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[[Image:2lay.jpg|left|200px]]
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{{STRUCTURE_2lay|  PDB=2lay  |  SCENE=  }}  
{{STRUCTURE_2lay|  PDB=2lay  |  SCENE=  }}  
===Structure of the first WW domain of human YAP in complex with a phosphorylated human Smad1 derived peptide===
===Structure of the first WW domain of human YAP in complex with a phosphorylated human Smad1 derived peptide===
{{ABSTRACT_PUBMED_21685363}}


==Disease==
[[http://www.uniprot.org/uniprot/SMAD1_HUMAN SMAD1_HUMAN]] Defects in SMAD1 may be a cause of primary pulmonary hypertension (PPH1) [MIM:[http://omim.org/entry/178600 178600]]. A rare disorder characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure, and death. The disease can occur from infancy throughout life and it has a mean age at onset of 36 years. Penetrance is reduced. Although familial PPH1 is rare, cases secondary to known etiologies are more common and include those associated with the appetite-suppressant drugs.<ref>PMID:21898662</ref>


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==Function==
The line below this paragraph, {{ABSTRACT_PUBMED_21685363}}, adds the Publication Abstract to the page
[[http://www.uniprot.org/uniprot/YAP1_HUMAN YAP1_HUMAN]] Transcriptional regulator which can act both as a coactivator and a corepressor and is the critical downstream regulatory target in the Hippo signaling pathway that plays a pivotal role in organ size control and tumor suppression by restricting proliferation and promoting apoptosis. The core of this pathway is composed of a kinase cascade wherein STK3/MST2 and STK4/MST1, in complex with its regulatory protein SAV1, phosphorylates and activates LATS1/2 in complex with its regulatory protein MOB1, which in turn phosphorylates and inactivates YAP1 oncoprotein and WWTR1/TAZ. Plays a key role to control cell proliferation in response to cell contact. Phosphorylation of YAP1 by LATS1/2 inhibits its translocation into the nucleus to regulate cellular genes important for cell proliferation, cell death, and cell migration. The presence of TEAD transcription factors are required for it to stimulate gene expression, cell growth, anchorage-independent growth, and epithelial mesenchymal transition (EMT) induction. Isoform 2 and isoform 3 can activate the C-terminal fragment (CTF) of ERBB4 (isoform 3).<ref>PMID:12807903</ref><ref>PMID:17974916</ref><ref>PMID:18579750</ref><ref>PMID:18158288</ref><ref>PMID:18280240</ref><ref>PMID:21364637</ref> [[http://www.uniprot.org/uniprot/SMAD1_HUMAN SMAD1_HUMAN]] Transcriptional modulator activated by BMP (bone morphogenetic proteins) type 1 receptor kinase. SMAD1 is a receptor-regulated SMAD (R-SMAD). SMAD1/OAZ1/PSMB4 complex mediates the degradation of the CREBBP/EP300 repressor SNIP1.<ref>PMID:12097147</ref>  
(as it appears on PubMed at http://www.pubmed.gov), where 21685363 is the PubMed ID number.
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{{ABSTRACT_PUBMED_21685363}}


==About this Structure==
==About this Structure==
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==Reference==
==Reference==
<ref group="xtra">PMID:021685363</ref><references group="xtra"/>
<ref group="xtra">PMID:021685363</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
[[Category: Aragon, E.]]
[[Category: Aragon, E.]]
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