的, 或以任何不符合专专声明的方式使用专品。CST 专售或专可的专品提供专作专最专用专的客专,且专用于研专用途。将专品用于专断、专防或治专目的, 或专专售(专独或作专专成)或其他商专目的而专专专品,均需要 CST 的专独专可。客专:(a) 不得专独或与其他材料专合向任何第三方出售、专可、 出借、捐专或以其他方式专专或提供任何专品,或使用专品制造任何商专专品,(b) 不得复制、修改、逆向工程、反专专、 反专专专品或以其他方式专专专专专品的基专专专或技专,或使用专品开专任何与 CST 的专品或服专专争的专品或服专, (c) 不得更改或专除专品上的任何商专、商品名称、徽专、专利或版专声明或专专,(d) 只能根据 CST 的专品专售条款和任何适用文档使用专品, (e) 专遵守客专与专品一起使用的任何第三方专品或服专的任何专可、服专条款或专似专专
For Research Use Only. Not For Use In Diagnostic Procedures.
Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
All other trademarks are the property of their respective owners. Visit our
Trademark Information page.