{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nSMC1A is a core subunit of the cohesin complex, a highly conserved multiprotein assembly essential for sister chromatid cohesion, accurate chromosome segregation, and the maintenance of genomic stability. In its canonical role, SMC1A partners with SMC3 and other cohesin components to establish and maintain proper chromatin architecture during interphase and mitosis. In response to DNA damage, SMC1A becomes phosphorylated in an ATM‐dependent manner, thereby mediating cell cycle checkpoint activation and facilitating DNA repair. In addition, its dynamic association with chromatin—including transient kinetochore localization and regulation by factors such as PTIP and Rad50—ensures a finely tuned response to double‐strand breaks and replication stress."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nMutations and subtle alterations in SMC1A function have been directly implicated in several developmental disorders. In Cornelia de Lange syndrome (CdLS) and CdLS‐like phenotypes, missense mutations and small in‐frame deletions in SMC1A often preserve the overall protein frame yet alter the dynamic binding of cohesin to chromatin, leading to dysregulated gene expression, developmental delay, and facial dysmorphisms. Furthermore, SMC1A variants have been associated with additional neurodevelopmental abnormalities—including epileptic encephalopathies with Rett‐like features and even midline forebrain defects as seen in holoprosencephaly—underscoring the protein’s role as a regulator of transcription during embryogenesis. These findings highlight that perturbed cohesin function through SMC1A mutations can affect both structural chromosome integrity and gene regulatory networks crucial for normal development."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "25"}, {"type": "fg_f", "ref": "13"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nDysregulation of SMC1A is also emerging as a critical contributor to cancer. Aberrant expression and somatic mutations in SMC1A have been linked to chromosomal instability observed in early colorectal adenomas and advanced carcinomas, and to the promotion of tumor cell proliferation, migration, and survival in various cancers including acute myeloid leukemia, prostate cancer, and hepatocellular carcinoma. Moreover, in the context of viral oncogenesis, constitutive activation and recruitment of phosphorylated SMC1A by factors such as CTCF facilitate viral genome amplification (as seen in high‐risk human papillomaviruses), while its potential role in recruiting Mediator and other transcription co-regulators underscores its broader impact on maintaining cancer cell identity and drug resistance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "26", "end_ref": "31"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its canonical roles, SMC1A participates in other non‐traditional cellular functions. It interacts with proteins such as the retinitis pigmentosa GTPase regulator (RPGR) in the maintenance and regulation of ciliary structures in photoreceptors and sperm flagella, and it functions as a negative regulator in nuclear receptor–mediated transcription—as exemplified by its involvement in the repression of drug metabolizing CYP2B6 gene transcription via interaction with the constitutive androstane receptor. Such findings suggest that SMC1A’s spectrum of function extends well beyond chromosome dynamics to include modulation of specialized transcriptional programs and cytoskeletal organization."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "32"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Matthew A Deardorff, Maninder Kaur, Dinah Yaeger, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mutations in cohesin complex members SMC3 and SMC1A cause a mild variant of cornelia de Lange syndrome with predominant mental retardation."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Am J Hum Genet (2007)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1086/511888"}], "href": "https://doi.org/10.1086/511888"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "17273969"}], "href": "https://pubmed.ncbi.nlm.nih.gov/17273969"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Thomas D Barber, Kirk McManus, Karen W Y Yuen, et al. 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