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concluding remarks and future directions
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The study of WW domains and Hippo pathway in recent years further highlighted important aspects of WW domain protein signaling including dimerization capability, regulation of WW domain-PRM interaction and networking (reviewed in Sudol>>5<<). WW domains are present in a wide variety of cellular proteins including E3 ligases, co-activators, co-repressors and adapter proteins that could potentially regulate members of the Hippo pathway.
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of this pathway. The use of GFP-expressing tumor cells in fresh tissue or live animals shall facilitate better characterization of the Hippo pathway proteins and their role, both in vitro and in vivo, in tumor initiation and progression.>>54<<, 55, 56, 57 Expansion of this information may aid in developing new therapeutic strategies based on the WW domain interactions in this pathway.
n3:mentions
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pathway. The use of GFP-expressing tumor cells in fresh tissue or live animals shall facilitate better characterization of the Hippo pathway proteins and their role, both in vitro and in vivo, in tumor initiation and progression.54, >>55<<, 56, 57 Expansion of this information may aid in developing new therapeutic strategies based on the WW domain interactions in this pathway.
n3:mentions
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pathway. The use of GFP-expressing tumor cells in fresh tissue or live animals shall facilitate better characterization of the Hippo pathway proteins and their role, both in vitro and in vivo, in tumor initiation and progression.54, 55, >>56<<, 57 Expansion of this information may aid in developing new therapeutic strategies based on the WW domain interactions in this pathway.
n3:mentions
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54, 55, 56, >>57<< Expansion of this information may aid in developing new therapeutic strategies based on the WW domain interactions in this pathway.
n3:mentions
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or activators of WW domain signaling complexes in the Hippo pathway could be facilitated by the considerable data available on the WW domain structure, the mechanism of interaction with its rigid ligands, and the complexes it forms.>>58<< Owing to the fact that the WW domain and its ligands' core motifs are relatively short, it might be possible to use small molecules that function as activators or inhibitors for the Hippo pathway signaling proteins; that is, small
n3:mentions
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ww domains
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WW domain, the smallest module that naturally occurs, consists of ∼35–40 amino acid residues, including two highly conserved tryptophan (W) residues separated by 20–23 amino acids in the polypeptide chain.>>6<<, 7, 8 These two W amino acids give the domain its name, WW domain.
n3:mentions
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WW domain, the smallest module that naturally occurs, consists of ∼35–40 amino acid residues, including two highly conserved tryptophan (W) residues separated by 20–23 amino acids in the polypeptide chain.6, >>7<<, 8 These two W amino acids give the domain its name, WW domain.
n3:mentions
n2:7782338
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Originally, WW domains were identified through detailed characterization of the Yes-associated protein (YAP) based on computer-aided analysis of imperfectly repeated sequences in the mouse isoform of YAP, and in yeast factor RSP5.>>7<<, 8 Functional screen of a cDNA expression library identified the first two putative WW domain ligands, WBP1 and 2.9, 10 To date, WW domains constitute five classes depending on the content of their cognate proline-rich binding motifs
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on computer-aided analysis of imperfectly repeated sequences in the mouse isoform of YAP, and in yeast factor RSP5.7, 8 Functional screen of a cDNA expression library identified the first two putative WW domain ligands, WBP1 and 2.9, >>10<< To date, WW domains constitute five classes depending on the content of their cognate proline-rich binding motifs (PRM).
n3:mentions
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Functional screen of a cDNA expression library identified the first two putative WW domain ligands, WBP1 and 2.9, 10 To date, WW domains constitute five classes depending on the content of their cognate proline-rich binding motifs (PRM).>>11<<, 12, 13, 14 The most abundant type of WW domains are class-I WW domains, which bind to PPxY motifs, where P is proline, x is any amino acid and Y is tyrosine.
n3:mentions
n2:9202023
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screen of a cDNA expression library identified the first two putative WW domain ligands, WBP1 and 2.9, 10 To date, WW domains constitute five classes depending on the content of their cognate proline-rich binding motifs (PRM).11, >>12<<, 13, 14 The most abundant type of WW domains are class-I WW domains, which bind to PPxY motifs, where P is proline, x is any amino acid and Y is tyrosine.
n3:mentions
n2:11911877
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_:vb11440583
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screen of a cDNA expression library identified the first two putative WW domain ligands, WBP1 and 2.9, 10 To date, WW domains constitute five classes depending on the content of their cognate proline-rich binding motifs (PRM).11, 12, >>13<<, 14 The most abundant type of WW domains are class-I WW domains, which bind to PPxY motifs, where P is proline, x is any amino acid and Y is tyrosine.
n3:mentions
n2:12592019
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11, 12, 13, >>14<< The most abundant type of WW domains are class-I WW domains, which bind to PPxY motifs, where P is proline, x is any amino acid and Y is tyrosine.
n3:mentions
n2:11163176
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WW domains falling in a tandem repeat manner have different binding properties to different proteins, suggesting that WW domains bind to a vast repertoire of different proteins and that they might be part of complexes bridging blocks.>>15<<, 16,
n3:mentions
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domains falling in a tandem repeat manner have different binding properties to different proteins, suggesting that WW domains bind to a vast repertoire of different proteins and that they might be part of complexes bridging blocks.15, >>16<<,
n3:mentions
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In fact, these domains gained their essential role after being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, >>19<< muscular dystrophy,20, 21 Alzheimer's,22, 23, 24 Huntington's diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate
n3:mentions
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In fact, these domains gained their essential role after being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, 19 muscular dystrophy,>>20<<, 21 Alzheimer's,22, 23, 24 Huntington's diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is
n3:mentions
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these domains gained their essential role after being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, 19 muscular dystrophy,20, >>21<< Alzheimer's,22, 23, 24 Huntington's diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is
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gained their essential role after being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, 19 muscular dystrophy,20, 21 Alzheimer's,>>22<<, 23, 24 Huntington's diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and
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gained their essential role after being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, 19 muscular dystrophy,20, 21 Alzheimer's,22, >>23<<, 24 Huntington's diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and more
n3:mentions
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their essential role after being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, 19 muscular dystrophy,20, 21 Alzheimer's,22, 23, >>24<< Huntington's diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and more
n3:mentions
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being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, 19 muscular dystrophy,20, 21 Alzheimer's,22, 23, 24 Huntington's diseases,>>25<<, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and more recently cancer.
n3:mentions
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being shown to be involved in human diseases including, Liddle's syndrome of hypertension, where the WW domain ligand (PPxY domain) is deleted or mutated,18, 19 muscular dystrophy,20, 21 Alzheimer's,22, 23, 24 Huntington's diseases,25, >>26<< Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and more recently cancer.
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23, 24 Huntington's diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,>>27<< and more recently cancer.3, 28, 29, 30 Moreover, WW domain-containing proteins have gained further interest after being identified in the Hippo tumor suppressor pathway.
n3:mentions
n2:20410308
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diseases,25, 26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and more recently cancer.>>3<<, 28, 29, 30 Moreover, WW domain-containing proteins have gained further interest after being identified in the Hippo tumor suppressor pathway.
n3:mentions
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26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and more recently cancer.3, >>28<<, 29, 30 Moreover, WW domain-containing proteins have gained further interest after being identified in the Hippo tumor suppressor pathway.
n3:mentions
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26 Golabi-Ito-Hall syndrome of mental retardation, in which the binding of Y65C-mutated WW domain of polyglutamine tract-binding protein 1 (PQBP1) to its cognate proline-rich ligands is abrogated,27 and more recently cancer.3, 28, >>29<<, 30 Moreover, WW domain-containing proteins have gained further interest after being identified in the Hippo tumor suppressor pathway.
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3, 28, 29, >>30<< Moreover, WW domain-containing proteins have gained further interest after being identified in the Hippo tumor suppressor pathway.
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hippo tumor suppressor pathway
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for protein ligands, and that a single polypeptide can bind multiple classes of WW domains through separate PRM suggested that WW domains provide a versatile platform to link individual proteins into physiologically important networks.>>16<<, 17 One such important network that has received much attention in the last few years is the Hippo tumor suppressor pathway.
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attention in the last few years is the Hippo tumor suppressor pathway. The Hippo pathway is a highly conserved pathway that regulates tissue growth and organ size by regulating cell growth, proliferation, differentiation and apoptosis.>>3<<, 29 Inactivation or mutations of some components of the pathway were identified in different types of cancer.
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in the last few years is the Hippo tumor suppressor pathway. The Hippo pathway is a highly conserved pathway that regulates tissue growth and organ size by regulating cell growth, proliferation, differentiation and apoptosis.3, >>29<< Inactivation or mutations of some components of the pathway were identified in different types of cancer.
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pathway that regulates tissue growth and organ size by regulating cell growth, proliferation, differentiation and apoptosis.3, 29 Inactivation or mutations of some components of the pathway were identified in different types of cancer.>>3<<, 29, 31 The Hippo pathway is composed of a kinase cascade core that includes MST1/2 serine/threonine kinase (ortholog of Hpo), WW45 scaffold protein (Sav), MOB (Mts) and LATS1/2 kinases (Wts) (Figure 1).
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n2:20439427
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_:vb11440605
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that regulates tissue growth and organ size by regulating cell growth, proliferation, differentiation and apoptosis.3, 29 Inactivation or mutations of some components of the pathway were identified in different types of cancer.3, >>29<<, 31 The Hippo pathway is composed of a kinase cascade core that includes MST1/2 serine/threonine kinase (ortholog of Hpo), WW45 scaffold protein (Sav), MOB (Mts) and LATS1/2 kinases (Wts) (Figure 1).
n3:mentions
n2:20951342
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_:vb11440606
rdf:type
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rdf:value
that regulates tissue growth and organ size by regulating cell growth, proliferation, differentiation and apoptosis.3, 29 Inactivation or mutations of some components of the pathway were identified in different types of cancer.3, 29, >>31<< The Hippo pathway is composed of a kinase cascade core that includes MST1/2 serine/threonine kinase (ortholog of Hpo), WW45 scaffold protein (Sav), MOB (Mts) and LATS1/2 kinases (Wts) (Figure 1).
n3:mentions
n2:17318211
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_:vb11440607
rdf:type
n3:Context
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by a mechanism that is not yet fully established, although some proteins were identified to feed into the core Hippo kinase cassette-like Fat, Dachsous (Dchs), Kibra, Expanded (Ex), Merlin (Mer) and others (reviewed in Grusche et al.>>32<<). Activation of the core cascade leads to phosphorylation of YAP33, 34, 35 and TAZ36 (Yki in flies) leading to their sequestration in the cytoplasm, preventing their translocation to the nucleus and binding to TEAD transcription factor,
n3:mentions
n2:20619814
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_:vb11440608
rdf:type
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rdf:value
32). Activation of the core cascade leads to phosphorylation of YAP>>33<<, 34, 35 and TAZ36 (Yki in flies) leading to their sequestration in the cytoplasm, preventing their translocation to the nucleus and binding to TEAD transcription factor, thereby inhibiting transcription of downstream target genes
n3:mentions
n2:18158288
Subject Item
_:vb11440609
rdf:type
n3:Context
rdf:value
32). Activation of the core cascade leads to phosphorylation of YAP33, >>34<<, 35 and TAZ36 (Yki in flies) leading to their sequestration in the cytoplasm, preventing their translocation to the nucleus and binding to TEAD transcription factor, thereby inhibiting transcription of downstream target genes implicated
n3:mentions
n2:18413746
Subject Item
_:vb11440610
rdf:type
n3:Context
rdf:value
32). Activation of the core cascade leads to phosphorylation of YAP33, 34, >>35<< and TAZ36 (Yki in flies) leading to their sequestration in the cytoplasm, preventing their translocation to the nucleus and binding to TEAD transcription factor, thereby inhibiting transcription of downstream target genes implicated in
n3:mentions
n2:17974916
Subject Item
_:vb11440611
rdf:type
n3:Context
rdf:value
Activation of the core cascade leads to phosphorylation of YAP33, 34, 35 and TAZ>>36<< (Yki in flies) leading to their sequestration in the cytoplasm, preventing their translocation to the nucleus and binding to TEAD transcription factor, thereby inhibiting transcription of downstream target genes implicated in
n3:mentions
n2:18227151
Subject Item
_:vb11440612
rdf:type
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rdf:value
their translocation to the nucleus and binding to TEAD transcription factor, thereby inhibiting transcription of downstream target genes implicated in proliferation, anti-apoptosis and epithelial-to-mesenchymal transition (EMT).>>37<<
n3:mentions
n2:19141641
Subject Item
_:vb11440613
rdf:type
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rdf:value
A unique feature of the Hippo pathway is the high prevalence of WW domain-mediated complexes, defined recently as WW modularity of the Hippo pathway.>>4<< The WW domain containing proteins occur at different levels of the Hippo pathway.
n3:mentions
n2:20598891
Subject Item
_:vb11440614
rdf:type
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rdf:value
In mammals, the core cassette also contains either PPxY/F motifs (Table 1), as in the case of LATS1/2 and MST1/2, or WW domains, as in case of WW45.>>4<< In addition, the nuclear effectors of the pathway, Yki in flies and YAP or TAZ in mammals, function through WW–PPxY interaction.
n3:mentions
n2:20598891
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_:vb11440615
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pathway, Yki in flies and YAP or TAZ in mammals, function through WW–PPxY interaction. Indeed, it has also been shown that the WW domains of YAP are crucial for YAP transcriptional co-activation function downstream of the Hippo pathway.>>37<< Not only do the core components or the downstream effectors contain WW domains but also several upstream regulators of the Hippo pathway, in both Drosophila and mammals, contain either WW or PPxY motifs.
n3:mentions
n2:19141641
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_:vb11440616
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domains but also several upstream regulators of the Hippo pathway, in both Drosophila and mammals, contain either WW or PPxY motifs. For example, the WW domain protein Kibra is a Hippo signaling component upstream of Hpo/MST and Merlin.>>38<<, 39 This modularity in the Hippo pathway might intend that this pathway is regulated by WW domain-containing proteins at different levels in the pathway, from the mediators down to the core components and effectors.
n3:mentions
n2:20159599
Subject Item
_:vb11440617
rdf:type
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but also several upstream regulators of the Hippo pathway, in both Drosophila and mammals, contain either WW or PPxY motifs. For example, the WW domain protein Kibra is a Hippo signaling component upstream of Hpo/MST and Merlin.38, >>39<< This modularity in the Hippo pathway might intend that this pathway is regulated by WW domain-containing proteins at different levels in the pathway, from the mediators down to the core components and effectors.
n3:mentions
n2:20159598
Subject Item
_:vb11440618
rdf:type
n5:Section
dc:title
ww domain proteins regulate members of the hippo pathway
n5:contains
_:vb11440620 _:vb11440621 _:vb11440622 _:vb11440623 _:vb11440619 _:vb11440636 _:vb11440637 _:vb11440638 _:vb11440639 _:vb11440632 _:vb11440633 _:vb11440634 _:vb11440635 _:vb11440628 _:vb11440629 _:vb11440630 _:vb11440631 _:vb11440624 _:vb11440625 _:vb11440626 _:vb11440627 _:vb11440652 _:vb11440653 _:vb11440654 _:vb11440655 _:vb11440648 _:vb11440649 _:vb11440650 _:vb11440651 _:vb11440644 _:vb11440645 _:vb11440646 _:vb11440647 _:vb11440640 _:vb11440641 _:vb11440642 _:vb11440643 _:vb11440660 _:vb11440661 _:vb11440656 _:vb11440657 _:vb11440658 _:vb11440659
Subject Item
_:vb11440619
rdf:type
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of the Hippo pathway. Some of these proteins can be broadly termed upstream Hippo pathway regulators and include proteins that signal via the atypical cadherin, Fat, which functions as a transmembrane receptor for the Hippo pathway.>>32<< Additionally, the Kibra–Expanded–Merlin complex links the apical membrane to the core of the pathway proteins and the apicobasal polarity proteins.
n3:mentions
n2:20619814
Subject Item
_:vb11440620
rdf:type
n3:Context
rdf:value
cadherin, Fat, which functions as a transmembrane receptor for the Hippo pathway.32 Additionally, the Kibra–Expanded–Merlin complex links the apical membrane to the core of the pathway proteins and the apicobasal polarity proteins.>>32<< These upstream regulators make different physical interactions with the pathway to manipulate its functions.
n3:mentions
n2:20619814
Subject Item
_:vb11440621
rdf:type
n3:Context
rdf:value
different null mutants of the Kibra gene are associated with increased cell number leading to tissue overgrowth. On the other hand, Kibra overexpressing clones contain fewer cells than control clones associated with induced apoptosis.>>40<< Kibra functions primarily upstream of Mer and contributes to Mer-independent regulation of Yki activity.
n3:mentions
n2:20159600
Subject Item
_:vb11440622
rdf:type
n3:Context
rdf:value
upstream of Mer and contributes to Mer-independent regulation of Yki activity. This effect on Mer seemed to be mediated by physical interaction of the two proteins. This interaction was found to be independent of the WW domains of Kibra.>>40<< On the other hand Ling Xiao et al.41 showed that the Kibra WW domains are essential for Kibra–LATS interaction and regulation of LATS1/2 functions in the context of the mammalian Hippo pathway.
n3:mentions
n2:20159600
Subject Item
_:vb11440623
rdf:type
n3:Context
rdf:value
regulation of Yki activity. This effect on Mer seemed to be mediated by physical interaction of the two proteins. This interaction was found to be independent of the WW domains of Kibra.40 On the other hand Ling Xiao et al.>>41<< showed that the Kibra WW domains are essential for Kibra–LATS interaction and regulation of LATS1/2 functions in the context of the mammalian Hippo pathway.
n3:mentions
n2:21233212
Subject Item
_:vb11440624
rdf:type
n3:Context
rdf:value
functions in the context of the mammalian Hippo pathway. Upon its expression, Kibra activates LATS1/2 as revealed by its increased phosphorylation, leading to increased phosphorylation of the ultimate effector of the pathway, YAP.>>41<< Not only was Kibra shown to enhance LATS function but it was also shown to be responsible for increased LATS2 protein levels.
n3:mentions
n2:21233212
Subject Item
_:vb11440625
rdf:type
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rdf:value
to enhance LATS function but it was also shown to be responsible for increased LATS2 protein levels. Kibra-LATS2 association increases LATS2 half-life, at least in part, by inhibiting LATS2 ubiquitination and its proteasomal degradation.>>41<< Implication of this functional interaction on tumorigenesis in vivo is still to be determined.
n3:mentions
n2:21233212
Subject Item
_:vb11440626
rdf:type
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rdf:value
two reports identified the E3 ligase responsible for the proteasomal degradation of LATS1. The first, coming from our lab, identified ITCH as a WW domain-containing protein that regulates the stability of LATS1 using WW domain arrays.>>42<< These findings were confirmed later by another group that utilized SILAC (Stable Isotope Labeling with Amino Acids in cell culture).
n3:mentions
n2:21212414
Subject Item
_:vb11440627
rdf:type
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rdf:value
identifying LATS1 as a target of the E3 ligase ITCH (Figure 1). In our work, we demonstrated that ITCH, mostly via its first WW domain, interacts with the PPxY motifs of LATS1 and enhances its ubiqitination and proteasomal degradation.>>42<< Of note, ITCH interaction with LATS1 was increased upon activation of the Hippo pathway either by MST2 overexpression or by high-cell density culture.
n3:mentions
n2:21212414
Subject Item
_:vb11440628
rdf:type
n3:Context
rdf:value
This interaction was associated with enhanced degradation of LATS1 and suggest that ITCH might specifically target the activated form of LATS1.>>42<< Expression of a kinase-dead mutant of MST2 (MSTD-KD), which is incapable of phosphorylating and activating LATS1, indeed rescued, at least in part, ITCH-mediated LATS1 degradation (Unpublished data, Salah and Aqeilan).
n3:mentions
n2:21212414
Subject Item
_:vb11440629
rdf:type
n3:Context
rdf:value
ITCH-mediated LATS1 degradation is also accompanied by reduced YAP phosphorylation on Ser127, mild YAP accumulation in the nucleus and increased co-activation function of TEAD-responsive genes.>>42<< As YAP phosphorylation has been shown to trigger its degradation by SCF-(βTRCP) E3 ubiquitin ligase, our results may suggest that ITCH expression might signal for YAP stabilization and TEAD co-activation.
n3:mentions
n2:21212414
Subject Item
_:vb11440630
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42 As YAP phosphorylation has been shown to trigger its degradation by SCF-(βTRCP) E3 ubiquitin ligase, our results may suggest that ITCH expression might signal for YAP stabilization and TEAD co-activation.>>42<<
n3:mentions
n2:21212414
Subject Item
_:vb11440631
rdf:type
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rdf:value
The findings by Salah et al.>>42<< further demonstrated that LATS1 degradation by ITCH enhances EMT in HeLa and MCF10A cells, phenocopying overexpression of YAP.
n3:mentions
n2:21212414
Subject Item
_:vb11440632
rdf:type
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The findings by Salah et al.42 further demonstrated that LATS1 degradation by ITCH enhances EMT in HeLa and MCF10A cells, phenocopying overexpression of YAP.>>1<<, 3 Increased levels of YAP-related EMT genes, including CTGF and fibronectin, and increased cellular migration and invasion are hallmarks of ITCH overexpression.
n3:mentions
n2:17889654
Subject Item
_:vb11440633
rdf:type
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rdf:value
The findings by Salah et al.42 further demonstrated that LATS1 degradation by ITCH enhances EMT in HeLa and MCF10A cells, phenocopying overexpression of YAP.1, >>3<< Increased levels of YAP-related EMT genes, including CTGF and fibronectin, and increased cellular migration and invasion are hallmarks of ITCH overexpression.
n3:mentions
n2:20439427
Subject Item
_:vb11440634
rdf:type
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are more tumorigenic both in vitro and in vivo. The findings of Ho et al.43 also confirmed that ITCH negatively regulates LATS1 level and function as related to cell proliferation and apoptosis in the same way as demonstrated earlier.>>42<< Because ITCH, as an E3 ligase, targets many substrates,44, 45 it is possible to speculate that the phenotypes observed after ITCH overexpression are related to the regulation of the different targets in a given context.
n3:mentions
n2:21212414
Subject Item
_:vb11440635
rdf:type
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42 Because ITCH, as an E3 ligase, targets many substrates,>>44<<, 45 it is possible to speculate that the phenotypes observed after ITCH overexpression are related to the regulation of the different targets in a given context.
n3:mentions
n2:15678106
Subject Item
_:vb11440636
rdf:type
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42 Because ITCH, as an E3 ligase, targets many substrates,44, >>45<< it is possible to speculate that the phenotypes observed after ITCH overexpression are related to the regulation of the different targets in a given context.
n3:mentions
n2:11278685
Subject Item
_:vb11440637
rdf:type
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rdf:value
to assume that changing the level, stability or subcellular localization of one WW protein would alter the function and outcome of WW domain targets, depending on the cellular context or the expression of the different proteins.17, >>30<< For example, p73 is a common ligand for ITCH and YAP. On one hand, ITCH degrades p73,44 while on the other hand it leads to enhanced YAP translocation to the nucleus to promote TEAD-dependent transcription.
n3:mentions
n2:20146584
Subject Item
_:vb11440638
rdf:type
n3:Context
rdf:value
On one hand, ITCH degrades p73,>>44<< while on the other hand it leads to enhanced YAP translocation to the nucleus to promote TEAD-dependent transcription.
n3:mentions
n2:15678106
Subject Item
_:vb11440639
rdf:type
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rdf:value
the different proteins.17, 30 For example, p73 is a common ligand for ITCH and YAP. On one hand, ITCH degrades p73,44 while on the other hand it leads to enhanced YAP translocation to the nucleus to promote TEAD-dependent transcription.>>3<< In addition, YAP is an important co-factor for p73-dependent transcriptional activity and exerts a tumor suppressor role in this context.
n3:mentions
n2:20439427
Subject Item
_:vb11440640
rdf:type
n3:Context
rdf:value
it leads to enhanced YAP translocation to the nucleus to promote TEAD-dependent transcription.3 In addition, YAP is an important co-factor for p73-dependent transcriptional activity and exerts a tumor suppressor role in this context.>>45<< Therefore, ITCH overexpression might serve as a molecular switch between opposing YAP functions.
n3:mentions
n2:11278685
Subject Item
_:vb11440641
rdf:type
n3:Context
rdf:value
the Hippo pathway is on the level of the effectors, YAP and TAZ. Indeed, LATS proteins, via their PPxY motifs, have been shown to bind to WW domains of YAP leading to YAP phosphorylation, sequestration in the cytoplasm and inactivation.>>33<<, 34, 46 This leads to reduce YAP-induced EMT phenotypes and is associated with reduced tumorigenicity.
n3:mentions
n2:18158288
Subject Item
_:vb11440642
rdf:type
n3:Context
rdf:value
Hippo pathway is on the level of the effectors, YAP and TAZ. Indeed, LATS proteins, via their PPxY motifs, have been shown to bind to WW domains of YAP leading to YAP phosphorylation, sequestration in the cytoplasm and inactivation.33, >>34<<, 46 This leads to reduce YAP-induced EMT phenotypes and is associated with reduced tumorigenicity.
n3:mentions
n2:18413746
Subject Item
_:vb11440643
rdf:type
n3:Context
rdf:value
pathway is on the level of the effectors, YAP and TAZ. Indeed, LATS proteins, via their PPxY motifs, have been shown to bind to WW domains of YAP leading to YAP phosphorylation, sequestration in the cytoplasm and inactivation.33, 34, >>46<< This leads to reduce YAP-induced EMT phenotypes and is associated with reduced tumorigenicity.
n3:mentions
n2:18640976
Subject Item
_:vb11440644
rdf:type
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rdf:value
motifs, have been shown to bind to WW domains of YAP leading to YAP phosphorylation, sequestration in the cytoplasm and inactivation.33, 34, 46 This leads to reduce YAP-induced EMT phenotypes and is associated with reduced tumorigenicity.>>1<<, 34 In fact, it was shown that the WW domain of YAP has a critical role in inducing a subset of YAP target genes independent of, or in cooperation with, TEAD.
n3:mentions
n2:17889654
Subject Item
_:vb11440645
rdf:type
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rdf:value
have been shown to bind to WW domains of YAP leading to YAP phosphorylation, sequestration in the cytoplasm and inactivation.33, 34, 46 This leads to reduce YAP-induced EMT phenotypes and is associated with reduced tumorigenicity.1, >>34<< In fact, it was shown that the WW domain of YAP has a critical role in inducing a subset of YAP target genes independent of, or in cooperation with, TEAD.
n3:mentions
n2:18413746
Subject Item
_:vb11440646
rdf:type
n3:Context
rdf:value
YAP-induced EMT phenotypes and is associated with reduced tumorigenicity.1, 34 In fact, it was shown that the WW domain of YAP has a critical role in inducing a subset of YAP target genes independent of, or in cooperation with, TEAD.>>37<< In addition, mutagenesis of the WW domains diminishes the ability of YAP to stimulate cell proliferation and oncogenic transformation.
n3:mentions
n2:19141641
Subject Item
_:vb11440647
rdf:type
n3:Context
rdf:value
critical role in inducing a subset of YAP target genes independent of, or in cooperation with, TEAD.37 In addition, mutagenesis of the WW domains diminishes the ability of YAP to stimulate cell proliferation and oncogenic transformation.>>37<< In support of this notion, two recent papers showed that WW domain-mediated interaction with WBP2 is important for the phenotypes induced by both Yki47 and TAZ.
n3:mentions
n2:19141641
Subject Item
_:vb11440648
rdf:type
n3:Context
rdf:value
of YAP to stimulate cell proliferation and oncogenic transformation.37 In support of this notion, two recent papers showed that WW domain-mediated interaction with WBP2 is important for the phenotypes induced by both Yki47 and TAZ.>>48<< In the first work, Zhang et al.47 reported that Yki, via its WW domain, binds to the PPxY motifs of Wbp2.
n3:mentions
n2:20972459
Subject Item
_:vb11440649
rdf:type
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rdf:value
phenotypes in wts null organisms, suggesting that Yki function is mediated by Wbp2.47 In mammalian cells, TAZ's WW domains' interaction with PPxY motifs of WBP2 suggested an indispensable role of WBP2 in TAZ transforming ability.>>48<< Although knockdown of WBP2 suppressed TAZ-driven transformation, its overexpression enhanced this transformation.
n3:mentions
n2:20972459
Subject Item
_:vb11440650
rdf:type
n3:Context
rdf:value
48 Although knockdown of WBP2 suppressed TAZ-driven transformation, its overexpression enhanced this transformation.>>48<<
n3:mentions
n2:20972459
Subject Item
_:vb11440651
rdf:type
n3:Context
rdf:value
Recently, the PPxY-containing Angiomotin (AMOT)-like proteins 1 and 2 (AMOTL1/AMOTL2) were identified as regulators of the downstream effectors of the Hippo pathway, YAP and TAZ.>>49<<, 50, 51 Three articles highlight the significance of this interaction and shed light on the role of AMOT cell junction proteins in regulating YAP and TAZ function.
n3:mentions
n2:21224387
Subject Item
_:vb11440652
rdf:type
n3:Context
rdf:value
Recently, the PPxY-containing Angiomotin (AMOT)-like proteins 1 and 2 (AMOTL1/AMOTL2) were identified as regulators of the downstream effectors of the Hippo pathway, YAP and TAZ.49, >>50<<, 51 Three articles highlight the significance of this interaction and shed light on the role of AMOT cell junction proteins in regulating YAP and TAZ function.
n3:mentions
n2:21187284
Subject Item
_:vb11440653
rdf:type
n3:Context
rdf:value
Recently, the PPxY-containing Angiomotin (AMOT)-like proteins 1 and 2 (AMOTL1/AMOTL2) were identified as regulators of the downstream effectors of the Hippo pathway, YAP and TAZ.49, 50, >>51<< Three articles highlight the significance of this interaction and shed light on the role of AMOT cell junction proteins in regulating YAP and TAZ function.
n3:mentions
n2:21205866
Subject Item
_:vb11440654
rdf:type
n3:Context
rdf:value
of the downstream effectors of the Hippo pathway, YAP and TAZ.49, 50, 51 Three articles highlight the significance of this interaction and shed light on the role of AMOT cell junction proteins in regulating YAP and TAZ function.>>49<<, 50, 51 These proteins were found to specifically interact with YAP in a WW domain-PPxY motif-dependent manner.
n3:mentions
n2:21224387
Subject Item
_:vb11440655
rdf:type
n3:Context
rdf:value
of the downstream effectors of the Hippo pathway, YAP and TAZ.49, 50, 51 Three articles highlight the significance of this interaction and shed light on the role of AMOT cell junction proteins in regulating YAP and TAZ function.49, >>50<<, 51 These proteins were found to specifically interact with YAP in a WW domain-PPxY motif-dependent manner.
n3:mentions
n2:21187284
Subject Item
_:vb11440656
rdf:type
n3:Context
rdf:value
of the downstream effectors of the Hippo pathway, YAP and TAZ.49, 50, 51 Three articles highlight the significance of this interaction and shed light on the role of AMOT cell junction proteins in regulating YAP and TAZ function.49, 50, >>51<< These proteins were found to specifically interact with YAP in a WW domain-PPxY motif-dependent manner.
n3:mentions
n2:21205866
Subject Item
_:vb11440657
rdf:type
n3:Context
rdf:value
be sufficient to sequester YAP and TAZ in the cytoplasm, independent of their phosphorylation status. Specifically, AMOT expression leads to YAP localization at the tight junction and cell membrane, preventing YAP nuclear translocation.>>51<< Moreover, it was shown that knockdown of AMOTL2 phenocopies YAP-induced EMT in MCF10A cells.
n3:mentions
n2:21205866
Subject Item
_:vb11440658
rdf:type
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51 Moreover, it was shown that knockdown of AMOTL2 phenocopies YAP-induced EMT in MCF10A cells.>>51<< Considering this scenario, loss of tight junction-localized YAP and TAZ increased their nuclear localization and was accompanied by induction of YAP/TAZ target gene expression, and most importantly, transformation and loss of cell contact
n3:mentions
n2:21205866
Subject Item
_:vb11440659
rdf:type
n3:Context
rdf:value
phenotypes were blocked by simultaneous knockdown of YAP and TAZ, demonstrating that the AMOT family proteins are new components of the Hippo pathway with tumor-suppressing potential, indicating a new mode of YAP and TAZ regulation.>>51<<
n3:mentions
n2:21205866
Subject Item
_:vb11440660
rdf:type
n3:Context
rdf:value
shown to stimulate TAZ dephosphorylation, partly by promoting the interaction between TAZ and PP1; this function of ASPP2 requires the TAZ WW domain. ASPP2–TAZ interaction promotes TAZ nuclear localization and TAZ target gene expression.>>52<< In another example, it was shown that ASPP1 was able to inhibit YAP/TAZ interaction with LATS1, leading to enhanced nuclear accumulation of YAP/TAZ and YAP/TAZ-dependent transcriptional regulation.
n3:mentions
n2:21189257
Subject Item
_:vb11440661
rdf:type
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This results in YAP/TAZ activation and thus inhibits apoptosis, in part, through the downregulation of Bim expression, leading to resistance to anoikis and enhanced cell migration.>>53<<
n3:mentions
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