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Article ; Online: p53: master of life, death, and the epigenome.

Laptenko, Oleg / Prives, Carol

2017 Volume 31, Issue 10, Page(s) 955–956

Abstract: Long understood as a bona fide tumor suppressor that safeguards the integrity of the genome via regulating numerous cellular outcomes, p53 may also exert its decisive and versatile functions by controlling DNA methylation. In this issue ... ...

Abstract	Long understood as a bona fide tumor suppressor that safeguards the integrity of the genome via regulating numerous cellular outcomes, p53 may also exert its decisive and versatile functions by controlling DNA methylation. In this issue of
MeSH term(s)	Animals ; DNA Methylation/genetics ; Epigenesis, Genetic/genetics ; Gene Expression Regulation, Neoplastic ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Tumor Suppressor Protein p53
Language	English
Publishing date	2017-05-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.302364.117
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Zs.MG 54: Show issues

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Article ; Online: Anything but simple: a phosphorylation-driven toggle within Brd4 triggers gene-specific transcriptional activation.

Laptenko, Oleg / Prives, Carol

Molecular cell

2013 Volume 49, Issue 5, Page(s) 838–839

Abstract: In this issue of Molecular Cell, Wu et al. (2013) report their extraordinary findings on the molecular mechanism that controls gene-specific targeting by Brd4, a universal epigenetic reader. ...

Abstract	In this issue of Molecular Cell, Wu et al. (2013) report their extraordinary findings on the molecular mechanism that controls gene-specific targeting by Brd4, a universal epigenetic reader.
Language	English
Publishing date	2013-03-11
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2013.02.021
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Article ; Online: p53 Frameshift Mutations Couple Loss-of-Function with Unique Neomorphic Activities.

Tong, David R / Zhou, Wen / Katz, Chen / Regunath, Kausik / Venkatesh, Divya / Ihuegbu, Chinyere / Manfredi, James J / Laptenko, Oleg / Prives, Carol

Molecular cancer research : MCR

2021 Volume 19, Issue 9, Page(s) 1522–1533

Abstract: p53 mutations that result in loss of transcriptional activity are commonly found in numerous types of cancer. While the majority of these are missense mutations that map within the central DNA-binding domain, truncations and/or frameshift mutations can ... ...

Abstract	p53 mutations that result in loss of transcriptional activity are commonly found in numerous types of cancer. While the majority of these are missense mutations that map within the central DNA-binding domain, truncations and/or frameshift mutations can also occur due to various nucleotide substitutions, insertions, or deletions. These changes result in mRNAs containing premature stop codons that are translated into a diverse group of C-terminally truncated proteins. Here we characterized three p53 frameshift mutant proteins expressed from the endogenous
MeSH term(s)	Apoptosis ; Biomarkers, Tumor/genetics ; Bone Neoplasms/genetics ; Bone Neoplasms/pathology ; Cell Cycle ; Cell Movement ; Cell Proliferation ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Frameshift Mutation ; Gene Expression Regulation, Neoplastic ; Humans ; Loss of Function Mutation ; Osteosarcoma/genetics ; Osteosarcoma/pathology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/genetics
Chemical Substances	Biomarkers, Tumor ; TP53 protein, human ; Tumor Suppressor Protein p53
Language	English
Publishing date	2021-05-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2098788-2
ISSN	1557-3125 ; 1541-7786
ISSN (online)	1557-3125
ISSN	1541-7786
DOI	10.1158/1541-7786.MCR-20-0691
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Article: Anything but Simple: A Phosphorylation-Driven Toggle within Brd4 Triggers Gene-Specific Transcriptional Activation

Laptenko, Oleg / Prives, Carol

Molecular cell. 2013 Mar. 07, v. 49

2013

Abstract	In this issue of Molecular Cell, Wu et al. (2013) report their extraordinary findings on the molecular mechanism that controls gene-specific targeting by Brd4, a universal epigenetic reader.
Keywords	epigenetics ; genes ; phosphorylation ; transcriptional activation
Language	English
Dates of publication	2013-0307
Size	p. 838-839.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2013.02.021
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Article ; Online: The p53-HAT connection: PCAF rules?

Laptenko, Oleg / Prives, Carol

Cell cycle (Georgetown, Tex.)

2012 Volume 11, Issue 16, Page(s) 2975–2976

MeSH term(s)	Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Histones/metabolism ; Humans ; Oxidative Stress ; p300-CBP Transcription Factors/metabolism
Chemical Substances	Cyclin-Dependent Kinase Inhibitor p21 ; Histones ; p300-CBP Transcription Factors (EC 2.3.1.48)
Language	English
Publishing date	2012-08-14
Publishing country	United States
Document type	News ; Comment
ZDB-ID	2146183-1
ISSN	1551-4005 ; 1538-4101 ; 1554-8627
ISSN (online)	1551-4005
ISSN	1538-4101 ; 1554-8627
DOI	10.4161/cc.21528
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Article: The Tail That Wags the Dog: How the Disordered C-Terminal Domain Controls the Transcriptional Activities of the p53 Tumor-Suppressor Protein.

Laptenko, Oleg / Tong, David R / Manfredi, James / Prives, Carol

Trends in biochemical sciences

2016 Volume 41, Issue 12, Page(s) 1022–1034

Abstract: The p53 tumor suppressor is a transcription factor (TF) that exerts antitumor functions through its ability to regulate the expression of multiple genes. Within the p53 protein resides a relatively short unstructured C-terminal domain (CTD) that ... ...

Abstract	The p53 tumor suppressor is a transcription factor (TF) that exerts antitumor functions through its ability to regulate the expression of multiple genes. Within the p53 protein resides a relatively short unstructured C-terminal domain (CTD) that remarkably participates in virtually every aspect of p53 performance as a TF. Because these aspects are often interdependent and it is not always possible to dissect them experimentally, there has been a great deal of controversy about the CTD. In this review we evaluate the significance and key features of this interesting region of p53 and its impact on the many aspects of p53 function in light of previous and more recent findings.
MeSH term(s)	Amino Acid Sequence ; Animals ; Binding Sites ; DNA/chemistry ; DNA/metabolism ; Humans ; Hydrophobic and Hydrophilic Interactions ; Intrinsically Disordered Proteins/chemistry ; Intrinsically Disordered Proteins/genetics ; Intrinsically Disordered Proteins/metabolism ; Protein Binding ; Protein Conformation, alpha-Helical ; Protein Conformation, beta-Strand ; Protein Domains ; Protein Structure, Tertiary ; Sequence Alignment ; Sequence Homology, Amino Acid ; Transcriptional Activation ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Intrinsically Disordered Proteins ; Tumor Suppressor Protein p53 ; DNA (9007-49-2)
Language	English
Publishing date	2016-09-23
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194216-5
ISSN	1362-4326 ; 0968-0004 ; 0376-5067
ISSN (online)	1362-4326
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2016.08.011
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Article: The Tail That Wags the Dog: How the Disordered C-Terminal Domain Controls the Transcriptional Activities of the p53 Tumor-Suppressor Protein

Laptenko, Oleg / Tong, David R / Manfredi, James / Prives, Carol

Trends in biochemical sciences. 2016 Dec., v. 41, no. 12

2016

Abstract	The p53 tumor suppressor is a transcription factor (TF) that exerts antitumor functions through its ability to regulate the expression of multiple genes. Within the p53 protein resides a relatively short unstructured C-terminal domain (CTD) that remarkably participates in virtually every aspect of p53 performance as a TF. Because these aspects are often interdependent and it is not always possible to dissect them experimentally, there has been a great deal of controversy about the CTD. In this review we evaluate the significance and key features of this interesting region of p53 and its impact on the many aspects of p53 function in light of previous and more recent findings.
Keywords	amino acid sequences ; dogs ; genes ; transcription (genetics) ; transcription factors
Language	English
Dates of publication	2016-12
Size	p. 1022-1034.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	194220-7
ISSN	0968-0004 ; 0376-5067
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2016.08.011
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Z 78/716: Show issues

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Article: Transcriptional regulation by p53: one protein, many possibilities.

Laptenko, O / Prives, C

Cell death and differentiation

2006 Volume 13, Issue 6, Page(s) 951–961

Abstract: The p53 tumor suppressor protein is a DNA sequence-specific transcriptional regulator that, in response to various forms of cellular stress, controls the expression of numerous genes involved in cellular outcomes including among others, cell cycle arrest ...

Abstract	The p53 tumor suppressor protein is a DNA sequence-specific transcriptional regulator that, in response to various forms of cellular stress, controls the expression of numerous genes involved in cellular outcomes including among others, cell cycle arrest and cell death. Two key features of the p53 protein are required for its transcriptional activities: its ability to recognize and bind specific DNA sequences and to recruit both general and specialized transcriptional co-regulators. In fact, multiple interactions with co-activators and co-repressors as well as with the components of the general transcriptional machinery allow p53 to either promote or inhibit transcription of different target genes. This review focuses on some of the salient features of the interactions of p53 with DNA and with factors that regulate transcription. We discuss as well the complexities of the functional domains of p53 with respect to these interactions.
MeSH term(s)	Animals ; Apoptosis Regulatory Proteins/genetics ; Apoptosis Regulatory Proteins/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; DNA/genetics ; DNA/metabolism ; Humans ; Protein Conformation ; Response Elements/genetics ; Transcription, Genetic ; Transcriptional Activation ; Tumor Suppressor Protein p53/chemistry ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Apoptosis Regulatory Proteins ; Cell Cycle Proteins ; Tumor Suppressor Protein p53 ; DNA (9007-49-2)
Language	English
Publishing date	2006-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1225672-9
ISSN	1350-9047
ISSN	1350-9047
DOI	10.1038/sj.cdd.4401916
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 80: Show issues

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Article ; Online: p53 binding to nucleosomes within the p21 promoter in vivo leads to nucleosome loss and transcriptional activation.

Laptenko, Oleg / Beckerman, Rachel / Freulich, Ella / Prives, Carol

Proceedings of the National Academy of Sciences of the United States of America

2011 Volume 108, Issue 26, Page(s) 10385–10390

Abstract: It is well established that p53 contacts DNA in a sequence-dependent manner in order to transactivate its myriad target genes. Yet little is known about how p53 interacts with its binding site/response element (RE) within such genes in vivo in the ... ...

Abstract	It is well established that p53 contacts DNA in a sequence-dependent manner in order to transactivate its myriad target genes. Yet little is known about how p53 interacts with its binding site/response element (RE) within such genes in vivo in the context of nucleosomal DNA. In this study we demonstrate that both distal (5') and proximal (3') p53 REs within the promoter of the p21 gene in unstressed HCT116 colon carcinoma cells are localized within a region of relatively high nucleosome occupancy. In the absence of cellular stress, p53 is prebound to both p21 REs within nucleosomal DNA in these cells. Treatment of cells with the DNA-damaging drug doxorubicin or the p53 stabilizing agent Nutlin-3, however, is accompanied by p53-dependent subsequent loss of nucleosomes associated with such p53 REs. We show that in vitro p53 can bind to mononucleosomal DNA containing the distal p21 RE, provided the binding site is not close to the diad center of the nucleosome. In line with this, our data indicate that the p53 distal RE within the p21 gene is located close to the end of the nucleosome. Thus, low- and high-resolution mapping of nucleosome boundaries around p53 REs within the p21 promoter have provided insight into the mechanism of p53 binding to its sites in cells and the consequent changes in nucleosome occupancy at such sites.
MeSH term(s)	Cell Line, Tumor ; Colonic Neoplasms/metabolism ; Colonic Neoplasms/pathology ; DNA/metabolism ; Humans ; Nucleosomes/metabolism ; Promoter Regions, Genetic ; Protein Binding ; Proto-Oncogene Proteins p21(ras)/genetics ; Transcriptional Activation ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Nucleosomes ; TP53 protein, human ; Tumor Suppressor Protein p53 ; DNA (9007-49-2) ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
Language	English
Publishing date	2011-05-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1105680108
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Article: p53 binding to nucleosomes within the p21 promoter in vivo leads to nucleosome loss and transcriptional activation

Laptenko, Oleg / Beckerman, Rachel / Freulich, Ella / Prives, Carol

Proceedings of the National Academy of Sciences of the United States of America. 2011 June 28, v. 108, no. 26

2011

Abstract	It is well established that p53 contacts DNA in a sequence-dependent manner in order to transactivate its myriad target genes. Yet little is known about how p53 interacts with its binding site/response element (RE) within such genes in vivo in the context of nucleosomal DNA. In this study we demonstrate that both distal (5') and proximal (3') p53 REs within the promoter of the p21 gene in unstressed HCT116 colon carcinoma cells are localized within a region of relatively high nucleosome occupancy. In the absence of cellular stress, p53 is prebound to both p21 REs within nucleosomal DNA in these cells. Treatment of cells with the DNA-damaging drug doxorubicin or the p53 stabilizing agent Nutlin-3, however, is accompanied by p53-dependent subsequent loss of nucleosomes associated with such p53 REs. We show that in vitro p53 can bind to mononucleosomal DNA containing the distal p21 RE, provided the binding site is not close to the diad center of the nucleosome. In line with this, our data indicate that the p53 distal RE within the p21 gene is located close to the end of the nucleosome. Thus, low- and high-resolution mapping of nucleosome boundaries around p53 REs within the p21 promoter have provided insight into the mechanism of p53 binding to its sites in cells and the consequent changes in nucleosome occupancy at such sites.
Keywords	DNA ; binding sites ; colorectal neoplasms ; doxorubicin ; genes ; neoplasm cells ; nucleosomes ; transcriptional activation
Language	English
Dates of publication	2011-0628
Size	p. 10385-10390.
Publishing place	National Academy of Sciences
Document type	Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1105680108
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