A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions

<p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral prot...
Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Demone Jordan [verfasserIn] Francis Sarah M [verfasserIn] Henley Shauna A [verfasserIn] Ainsworth Peter [verfasserIn] Dick Frederick A [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2010

Übergeordnetes Werk:	In: Cancer Cell International - BMC, 2003, 10(2010), 1, p 8
Übergeordnetes Werk:	volume:10 ; year:2010 ; number:1, p 8

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/1475-2867-10-8

Katalog-ID:	DOAJ065799887

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520			\|a <p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p<
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allfields	10.1186/1475-2867-10-8 doi (DE-627)DOAJ065799887 (DE-599)DOAJ4a2651a0d6934d6aadabf2239a6f04c8 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Demone Jordan verfasserin aut A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Francis Sarah M verfasserin aut Henley Shauna A verfasserin aut Ainsworth Peter verfasserin aut Dick Frederick A verfasserin aut In Cancer Cell International BMC, 2003 10(2010), 1, p 8 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:10 year:2010 number:1, p 8 https://doi.org/10.1186/1475-2867-10-8 kostenfrei https://doaj.org/article/4a2651a0d6934d6aadabf2239a6f04c8 kostenfrei http://www.cancerci.com/content/10/1/8 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 10 2010 1, p 8
spelling	10.1186/1475-2867-10-8 doi (DE-627)DOAJ065799887 (DE-599)DOAJ4a2651a0d6934d6aadabf2239a6f04c8 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Demone Jordan verfasserin aut A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Francis Sarah M verfasserin aut Henley Shauna A verfasserin aut Ainsworth Peter verfasserin aut Dick Frederick A verfasserin aut In Cancer Cell International BMC, 2003 10(2010), 1, p 8 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:10 year:2010 number:1, p 8 https://doi.org/10.1186/1475-2867-10-8 kostenfrei https://doaj.org/article/4a2651a0d6934d6aadabf2239a6f04c8 kostenfrei http://www.cancerci.com/content/10/1/8 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 10 2010 1, p 8
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allfieldsGer	10.1186/1475-2867-10-8 doi (DE-627)DOAJ065799887 (DE-599)DOAJ4a2651a0d6934d6aadabf2239a6f04c8 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Demone Jordan verfasserin aut A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Francis Sarah M verfasserin aut Henley Shauna A verfasserin aut Ainsworth Peter verfasserin aut Dick Frederick A verfasserin aut In Cancer Cell International BMC, 2003 10(2010), 1, p 8 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:10 year:2010 number:1, p 8 https://doi.org/10.1186/1475-2867-10-8 kostenfrei https://doaj.org/article/4a2651a0d6934d6aadabf2239a6f04c8 kostenfrei http://www.cancerci.com/content/10/1/8 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 10 2010 1, p 8
allfieldsSound	10.1186/1475-2867-10-8 doi (DE-627)DOAJ065799887 (DE-599)DOAJ4a2651a0d6934d6aadabf2239a6f04c8 DE-627 ger DE-627 rakwb eng RC254-282 QH573-671 Demone Jordan verfasserin aut A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions 2010 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier <p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p< Neoplasms. Tumors. Oncology. Including cancer and carcinogens Cytology Francis Sarah M verfasserin aut Henley Shauna A verfasserin aut Ainsworth Peter verfasserin aut Dick Frederick A verfasserin aut In Cancer Cell International BMC, 2003 10(2010), 1, p 8 (DE-627)355989204 (DE-600)2091573-1 14752867 nnns volume:10 year:2010 number:1, p 8 https://doi.org/10.1186/1475-2867-10-8 kostenfrei https://doaj.org/article/4a2651a0d6934d6aadabf2239a6f04c8 kostenfrei http://www.cancerci.com/content/10/1/8 kostenfrei https://doaj.org/toc/1475-2867 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 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_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 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 10 2010 1, p 8
language	English
source	In Cancer Cell International 10(2010), 1, p 8 volume:10 year:2010 number:1, p 8
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callnumber-first	R - Medicine
author	Demone Jordan
spellingShingle	Demone Jordan misc RC254-282 misc QH573-671 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens misc Cytology A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions
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topic_title	RC254-282 QH573-671 A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions
topic	misc RC254-282 misc QH573-671 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens misc Cytology
topic_unstemmed	misc RC254-282 misc QH573-671 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens misc Cytology
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title	A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions
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title_full	A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions
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author_browse	Demone Jordan Francis Sarah M Henley Shauna A Ainsworth Peter Dick Frederick A
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title_sort	cancer derived mutation in the retinoblastoma gene with a distinct defect for lxcxe dependent interactions
callnumber	RC254-282
title_auth	A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions
abstract	<p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p<
abstractGer	<p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p<
abstract_unstemmed	<p<Abstract</p< <p<Background</p< <p<The interaction between viral oncoproteins such as Simian virus 40 TAg, adenovirus E1A, and human papilloma virus E7, and the retinoblastoma protein (pRB) occurs through a well characterized peptide sequence, LXCXE, on the viral protein and a well conserved groove in the pocket domain of pRB. Cellular proteins, such as histone deacetylases, also use this mechanism to interact with the retinoblastoma protein to repress transcription at cell cycle regulated genes. For these reasons this region of the pRB pocket domain is thought to play a critical role in growth suppression.</p< <p<Results</p< <p<In this study, we identify and characterize a tumor derived allele of the retinoblastoma gene (<it<RB1</it<) that possesses a discrete defect in its ability to interact with LXCXE motif containing proteins that compromises proliferative control. To assess the frequency of similar mutations in the <it<RB1 </it<gene in human cancer, we screened blood and tumor samples for similar alleles. We screened almost 700 samples and did not detect additional mutations, indicating that this class of mutation is rare.</p< <p<Conclusions</p< <p<Our work provides proof of principal that alleles encoding distinct, partial loss of function mutations in the retinoblastoma gene that specifically lose LXCXE dependent interactions, are found in human cancer.</p<
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title_short	A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions
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up_date	2024-07-03T16:39:44.964Z
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A cancer derived mutation in the Retinoblastoma gene with a distinct defect for LXCXE dependent interactions

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