{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\n HROB—also known as C17orf53 or MCM8IP—is an OB‐fold–containing protein that plays a pivotal role in maintaining genome integrity by facilitating homologous recombination (HR)–mediated DNA repair. Studies have shown that HROB promotes HR by recruiting the MCM8–MCM9 helicase complex to sites of DNA damage, thereby stimulating recombination‐associated DNA synthesis downstream of RAD51 loading."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "3"}]}, {"type": "t", "text": " In addition, HROB directly binds single‐stranded DNA as well as the replication protein A (RPA), which supports its function in promoting replication fork progression and cellular survival in the face of DNA replication stress, including interstrand crosslink damage.\n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n Beyond its well‐established role in genome maintenance, genetic analyses have implicated HROB in bone biology. Nonsynonymous variants and a specific phosphorylation single-nucleotide polymorphism (phosSNP) in the HROB (C17orf53) gene have been associated with increased bone mineral density and enhanced osteoblast function, as evidenced by elevated expression of osteoblastic markers and improved cell growth and alkaline phosphatase activity."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "4"}]}, {"type": "t", "text": " \n "}]}, {"type": "t", "text": "\n "}, {"type": "p", "children": [{"type": "t", "text": "\n In summary, HROB serves as a key regulator of HR-dependent DNA repair by recruiting and activating a helicase complex essential for DNA synthesis during repair, while its genetic variation may also influence osteoblast activity and bone mineral density.\n "}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Nicole Hustedt, Yuichiro Saito, Michal Zimmermann, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Control of homologous recombination by the HROB-MCM8-MCM9 pathway."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genes Dev (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1101/gad.329508.119"}], "href": "https://doi.org/10.1101/gad.329508.119"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "31467087"}], "href": "https://pubmed.ncbi.nlm.nih.gov/31467087"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Jen-Wei Huang, Ananya Acharya, Angelo Taglialatela, et al. "}, {"type": "b", "children": [{"type": "t", "text": "MCM8IP activates the MCM8-9 helicase to promote DNA synthesis and homologous recombination upon DNA damage."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Commun (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/s41467-020-16718-3"}], "href": "https://doi.org/10.1038/s41467-020-16718-3"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32528060"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32528060"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "Chao Wang, Zhen Chen, Dan Su, et al. "}, {"type": "b", "children": [{"type": "t", "text": "C17orf53 is identified as a novel gene involved in inter-strand crosslink repair."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "DNA Repair (Amst) (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.dnarep.2020.102946"}], "href": "https://doi.org/10.1016/j.dnarep.2020.102946"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32853826"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32853826"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Xu Zhou, Ying-Hua Qiu, Pei He, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Why SNP rs227584 is associated with human BMD and fracture risk? A molecular and cellular study in bone cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "J Cell Mol Med (2019)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/jcmm.13991"}], "href": "https://doi.org/10.1111/jcmm.13991"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30370607"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30370607"}]}]}]}