• Humans
• Phenotype
• Genotype
• Genetic Association Studies/methods
• von Willebrand Factor/genetics
• Computational Biology/methods
• Transcriptome/genetics
• Gene Expression Profiling
• Machine Learning
• Single-Cell Analysis

• HL161069 U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI)

• CP: Cancer
• CP: Molecular biology
• DNA damage
• DNA repair
• DNA replication
• Transcription
• bi-directional promoters
• epithelia
• skin

• Serine-Arginine Splicing Factors/metabolism
• Serine-Arginine Splicing Factors/genetics
• DNA Damage
• Animals
• DNA Repair
• Mice
• Transcription, Genetic
• Humans
• Carcinoma, Squamous Cell/genetics
• Carcinoma, Squamous Cell/pathology
• Carcinoma, Squamous Cell/metabolism
• Cell Cycle Checkpoints/genetics
• Cell Cycle Checkpoints/drug effects

• C10701/A15181 Cancer Research UK

• LZTR1
• Candidate genes
• Copy number variations
• Spontaneous abortion

• 2023ZD65 the science and technology innovation Program of Changde city
• HPKL2023023 Hunan Provincial Key Laboratory of Regional Hereditary Birth Defects Prevention and Control
• 2024JJ7014 Hunan Provincial Natural Science Foundation Of China
• D202301037694 Scientific Research Project of Hunan Provincial Health Commission

• H2020 Marie Skłodowska-Curie Actions
• Ministerio de Ciencia e Innovación
• Agencia Estatal de Investigación
• Fundació la Marató de TV3
• Fundación Cientà fica Asociación Española Contra el Cáncer
• Austrian Science Fund

• Physarum
• cell cycle
• histone chaperones
• phylogeny
• protein domains

• Animals
• Histones/metabolism
• Physarum polycephalum/genetics
• Physarum polycephalum/metabolism
• Histone Chaperones/metabolism
• Saccharomyces cerevisiae/metabolism
• Chromatin/metabolism
• Molecular Chaperones/genetics
• Molecular Chaperones/metabolism

• R35 GM128619 NIGMS NIH HHS
• R35 GM128661 NIGMS NIH HHS
• R35GM128661 NIH HHS
• R35GM128619 NIH HHS

Aqueous humor (AH) can be easily and safely used to evaluate disease-specific biomarkers in ocular disease. The aim of this study was to identify specific proteins biomarkers in the AH of retinoblastoma (RB) patients at various stages of the disease. We analyzed the proteome of 53 AH samples using high-resolution mass spectrometry. We grouped the samples according to active vitreous seeding (Group 1), active aqueous seeding (Group 2), naive RB (group 3), inactive RB (group 4), and congenital cataracts as the control (Group 5). We found a total of 889 proteins in all samples. Comparative parametric analyses among the different groups revealed three additional proteins expressed in the RB groups that were not expressed in the control group. These were histone H2B type 2-E (HISTH2B2E), InaD-like protein (PATJ), and ubiquitin conjugating enzyme E2 V1 (UBE2V1). Upon processing the data of our study with the OpenTarget Tool software, we found that glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and CD44 were more highly expressed in the RB groups. Our results provide a proteome database regarding AH related to RB disease that may be used as a source of biomarkers. Further prospective studies should validate our finding in a large cohort of RB patients.

• Humans
• Retinoblastoma/metabolism
• Aqueous Humor/metabolism
• Proteomics
• Proteome/metabolism
• Prospective Studies
• Biomarkers/metabolism
• Retinal Neoplasms/metabolism

• TCGA
• THAP9
• THAP9-AS1
• co-expression
• guilt-by-association
• head-to-head genes
• pan-cancer
• survival

• CG# 2207376 Cisco Research Center

• Chaperones
• Chromatin
• H2A.B
• H2A.X
• H2A.Z
• Histone variants
• Posttranslational modifications
• disease

• rna
• cell biology
• skin stem cells

• Animals
• Cell Cycle
• Cell Differentiation
• Cell Proliferation
• Chromatin
• Chromatin Assembly and Disassembly
• Epidermis
• Female
• Gene Expression Regulation
• Humans
• Keratinocytes/metabolism
• Mice
• Mice, Inbred C57BL
• Mice, Knockout
• Promoter Regions, Genetic
• RNA Polymerase II/metabolism
• RNA Splicing
• RNA, Small Nuclear/genetics
• RNA, Small Nuclear/metabolism
• Skin/metabolism
• Skin/pathology
• Stem Cells
• Transcription, Genetic

• 15181 Cancer Research UK
• Wellcome Trust
• Medical Research Council
• C10701/A15181 Cancer Research UK
• Cancer Research UK (CRUK)

To investigate the role of fucoxanthin, reported to have significant anticancer effects, and histone Cluster 1 H3 Family Member D (HIST1H3D; implicated in tumorigenesis) in cervical cancer.

The half maximal inhibitory concentration (IC50) of fucoxanthin against HeLa and SiHa cervical cancer cells was determined. Differentially expressed genes (DEGs) in SiHa cells treated with IC50 fucoxanthin were screened by high-throughput techniques and subjected to signal enrichment. Following identification of HIST1H3D as a candidate gene, HIST1H3D-knockdown models were created via transfection with a short hairpin HIST1H3D payload. Impacts on cell proliferation, cell-cycle distribution, colony formation, and apoptosis were studied.

The fucoxanthin IC50 was 1 445 and 1 641 µM (Hela and SiHa cells, respectively). Chip results revealed 2 255 DEGs, including 943 upregulated and 1 312 downregulated genes, in fucoxanthin-treated versus untreated SiHa cells. Disease and function analysis indicated that these DEGs are primarily associated with cancer and organismal injuries and abnormalities, and online integrated pathway analysis showed that the DEGs were mainly enriched in p53 signalling. HIST1H3D was significantly downregulated in response to fucoxanthin. Inhibition of HIST1H3D mRNA significantly reduced cell proliferation and colony formation, significantly augmented the percentage of apoptotic HeLa and SiHa cells, and cells were arrested in G₀/G₁ cell cycle phase.

The results suggest that HIST1H3D may be an oncogene in cervical carcinogenesis and a potential fucoxanthin target in treating cervical cancer.

• Fucoxanthin
• cervical cancer
• colony formation
• proliferation

Down syndrome (DS) is characterized by neurodevelopmental abnormalities caused by partial or complete trisomy of human chromosome 21 (T21). Analysis of Down syndrome brain specimens has shown global epigenetic and transcriptional changes but their interplay during early neurogenesis remains largely unknown. We differentiated induced pluripotent stem cells (iPSCs) established from two DS patients with complete T21 and matched euploid donors into two distinct neural stages corresponding to early- and mid-gestational ages.

Using the Illumina Infinium 450K array, we assessed the DNA methylation pattern of known CpG regions and promoters across the genome in trisomic neural iPSC derivatives, and we identified a total of 500 stably and differentially methylated CpGs that were annotated to CpG islands of 151 genes. The genes were enriched within the DNA binding category, uncovering 37 factors of importance for transcriptional regulation and chromatin structure. In particular, we observed regional epigenetic changes of the transcription factor genes ZNF69, ZNF700 and ZNF763 as well as the HOXA3, HOXB3 and HOXD3 genes. A similar clustering of differential methylation was found in the CpG islands of the HIST1 genes suggesting effects on chromatin remodeling.

The study shows that early established differential methylation in neural iPSC derivatives with T21 are associated with a set of genes relevant for DS brain development, providing a novel framework for further studies on epigenetic changes and transcriptional dysregulation during T21 neurogenesis.

• DNA-methylation
• Down syndrome
• Gene expression
• Induced pluripotent stem cells
• Neurogenesis
• Transcription factors

Mutations of the Glu76 residue of canonical histone H2B are frequently found in cancer cells. However, it is quite mysterious how a single amino acid substitution in one of the multiple H2B genes affects cell fate. Here we found that the H2B E76K mutation, in which Glu76 is replaced by Lys (E76K), distorted the interface between H2B and H4 in the nucleosome, as revealed by the crystal structure and induced nucleosome instability in vivo and in vitro. Exogenous production of the H2B E76K mutant robustly enhanced the colony formation ability of the expressing cells, indicating that the H2B E76K mutant has the potential to promote oncogenic transformation in the presence of wild-type H2B. We found that other cancer-associated mutations of histones, H3.1 E97K and H2A.Z.1 R80C, also induced nucleosome instability. Interestingly, like the H2B E76K mutant, the H3.1 E97K mutant was minimally incorporated into chromatin in cells, but it enhanced the colony formation ability. In contrast, the H2A.Z.1 R80C mutant was incorporated into chromatin in cells, and had minor effects on the colony formation ability of the cells. These characteristics of histones with cancer-associated mutations may provide important information toward understanding how the mutations promote cancer progression.

δ-Tocotrienol is a naturally occurring proteasome inhibitor, which has the capacity to inhibit proliferation and induce apoptosis in several cancer cells obtained from several organs of humans, and other cancer cell lines. Moreover, results of plasma total mRNAs after δ-tocotrienol feeding to hepatitis C patients revealed significant inhibition in the expression of pro-inflammatory cytokines (TNF-α, VCAM1, proteasome subunits) and induction in the expression of ICAM1 and IFN-γ after post-treatment. This down-regulation of proteasome subunits leads to autophagy, apoptosis of immune cells and several genes. The present study describes RNA-sequence analysis of plasma total mRNAs obtained from δ-tocotrienol treatment of hepatitis C patients on gene expression regulated by proteasome.

Pooled specimens of plasma total mRNAs of pre-dose versus post-dose of δ-tocotrienol treatment of hepatitis C patients were submitted to RNA-sequence analyses. The data based on > 1 and 8-fold expression changes of 2136 genes were uploaded into “Ingenuity Pathway Analyses (IPA)” for core analysis, which describes possible canonical pathways, upstream regulators, diseases and functional metabolic networks.

The IPA of “molecules” indicated fold change in gene expression of 953 molecules, which covered several categories of biological biomarkers. Out of these, gene expression of 220 related to present study, 12 were up-regulated, and 208 down-regulated after δ-tocotrienol treatment. The gene expression of transcription regulators (ceramide synthase 3 and Mohawk homeobox) were up-regulated, and gene expression of 208 molecules were down-regulated, involved in several biological functions (HSP90AB1, PSMC3, CYB5R4, NDUFB1, CYP2R1, TNFRF1B, VEGFA, GPR65, PIAS1, SFPQ, GPS2, EIF3F, GTPBP8, EIF4A1, HSPA14, TLR8, TUSSC2). IPA of “causal network” indicated gene regulators (676), in which 76 down-regulated (26 s proteasomes, interleukin cytokines, and PPAR-ligand-PPA-Retinoic acid-RXRα, PPARγ-ligand-PPARγ-Retinoic acid-RARα, IL-21, IL-23) with significant P-values. The IPA of “diseases and functions” regulators (85) were involved with cAMP, STAT2, 26S proteasome, CSF1, IFNγ, LDL, TGFA, and microRNA-155-5p, miR-223, miR-21-5p. The IPA of “upstream analysis” (934) showed 57 up-regulated (mainly 38 microRNAs) and 64 gene regulators were down-regulated (IL-2, IL-5, IL-6, IL-12, IL-13, IL-15, IL-17, IL-18, IL-21, IL-24, IL-27, IL-32), interferon β-1a, interferon γ, TNF-α, STAT2, NOX1, prostaglandin J2, NF-κB, 1κB, TCF3, and also miRNA-15, miRNA-124, miRNA-218-5P with significant activation of Z-Score (P < 0.05).

This is first report describing RNA-sequence analysis of δ-tocotrienol treated plasma total mRNAs obtained from chronic hepatitis C patients, that acts via multiple-signaling pathways without any side-effects. These studies may lead to development of novel classes of drugs for treatment of chronic hepatitis C patients.

The online version of this article (10.1186/s12944-018-0804-7) contains supplementary material, which is available to authorized users.

• Canonical pathways
• Causal network
• Chronic hepatitis C
• Diseases and functions
• Gene expression of biomarkers
• RNA-sequence
• Up-stream regulators
• δ-Tocotrienol

The effects of the high-dose ionizing radiation used in radiotherapy have been thoroughly demonstrated in vitro and in vivo. However, the effects of low-dose ionizing radiation (LDIR) such as computed tomography-guided biopsies and X-ray fluoroscopy on skin cells remain controversial. This study investigated the molecular effects of LDIR on the human primary keratinocytes (HPKs) and U937 cells, monocytes-like cell lines. These cells were exposed to 0.1 Gray (Gy) X-ray as LDIR. The modulation of transcription was assessed using a cDNA array, and the protein expression after LDIR exposure was investigated using isobaric tags for relative and absolute quantification (iTRAQ) proteomic analysis at 24 hours. These effects were confirmed by immunoblotting analysis. The direct effects of LDIR on the U937 cells and HPKs and the bystander effects of irradiated HPKs on U937 cells were also investigated. LDIR downregulated c-Myc in both U937 cells and HPKs, and upregulated the p21^WAF1/CIP1 protein expression in U937 cells along with the activation of TGFβ and protein phosphatase 2A (PP2A). In HPKs, LDIR downregulated the mTOR signaling with repression of S6 and 4EBP1 activation. Similar changes were observed as bystander effects of LDIR. Our findings suggest that LDIR inhibits protein synthesis and induces the cytokines activation associated with inflammation via direct and bystander effects, which might recapitulate the effects of LDIR in inflammated skin structures.

The expression of core histone genes is cell cycle regulated. Large amounts of histones are required to restore duplicated chromatin during S phase when DNA replication occurs. Over-expression and excess accumulation of histones outside S phase are toxic to cells and therefore cells need to restrict histone expression to S phase. Misregulation of histone gene expression leads to defects in cell cycle progression, genome stability, DNA damage response and transcriptional regulation. Here, we discussed the factors involved in histone gene regulation as well as the underlying mechanism. Understanding the histone regulation mechanism will shed lights on elucidating the side effects of certain cancer chemotherapeutic drugs and developing potential biomarkers for tumor cells.

• DNA replication
• cell cycle
• histone gene transcription

• functional differentiation
• histone H1
• insertions/deletions
• maximum-likelihood analysis
• positive selection.
• recombination

• Amino Acid Sequence
• Animals
• Biological Evolution
• Chromatin/genetics
• Codon
• DNA/genetics
• DNA/metabolism
• Evolution, Molecular
• Histones/genetics
• Histones/metabolism
• INDEL Mutation
• Mammals/genetics
• Mammals/metabolism
• Sequence Alignment/methods
• Sequence Analysis, DNA/methods
• Structure-Activity Relationship

• cancer
• chromatin
• epigenetics
• histone
• histone variants
• mass spectrometry
• post-translational modifications
• proteomics
• translational medicine

Epigenetic reprogramming is necessary in somatic cell nuclear transfer (SCNT) embryos in order to erase the differentiation-associated epigenetic marks of donor cells. However, such epigenetic memories often persist throughout the course of clonal development, thus decreasing cloning efficiency. Here, we explored reprogramming-refractory regions in bovine SCNT blastocyst transcriptomes. We observed that histone genes residing in the 1.5 Mb spanning the cow HIST1 cluster were coordinately downregulated in SCNT blastocysts. In contrast, both the nonhistone genes of this cluster, and histone genes elsewhere remained unaffected. This indicated that the downregulation was specific to HIST1 histone genes. We found that, after trichostatin A treatment, HIST1 histone genes were derepressed, and DNA methylation at their promoters was decreased to the level of in vitro fertilization embryos. Therefore, our results indicate that the reduced expression of HIST1 histone genes is a consequence of poor epigenetic reprogramming in SCNT blastocysts.

• DNA methylation
• HDAC inhibitor
• HIST1 cluster
• RNA-seq
• SCNT
• epigenetics
• reprogramming

• Chromatin
• Epigenetic gene regulation
• H1 variants
• Linker histones
• Mammalian development
• Stem cell differentiation

Heart failure is one of the leading causes of death today. It is a complex clinical syndrome in which the heart has a reduced contraction ability and decreased viable myocytes. Novel approaches to the clinical management of heart failure have been achieved through an understanding of the molecular pathways necessary for normal heart development. Neuregulin-1 (NRG-1) has emerged as a potential therapeutic target based on the fact that mice null for NRG-1 or receptors mediating its activity, ErbB2 and ErbB4, are embryonic lethal and exhibit severe cardiac defects. Preclinical studies performed with animal models of heart failure demonstrate that treatment with NRG-1 significantly improves heart function and survival. Clinical data further support NRG-1 as a promising drug candidate for the treatment of cardiac dysfunction in patients. Recent studies have revealed the mechanism underlying the therapeutic effects of NRG-1/ErbB signaling in the treatment of heart failure. Through activation of upstream signaling molecules such as phosphoinositide 3-kinase, mitogen-activated protein kinase, and focal adhesion kinase, NRG-1/ErbB pathway activation results in increased cMLCK expression and enhanced intracellular calcium cycling. The former is a regulator of the contractile machinery, and the latter triggers cell contraction and relaxation. In addition, NRG-1/ErbB signaling also influences energy metabolism and induces epigenetic modification in cardiac myocytes in a way that more closely resembles healthy heart. These observations reveal potentially new treatment options for heart failure.

• ErbB
• Epigenetic modification
• Heart failure
• Metabolism
• Neuregulin-1

• Animals
• Chromatin/chemistry
• Chromatin/metabolism
• Chromatin Assembly and Disassembly/physiology
• DNA Replication/physiology
• Histone Chaperones/metabolism
• Histones/metabolism
• Humans
• Protein Processing, Post-Translational
• Protein Transport/physiology

H1 and related linker histones are important both for maintenance of higher-order chromatin structure and for the regulation of gene expression. The biology of the linker histones is complex, as they are evolutionarily variable, exist in multiple isoforms and undergo a large variety of posttranslational modifications in their long, unstructured, NH₂- and COOH-terminal tails. We review recent progress in understanding the structure, genetics and posttranslational modifications of linker histones, with an emphasis on the dynamic interactions of these proteins with DNA and transcriptional regulators. We also discuss various experimental challenges to the study of H1 and related proteins, including limitations of immunological reagents and practical difficulties in the analysis of posttranslational modifications by mass spectrometry.

Community associated methicillin-resistant Staphylococcus aureus (CA-MRSA) is an emerging threat to human health throughout the world. Rodent MRSA pneumonia models mainly focus on the early innate immune responses to MRSA lung infection. However, the molecular pattern and mechanisms of recovery from MRSA lung infection are largely unknown. In this study, a sublethal mouse MRSA pneumonia model was employed to investigate late events during the recovery from MRSA lung infection. We compared lung bacterial clearance, bronchoalveolar lavage fluid (BALF) characterization, lung histology, lung cell proliferation, lung vascular permeability and lung gene expression profiling between days 1 and 3 post MRSA lung infection. Compared to day 1 post infection, bacterial colony counts, BALF total cell number and BALF protein concentration significantly decreased at day 3 post infection. Lung cDNA microarray analysis identified 47 significantly up-regulated and 35 down-regulated genes (p<0.01, 1.5 fold change [up and down]). The pattern of gene expression suggests that lung recovery is characterized by enhanced cell division, vascularization, wound healing and adjustment of host adaptive immune responses. Proliferation assay by PCNA staining further confirmed that at day 3 lungs have significantly higher cell proliferation than at day 1. Furthermore, at day 3 lungs displayed significantly lower levels of vascular permeability to albumin, compared to day 1. Collectively, this data helps us elucidate the molecular mechanisms of the recovery after MRSA lung infection.

• (4-(2-hydroxyethyl)-1-piperazineethanesulfonic acid)
• 5′-Untranslated region
• 6-carboxyfluorescein
• 6FAM
• Agrobacterium mediated transient expression assay
• AmTEA
• BDPs
• BSA
• Bidirectional promoters
• Bovine serum albumin
• CREs
• Cis regulatory elements
• Degree centigrade
• Enhanced green fluorescent protein gene
• HEPES
• HEX
• Hexachloro-fluorescein
• INTS7
• Integrator complex subunit 7
• MS
• Microliter
• Micromolar
• Milliliter
• Murashige and Skoog
• OD
• Optical density
• PBS
• Phosphate buffered saline
• Protein binding site
• Quantitative polymerase chain reaction
• RPM
• RT-PCR
• Red fluorescent protein gene
• Reporter genes
• Reverse transcription polymerase chain reaction
• Revolutions per minute
• Rice
• TSS
• Transcriptional start site
• UTR
• Untranslated region
• egfp
• gus
• mL
• qPCR
• rfp
• °C
• β-glucuronidase gene
• μL
• μM

Histone variants are non-allelic protein isoforms that play key roles in diversifying chromatin structure. The known number of such variants has greatly increased in recent years, but the lack of naming conventions for them has led to a variety of naming styles, multiple synonyms and misleading homographs that obscure variant relationships and complicate database searches. We propose here a unified nomenclature for variants of all five classes of histones that uses consistent but flexible naming conventions to produce names that are informative and readily searchable. The nomenclature builds on historical usage and incorporates phylogenetic relationships, which are strong predictors of structure and function. A key feature is the consistent use of punctuation to represent phylogenetic divergence, making explicit the relationships among variant subtypes that have previously been implicit or unclear. We recommend that by default new histone variants be named with organism-specific paralog-number suffixes that lack phylogenetic implication, while letter suffixes be reserved for structurally distinct clades of variants. For clarity and searchability, we encourage the use of descriptors that are separate from the phylogeny-based variant name to indicate developmental and other properties of variants that may be independent of structure.

• Carcinoma, Hepatocellular
• CpG Islands
• DNA Methylation
• Microarray
• Prognosis

• Azacitidine/analogs & derivatives
• Azacitidine/pharmacology
• Biomarkers, Tumor/genetics
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/mortality
• Cell Line, Tumor
• CpG Islands
• DNA Methylation/drug effects
• Decitabine
• Down-Regulation
• Female
• Hep G2 Cells
• Humans
• Hydroxamic Acids/pharmacology
• Liver/metabolism
• Liver Neoplasms/genetics
• Liver Neoplasms/mortality
• Male
• Middle Aged
• Oligonucleotide Array Sequence Analysis
• Promoter Regions, Genetic
• Survival Analysis

• Animals
• Chromatin/genetics
• Chromatin/metabolism
• Histones/chemistry
• Histones/genetics
• Histones/metabolism
• Humans
• Models, Biological
• Nucleosomes/genetics
• Nucleosomes/metabolism
• Protein Binding
• Transcription, Genetic

• 3' Untranslated Regions
• Animals
• Chromatin Immunoprecipitation
• CpG Islands
• Evolution, Molecular
• Genome
• Genome, Human
• Humans
• Mice
• Promoter Regions, Genetic
• RNA Polymerase II/genetics
• TATA Box
• Transcription Initiation Site

• MC_U137761446 Medical Research Council

• histone
• rplc-ms
• post-translational modification
• au-page
• nano-lc-ms/ms

• Amino Acid Sequence
• Chromatography, High Pressure Liquid/methods
• Electrophoresis, Polyacrylamide Gel
• Histones/analysis
• Histones/chemistry
• Molecular Sequence Data
• Nanotechnology
• Reproducibility of Results
• Tandem Mass Spectrometry/methods

• R01 GM080176 NIGMS NIH HHS
• CA56542 NCI NIH HHS
• CA67007 NCI NIH HHS
• R01 CA056542 NCI NIH HHS
• R21 CA110496 NCI NIH HHS
• R01 CA107106 NCI NIH HHS
• GM63556 NIGMS NIH HHS
• R01 CA067007 NCI NIH HHS

• Base Sequence
• Cell Line, Tumor
• Chromosomes, Human, Pair 3/genetics
• Gene Expression Regulation, Neoplastic/drug effects
• Humans
• Interferon-gamma/metabolism
• Interferon-gamma/pharmacology
• Janus Kinase 2
• Lymphoma, B-Cell/genetics
• Lymphoma, B-Cell/immunology
• Lymphoma, B-Cell/pathology
• Lymphoma, Large B-Cell, Diffuse/genetics
• Lymphoma, Large B-Cell, Diffuse/immunology
• Lymphoma, Large B-Cell, Diffuse/pathology
• Mutation
• Neoplasm Proteins/genetics
• Poly(ADP-ribose) Polymerases
• Promoter Regions, Genetic
• Protein-Tyrosine Kinases/metabolism
• Proto-Oncogene Proteins/metabolism
• RNA Interference
• RNA, Small Interfering/genetics
• Recombinant Proteins
• Subcellular Fractions/metabolism
• Ubiquitin-Protein Ligases/antagonists & inhibitors
• Ubiquitin-Protein Ligases/genetics

• Acetylation
• Chromatin/physiology
• Cytosol/chemistry
• DNA Replication
• HeLa Cells
• Histones/metabolism
• Humans
• Immunoprecipitation
• Nucleosomes
• Protein Processing, Post-Translational

• GM35837 NIGMS NIH HHS
• GM53122 NIGMS NIH HHS

• Amino Acid Sequence
• Base Sequence
• DNA Primers
• DNA-Binding Proteins/genetics
• DNA-Binding Proteins/metabolism
• Histones/metabolism
• Immunoprecipitation
• Molecular Sequence Data
• Mutation
• Nuclear Proteins/genetics
• Nuclear Proteins/metabolism
• Protein Binding
• Recombinant Proteins/metabolism
• Sequence Homology, Amino Acid
• Transfection

• R01 GM48646 NIGMS NIH HHS

• Animals
• Evolution, Molecular
• Genome
• Histones/classification
• Histones/genetics
• Humans
• Invertebrates/genetics
• Phylogeny
• Promoter Regions, Genetic/genetics
• Protein Isoforms/classification
• Protein Isoforms/genetics
• Transcription, Genetic/genetics
• Vertebrates/genetics

• Base Sequence/genetics
• Binding Sites/genetics
• CCAAT-Enhancer-Binding Proteins/genetics
• Cloning, Molecular
• DNA/chemistry
• DNA/genetics
• DNA Replication/physiology
• Electrophoretic Mobility Shift Assay/methods
• Enhancer Elements, Genetic/genetics
• Gene Expression Regulation/physiology
• Histones/genetics
• Histones/physiology
• Humans
• Kidney/chemistry
• Kidney/cytology
• Kidney/embryology
• Kidney/metabolism
• Molecular Sequence Data
• Mutagenesis/genetics
• Promoter Regions, Genetic/genetics
• Sequence Analysis, DNA/methods
• Tandem Repeat Sequences/physiology
• Transcription, Genetic/physiology

• 3T3 Cells
• Animals
• Blotting, Western
• Bromodeoxyuridine/pharmacology
• Cell Differentiation
• Cell Nucleus/metabolism
• Cell Proliferation
• Centromere/ultrastructure
• Chromatin/chemistry
• Chromatin/metabolism
• Chromobox Protein Homolog 5
• Chromosomal Proteins, Non-Histone/metabolism
• Coloring Agents/pharmacology
• Fibroblasts/metabolism
• Heterochromatin/chemistry
• Heterochromatin/metabolism
• Histones/chemistry
• Histones/metabolism
• Image Processing, Computer-Assisted
• Lymphocyte Activation
• Lymphocytes/immunology
• Lymphocytes/metabolism
• Mice
• Plasmids/metabolism
• Spleen/metabolism
• Transfection

• GM-43786 NIGMS NIH HHS
• GM-59118 NIGMS NIH HHS

• Amino Acid Sequence
• Animals
• Base Sequence
• Bivalvia/genetics
• Blotting, Southern
• Chromosome Mapping
• Codon/genetics
• DNA Primers
• Evolution, Molecular
• Gene Components
• Genomic Library
• Histones/genetics
• In Situ Hybridization, Fluorescence
• Interspersed Repetitive Sequences/genetics
• Molecular Sequence Data
• Multigene Family/genetics
• Phylogeny
• Point Mutation
• RNA, Ribosomal, 5S/genetics
• Selection, Genetic
• Sequence Analysis, DNA
• Species Specificity

• Alternative Splicing
• Amino Acid Sequence
• Animals
• CHO Cells
• Cell Nucleus/metabolism
• Cells, Cultured
• Cricetinae
• Electrophoretic Mobility Shift Assay
• Evolution, Molecular
• Gene Expression Regulation
• Green Fluorescent Proteins/metabolism
• Histones/genetics
• Histones/metabolism
• Humans
• Introns/genetics
• Male
• Molecular Sequence Data
• Pan troglodytes/genetics
• Promoter Regions, Genetic
• Sequence Homology, Nucleic Acid
• Spermatozoa/metabolism
• Telomere/genetics
• Telomere/metabolism
• Testis/cytology
• Testis/physiology
• X Chromosome/genetics

• HD 39830 NICHD NIH HHS

• Adult
• Aged
• Alternative Splicing
• Astrocytoma/genetics
• Astrocytoma/pathology
• Base Sequence
• Brain Neoplasms/genetics
• Brain Neoplasms/pathology
• Cell Division
• Histones/genetics
• Humans
• Ki-67 Antigen/analysis
• Ki-67 Antigen/metabolism
• Middle Aged
• Molecular Sequence Data
• Neoplasm Staging
• RNA, Messenger/genetics
• RNA, Messenger/metabolism
• Reverse Transcriptase Polymerase Chain Reaction
• Sequence Alignment

• Amino Acid Sequence
• Animals
• Base Sequence
• Databases, Genetic
• Evolution, Molecular
• Fungi/genetics
• Gene Conversion
• Histones/genetics
• Humans
• Multigene Family
• Phylogeny
• Plants/genetics
• Point Mutation
• Selection, Genetic
• Sequence Alignment

• Animals
• Cell Line
• Cell Line, Tumor
• DNA Repair/genetics
• DNA Repair/physiology
• Embryo, Mammalian
• Fibroblasts/chemistry
• Fibroblasts/metabolism
• Gene Expression Regulation/genetics
• Genes/genetics
• Genes/physiology
• Genome
• Genome, Human
• HeLa Cells
• Humans
• Mice
• Promoter Regions, Genetic/genetics
• Promoter Regions, Genetic/physiology
• Sequence Analysis, DNA/methods
• Transcription, Genetic/genetics

• Amino Acid Sequence
• Antimicrobial Cationic Peptides/chemistry
• Antimicrobial Cationic Peptides/isolation & purification
• Antimicrobial Cationic Peptides/pharmacology
• Chromatography, High Pressure Liquid
• Colon/chemistry
• Epithelium/chemistry
• Escherichia coli/drug effects
• Humans
• Intestinal Mucosa/chemistry
• Molecular Sequence Data

• AI32738 NIAID NIH HHS