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anti-Rat (Rattus) HIRA Anticorps:
anti-Mouse (Murine) HIRA Anticorps:
anti-Human HIRA Anticorps:
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Yeast (Saccharomyces cerevisiae) Monoclonal HIRA Primary Antibody pour WB - ABIN533550
Yang, Zhang, Kudlow: Recruitment of O-GlcNAc transferase to promoters by corepressor mSin3A: coupling protein O-GlcNAcylation to transcriptional repression. dans Cell 2002
Show all 3 Pubmed References
Human Polyclonal HIRA Primary Antibody pour ELISA, WB - ABIN545785
Zhang, Chen, Adams: Molecular dissection of formation of senescence-associated heterochromatin foci. dans Molecular and cellular biology 2007
Show all 2 Pubmed References
Human Monoclonal HIRA Primary Antibody pour ICC, IF - ABIN4889661
Inoue, Zhang: Nucleosome assembly is required for nuclear pore complex assembly in mouse zygotes. dans Nature structural & molecular biology 2014
Human Polyclonal HIRA Primary Antibody pour IF, WB - ABIN521162
Jiang, Nguyen, Cao, Chang, Reddel: HP1-mediated formation of alternative lengthening of telomeres-associated PML bodies requires HIRA but not ASF1a. dans PLoS ONE 2011
These data suggest that elimination of HIRA produces a hypertrophic response in skeletal muscle and leaves myofibers susceptible to stress-induced degeneration.
HIRA, in cooperation with Setd1A, modulates beta-catenin expression to regulate neural stem cell proliferation and neurogenesis.
transcriptional regulation by HIRA is crucial for cardiomyocyte homeostasis.
Data show that Hira is important to mediates Histone H3/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 expression but is also required for activation of the erythropoietic regulators EKLF 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 links transcription elongation to HIRA-mediated histone H3.3 deposition.
HIRA interacts with H3.3/H4 in the absence of Daxx.
HIRA is an essential factor for muscle development by establishing MyoD 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 data show that HIRA phosphorylation limits the expression of myogenic genes, while the dephosphorylation of HIRA is required for proficient H3.3 deposition and gene activation, demonstrating that the phosphorylation switch is exploited to modulate HIRA/H3.3-mediated muscle gene regulation during myogenesis.
Data show that histone chaperone HIRA co-localizes with viral genomes, binds to incoming viral and deposits histone H3.3 onto these.
Chromatin reassembly during double-strand break repair was dependent on the HIRA histone chaperone that is specific to the replication-independent histone variant H3.3 and on CAF-1 that is specific to the replication-dependent canonical histones H3.1/H3.2.
RPA, best known for its role in DNA replication and repair, recruits HIRA to promoters and enhancers and regulates deposition of newly synthesized H3.3 to these regulatory elements for gene regulation.
H3.Y discriminates between HIRA and DAXX chaperone complexes and reveals unexpected insights into human DAXX-H3.3-H4 binding and deposition requirements.
PHB has an unexpected nuclear role in human embryonic stem cells that is required for self-renewal and that it acts with HIRA in chromatin organization to link epigenetic organization to a metabolic circuit.
The abnormal lower expression of the HIRA gene in the myocardium may participate in the pathogenesis of Tetralogy of Fallot.
These results support a model in which OGT modifies HIRA to regulate HIRA-H3.3 complex formation and H3.3 nucleosome assembly and reveal the mechanism by which OGT 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 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-independent role, which is required for the localization of HP1
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 and ASF1b determine the different affinities of these two proteins for HIRA, by contacting regions outside the HIRA B domain. CAF-1 also uses B domain-like motifs for binding to ASF1a, thereby competing with HIRA.
Hpc2-related domain of UBN1, UBN2, and Hpc2p is an evolutionarily conserved HIRA/Hir-binding domain, which directly interacts with the N-terminal WD repeats of HIRA/Hir.
FISH analysis of metaphases revealed a duplication of TUPLE1 probe on one chromosome 22q (Fig. 1).
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