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CHAF1A and PCNA are highly expressed in cervical squamous cell carcinoma and associated with the malignancy
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Recent work has identified the chromatin assembly factor complex CAF-1 as a potent barrier to cellular reprogramming. In addition, CAF-1 has been implicated in the reversion of pluripotent cells to a totipotent-like state and in various lineage conversion paradigms, suggesting that modulation of CAF-1 levels may endow cells with a developmentally more plastic state.
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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.
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Data show that the high expression of chromatin assembly factor 1, subunit A (p150) (CHAF1A) promotes cell proliferation and inhibits cell apoptosis, suggesting that CHAF1A may be developed as a prognosis biomarker and potential therapeutic target of epithelial ovarian cancer (EOC).
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CHAF1A inhibits NEIL1 initiated repair in vitro Subsequent restoration of the chaperone-BER complex in cell, presumably after completion of repair, suggests that histone chaperones sequester the repair complex for oxidized bases in non-replicating chromatin, and allow repair when oxidized bases are induced in the genome.
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Loss of CAF1 is associated with increased motility and invasive phenotypes seen in transformed cells.
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These data suggest that CAF-1- and ASF1A-H3-H4-dependent deposition of the histone (H3-H4)2 tetramers is compatible with MMR and protects the discontinuous daughter strand from unnecessary degradation by MMR machinery.
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Taken together, these results show that CHAF1A contributes to the proliferation of glioblastoma cells and may be developed as a de novo drug target and prognosis biomarker of glioblastoma.
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Novel functions for a separable domain of the p150 protein, regulating protein and DNA interactions at the nucleolus.
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The frequency of positive CHAF1A staining in primary tumor mucosa (45.8% of 203 samples) was significantly elevated compared to normal mucosa (18.7% of samples). Increased expression was associated with cancer stage, tumor invasion and histological grade.
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Histone chaperone CHAF1A inhibits differentiation and promotes aggressive neuroblastoma.
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CAF1 was hijacked by IE2 to facilitate the replication of the HCMV genome, suggesting chromatin assembly plays an important role in herpesviral DNA synthesis, but also provide a model of the virus-induced chromatin instability through CAF1.
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CAF-I-dependent control of degradation of the discontinuous strands during mismatch repair.
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these findings suggest an expanded role of p150 as a SUMO2/3-interacting factor, and raise the intriguing possibility that p150 plays a role in promoting delivery of SUMO2/3 or SUMO2/3-modified proteins (or both) on chromatin fibers during replication.
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p150 was efficiently phosphorylated by Cdc7-Dbf4 kinase.
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ACF generates the characteristic 50- to 60-base-pair internucleosomal spacing in silent chromatin by kinetically discriminating against shorter linker DNAs
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rs9352 of CHAF1A was repeatedly includes (78% of the 200 bootstrap samples) in the best set of SNPs. CHAF1A may contribute to gliomagenesis.
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p150 directly activates transcription, independently of its histone deposition function.
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Data show that human CAF-1 (p150) contains two PCNA interaction peptides, and suggest that these peptides are part of the mechanism that enables CAF-1 to function behind replication forks without interfering with other PCNA-mediated processes.
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Altered mRNA expression is associated with prostate cancer recurrence.
