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Article ; Online: Histone editing elucidates the functional roles of H3K27 methylation and acetylation in mammals.

Sankar, Aditya / Mohammad, Faizaan / Sundaramurthy, Arun Kumar / Wang, Hua / Lerdrup, Mads / Tatar, Tulin / Helin, Kristian

Nature genetics

2022 Volume 54, Issue 6, Page(s) 754–760

Abstract: Posttranslational modifications of histones (PTMs) are associated with specific chromatin and gene expression ... ...

Abstract	Posttranslational modifications of histones (PTMs) are associated with specific chromatin and gene expression states
MeSH term(s)	Acetylation ; Animals ; Chromatin/genetics ; Chromatin/metabolism ; Drosophila melanogaster/genetics ; Histones/genetics ; Histones/metabolism ; Mammals/genetics ; Methylation ; Mice ; Polycomb Repressive Complex 2/genetics ; Protein Processing, Post-Translational/genetics
Chemical Substances	Chromatin ; Histones ; Polycomb Repressive Complex 2 (EC 2.1.1.43)
Language	English
Publishing date	2022-06-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-022-01091-2
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Zs.A 3613: 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)
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Article ; Online: Oncohistones: drivers of pediatric cancers.

Mohammad, Faizaan / Helin, Kristian

Genes & development

2017 Volume 31, Issue 23-24, Page(s) 2313–2324

Abstract: One of the most striking results in the area of chromatin and cancer in recent years has been the identification of recurrent mutations in histone genes in pediatric cancers. These mutations occur at high frequency and lead to the expression of mutant ... ...

Abstract	One of the most striking results in the area of chromatin and cancer in recent years has been the identification of recurrent mutations in histone genes in pediatric cancers. These mutations occur at high frequency and lead to the expression of mutant histones that exhibit oncogenic features. Thus, they are termed oncohistones. Thus far, mutations have been found in the genes encoding histone H3 and its variants. The expression of the oncohistones affects the global chromatin landscape through mechanisms that have just begun to be unraveled. In this review, we provide an overview of histone mutations that have been identified and discuss the possible mechanisms by which they contribute to tumor development. We further discuss the targeted therapies that have been proposed to treat cancers expressing oncohistones.
MeSH term(s)	Carcinogenesis/genetics ; Chondroblastoma/genetics ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic/genetics ; Genetic Therapy ; Histones/genetics ; Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/therapy
Chemical Substances	Histones
Language	English
Publishing date	2017-12-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.309013.117
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Zs.MG 54: Show issues

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Article ; Online: Accurate H3K27 methylation can be established de novo by SUZ12-directed PRC2.

Højfeldt, Jonas W / Laugesen, Anne / Willumsen, Berthe M / Damhofer, Helene / Hedehus, Lin / Tvardovskiy, Andrey / Mohammad, Faizaan / Jensen, Ole N / Helin, Kristian

Nature structural & molecular biology

2018 Volume 25, Issue 3, Page(s) 225–232

Abstract: Polycomb repressive complex 2 (PRC2) catalyzes methylation on lysine 27 of histone H3 (H3K27) and is required for maintaining transcriptional patterns and cellular identity, but the specification and maintenance of genomic PRC2 binding and H3K27 ... ...

Abstract	Polycomb repressive complex 2 (PRC2) catalyzes methylation on lysine 27 of histone H3 (H3K27) and is required for maintaining transcriptional patterns and cellular identity, but the specification and maintenance of genomic PRC2 binding and H3K27 methylation patterns remain incompletely understood. Epigenetic mechanisms have been proposed, wherein pre-existing H3K27 methylation directs recruitment and regulates the catalytic activity of PRC2 to support its own maintenance. Here we investigate whether such mechanisms are required for specifying H3K27 methylation patterns in mouse embryonic stem cells (mESCs). Through re-expression of PRC2 subunits in PRC2-knockout cells that have lost all H3K27 methylation, we demonstrate that methylation patterns can be accurately established de novo. We find that regional methylation kinetics correlate with original methylation patterns even in their absence, and specification of the genomic PRC2 binding pattern is retained and specifically dependent on the PRC2 core subunit SUZ12. Thus, the H3K27 methylation patterns in mESCs are not dependent on self-autonomous epigenetic inheritance.
MeSH term(s)	Animals ; Cells, Cultured ; CpG Islands ; Embryonic Stem Cells/metabolism ; Histones/metabolism ; Kinetics ; Methylation ; Mice ; Polycomb Repressive Complex 2/metabolism
Chemical Substances	Histones ; Suz12 protein, mouse ; Polycomb Repressive Complex 2 (EC 2.1.1.43)
Language	English
Publishing date	2018-02-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2126708-X
ISSN	1545-9985 ; 1545-9993
ISSN (online)	1545-9985
ISSN	1545-9993
DOI	10.1038/s41594-018-0036-6
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Zs.A 4101: 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)
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Article ; Online: Mutant FOXL2

Weis-Banke, Stine E / Lerdrup, Mads / Kleine-Kohlbrecher, Daniela / Mohammad, Faizaan / Sidoli, Simone / Jensen, Ole N / Yanase, Toshihiko / Nakamura, Tomoko / Iwase, Akira / Stylianou, Anthe / Abu-Rustum, Nadeem R / Aghajanian, Carol / Soslow, Robert / Da Cruz Paula, Arnaud / Koche, Richard P / Weigelt, Britta / Christensen, Jesper / Helin, Kristian / Cloos, Paul A C

Cancer research

2020 Volume 80, Issue 17, Page(s) 3466–3479

Abstract: The mutant protein ... ...

Abstract	The mutant protein FOXL2
MeSH term(s)	Cell Line, Tumor ; Cells, Cultured ; Epithelial-Mesenchymal Transition/genetics ; Female ; Forkhead Box Protein L2/genetics ; Forkhead Box Protein L2/metabolism ; Gene Expression Regulation, Neoplastic/genetics ; Granulosa Cell Tumor/genetics ; Granulosa Cell Tumor/metabolism ; Granulosa Cell Tumor/pathology ; Humans ; Mutation ; Smad Proteins/metabolism ; Smad2 Protein/metabolism ; Smad3 Protein/metabolism ; Smad4 Protein/metabolism
Chemical Substances	FOXL2 protein, human ; Forkhead Box Protein L2 ; SMAD2 protein, human ; SMAD3 protein, human ; SMAD4 protein, human ; Smad Proteins ; Smad2 Protein ; Smad3 Protein ; Smad4 Protein
Language	English
Publishing date	2020-07-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-0259
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Article ; Online: The long and the short of it: RNA-directed chromatin asymmetry in mammalian X-chromosome inactivation.

Kanduri, Chandrasekhar / Whitehead, Joanne / Mohammad, Faizaan

FEBS letters

2009 Volume 583, Issue 5, Page(s) 857–864

Abstract: Mammalian X-chromosome inactivation is controlled by a multilayered silencing pathway involving both short and long non-coding RNAs, which differentially recruit the epigenetic machinery to establish chromatin asymmetries. In response to developmentally ... ...

Abstract	Mammalian X-chromosome inactivation is controlled by a multilayered silencing pathway involving both short and long non-coding RNAs, which differentially recruit the epigenetic machinery to establish chromatin asymmetries. In response to developmentally regulated small RNAs, dicer, a key effector of RNA interference, locally silences Xist on the active X-chromosome and establishes the heterochromatin conformation along the silent X-chromosome. The 1.6 kb RepA RNA initiates silencing by targeting the PRC2 polycomb complex to the inactive X-chromosome. In addition, the nuclear microenvironment is implicated in the initiation and maintenance of X-chromosome asymmetries. Here we review new findings involving these various RNA species in terms of understanding Xist gene regulation and the establishment of X-chromosome inactivation.
MeSH term(s)	Animals ; Chromatin/genetics ; Chromatin/metabolism ; Humans ; Models, Genetic ; Nucleic Acid Conformation ; RNA/genetics ; RNA/metabolism ; X Chromosome Inactivation/genetics
Chemical Substances	Chromatin ; RNA (63231-63-0)
Language	English
Publishing date	2009-03-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2009.02.004
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Article ; Online: Epigenetics of imprinted long non-coding RNAs.

Mohammad, Faizaan / Mondal, Tanmoy / Kanduri, Chandrasekhar

Epigenetics

2009 Volume 4, Issue 5, Page(s) 277–286

Abstract: It is becoming increasingly evident that noncoding RNA (ncRNA) constitutes an important component of chromatin and that ncRNA has a critical role in organizing the chromatin architecture and epigenetic memory by acting as an interface with the chromatin ... ...

Abstract	It is becoming increasingly evident that noncoding RNA (ncRNA) constitutes an important component of chromatin and that ncRNA has a critical role in organizing the chromatin architecture and epigenetic memory by acting as an interface with the chromatin modifying machinery. Xist is the only RNA that has been shown to regulate gene expression by modulating chromatin structure using a multilayered silencing pathway. Recent emerging evidence indicates that long ncRNAs such as Kcnq1ot1 and Air which map to the Kcnq1 and Igf2r imprinted gene clusters, respectively, mediate the transcriptional silencing of multiple genes by interacting with chromatin and recruiting the chromatin modifying machinery. Though there are some parallels in the mechanistic actions of Kcnq1ot1 and Air, they seem to differ greatly in the way they achieve the silencing of overlapping and nonoverlapping genes. By reviewing the latest available evidence, we propose that Kcnq1ot1 RNA itself seems to play a critical role in the bidirectional silencing of genes in the Kcnq1 domain, thus resembling the Xist RNA; whereas in the case of Air, the act of transcription plays a critical role in the silencing of the overlapping gene, whilst Air RNA itself mediates the silencing of nonoverlapping genes in a fashion similar to Kcnq1ot1 and Xist RNAs.
Language	English
Publishing date	2009-07-01
Publishing country	United States
Document type	Journal Article
ISSN	1559-2308
ISSN (online)	1559-2308
DOI	10.4161/epi.4.5.9242
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Article ; Online: Epigenetics of imprinted long noncoding RNAs.

Mohammad, Faizaan / Mondal, Tanmoy / Kanduri, Chandrasekhar

Epigenetics

2009 Volume 4, Issue 5, Page(s) 277–286

Abstract	It is becoming increasingly evident that noncoding RNA (ncRNA) constitutes an important component of chromatin and that ncRNA has a critical role in organizing the chromatin architecture and epigenetic memory by acting as an interface with the chromatin modifying machinery. Xist is the only RNA that has been shown to regulate gene expression by modulating chromatin structure using a multilayered silencing pathway. Recent emerging evidence indicates that long ncRNAs such as Kcnq1ot1 and Air which map to the Kcnq1 and Igf2r imprinted gene clusters, respectively, mediate the transcriptional silencing of multiple genes by interacting with chromatin and recruiting the chromatin modifying machinery. Though there are some parallels in the mechanistic actions of Kcnq1ot1 and Air, they seem to differ greatly in the way they achieve the silencing of overlapping and nonoverlapping genes. By reviewing the latest available evidence, we propose that Kcnq1ot1 RNA itself seems to play a critical role in the bidirectional silencing of genes in the Kcnq1 domain, thus resembling the Xist RNA; whereas in the case of Air, the act of transcription plays a critical role in the silencing of the overlapping gene, whilst Air RNA itself mediates the silencing of nonoverlapping genes in a fashion similar to Kcnq1ot1 and Xist RNAs.
MeSH term(s)	Animals ; Chromatin Assembly and Disassembly/genetics ; Gene Silencing ; Genomic Imprinting/genetics ; Humans ; RNA Polymerase II/metabolism ; RNA, Untranslated/genetics ; Transcription, Genetic
Chemical Substances	RNA, Untranslated ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2009-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ISSN	1559-2308
ISSN (online)	1559-2308
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Article ; Online: Histone acetyltransferase PCAF is required for Hedgehog-Gli-dependent transcription and cancer cell proliferation.

Malatesta, Martina / Steinhauer, Cornelia / Mohammad, Faizaan / Pandey, Deo P / Squatrito, Massimo / Helin, Kristian

Cancer research

2013 Volume 73, Issue 20, Page(s) 6323–6333

Abstract: The Hedgehog (Hh) signaling pathway plays an important role in embryonic patterning and development of many tissues and organs as well as in maintaining and repairing mature tissues in adults. Uncontrolled activation of the Hh-Gli pathway has been ... ...

Abstract	The Hedgehog (Hh) signaling pathway plays an important role in embryonic patterning and development of many tissues and organs as well as in maintaining and repairing mature tissues in adults. Uncontrolled activation of the Hh-Gli pathway has been implicated in developmental abnormalities as well as in several cancers, including brain tumors like medulloblastoma and glioblastoma. Inhibition of aberrant Hh-Gli signaling has, thus, emerged as an attractive approach for anticancer therapy; however, the mechanisms that mediate Hh-Gli signaling in vertebrates remain poorly understood. Here, we show that the histone acetyltransferase PCAF/KAT2B is an important factor of the Hh pathway. Specifically, we show that PCAF depletion impairs Hh activity and reduces expression of Hh target genes. Consequently, PCAF downregulation in medulloblastoma and glioblastoma cells leads to decreased proliferation and increased apoptosis. In addition, we found that PCAF interacts with GLI1, the downstream effector in the Hh-Gli pathway, and that PCAF or GLI1 loss reduces the levels of H3K9 acetylation on Hh target gene promoters. Finally, we observed that PCAF silencing reduces the tumor-forming potential of neural stem cells in vivo. In summary, our study identified the acetyltransferase PCAF as a positive cofactor of the Hh-Gli signaling pathway, leading us to propose PCAF as a candidate therapeutic target for the treatment of patients with medulloblastoma and glioblastoma.
MeSH term(s)	Animals ; Cell Growth Processes/physiology ; Cell Line, Tumor ; Glioblastoma/enzymology ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Hedgehog Proteins/biosynthesis ; Hedgehog Proteins/genetics ; Hedgehog Proteins/metabolism ; Humans ; Medulloblastoma/enzymology ; Medulloblastoma/genetics ; Medulloblastoma/metabolism ; Medulloblastoma/pathology ; Mice ; NIH 3T3 Cells ; Promoter Regions, Genetic ; RNA, Small Interfering ; Signal Transduction ; Transcription Factors/genetics ; Transcription Factors/metabolism ; Transcription, Genetic ; Transfection ; Zinc Finger Protein GLI1 ; p300-CBP Transcription Factors/genetics ; p300-CBP Transcription Factors/metabolism
Chemical Substances	GLI1 protein, human ; Hedgehog Proteins ; RNA, Small Interfering ; Transcription Factors ; Zinc Finger Protein GLI1 ; p300-CBP Transcription Factors (EC 2.3.1.48) ; p300-CBP-associated factor (EC 2.3.1.48)
Language	English
Publishing date	2013-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-12-4660
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Article: Inflammatory system gene polymorphism and the risk of stroke: a case-control study in an Indian population.

Banerjee, Indranil / Gupta, Veena / Ahmed, Tanveer / Faizaan, Mohammad / Agarwal, Puneet / Ganesh, Subramaniam

Brain research bulletin

2008 Volume 75, Issue 1, Page(s) 158–165

Abstract: Sequence variations in genes involved in inflammation system are known to contribute to the risk of cardiovascular diseases (CVD) including stroke. In this study, we performed a genetic association study on the single nucleotide polymorphisms (SNPs) ... ...

Abstract	Sequence variations in genes involved in inflammation system are known to contribute to the risk of cardiovascular diseases (CVD) including stroke. In this study, we performed a genetic association study on the single nucleotide polymorphisms (SNPs) present in the genes CD14 (-159 C/T), TNFalpha (-308 G/A), IL-1alpha (-889 C/T), IL-6 (-174 G/C), PSMA6 (-8 C/G), and PDE4D (SNP83 T/C, respectively) in order to discern their possible role in the susceptibility to stroke in a North Indian population. These SNPs were previously found to be associated with CVD through their contribution to inflammation. A case-control design was used to examine 176 stroke patients (112 ischemic and 64 hemorrhagic stroke patients) and 212 unrelated healthy control individuals. After adjustment for the confounding risk factors, the IL-1alpha -889 T allele carriers (TT+CT) were found to be strongly associated with both forms of stroke (OR=2.56; 95% CI=1.53-4.29; P=0.0004). The CC genotype of PDE4D was found to be associated only with ischemic stroke (OR=2.02; 95% CI=1.08-3.76; P=0.03). None of the variants tested for the CD14, TNFalpha, IL-6, and PSMA6 genes found to confer risk for stroke in the study population. In conclusion, the -889 C/T and SNP83 T/C SNPs of the IL-1alpha and PDE4D genes, respectively, appear to be genetic risk factors for stroke in our study population.
MeSH term(s)	Adult ; Aged ; Case-Control Studies ; Cyclic Nucleotide Phosphodiesterases, Type 3/genetics ; Cyclic Nucleotide Phosphodiesterases, Type 3/metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 4 ; Cytokines/genetics ; Cytokines/metabolism ; Female ; Genetic Predisposition to Disease ; Genotype ; Humans ; India/epidemiology ; Male ; Middle Aged ; Multienzyme Complexes/genetics ; Multienzyme Complexes/metabolism ; Polymorphism, Genetic ; Proteasome Endopeptidase Complex/genetics ; Proteasome Endopeptidase Complex/metabolism ; Risk ; Stroke/epidemiology ; Stroke/genetics
Chemical Substances	Cytokines ; Multienzyme Complexes ; Cyclic Nucleotide Phosphodiesterases, Type 3 (EC 3.1.4.17) ; Cyclic Nucleotide Phosphodiesterases, Type 4 (EC 3.1.4.17) ; PDE4D protein, human (EC 3.1.4.17) ; PSMA6 protein, human (EC 3.4.25.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2008-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	197620-5
ISSN	1873-2747 ; 0361-9230
ISSN (online)	1873-2747
ISSN	0361-9230
DOI	10.1016/j.brainresbull.2007.08.007
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Article ; Online: Kcnq1ot1 noncoding RNA mediates transcriptional gene silencing by interacting with Dnmt1.

Mohammad, Faizaan / Mondal, Tanmoy / Guseva, Natalia / Pandey, Gaurav Kumar / Kanduri, Chandrasekhar

Development (Cambridge, England)

2010 Volume 137, Issue 15, Page(s) 2493–2499

Abstract: A long noncoding RNA, Kcnq1ot1, regulates the expression of both ubiquitously and tissue-specific imprinted genes within the Kcnq1 domain. However, the functional sequences of the Kcnq1ot1 RNA that mediate lineage-specific imprinting are unknown. Here, ... ...

Abstract	A long noncoding RNA, Kcnq1ot1, regulates the expression of both ubiquitously and tissue-specific imprinted genes within the Kcnq1 domain. However, the functional sequences of the Kcnq1ot1 RNA that mediate lineage-specific imprinting are unknown. Here, we have generated a knockout mouse with a deletion encompassing an 890-bp silencing domain (Delta890) downstream of the Kcnq1ot1 promoter. Maternal transmission of the Delta890 allele has no effect on imprinting, whereas paternal inheritance of the deletion leads to selective relaxation of the imprinting of ubiquitously imprinted genes to a variable extent in a tissue-specific manner. Interestingly, the deletion affects DNA methylation at somatically acquired differentially methylated regions (DMRs), but does not affect the histone modifications of the ubiquitously imprinted genes. Importantly, we found that Kcnq1ot1 recruits Dnmt1 to somatic DMRs by interacting with Dnmt1, and that this interaction was significantly reduced in the Delta890 mice. Thus, the ubiquitous and placental-specific imprinting of genes within the Kcnq1 domain might be mediated by distinct mechanisms, and Kcnq1ot1 RNA might mediate the silencing of ubiquitously imprinted genes by maintaining allele-specific methylation through its interactions with Dnmt1.
MeSH term(s)	Alleles ; Animals ; Chromatin ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/genetics ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Gene Silencing ; Genomic Imprinting ; Mice ; Mutation ; Protein Structure, Tertiary ; RNA, Long Noncoding ; RNA, Untranslated/genetics ; Transcription, Genetic
Chemical Substances	Chromatin ; KCNQ1OT1 RNA ; RNA, Long Noncoding ; RNA, Untranslated ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; Dnmt1 protein, mouse (EC 2.1.1.37)
Language	English
Publishing date	2010-08-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	90607-4
ISSN	1477-9129 ; 0950-1991
ISSN (online)	1477-9129
ISSN	0950-1991
DOI	10.1242/dev.048181
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