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anti-Rat (Rattus) HIRA Anticorps:
anti-Mouse (Murine) HIRA Anticorps:
anti-Human HIRA Anticorps:
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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
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
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 (Montrer SETD1A Anticorps), modulates beta-catenin (Montrer CTNNB1 Anticorps) 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 (Montrer HIST3H3 Anticorps)/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 (Montrer HBB Anticorps) expression but is also required for activation of the erythropoietic regulators EKLF (Montrer KLF1 Anticorps) 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 (Montrer WHSC1 Anticorps) links transcription elongation to HIRA-mediated histone H3.3 (Montrer H3F3A Anticorps) deposition.
HIRA interacts with H3.3/H4 in the absence of Daxx (Montrer DAXX Anticorps).
HIRA is an essential factor for muscle development by establishing MyoD (Montrer MYOD1 Anticorps) 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 (Montrer H3F3A Anticorps) 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 (Montrer PHB Anticorps) 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 (Montrer OGT Anticorps) modifies HIRA to regulate HIRA-H3.3 complex formation and H3.3 nucleosome assembly and reveal the mechanism by which OGT (Montrer OGT Anticorps) 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.
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