YAP1 - a transcription co-activator and the downstream target of Hippo pathway

Wed, 11/04/2015 - 15:07

YAP1 (Yes-associated protein 1) is a  transcriptional co-activator which acts as a major effector of Hippo signaling pathway that regulates organ size/ tissue homeostasis and cell proliferation, and is an established oncogene (1).  Hippo signaling activation results in the phosphorylation mediated inactivation of YAP1, and restriction of YAP1’s transcriptional activity is the principal mechanism of growth and tumor suppression by Hippo pathway. Accordingly, loss of Hippo signaling by mutations or down-regulation of core pathway components is associated with cancer development, while YAP1 is reported as a potent oncogene that can promote tumorigenesis in a wide range of tissues (2).




YAP1 Antibody [NB110-58358]
YAP antibody was tested in Hela cells at a 1:500 dilution with Dylight 488 (Green) labelled secondary antibody. Alpha tubulin and nuclei were counterstained against Dylight 550 (red) and DAPI (blue), respectively.


YAP1 Antibody (1A12) [NBP2-22117]
Flow cytometric analysis of Hela cells using mouse monoclonal YAP1 antibody (clone 1A12). Green line represents YAP1+ cells & negative control pool is depicted by red line.

For exploring the role of Glypican 3 (GPC3) in the development of hepatocellular carcinoma and its relationship to YAP1, Miao et al 2013 used siRNA to knock down GPC3 in Huh7 HCC cells, added recombinant human YAP-1, and assayed parameters linked to apoptosis, cell division and migration/invasion. GPC3 knockdown was found to suppress YAP mRNA /protein expression levels while addition of recombinant human YAP-1 effectively rescued the cells from biological effects of lack of GPC3 (3).  Tsujiura and coworkers used YAP1 antibody (NB110-58358) for IHC-P analysis of 150 primary tumor tissues from endometrial cancer/ EMCA patients and for WB as well as ICC/IF assays in studies evaluating of biological role of YAP in EMCA cell lines (HEC-1-A, HEC-1-B and Ishikawa). YAP’s nuclear positivity was found to correlate well with higher grade, stage, lympho-vascular space invasion, postoperative recurrence/metastasis and overall survival in estrogen mediated EMCA. Knockdown of YAP lead to decreased cell proliferation, anchorage-dependent growth and migration/invasion while YAP overexpression promoted cell proliferation (4). Chen et al 2015 used our YAP1 antibody for ICC/IF and IHC-P assays in studies involving evaluation of the effect of matrix stiffness on cellular proliferation and Klf5/Klf4 expression in murine model of renal fibrosis pathogenesis.  Stiff matrix-activated ERK was found to enhance the expression levels as well as the nuclear translocation of YAP1. Moreover, the dilated tubules of obstructed kidney depicted an up-regulated ERK/YAP1/Klf5/cyclin D1 axis proteins (5).  

Novus Biologicals offers YAP1 reagents for your research needs including:


  1. Stein et al. 2015. YAP1 Exerts Its Transcriptional Control via TEAD-Mediated Activation of Enhancers.  PLoS Genet. 11(8):e1005465
  2. Harvey et al. 2013. The Hippo pathway and human cancer. Nat Rev Cancer.  13(4):246-57
  3. Miao et al 2013. Knockdown of GPC3 inhibits the proliferation of Huh7 hepatocellular carcinoma cells through down-regulation of YAP. J Cell Biochem. 114(3):625-31
  4. Tsujiura et al 2014. Yes-associated protein (YAP) modulates oncogenic features and radiation sensitivity in endometrial cancer. PLoS One. 9(6):e100974
  5. Chen et al. 2015. Matrix-Stiffness-Regulated Inverse Expression of Krüppel-Like Factor 5 and Krüppel-Like Factor 4 in the Pathogenesis of Renal Fibrosis. Am J Pathol. 185(9):2468-81

By: Subhash Gangar

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