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Validated All-in-One™ qPCR Primer for YAP1(NM_001130145.2) Search again
Product ID:
HQP055077
(click here to view gene annotation page)
Species:
Human
Symbol:
Alias:
COB1, YAP, YAP-1, YAP2, YAP65, YKI
Gene Description:
Yes1 associated transcriptional regulator
Target Gene Accession:
NM_001130145.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
Summary
This gene encodes the human ortholog of chicken YAP protein which binds to the SH3 domain of the Yes proto-oncogene product. This protein contains a WW domain that is found in various structural, regulatory and signaling molecules in yeast, nematode, and mammals, and may be involved in protein-protein interaction.
Gene References into function
- NMR structures of the YAP65 WW domain and the variant L30 K in complex with the peptides GTPPPPYTVG, N-(n-octyl)-GPPPY and PLPPY and the application of peptide libraries reveal a minimal binding epitope
- YAP is a potential signaling partner of the full-length ErbB4 receptor at the membrane and of the COOH-terminal fragment of ErbB-4 that translocates to the nucleus to regulate transcription
- Yap binds to HNRNPU and regulates its co-activation of Bax transcription
- the minimum binding domain is larger than the latter two strands of the WW domain beta-sheet
- WWOX antagonizes the function of YAP by competing for interaction with ErbB-4 and other targets and thus affect its transcriptional activity.
- Results suggested that YAP65 plays a role in the normal and diseased pancreas.
- WBP-2 and YAP are coactivators for estrogen and progesterone receptor transactivation pathways.
- Results point to a potential oncogenic role for YAP in 11q22-amplified human cancers, and suggest that this signaling pathway regulates both cellular proliferation and apoptosis in mammalian epithelial cells.
- The Yes-associated protein 1 stabilizes p73 by preventing Itch-mediated ubiquitination of p73.
- the RUNX2 and YAP65 interaction has a novel role in oncogenic transformation that may be mediated by modulation of p21(CIP1) protein expression
- Proline-rich Gla protein 2 may be involved in a signal transduction pathway, the impairment of which may be an unintended consequence of warfarin therapy
- YAP identified as a novel and critical downstream effector of c-Jun-mediated apoptosis following cisplatin treatment
- Delineate a mammalian Hippo signaling pathway that culminates in the phosphorylation of YAP, the mammalian homolog of Yki. Is a potent regulator of organ size, and its dysregulation leads to tumorigenesis.
- findings report that YAP1 increases organ size and causes aberrant tissue expansion
- LATS1 inactivates YAP oncogenic function by suppressing its transcription regulation of cellular genes via sequestration of YAP in the cytoplasm after phosphorylation of YAP.
- Increased YAP protein is associated with esophageal and gastric epithelial tumorigenesis.
- c-Abl directly phosphorylates Yap1 at position Y357 in response to DNA damage. Tyrosine-phosphorylated Yap1 is a more stable protein that displays higher affinity to p73 and selectively coactivates p73 proapoptotic target genes.
- Expression profiling of genes induced by ectopic expression of YAP or by knockdown of LATS1 reveals a subset of the potential Drosophila Hippo pathway targets implicated in epithelial-to-mesenchymal transition.
- This is the first report indicating YAP as a tumor suppressor, revealing its decreased expression in breast cancer as well as demonstrating the functional implications of YAP loss in several aspects of cancer signaling.
- Overexpression of YAP2 in cells promoted apoptosis, whereas the Mst2/Lats1-induced phosphorylation of YAP partially rescued the cells from apoptotic death.
- The modified Yap1 does not co-activate Runx in supporting Itch transcription. The subsequent reduction in the Itch level gives rise to p73 accumulation.
- this is the first report of negative regulatory signaling from Merlin to YAP1 in mammalian cells and may shed light on mechanisms of malignant pleural mesothelioma development
- results represent the first demonstration that merlin regulates cell growth in meningioma cells by suppressing YAP
- YAP and TEAD gain of function causes marked expansion of the neural progenitor population, partly owing to their ability to promote cell cycle progression by inducing cyclin D1 and to inhibit differentiation by suppressing NeuroM.
- The existence of a proapoptotic autoregulatory feedback loop between p73, YAP, and the promyelocytic leukemia (PML) tumor suppressor gene, is shown.
