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H2A.Z associates with epigenetic gene activation in prostate cancer.Acetylated H2A.Z role in activation of newly formed enhancers in prostate cancer.
The present study demonstrated that H2A.Z is overexpressed in ICC and expression of H2A.Z correlated with poor prognosis in patients with ICC. H2A.Z regulated cell proliferation in vitro and in vivo via H2A.Z/S-phase kinase-associated protein 2/p27/p21 signaling.
study identifies GAS41 as a histone acetylation reader that promotes histone H2A.Z deposition in non-small cell lung cancer.
Two possible modes of pioneering associated with combinations of H2A.Z and p300/CBP at nucleosome-occupied enhancers.
Results indicate that accumulation of H2A.Z within repressed genes can also be a consequence of the repression of gene transcription rather than an active mechanism required to establish the repression.
Findings suggest the oncogenic potential of H2A.Z.1 in liver tumorigenesis and that it plays established role in accelerating cell cycle transition and EMT during hepatocarcinogenesis.
Crystal structure results show that the flexible character of the H2A.Z L1 loop plays an essential role in forming the stable heterotypic H2A.Z/H2A nucleosome.
Monoubiquitination of histone H2B blocks eviction of histone variant H2A.Z from inducible enhancers.
Thus, PWWP2A is a novel H2A.Z-specific multivalent chromatin binder providing a surprising link between H2A.Z, chromosome segregation, and organ development.
SMYD3-mediated H2A.Z.1K101 dimethylation activates cyclin A1 expression and contributes to driving the proliferation of breast cancer cells.
Results suggest that the N-terminal tail of H2A.Z makes distinctively different contributions to epigenetic events.
the H2AFZ gene may confer a risk for schizophrenia and contribute to the impairment of executive function in Han Chinese patients with schizophrenia.
The 2.7-A-resolution crystal structure of the human YL1-H2A.Z-H2B complex shows that YL1 binding, similarly to ANP32E binding, triggers an extension of the H2A.Z alphaC helix.
H2A.Z removal from chromatin is the primary function of INO80 and ANP32E in promoting homologous recombination.
Results demonstrated male-selective association of the H2AFZ gene with schizophrenia, and that modification of the H2AFZ signaling pathway warrants further study in terms of the pathophysiology of schizophrenia
Dynamic modulation of H2A.Z exchange and removal by Anp32e reveals the importance of the nucleosome surface and nucleosome dynamics in processing the damaged chromatin template during DSB repair.
The findings implicate H2A.Z.2 as a mediator of cell proliferation and drug sensitivity in malignant melanoma.
the predictive values regarding low expressions of H2AFZ and CASP8AP2 and high white blood cell count suggest that these features could help to identify more accurately patients at greater risk of relapse.
Anp32e may help to resolve the non-nucleosomal H2A.Z aggregates and also facilitate the removal of H2A.Z at the +1 nucleosomes, and the latter may help RNA polymerase II to pass the first nucleosomal barrier.
Study mapped H2A.Z genome-wide in embryonic stem cells and neural progenitors; H2A.Z is deposited at promoters and enhancers, and correlates strongly with H3K4 methylation. H2A.Z is present at poised promoters with bivalent chromatin and at active promoters with H3K4 methylation, but is absent from stably repressed promoters that are enriched for H3K27 trimethylation.
The data also suggest that H2A.Z restricts transcription, which is moderated by ANP32e at the promoter and gene bodies of expressed genes. Thus, ANP32e, through inhibition of PP2A, is required for nucleosomal inclusion of H2A.Z and the regulation of gene expression
In contrast to H2A-interacting proteins, the H2A.Z-interacting proteins are involved in transcriptional regulation. We found that the transcription factor Osr1 interacts with H2A.Z both in vitro and in vivo. It also mediates H2A.Z incorporation to a large number of target sites and regulates gene expression
This study reveals an antagonistic relationship between H2A.Z.1ub and BRD2 to regulate the transcriptional balance at bivalent genes to enable proper execution of developmental programs.
Embryonic stem cell BAF is required for normal H2A.Z localization in these cells, suggesting BAF either stabilizes H2A.Z containing nucleosomes or promotes subnucleosome to nucleosome conversion by facilitating H2A.Z deposition.
our work suggests that the divergent residues in the H2A.Z acidic patch comprise a unique domain that couples control of chromatin dynamics to the regulation of developmental gene expression patterns during lineage commitment.
Data propose that H2A.Z mediates such contrasting activities by acting as a general facilitator that generates access for a variety of complexes, both activating and repressive.
The variant histone H2A.Z and the winged helix transcription factor Foxa2 both act to regulate nucleosome depletion and gene activation, thus promoting embryonic stem cell differentiation, whereas DNA methylation promotes nucleosome occupation and suppresses gene expression.
incorporation of the histone variant H2A.Z at the promoter regions of PPARgamma target genes by p400/Brd8 is essential to allow fat cell differentiation
In mouse trophoblast stem cells, the amount of histone H2A.Z at promoters decreased during S phase, coinciding with homotypic (H2A.Z-H2A.Z) nucleosomes flanking the TSS becoming heterotypic (H2A.Z-H2A).
It was shown that Ring1B interacted with multiple complexes in embryonic stem cells. Although H2A.Z co-localized with Eed, Ring1B and CpG islands in chromatin, H2A.Z still blanketed polycomb target loci in the absence of Suz12, Eed, or Ring1B.
Studies indicate that the unique chromatin landscape also includes a second histone variant, H2A.Z.
H2A.Z detection is asymmetrically associated with segregating sets of chromosomes in asymmetric self-renewing mitotic cells.
Our results imply that antagonism between H2A.Z deposition and DNA methylation is a conserved feature of eukaryotic genes, and that transcription-coupled H2A.Z changes may play a role in cancer initiation and progression.
Data show that RARgamma is required for deposition of H2A.Z and Suz12 at RA target genes, and that in embryonic stem cells both RARgamma and Suz12 exist in a multi-protein complex in the absence of ligand.
C-terminal amino acids of H2A.X function specifically to target this variant histone into chromatin in embryos after fertilization and that the absence of H2A.Z and macroH2A from the chromatin is required for normal development.
These results identify SRCAP/H2A.Z-mediated chromatin remodelling as a key early event in muscle differentiation-specific gene expression.
Pericentric heterochromatin becomes enriched with H2A.Z during early mammalian development
Histone H2A.z is required for cardiac hypertrophy, where its stability and the extent of cell growth and apoptosis are moderated by Sir2alpha
the X and the Y chromosome are assembled into facultative heterochromatic structures postmeiotically that are enriched with H2A.Z, thereby replacing macroH2A
Depletion of H2A.Z by RNA interference perturbs Xenopus laevis development at gastrulation leading to embryos with malformed, shortened trunks.
Histones are basic nuclear proteins that are responsible for the nucleosome structure of the chromosomal fiber in eukaryotes. Nucleosomes consist of approximately 146 bp of DNA wrapped around a histone octamer composed of pairs of each of the four core histones (H2A, H2B, H3, and H4). The chromatin fiber is further compacted through the interaction of a linker histone, H1, with the DNA between the nucleosomes to form higher order chromatin structures. This gene encodes a replication-independent member of the histone H2A family that is distinct from other members of the family. Studies in mice have shown that this particular histone is required for embryonic development and indicate that lack of functional histone H2A leads to embryonic lethality.
, histone H2A.Z
, H2A histone family, member Z
, H2A histone family, member V
, histone H2A.Z-like
, histone H2A.Zl2
, histone H2AF