The amplifier effect: how Pin1 empowers mutant p53

Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 m...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Hu, Hai [verfasserIn] Wulf, Gerburg M

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2011

Schlagwörter:	Prolyl Transcriptional Program Adrenal Cortical Carcinoma Prolyl Isomerase PPIase Domain

Anmerkung:	© BioMed Central Ltd 2011

Übergeordnetes Werk:	Enthalten in: Breast cancer research - London : BioMed Central, 1999, 13(2011), 5 vom: 13. Okt.
Übergeordnetes Werk:	volume:13 ; year:2011 ; number:5 ; day:13 ; month:10

Links:	Volltext

DOI / URN:	10.1186/bcr2941

Katalog-ID:	SPR029944376

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allfields	10.1186/bcr2941 doi (DE-627)SPR029944376 (SPR)bcr2941-e DE-627 ger DE-627 rakwb eng Hu, Hai verfasserin aut The amplifier effect: how Pin1 empowers mutant p53 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2011 Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. Prolyl (dpeaa)DE-He213 Transcriptional Program (dpeaa)DE-He213 Adrenal Cortical Carcinoma (dpeaa)DE-He213 Prolyl Isomerase (dpeaa)DE-He213 PPIase Domain (dpeaa)DE-He213 Wulf, Gerburg M aut Enthalten in Breast cancer research London : BioMed Central, 1999 13(2011), 5 vom: 13. Okt. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:13 year:2011 number:5 day:13 month:10 https://dx.doi.org/10.1186/bcr2941 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2011 5 13 10
spelling	10.1186/bcr2941 doi (DE-627)SPR029944376 (SPR)bcr2941-e DE-627 ger DE-627 rakwb eng Hu, Hai verfasserin aut The amplifier effect: how Pin1 empowers mutant p53 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2011 Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. Prolyl (dpeaa)DE-He213 Transcriptional Program (dpeaa)DE-He213 Adrenal Cortical Carcinoma (dpeaa)DE-He213 Prolyl Isomerase (dpeaa)DE-He213 PPIase Domain (dpeaa)DE-He213 Wulf, Gerburg M aut Enthalten in Breast cancer research London : BioMed Central, 1999 13(2011), 5 vom: 13. Okt. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:13 year:2011 number:5 day:13 month:10 https://dx.doi.org/10.1186/bcr2941 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2011 5 13 10
allfields_unstemmed	10.1186/bcr2941 doi (DE-627)SPR029944376 (SPR)bcr2941-e DE-627 ger DE-627 rakwb eng Hu, Hai verfasserin aut The amplifier effect: how Pin1 empowers mutant p53 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2011 Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. Prolyl (dpeaa)DE-He213 Transcriptional Program (dpeaa)DE-He213 Adrenal Cortical Carcinoma (dpeaa)DE-He213 Prolyl Isomerase (dpeaa)DE-He213 PPIase Domain (dpeaa)DE-He213 Wulf, Gerburg M aut Enthalten in Breast cancer research London : BioMed Central, 1999 13(2011), 5 vom: 13. Okt. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:13 year:2011 number:5 day:13 month:10 https://dx.doi.org/10.1186/bcr2941 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2011 5 13 10
allfieldsGer	10.1186/bcr2941 doi (DE-627)SPR029944376 (SPR)bcr2941-e DE-627 ger DE-627 rakwb eng Hu, Hai verfasserin aut The amplifier effect: how Pin1 empowers mutant p53 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2011 Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. Prolyl (dpeaa)DE-He213 Transcriptional Program (dpeaa)DE-He213 Adrenal Cortical Carcinoma (dpeaa)DE-He213 Prolyl Isomerase (dpeaa)DE-He213 PPIase Domain (dpeaa)DE-He213 Wulf, Gerburg M aut Enthalten in Breast cancer research London : BioMed Central, 1999 13(2011), 5 vom: 13. Okt. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:13 year:2011 number:5 day:13 month:10 https://dx.doi.org/10.1186/bcr2941 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2011 5 13 10
allfieldsSound	10.1186/bcr2941 doi (DE-627)SPR029944376 (SPR)bcr2941-e DE-627 ger DE-627 rakwb eng Hu, Hai verfasserin aut The amplifier effect: how Pin1 empowers mutant p53 2011 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2011 Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. Prolyl (dpeaa)DE-He213 Transcriptional Program (dpeaa)DE-He213 Adrenal Cortical Carcinoma (dpeaa)DE-He213 Prolyl Isomerase (dpeaa)DE-He213 PPIase Domain (dpeaa)DE-He213 Wulf, Gerburg M aut Enthalten in Breast cancer research London : BioMed Central, 1999 13(2011), 5 vom: 13. Okt. (DE-627)326645950 (DE-600)2041618-0 1465-542X nnns volume:13 year:2011 number:5 day:13 month:10 https://dx.doi.org/10.1186/bcr2941 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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2011 5 13 10
language	English
source	Enthalten in Breast cancer research 13(2011), 5 vom: 13. Okt. volume:13 year:2011 number:5 day:13 month:10
sourceStr	Enthalten in Breast cancer research 13(2011), 5 vom: 13. Okt. volume:13 year:2011 number:5 day:13 month:10
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topic_facet	Prolyl Transcriptional Program Adrenal Cortical Carcinoma Prolyl Isomerase PPIase Domain
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container_title	Breast cancer research
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author	Hu, Hai
spellingShingle	Hu, Hai misc Prolyl misc Transcriptional Program misc Adrenal Cortical Carcinoma misc Prolyl Isomerase misc PPIase Domain The amplifier effect: how Pin1 empowers mutant p53
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topic_title	The amplifier effect: how Pin1 empowers mutant p53 Prolyl (dpeaa)DE-He213 Transcriptional Program (dpeaa)DE-He213 Adrenal Cortical Carcinoma (dpeaa)DE-He213 Prolyl Isomerase (dpeaa)DE-He213 PPIase Domain (dpeaa)DE-He213
topic	misc Prolyl misc Transcriptional Program misc Adrenal Cortical Carcinoma misc Prolyl Isomerase misc PPIase Domain
topic_unstemmed	misc Prolyl misc Transcriptional Program misc Adrenal Cortical Carcinoma misc Prolyl Isomerase misc PPIase Domain
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title	The amplifier effect: how Pin1 empowers mutant p53
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title_full	The amplifier effect: how Pin1 empowers mutant p53
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title_sort	amplifier effect: how pin1 empowers mutant p53
title_auth	The amplifier effect: how Pin1 empowers mutant p53
abstract	Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. © BioMed Central Ltd 2011
abstractGer	Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. © BioMed Central Ltd 2011
abstract_unstemmed	Abstract Mutation of p53 occurs in 15 to 20% of all breast cancers, and with higher frequency in estrogen-receptor negative and high-grade tumors. Certain p53 mutations contribute to malignant transformation not only through loss of wild-type p53 but also through a gain of function of specific p53 mutations. How these hotspot mutations turn p53 from a tumor suppressor into an oncogene had until now remained incompletely understood. In an elegant paper published in the July 12 issue of Cancer Cell, Girardini and colleagues show how Pin1-mediated prolylisomerization, a regulatory mechanism intended by evolution to support p53's function as a guardian of the genome, can go haywire and accelerate malignant transformation when p53 carries a dominant-negative mutation. © BioMed Central Ltd 2011
collection_details	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_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2014 GBV_ILN_2106 GBV_ILN_2232 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 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_4338 GBV_ILN_4367 GBV_ILN_4700
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title_short	The amplifier effect: how Pin1 empowers mutant p53
url	https://dx.doi.org/10.1186/bcr2941
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