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anti-Human H2AFZ Antibodies:
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Human Polyclonal H2AFZ Primary Antibody for ChIPSeq, ChIP - ABIN4889649
El Gazzar, Liu, Yoza, McCall: Dynamic and selective nucleosome repositioning during endotoxin tolerance. in The Journal of biological chemistry 2010
Show all 9 Pubmed References
Human Polyclonal H2AFZ Primary Antibody for ChIPSeq, ChIP - ABIN2668307
Lodhi, Kossenkov, Tulin: Bookmarking promoters in mitotic chromatin: poly(ADP-ribose)polymerase-1 as an epigenetic mark. in Nucleic acids research 2014
Show all 2 Pubmed References
Mammalian Monoclonal H2AFZ Primary Antibody for - ABIN1304703
Satterlee, Beckel-Mitchener, McAllister, Procaccini, Rutter, Tyson, Chadwick: Community resources and technologies developed through the NIH Roadmap Epigenomics Program. in Methods in molecular biology (Clifton, N.J.) 2014
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 (show SMYD3 Antibodies)-mediated H2A.Z.1K101 dimethylation activates cyclin A1 (show CCNA1 Antibodies) 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 (show VPS72 Antibodies)-H2A.Z-H2B complex shows that YL1 (show VPS72 Antibodies) binding, similarly to ANP32E (show ANP32E Antibodies) binding, triggers an extension of the H2A.Z alphaC helix.
H2A.Z removal from chromatin is the primary function of INO80 (show INO80 Antibodies) and ANP32E (show ANP32E Antibodies) 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 (show ANP32E Antibodies) 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.
This study reveals an antagonistic relationship between H2A.Z.1ub and BRD2 (show BRD2 Antibodies) to regulate the transcriptional balance at bivalent genes to enable proper execution of developmental programs.
Embryonic stem cell BAF (show BANF1 Antibodies) is required for normal H2A.Z localization in these cells, suggesting BAF (show BANF1 Antibodies) either stabilizes H2A.Z containing nucleosomes or promotes subnucleosome to nucleosome conversion by facilitating H2A.Z deposition.
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.
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 (show FOXC1 Antibodies) Foxa2 (show FOXA2 Antibodies) both act to regulate nucleosome depletion and gene activation, thus promoting embryonic stem cell differentiation, whereas DNA methylation (show HELLS Antibodies) promotes nucleosome occupation and suppresses gene expression.
incorporation of the histone variant H2A.Z at the promoter regions of PPARgamma (show PPARG Antibodies) target genes by p400 (show ITPR1 Antibodies)/Brd8 (show BRD8 Antibodies) 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 (show RPL38 Antibodies) becoming heterotypic (H2A.Z-H2A).
It was shown that Ring1B (show RNF2 Antibodies) interacted with multiple complexes in embryonic stem cells. Although H2A.Z co-localized with Eed (show EED Antibodies), Ring1B (show RNF2 Antibodies) and CpG islands in chromatin, H2A.Z still blanketed polycomb (show CBX2 Antibodies) target loci in the absence of Suz12 (show SUZ12 Antibodies), Eed (show EED Antibodies), or Ring1B (show RNF2 Antibodies).
Studies indicate that the unique chromatin landscape also includes a second histone variant, H2A.Z.
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.
H2A histone family, member Z
, H2A histone family, member V
, H2A histone family member V
, histone H2A.Z
, H2AZ histone
, histone H2AF
, histone H2A.Z-like
, histone H2A.Zl2