{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n Histone H2B variants – including the replication‐dependent H2BC13 – are emerging as key modulators of chromatin architecture and gene expression. Several studies have demonstrated that fluctuations in the expression of H2B family members are intimately linked to changes in nucleosome stability, transcriptional regulation, and DNA repair processes. For instance, altered expression of H2B subtypes has been observed during carcinogenesis, where aberrant levels correlate with differences in tumor stage, genomic instability, and patient prognosis (1,2,4). In lung cancer models, the downregulation of select histone H2B variants through targeted silencing of enzymes such as poly(ADP‐ribose) glycohydrolase has been associated with reduced BaP‐induced carcinogenesis and appears to impact pathways governing genome stability (1). Similarly, in cervical cancer, a dysregulated pattern of histone cluster expression—including H2B variants—is linked to the cellular response to DNA damage and may provide prognostic information (2). Moreover, efforts to define novel histone haplotypes have underscored the complexity and specialization within the H2B family, with H2BC13 representing one example of a variant that may be differentially utilized in establishing a specific chromatin environment (3). Collectively, these findings support a role for H2BC13 not only in structuring chromatin and maintaining genomic integrity, but also in orchestrating the dynamic transcriptional responses that underlie cell differentiation, stress adaptation, and oncogenic transformation."}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "4"}]}, {"type": "t", "text": ""}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Zhuoying Zeng, Jingjing Lu, Desheng Wu, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Poly(ADP-ribose) glycohydrolase silencing-mediated H2B expression inhibits benzo(a)pyrene-induced carcinogenesis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Environ Toxicol (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/tox.23034"}], "href": "https://doi.org/10.1002/tox.23034"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33044785"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33044785"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Xiaofang Li, Run Tian, Hugh Gao, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Identification of a histone family gene signature for predicting the prognosis of cervical cancer patients."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Sci Rep (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41598-017-16472-5"}], "href": "https://doi.org/10.1038/s41598-017-16472-5"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29184082"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29184082"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Kozo Ohkusu-Tsukada, Daiki Ito, Yuki Okuno, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Signs of atopic dermatitis and contact dermatitis affected by distinct H2-haplotype in the NC/Nga genetic background."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Sci Rep (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41598-018-21049-x"}], "href": "https://doi.org/10.1038/s41598-018-21049-x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "29416104"}], "href": "https://pubmed.ncbi.nlm.nih.gov/29416104"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Muhammad A Shah, Emily L Denton, Cheryl H Arrowsmith, et al. "}, {"type": "b", "children": [{"type": "t", "text": "A global assessment of cancer genomic alterations in epigenetic mechanisms."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Epigenetics Chromatin (2014)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1186/1756-8935-7-29"}], "href": "https://doi.org/10.1186/1756-8935-7-29"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "25484917"}], "href": "https://pubmed.ncbi.nlm.nih.gov/25484917"}]}]}]}