IndraLab

Statements

PAN2 activates ASF1A. 15 / 15
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"USP52 promoted ASF1A stabilization facilitates chromatin assembly and favors cell cycle progression."
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"These results favor the argument that USP52 promoted ASF1A stabilization regulates DNA synthesis coupled chromatin assembly through ASF1A mediated deposition of H3K56Ac."
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"Taken together, these data indicate that USP52 targets ASF1A and K129 for deubiquitination and USP52 is a bona fide deubiquitinase for ASF1A."
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"In light of our observation that USP52 mediated ASF1A stabilization regulates the level of H3K56Ac, it is reasonable to postulate that USP52 and ASF1A signaling pathway plays a role in tumorigenesis."
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"These results are in favor of the role of USP52 promoted ASF1A stabilization in chromatin assembly thus cell cycle progression, and indicate that USP52 and ASF1A axis is required for breast cancer cell proliferation."
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"To corroborate the role of USP52 promoted ASF1A stabilization in chromatin replication, cellular extracts from cells used in MNase digestion assays were collected and analyzed by western blotting."
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"USP52 acts as a deubiquitinase and promotes histone chaperone ASF1A stabilization."
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"Considering that ASF1A also plays an important role in replication independent chromatin assembly and chromatin disassembly during transcriptional activation XREF_BIBR, XREF_BIBR, XREF_BIBR, it is interesting to investigate whether USP52 promoted ASF1A stabilization plays a role in these processes."
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"Collectively, these results point a role of the USP52 promoted ASF1A stabilization in promoting breast carcinogenesis."
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"Collectively, these observations suggest that USP52 promoted ASF1A stabilization is potentially associated with breast carcinogenesis."
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"In this study, we revealed that the expression level of USP52 and ASF1A is upregulated in breast cancer and positively correlates with each other, and, indeed, USP52 promoted ASF1A stabilization is required for breast cancer cells to combat with genotoxic insults."
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"These results suggest that USP52 promotes chromatin assembly in an ASF1A dependent manner."
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"Taken together, these results support the argument that USP52 promoted ASF1A stabilization is required for efficient DNA replication and proper S-phase progression."
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"Collectively, these results support the notion that USP52 promoted ASF1A stabilization confers cellular resistance of breast cancer cells to genotoxic insults."
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"Remarkably, we also revealed that histone H3K56Ac levels were downregulated upon impairment of USP52 promoted ASF1A stabilization."
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