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Article: Use of penicillin O in patients hypersensitive to pencilling G.

VOLINI, I F / SHLAES, W H / FELSENFELD, O

Journal of the American Medical Association

2004 Volume 143, Issue 9, Page(s) 794–797

MeSH term(s)	Humans ; Penicillins
Chemical Substances	Penicillins
Language	English
Publishing date	2004-05-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	2958-0
ISSN	1538-3598 ; 0002-9955 ; 0254-9077 ; 0098-7484
ISSN (online)	1538-3598
ISSN	0002-9955 ; 0254-9077 ; 0098-7484
DOI	10.1001/jama.1950.02910440012006
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Article ; Online: The Myc-associated zinc finger protein epigenetically controls expression of interferon-γ-stimulated genes by recruiting STAT1 to chromatin.

Xiao, Tiaojiang / Li, Xin / Felsenfeld, Gary

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

2024 Volume 121, Issue 17, Page(s) e2320938121

Abstract: The MYC-Associated Zinc Finger Protein (MAZ) plays important roles in chromatin organization and gene transcription regulation. Dysregulated expression of MAZ causes diseases, such as glioblastoma, breast cancer, prostate cancer, and liposarcoma. ... ...

Abstract	The MYC-Associated Zinc Finger Protein (MAZ) plays important roles in chromatin organization and gene transcription regulation. Dysregulated expression of MAZ causes diseases, such as glioblastoma, breast cancer, prostate cancer, and liposarcoma. Previously, it has been reported that MAZ controls the proinflammatory response in colitis and colon cancer via STAT3 signaling, suggesting that MAZ is involved in regulating immunity-related pathways. However, the molecular mechanism underlying this regulation remains elusive. Here, we investigate the regulatory effect of MAZ on interferon-gamma (IFN-γ)-stimulated genes via STAT1, a protein that plays an essential role in immune responses to viral, fungal, and mycobacterial pathogens. We demonstrate that about 80% of occupied STAT1-binding sites colocalize with occupied MAZ-binding sites in HAP1/K562 cells after IFN
MeSH term(s)	Male ; Humans ; Interferon-gamma/genetics ; Interferon-gamma/pharmacology ; Chromatin/genetics ; Gene Expression Regulation ; Protein Binding ; Zinc Fingers/genetics ; STAT1 Transcription Factor/genetics
Chemical Substances	Interferon-gamma (82115-62-6) ; Chromatin ; STAT1 Transcription Factor
Language	English
Publishing date	2024-04-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2320938121
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Article: G protein-induced trafficking of voltage-dependent calcium channels.

Tombler, Eugene / Cabanilla, Nory Jun / Carman, Paul / Permaul, Natasha / Hall, John J / Richman, Ryan W / Lee, Jessica / Rodriguez, Jennifer / Felsenfeld, Dan P / Hennigan, Robert F / Diversé-Pierluissi, María A

publication RETRACTED

The Journal of biological chemistry

2005 Volume 281, Issue 3, Page(s) 1827–1839

Abstract: Calcium channels are well known targets for inhibition by G protein-coupled receptors, and multiple ... forms of inhibition have been described. Here we report a novel mechanism for G protein-mediated ... trafficking of the channels, reduces calcium influx, and decreases exocytosis. Our results suggest that G protein-induced ...

Abstract	Calcium channels are well known targets for inhibition by G protein-coupled receptors, and multiple forms of inhibition have been described. Here we report a novel mechanism for G protein-mediated modulation of neuronal voltage-dependent calcium channels that involves the destabilization and subsequent removal of calcium channels from the plasma membrane. Imaging experiments in living sensory neurons show that, within seconds of receptor activation, calcium channels are cleared from the membrane and sequestered in clathrin-coated vesicles. Disruption of the L1-CAM-ankyrin B complex with the calcium channel mimics transmitter-induced trafficking of the channels, reduces calcium influx, and decreases exocytosis. Our results suggest that G protein-induced removal of plasma membrane calcium channels is a consequence of disrupting channel-cytoskeleton interactions and might represent a novel mechanism of presynaptic inhibition.
MeSH term(s)	Animals ; Calcium Channels/drug effects ; Calcium Channels/physiology ; Chick Embryo ; Electrophysiology ; GTP-Binding Proteins/physiology ; Ganglia, Spinal/physiology ; Neurons, Afferent/physiology ; Peptide Fragments ; omega-Conotoxin GVIA/pharmacology
Chemical Substances	Calcium Channels ; Peptide Fragments ; omega-Conotoxin GVIA (92078-76-7) ; GTP-Binding Proteins (EC 3.6.1.-)
Language	English
Publishing date	2005-11-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Retracted Publication
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M508829200
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Article ; Online: Large parental differences in chromatin organization in pancreatic beta cell line explaining diabetes susceptibility effects.

Jian, Xing / Felsenfeld, Gary

Nature communications

2021 Volume 12, Issue 1, Page(s) 4338

Abstract: Previous GWAS studies identified non-coding loci with parent-of-origin-specific effects on Type 2 diabetes susceptibility. Here we report the molecular basis for one such locus near the KRTAP5-6 gene on chromosome 11. We determine the pattern of long- ... ...

Abstract	Previous GWAS studies identified non-coding loci with parent-of-origin-specific effects on Type 2 diabetes susceptibility. Here we report the molecular basis for one such locus near the KRTAP5-6 gene on chromosome 11. We determine the pattern of long-range contacts between an enhancer in this locus and the human INS promoter 460 kb away, in the human pancreatic β-cell line, EndoC-βH1. 3C long range contact experiments distinguish contacts on the two sister chromosomes. Coupling with allele-specific SNPs allows construction of maps revealing marked differences in organization of the two sister chromosomes in the entire region between KRTAP5-6 and INS. Further mapping distinguishes maternal and paternal alleles. This reveals a domain of parent-of-origin-specific chromatin structure extending in the telomeric direction from the INS locus. This suggests more generally that imprinted loci may extend their influence over gene expression beyond those loci through long range chromatin structure, resulting in parent-of-origin-biased expression patterns over great distances.
MeSH term(s)	Adult ; Cell Line ; Chromatin/genetics ; Chromatin/metabolism ; CpG Islands ; Cytoskeletal Proteins/genetics ; DNA Methylation ; Diabetes Mellitus, Type 2/genetics ; Female ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Insulin/genetics ; Insulin-Like Growth Factor II/genetics ; Insulin-Secreting Cells/physiology ; Male ; Mutant Chimeric Proteins/genetics ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic
Chemical Substances	Chromatin ; Cytoskeletal Proteins ; IGF2 protein, human ; INS-IGF2 protein, human ; Insulin ; Mutant Chimeric Proteins ; keratin-associated protein 5 family, human ; Insulin-Like Growth Factor II (67763-97-7)
Language	English
Publishing date	2021-07-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-24635-2
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Article ; Online: A brief history of epigenetics.

Felsenfeld, Gary

Cold Spring Harbor perspectives in biology

2014 Volume 6, Issue 1

Abstract: The term "epigenetics" was originally used to denote the poorly understood processes by which a fertilized zygote developed into a mature, complex organism. With the understanding that all cells of an organism carry the same DNA, and with increased ... ...

Abstract	The term "epigenetics" was originally used to denote the poorly understood processes by which a fertilized zygote developed into a mature, complex organism. With the understanding that all cells of an organism carry the same DNA, and with increased knowledge of mechanisms of gene expression, the definition was changed to focus on ways in which heritable traits can be associated not with changes in nucleotide sequence, but with chemical modifications of DNA, or of the structural and regulatory proteins bound to it. Recent discoveries about the role of these mechanisms in early development may make it desirable to return to the original definition of epigenetics.
MeSH term(s)	Chromatin/physiology ; DNA/genetics ; DNA Methylation ; Epigenesis, Genetic ; History, 20th Century ; History, 21st Century
Chemical Substances	Chromatin ; DNA (9007-49-2)
Language	English
Publishing date	2014-01-01
Publishing country	United States
Document type	Historical Article ; Journal Article ; Research Support, N.I.H., Intramural
ISSN	1943-0264
ISSN (online)	1943-0264
DOI	10.1101/cshperspect.a018200
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Article ; Online: The evolution of epigenetics.

Felsenfeld, Gary

Perspectives in biology and medicine

2014 Volume 57, Issue 1, Page(s) 132–148

Abstract: Early studies of the developing embryo raised the question of how a fertilized egg could give rise to a complex multicellular organism containing many different kinds of cells. The term epigenetics originally referred to the study of these processes. ... ...

Abstract	Early studies of the developing embryo raised the question of how a fertilized egg could give rise to a complex multicellular organism containing many different kinds of cells. The term epigenetics originally referred to the study of these processes. With the advent of detailed knowledge of mechanisms of gene expression, this definition was superseded by another: epigenetics concerned the transmission of phenotype through mitosis or the germ line by mechanisms that did not involve changes in the DNA sequence. Much effort has been spent in attempting to identify and characterize these events. Work initially focused on DNA methylation as an epigenetic mark, but more recently there has been an emphasis on histone modifications as possible carriers of epigenetic information. However, there is confusion between situations in which the modifications may be propagated through cell division, thus helping to maintain a pattern of gene expression, and situations in which the modifications are simply part of the transcriptional apparatus. Arguments about the role of the histones have led to a reexamination of the definition of epigenetics and the primary events in development leading to cell type specific gene expression patterns.
MeSH term(s)	Chromatin/chemistry ; Chromatin/genetics ; DNA Methylation ; Epigenesis, Genetic ; Evolution, Molecular ; Sequence Analysis, DNA
Chemical Substances	Chromatin
Language	English
Publishing date	2014
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	80373-x
ISSN	1529-8795 ; 0031-5982
ISSN (online)	1529-8795
ISSN	0031-5982
DOI	10.1353/pbm.2014.0004
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Article ; Online: The RNA helicases DDX5 and DDX17 facilitate neural differentiation of human pluripotent stem cells NTERA2.

Suthapot, Praewa / Xiao, Tiaojiang / Felsenfeld, Gary / Hongeng, Suradej / Wongtrakoongate, Patompon

Life sciences

2022 Volume 291, Page(s) 120298

Abstract: Aims: Understanding human neurogenesis is critical toward regenerative medicine for neurodegeneration. However, little is known how neural differentiation is regulated by DEAD box-containing RNA helicases, which comprise a diverse class of RNA ... ...

Abstract	Aims: Understanding human neurogenesis is critical toward regenerative medicine for neurodegeneration. However, little is known how neural differentiation is regulated by DEAD box-containing RNA helicases, which comprise a diverse class of RNA remodeling enzymes. Materials and methods: ChIP-seq was utilized to identify binding sites of DDX5 and DDX17 in both human pluripotent stem cell (hPSC) line NTERA2 and their retinoic acid-induced neural derivatives. RNA-seq was used to elucidate genes differentially expressed upon depletion of DDX5 and DDX17. Neurosphere assay, flow cytometry, and immunofluorescence staining were performed to test the effect of depletion of the two RNA helicases in neural differentiation. Key findings: We show here that expression of DDX5 and DDX17 is abundant throughout neural differentiation of NTERA2, and is mostly localized within the nucleus. The two RNA helicases occupy chromatin genome-wide at regions associated with neurogenesis-related genes in both hPSCs and their neural derivatives. Further, both DDX5 and DDX17 are mutually required for controlling transcriptional expression of these genes, but are not important for maintenance of stem cell state of hPSCs. In contrast, they facilitate early neural differentiation of hPSCs, generation of neurospheres from the stem cells, and transcriptional expression of key neurogenic transcription factors such as SOX1 and PAX6 during neural differentiation. Importantly, DDX5 and DDX17 are critical for differentiation of hPSCs toward NESTIN- and TUBB3-positive cells, which represent neural progenitors and mature neurons, respectively. Significance: Collectively, our findings suggest the role of DDX5 and DDX17 in transcriptional regulation of genes involved in neurogenesis, and hence in neural differentiation of hPSCs.
MeSH term(s)	Cell Differentiation/physiology ; Chromatin ; Chromatin Immunoprecipitation Sequencing/methods ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism ; Gene Expression/genetics ; Gene Expression Profiling/methods ; Gene Expression Regulation/genetics ; Humans ; MCF-7 Cells ; Neural Stem Cells/metabolism ; Neurogenesis/genetics ; Pluripotent Stem Cells/metabolism ; RNA Helicases/metabolism ; Transcription Factors/metabolism ; Transcriptome/genetics
Chemical Substances	Chromatin ; Transcription Factors ; DDX17 protein, human (EC 3.6.1.-) ; Ddx5 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13) ; RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2022-01-07
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2021.120298
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Article ; Online: The Myc-associated zinc finger protein (MAZ) works together with CTCF to control cohesin positioning and genome organization.

Xiao, Tiaojiang / Li, Xin / Felsenfeld, Gary

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

2021 Volume 118, Issue 7

Abstract: The Myc-associated zinc finger protein (MAZ) is often found at genomic binding sites adjacent to CTCF, a protein which affects large-scale genome organization through its interaction with cohesin. We show here that, like CTCF, MAZ physically interacts ... ...

Abstract	The Myc-associated zinc finger protein (MAZ) is often found at genomic binding sites adjacent to CTCF, a protein which affects large-scale genome organization through its interaction with cohesin. We show here that, like CTCF, MAZ physically interacts with a cohesin subunit and can arrest cohesin sliding independently of CTCF. It also shares with CTCF the ability to independently pause the elongating form of RNA polymerase II, and consequently affects RNA alternative splicing. CTCF/MAZ double sites are more effective at sequestering cohesin than sites occupied only by CTCF. Furthermore, depletion of CTCF results in preferential loss of CTCF from sites not occupied by MAZ. In an assay for insulation activity like that used for CTCF, binding of MAZ to sites between an enhancer and promoter results in down-regulation of reporter gene expression, supporting a role for MAZ as an insulator protein. Hi-C analysis of the effect of MAZ depletion on genome organization shows that local interactions within topologically associated domains (TADs) are disrupted, as well as contacts that establish the boundaries of individual TADs. We conclude that MAZ augments the action of CTCF in organizing the genome, but also shares properties with CTCF that allow it to act independently.
MeSH term(s)	Alternative Splicing ; CCCTC-Binding Factor/metabolism ; Cell Cycle Proteins/metabolism ; Chromosomal Proteins, Non-Histone/metabolism ; DNA-Binding Proteins/chemistry ; DNA-Binding Proteins/metabolism ; Enhancer Elements, Genetic ; HEK293 Cells ; Humans ; K562 Cells ; Promoter Regions, Genetic ; Protein Binding ; RNA Polymerase II/metabolism ; Transcription Factors/chemistry ; Transcription Factors/metabolism ; Cohesins
Chemical Substances	CCCTC-Binding Factor ; CTCF protein, human ; Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; DNA-Binding Proteins ; Transcription Factors ; c-MYC-associated zinc finger protein ; RNA Polymerase II (EC 2.7.7.-)
Language	English
Publishing date	2021-02-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.2023127118
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Article: Association of arginine-rich histones with G-C-rich regions of DNA in chromatin.

Clark, R J / Felsenfeld, G

Nature: New biology

1972 Volume 240, Issue 103, Page(s) 226–229

MeSH term(s)	Animals ; Arginine/analysis ; Base Sequence ; Binding Sites ; Calcium/metabolism ; Cattle ; Centrifugation, Density Gradient ; Chromatin/analysis ; Cytosine Nucleotides/metabolism ; DNA/analysis ; DNA/metabolism ; Electrophoresis, Disc ; Endonucleases/metabolism ; Formaldehyde ; Guanine Nucleotides/metabolism ; Histones/analysis ; Histones/isolation & purification ; Histones/metabolism ; Protein Binding ; Spectrophotometry ; Staphylococcus/enzymology ; Thymus Gland/analysis ; Tritium ; Urea/metabolism
Chemical Substances	Chromatin ; Cytosine Nucleotides ; Guanine Nucleotides ; Histones ; Tritium (10028-17-8) ; Formaldehyde (1HG84L3525) ; Urea (8W8T17847W) ; DNA (9007-49-2) ; Arginine (94ZLA3W45F) ; Endonucleases (EC 3.1.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	1972-12-20
Publishing country	England
Document type	Journal Article
ZDB-ID	120715-5
ISSN	0090-0028 ; 0369-4887
ISSN	0090-0028 ; 0369-4887
DOI	10.1038/newbio240226a0
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Article ; Online: Insulin

Jian, Xing / Felsenfeld, Gary

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

2018 Volume 115, Issue 20, Page(s) E4633–E4641

Abstract: Both type 1 and type 2 diabetes involve a complex interplay between genetic, epigenetic, and environmental factors. Our laboratory has been interested in the physical interactions, in nuclei of human pancreatic β cells, between the insulin ( ...

Abstract	Both type 1 and type 2 diabetes involve a complex interplay between genetic, epigenetic, and environmental factors. Our laboratory has been interested in the physical interactions, in nuclei of human pancreatic β cells, between the insulin (
MeSH term(s)	Cells, Cultured ; Chromosomes, Human, Pair 11/genetics ; Chromosomes, Human, Pair 11/metabolism ; Diabetes Mellitus/genetics ; Diabetes Mellitus/metabolism ; Diabetes Mellitus/pathology ; Disease Susceptibility ; Gene Expression Regulation/drug effects ; Glucose/metabolism ; Humans ; Insulin/genetics ; Insulin/metabolism ; Insulin Secretion ; Insulin-Secreting Cells/drug effects ; Insulin-Secreting Cells/metabolism ; Oligonucleotides, Antisense/pharmacology ; Promoter Regions, Genetic ; Receptors, Somatostatin/antagonists & inhibitors ; Receptors, Somatostatin/genetics ; Receptors, Somatostatin/metabolism ; Somatostatin-28/pharmacology
Chemical Substances	Insulin ; Oligonucleotides, Antisense ; Receptors, Somatostatin ; Somatostatin-28 (75037-27-3) ; somatostatin receptor 5 (8X85ZJG6XJ) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2018-04-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1803146115
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