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PMID |
Sentence |
1 |
15007383
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Nore1 inhibits tumor cell growth independent of Ras or the MST1/2 kinases.
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2 |
15007383
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Nore1, a noncatalytic protein identified by its ability to bind selectively to active Ras, is most closely related in amino-acid sequence to the tumor suppressor RASSF1.
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3 |
15007383
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Both are expressed predominantly as a longer (Nore1A/RASSF1A) and/or shorter (Nore1B/RASSF1C) polypeptide; all four polypeptides contain a Ras-association domain and bind, through their conserved carboxytermini, the proapoptotic protein kinases MST1 and MST2.
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4 |
15007383
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Moreover, the expression of the longer polypeptide is downregulated in human tumor cell lines through promoter methylation (frequently for RASSF1A, less regularly for Nore1A).
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5 |
15007383
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The expression of Nore1A or Nore1B suppresses colony formation by the A549 and G361 lines, as effectively in A549 as does RASSF1A; colony formation in the NCI-H460 and M14 lines is unaffected.
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6 |
15007383
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Thus, Nore1 suppresses the growth of some tumor cell lines through as yet unidentified effectors, independent of Ras-like proteins or MST1/2.
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7 |
15007383
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Nore1 inhibits tumor cell growth independent of Ras or the MST1/2 kinases.
|
8 |
15007383
|
Nore1, a noncatalytic protein identified by its ability to bind selectively to active Ras, is most closely related in amino-acid sequence to the tumor suppressor RASSF1.
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9 |
15007383
|
Both are expressed predominantly as a longer (Nore1A/RASSF1A) and/or shorter (Nore1B/RASSF1C) polypeptide; all four polypeptides contain a Ras-association domain and bind, through their conserved carboxytermini, the proapoptotic protein kinases MST1 and MST2.
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10 |
15007383
|
Moreover, the expression of the longer polypeptide is downregulated in human tumor cell lines through promoter methylation (frequently for RASSF1A, less regularly for Nore1A).
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11 |
15007383
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The expression of Nore1A or Nore1B suppresses colony formation by the A549 and G361 lines, as effectively in A549 as does RASSF1A; colony formation in the NCI-H460 and M14 lines is unaffected.
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12 |
15007383
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Thus, Nore1 suppresses the growth of some tumor cell lines through as yet unidentified effectors, independent of Ras-like proteins or MST1/2.
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13 |
15007383
|
Nore1 inhibits tumor cell growth independent of Ras or the MST1/2 kinases.
|
14 |
15007383
|
Nore1, a noncatalytic protein identified by its ability to bind selectively to active Ras, is most closely related in amino-acid sequence to the tumor suppressor RASSF1.
|
15 |
15007383
|
Both are expressed predominantly as a longer (Nore1A/RASSF1A) and/or shorter (Nore1B/RASSF1C) polypeptide; all four polypeptides contain a Ras-association domain and bind, through their conserved carboxytermini, the proapoptotic protein kinases MST1 and MST2.
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16 |
15007383
|
Moreover, the expression of the longer polypeptide is downregulated in human tumor cell lines through promoter methylation (frequently for RASSF1A, less regularly for Nore1A).
|
17 |
15007383
|
The expression of Nore1A or Nore1B suppresses colony formation by the A549 and G361 lines, as effectively in A549 as does RASSF1A; colony formation in the NCI-H460 and M14 lines is unaffected.
|
18 |
15007383
|
Thus, Nore1 suppresses the growth of some tumor cell lines through as yet unidentified effectors, independent of Ras-like proteins or MST1/2.
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19 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
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20 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
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21 |
16757333
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RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
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22 |
16757333
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The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
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23 |
16757333
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By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
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24 |
16757333
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Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
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25 |
16757333
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The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
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26 |
16757333
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Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
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27 |
16757333
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Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
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28 |
16757333
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Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
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29 |
16757333
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Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
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30 |
16757333
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Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
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31 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
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32 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
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33 |
16757333
|
RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
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34 |
16757333
|
The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
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35 |
16757333
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By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
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36 |
16757333
|
Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
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37 |
16757333
|
The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
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38 |
16757333
|
Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
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39 |
16757333
|
Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
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40 |
16757333
|
Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
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41 |
16757333
|
Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
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42 |
16757333
|
Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
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43 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
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44 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
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45 |
16757333
|
RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
|
46 |
16757333
|
The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
|
47 |
16757333
|
By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
|
48 |
16757333
|
Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
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49 |
16757333
|
The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
|
50 |
16757333
|
Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
|
51 |
16757333
|
Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
|
52 |
16757333
|
Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
|
53 |
16757333
|
Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
|
54 |
16757333
|
Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
|
55 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
|
56 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
|
57 |
16757333
|
RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
|
58 |
16757333
|
The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
|
59 |
16757333
|
By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
|
60 |
16757333
|
Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
|
61 |
16757333
|
The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
|
62 |
16757333
|
Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
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63 |
16757333
|
Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
|
64 |
16757333
|
Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
|
65 |
16757333
|
Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
|
66 |
16757333
|
Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
|
67 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
|
68 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
|
69 |
16757333
|
RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
|
70 |
16757333
|
The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
|
71 |
16757333
|
By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
|
72 |
16757333
|
Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
|
73 |
16757333
|
The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
|
74 |
16757333
|
Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
|
75 |
16757333
|
Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
|
76 |
16757333
|
Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
|
77 |
16757333
|
Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
|
78 |
16757333
|
Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
|
79 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
|
80 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
|
81 |
16757333
|
RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
|
82 |
16757333
|
The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
|
83 |
16757333
|
By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
|
84 |
16757333
|
Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
|
85 |
16757333
|
The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
|
86 |
16757333
|
Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
|
87 |
16757333
|
Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
|
88 |
16757333
|
Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
|
89 |
16757333
|
Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
|
90 |
16757333
|
Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
|
91 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
|
92 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
|
93 |
16757333
|
RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
|
94 |
16757333
|
The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
|
95 |
16757333
|
By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
|
96 |
16757333
|
Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
|
97 |
16757333
|
The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
|
98 |
16757333
|
Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
|
99 |
16757333
|
Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
|
100 |
16757333
|
Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
|
101 |
16757333
|
Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
|
102 |
16757333
|
Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
|
103 |
16757333
|
Nore1 and RASSF1 regulation of cell proliferation and of the MST1/2 kinases.
|
104 |
16757333
|
The expression of the RASSF1A and Nore1A isoforms is extinguished selectively by gene loss and/or epigenetic mechanisms in a considerable fraction of epithelial cancers and cell lines derived therefrom, and reexpression usually suppresses the proliferation and tumorigenicity of these cells.
|
105 |
16757333
|
RASSF1A/Nore1A can cause cell cycle delay in G1 and/or M and may promote apoptosis.
|
106 |
16757333
|
The founding member, Nore1A, binds preferentially through its RA domain to the GTP-charged forms of Ras, Rap-1, and several other Ras subfamily GTPases with high affinity.
|
107 |
16757333
|
By contrast, RASSF1, despite an RA domain 50% identical to Nore1, exhibits relatively low affinity for Ras-like GTPases but may associate with Ras-GTP indirectly.
|
108 |
16757333
|
Each of the RASSF polypeptides, including the C. elegans ortholog encoded by T24F1.3, binds to the Ste20-related protein kinases MST1 and MST2 through the SARAH domains of each partner.
|
109 |
16757333
|
The recombinant MST1/2 kinases, spontaneous dimers, autoactivate in vitro through an intradimer transphosphorylation of the activation loop, and the Nore1/RASSF1 polypeptides inhibit this process.
|
110 |
16757333
|
Recombinant MST1 is strongly activated in vivo by recruitment to the membrane; the recombinant MST1 that is bound to RasG12V through Nore1A is activated; however, the bulk of MST1 is not.
|
111 |
16757333
|
Endogenous complexes of MST1 with both Nore1A and RASSF1A are detectable, and Nore1A/MST1 can associate with endogenous Ras in response to serum addition.
|
112 |
16757333
|
Nevertheless, the physiological functions of the Nore1/RASSF polypeptides in mammalian cells, as well as the role of the MST1/2 kinases in their growth-suppressive actions, remain to be established.
|
113 |
16757333
|
Overexpression of mammalian MST1 or MST2 promotes apoptosis, as does overexpression of mutant active Ki-Ras.
|
114 |
16757333
|
Interference with the ability of endogenous MST1/2 to associate with the Nore1/RASSF polypeptides inhibits Ras-induced apoptosis.
|
115 |
18328708
|
MOBKL1A/MOBKL1B phosphorylation by MST1 and MST2 inhibits cell proliferation.
|