Disease relevance of Hist3

• There was an increase in podocyte expression of Cdc2, cyclin B1 and B2 and phosphorylated histone 3 in PHN rats, and in HIV transgenic mice [1].
• METHODS: The expression of mitotic cell cycle proteins (phosphorylated Histone 3, Cdc2, cyclin B1 and B2) was examined by immunohistochemistry in kidneys of embryonal mice, transgenic HIV-mice, and rats with experimental membranous nephropathy (passive Heymann nephritis, PHN) [1].

High impact information on Hist3

• B cell-specific loss of histone 3 lysine 9 methylation in the V(H) locus depends on Pax5 [2].
• We show that other heterochromatic marks, such as histone 3 Lys 9 (H3K9) and histone 4 Lys 20 (H4K20) trimethylation, remain at both subtelomeric and telomeric regions in these cells [3].
• Loss of Lsh, in Lsh-deficient mice, results in accumulation of di- and tri-methylated histone 3 at lysine 4 (H3-K4me) at pericentromeric DNA and other repetitive sequences [4].
• Keratinocyte proliferation was drastically stimulated by dermal cells (histone 3 mRNA expression and BrdU labeling) which continued to proliferate as well in the gel [5].
• Menin has been shown to interact with SET-1 domain-containing histone 3 lysine 4 (H3K4) methyltransferases including mixed lineage leukemia proteins to regulate homeobox (Hox) gene expression in vitro [6].

Biological context of Hist3

• Orthologous Hist2 and Hist3 clusters are present on mouse chromosomes 3 and 11, respectively [7].
• Insertion of a 150-nucleotide fragment containing the termination site between the histone 3' end and downstream polyadenylation sites reduces usage of polyadenylation sites 85 to 90% [8].
• In parallel to the beneficial effect observed, a dose-dependent increase in histone 3 acetylation at the site of inflammation was shown under VPA treatment [9].
• Ca(2+)-calmodulin-dependent phosphorylation of arginine in histone 3 by a nuclear kinase from mouse leukemia cells [10].
• EZH2 and histone 3 trimethyl lysine 27 associated with Il4 and Il13 gene silencing in Th1 cells [11].

Anatomical context of Hist3

• We introduced modified mouse histone H3 genes into mouse fibroblasts and studied the regulation of several different H3 mRNAs that are not terminated with a normal histone 3' end [12].
• However, transcripts containing the same sequences including the snRNA 3' end followed by the histone 3' end were present in the cytoplasm on polyribosomes [13].

Associations of Hist3 with chemical compounds

• To identify the phosphorylated peptide(s), histone 3 was cleaved with cyanogen bromide prior to phosphorylation [10].
• Treatment of ES cells with trichostatin A (TSA), a specific HDAC inhibitor, induced acetylation of histone-3/4 near GATA sites within the atrial natriuretic factor promoter [14].
• S-adenosylmethionine, acetylated histone 3, reelin promoter methylation, and reelin mRNA were assayed in the frontal cortex [15].

Regulatory relationships of Hist3

• Changes in mRNA copy numbers were not associated with altered cell kinetics as determined by immunohistochemistry using antibodies to phospho-histone 3 and activated caspase-3 [16].

Other interactions of Hist3

• G9a, which was coimmunoprecipitated with hepatic SHP, methylated Lys-9 of histone 3 (H3K9) in vitro [17].
• Although accumulating evidence suggests that methylation of histone 3, lysine 36 (H3K36) is associated with actively transcribed genes, we show that the SET domain of Smyd2 mediates H3K36 dimethylation and that Smyd2 represses transcription from an SV40-luciferase reporter [18].
• These results show that the histone 3' end processing signals can function independently of the histone promoter and the transcripts which are normally polyadenylated (alpha globin) can be stabilized by a poly(A)- histone mRNA 3' terminus [19].

Analytical, diagnostic and therapeutic context of Hist3

• A Ca(2+)-calmodulin dependent histone 3 kinase was partially purified from a low salt (150 mM NaCl) nuclear extract of mouse leukemia cells by calmodulin-Sepharose affinity chromatography [10].

References