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HIRA encodes a histone chaperone that preferentially places the variant histone H3.3 in nucleosomes. Additionally we are shipping HIRA Antibodies (61) and many more products for this protein.
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transcriptional regulation by HIRA is crucial for cardiomyocyte homeostasis.
Data show that Hira is important to mediates Histone H3 (show HIST3H3 Proteins)/H4 replacement during mouse oogenesis which is required for normal 5mC deposition in oocytes. Its loss results in chromatin abnormalities and extensive oocyte loss.
HIRA is not only critical for beta-globin (show HBB Proteins) expression but is also required for activation of the erythropoietic regulators EKLF (show KLF1 Proteins) and GATA binding protein 1 (GATA1).
Hira-mediated H3.3 incorporation is essential for parental genome reprogramming and reveal an unexpected role for rRNA transcription in the mouse zygote
WHSC1 (show WHSC1 Proteins) links transcription elongation to HIRA-mediated histone H3.3 (show H3F3A Proteins) deposition.
HIRA interacts with H3.3/H4 in the absence of Daxx (show DAXX Proteins).
HIRA is an essential factor for muscle development by establishing MyoD (show MYOD1 Proteins) activation in myotubes.
Targeted mutagenesis of the Hira gene results in gastrulation defects and patterning abnormalities of mesoendodermal derivatives prior to early embryonic lethality
These results support a model in which OGT (show OGT Proteins) modifies HIRA to regulate HIRA-H3.3 complex formation and H3.3 nucleosome assembly and reveal the mechanism by which OGT (show OGT Proteins) functions in cellular senescence.
HIRA controls a specialized, dynamic H4K16ac-decorated chromatin landscape in senescent cells and enforces tumor suppression.
Mechanistic studies reveal that HIRA accumulates at sites of UVC irradiation upon detection of DNA damage prior to repair and deposits newly synthesized H3.3 histones. This local action of HIRA depends on ubiquitylation events associated with damage recognition.
HIRA is required for deposition of histone H3.3 (show H3F3A Proteins) at its binding sites.
NHRD domain of UBN1 as being an essential region for HIRA interaction and chromatin organization by the HUCA complex
HIRA plays a unique, ASF1a (show ASF1A Proteins)-independent role, which is required for the localization of HP1 (show DEFA1 Proteins)
Data show that, like HIRA, UBN1, and ASF1a, CABIN1 is involved in heterochromatinization of the genome of senescent human cells.
phosphorylation of histone H4 Ser 47 catalyzed by the PAK2 kinase, promotes nucleosome assembly of H3.3-H4 and inhibits nucleosome assembly of H3.1-H4 by increasing the binding affinity of HIRA to H3.3-H4 and reducing association of CAF-1 with H3.1-H4
the N-terminal half of HIRA should contribute positively to the growth rate via up-regulation of a set of cell cycle-related genes, whereas the C-terminal half down-regulated another set of them without exhibiting any effect on the cell growth
The N- and C-terminal regions of ASF1a (show ASF1A Proteins) and ASF1b (show ASF1B Proteins) determine the different affinities of these two proteins for HIRA, by contacting regions outside the HIRA B domain. CAF-1 (show CHAF1B Proteins) also uses B domain-like motifs for binding to ASF1a (show ASF1A Proteins), thereby competing with HIRA.
Downregulation of the H3.3 histone chaperone HIRA similarly impairs late gastrulation.
Loss of HIRA reduces extractable histone H3 protein levels and decreases nucleosome occupancy at both actively transcribed genes and heterochromatic regions.
This gene encodes a histone chaperone that preferentially places the variant histone H3.3 in nucleosomes. Orthologs of this gene in yeast, flies, and plants are necessary for the formation of transcriptionally silent heterochomatin. This gene plays an important role in the formation of the senescence-associated heterochromatin foci. These foci likely mediate the irreversible cell cycle changes that occur in senescent cells. It is considered the primary candidate gene in some haploinsufficiency syndromes such as DiGeorge syndrome, and insufficient production of the gene may disrupt normal embryonic development.
HIR histone cell cycle regulation defective homolog A (S. cerevisiae)
, HIR histone cell cycle regulation defective homolog A-like
, protein HIRA-like
, histone cell cycle regulation defective homolog A
, protein HIRA
, TUP1-like enhancer of split protein 1
, histone regulator protein
, TUP1-like enhancer of split gene 1
, DiGeorge critical region gene 1
, HIR histone cell cycle regulation defective homolog A