An emerging role of PARK2 in cancer

Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 i...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Xu, Liang [verfasserIn] Lin, De-chen Yin, Dong Koeffler, H. Phillip

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2013

Schlagwörter:	PARK2 Mutation Deletion Tumor suppressor Mitophagy Metabolism

Anmerkung:	© Springer-Verlag Berlin Heidelberg 2013

Übergeordnetes Werk:	Enthalten in: Journal of molecular medicine - Berlin : Springer, 1922, 92(2013), 1 vom: 03. Dez., Seite 31-42
Übergeordnetes Werk:	volume:92 ; year:2013 ; number:1 ; day:03 ; month:12 ; pages:31-42

Links:	Volltext

DOI / URN:	10.1007/s00109-013-1107-0

Katalog-ID:	SPR00076552X

Internformat


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245	1	3	\|a An emerging role of PARK2 in cancer
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520			\|a Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer.
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912			\|a GBV_ILN_151
912			\|a GBV_ILN_152
912			\|a GBV_ILN_161
912			\|a GBV_ILN_170
912			\|a GBV_ILN_171
912			\|a GBV_ILN_187
912			\|a GBV_ILN_213
912			\|a GBV_ILN_224
912			\|a GBV_ILN_230
912			\|a GBV_ILN_250
912			\|a GBV_ILN_267
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912			\|a GBV_ILN_293
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912			\|a GBV_ILN_602
912			\|a GBV_ILN_636
912			\|a GBV_ILN_702
912			\|a GBV_ILN_2001
912			\|a GBV_ILN_2003
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912			\|a GBV_ILN_2006
912			\|a GBV_ILN_2007
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912			\|a GBV_ILN_2010
912			\|a GBV_ILN_2011
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912			\|a GBV_ILN_2021
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912			\|a GBV_ILN_2026
912			\|a GBV_ILN_2027
912			\|a GBV_ILN_2031
912			\|a GBV_ILN_2034
912			\|a GBV_ILN_2037
912			\|a GBV_ILN_2038
912			\|a GBV_ILN_2039
912			\|a GBV_ILN_2044
912			\|a GBV_ILN_2048
912			\|a GBV_ILN_2049
912			\|a GBV_ILN_2050
912			\|a GBV_ILN_2055
912			\|a GBV_ILN_2057
912			\|a GBV_ILN_2059
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912			\|a GBV_ILN_2064
912			\|a GBV_ILN_2065
912			\|a GBV_ILN_2068
912			\|a GBV_ILN_2070
912			\|a GBV_ILN_2086
912			\|a GBV_ILN_2088
912			\|a GBV_ILN_2093
912			\|a GBV_ILN_2106
912			\|a GBV_ILN_2107
912			\|a GBV_ILN_2108
912			\|a GBV_ILN_2110
912			\|a GBV_ILN_2111
912			\|a GBV_ILN_2112
912			\|a GBV_ILN_2113
912			\|a GBV_ILN_2116
912			\|a GBV_ILN_2118
912			\|a GBV_ILN_2119
912			\|a GBV_ILN_2122
912			\|a GBV_ILN_2129
912			\|a GBV_ILN_2143
912			\|a GBV_ILN_2144
912			\|a GBV_ILN_2147
912			\|a GBV_ILN_2148
912			\|a GBV_ILN_2152
912			\|a GBV_ILN_2153
912			\|a GBV_ILN_2188
912			\|a GBV_ILN_2190
912			\|a GBV_ILN_2232
912			\|a GBV_ILN_2336
912			\|a GBV_ILN_2446
912			\|a GBV_ILN_2470
912			\|a GBV_ILN_2472
912			\|a GBV_ILN_2507
912			\|a GBV_ILN_2522
912			\|a GBV_ILN_2548
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Indexfelder

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matchkey_str	article:14321440:2013----::nmrigoefak
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publishDate	2013
allfields	10.1007/s00109-013-1107-0 doi (DE-627)SPR00076552X (SPR)s00109-013-1107-0-e DE-627 ger DE-627 rakwb eng Xu, Liang verfasserin aut An emerging role of PARK2 in cancer 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. PARK2 (dpeaa)DE-He213 Mutation (dpeaa)DE-He213 Deletion (dpeaa)DE-He213 Tumor suppressor (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Metabolism (dpeaa)DE-He213 Lin, De-chen aut Yin, Dong aut Koeffler, H. Phillip aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 92(2013), 1 vom: 03. Dez., Seite 31-42 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:92 year:2013 number:1 day:03 month:12 pages:31-42 https://dx.doi.org/10.1007/s00109-013-1107-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 92 2013 1 03 12 31-42
spelling	10.1007/s00109-013-1107-0 doi (DE-627)SPR00076552X (SPR)s00109-013-1107-0-e DE-627 ger DE-627 rakwb eng Xu, Liang verfasserin aut An emerging role of PARK2 in cancer 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. PARK2 (dpeaa)DE-He213 Mutation (dpeaa)DE-He213 Deletion (dpeaa)DE-He213 Tumor suppressor (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Metabolism (dpeaa)DE-He213 Lin, De-chen aut Yin, Dong aut Koeffler, H. Phillip aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 92(2013), 1 vom: 03. Dez., Seite 31-42 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:92 year:2013 number:1 day:03 month:12 pages:31-42 https://dx.doi.org/10.1007/s00109-013-1107-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 92 2013 1 03 12 31-42
allfields_unstemmed	10.1007/s00109-013-1107-0 doi (DE-627)SPR00076552X (SPR)s00109-013-1107-0-e DE-627 ger DE-627 rakwb eng Xu, Liang verfasserin aut An emerging role of PARK2 in cancer 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. PARK2 (dpeaa)DE-He213 Mutation (dpeaa)DE-He213 Deletion (dpeaa)DE-He213 Tumor suppressor (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Metabolism (dpeaa)DE-He213 Lin, De-chen aut Yin, Dong aut Koeffler, H. Phillip aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 92(2013), 1 vom: 03. Dez., Seite 31-42 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:92 year:2013 number:1 day:03 month:12 pages:31-42 https://dx.doi.org/10.1007/s00109-013-1107-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 92 2013 1 03 12 31-42
allfieldsGer	10.1007/s00109-013-1107-0 doi (DE-627)SPR00076552X (SPR)s00109-013-1107-0-e DE-627 ger DE-627 rakwb eng Xu, Liang verfasserin aut An emerging role of PARK2 in cancer 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. PARK2 (dpeaa)DE-He213 Mutation (dpeaa)DE-He213 Deletion (dpeaa)DE-He213 Tumor suppressor (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Metabolism (dpeaa)DE-He213 Lin, De-chen aut Yin, Dong aut Koeffler, H. Phillip aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 92(2013), 1 vom: 03. Dez., Seite 31-42 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:92 year:2013 number:1 day:03 month:12 pages:31-42 https://dx.doi.org/10.1007/s00109-013-1107-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 92 2013 1 03 12 31-42
allfieldsSound	10.1007/s00109-013-1107-0 doi (DE-627)SPR00076552X (SPR)s00109-013-1107-0-e DE-627 ger DE-627 rakwb eng Xu, Liang verfasserin aut An emerging role of PARK2 in cancer 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Springer-Verlag Berlin Heidelberg 2013 Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. PARK2 (dpeaa)DE-He213 Mutation (dpeaa)DE-He213 Deletion (dpeaa)DE-He213 Tumor suppressor (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Metabolism (dpeaa)DE-He213 Lin, De-chen aut Yin, Dong aut Koeffler, H. Phillip aut Enthalten in Journal of molecular medicine Berlin : Springer, 1922 92(2013), 1 vom: 03. Dez., Seite 31-42 (DE-627)254630804 (DE-600)1462132-0 1432-1440 nnns volume:92 year:2013 number:1 day:03 month:12 pages:31-42 https://dx.doi.org/10.1007/s00109-013-1107-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_267 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 92 2013 1 03 12 31-42
language	English
source	Enthalten in Journal of molecular medicine 92(2013), 1 vom: 03. Dez., Seite 31-42 volume:92 year:2013 number:1 day:03 month:12 pages:31-42
sourceStr	Enthalten in Journal of molecular medicine 92(2013), 1 vom: 03. Dez., Seite 31-42 volume:92 year:2013 number:1 day:03 month:12 pages:31-42
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	PARK2 Mutation Deletion Tumor suppressor Mitophagy Metabolism
isfreeaccess_bool	false
container_title	Journal of molecular medicine
authorswithroles_txt_mv	Xu, Liang @@aut@@ Lin, De-chen @@aut@@ Yin, Dong @@aut@@ Koeffler, H. Phillip @@aut@@
publishDateDaySort_date	2013-12-03T00:00:00Z
hierarchy_top_id	254630804
id	SPR00076552X
language_de	englisch
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author	Xu, Liang
spellingShingle	Xu, Liang misc PARK2 misc Mutation misc Deletion misc Tumor suppressor misc Mitophagy misc Metabolism An emerging role of PARK2 in cancer
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topic_title	An emerging role of PARK2 in cancer PARK2 (dpeaa)DE-He213 Mutation (dpeaa)DE-He213 Deletion (dpeaa)DE-He213 Tumor suppressor (dpeaa)DE-He213 Mitophagy (dpeaa)DE-He213 Metabolism (dpeaa)DE-He213
topic	misc PARK2 misc Mutation misc Deletion misc Tumor suppressor misc Mitophagy misc Metabolism
topic_unstemmed	misc PARK2 misc Mutation misc Deletion misc Tumor suppressor misc Mitophagy misc Metabolism
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title	An emerging role of PARK2 in cancer
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title_full	An emerging role of PARK2 in cancer
author_sort	Xu, Liang
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author_browse	Xu, Liang Lin, De-chen Yin, Dong Koeffler, H. Phillip
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author-letter	Xu, Liang
doi_str_mv	10.1007/s00109-013-1107-0
title_sort	emerging role of park2 in cancer
title_auth	An emerging role of PARK2 in cancer
abstract	Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. © Springer-Verlag Berlin Heidelberg 2013
abstractGer	Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. © Springer-Verlag Berlin Heidelberg 2013
abstract_unstemmed	Abstract PARK2 (PARKIN) is an E3 ubiquitin ligase involved in multiple signaling pathways and cellular processes. Activity of PARK2 is tightly regulated through inter- and intra-molecular interactions. Dysfunction of PARK2 is associated with the progression of parkinsonism. Notably, frequent PARK2 inactivation has been identified in various human cancers. Park2-deficient mice are more susceptible to tumorigenesis, indicating its crucial role as a tumor suppressor. However, biological studies also show that PARK2 possesses both pro-survival and growth suppressive functions. Here, we summarize the genetic lesions of PARK2 in human cancers and discuss the current knowledge of PARK2 in cancer progression. We further highlight future efforts for the study of PARK2 in cancer. © Springer-Verlag Berlin Heidelberg 2013
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container_issue	1
title_short	An emerging role of PARK2 in cancer
url	https://dx.doi.org/10.1007/s00109-013-1107-0
remote_bool	true
author2	Lin, De-chen Yin, Dong Koeffler, H. Phillip
author2Str	Lin, De-chen Yin, Dong Koeffler, H. Phillip
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doi_str	10.1007/s00109-013-1107-0
up_date	2024-07-03T18:08:02.110Z
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