{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nAlthough the query requested a summary of SNORD20 function, none of the provided abstracts address SNORD20. Instead, these studies focus on FKBP8 (also known as FKBP38), a multifunctional immunophilin that plays diverse roles in development and cellular homeostasis. Several studies describe its critical function as an antagonist of Sonic hedgehog (Shh) signaling during neural development, where loss or disruption of FKBP8 results in ectopic or hyperactivated Shh pathway activity, altered ventral cell fates, and neural tube closure defects such as spina bifida. In addition, FKBP8 is implicated in regulating neural patterning and promoting proper neurite extension by modulating apoptosis and membrane trafficking in the developing central nervous system."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nOther abstracts reveal that FKBP8 plays essential roles in cellular quality control and organellar homeostasis. It interacts with proteasomal subunits to tether the 26S proteasome to mitochondrial and endoplasmic reticulum membranes, influencing local protein degradation. Moreover, FKBP8 is involved in regulating the stability of key proteins such as prolyl-4-hydroxylase domain protein 2 (PHD2) via ubiquitin-independent proteasomal pathways, thereby modulating cellular responses to oxygen levels. Its role in mitochondrial dynamics and mitophagy further underscores its importance in maintaining mitochondrial quality and cellular integrity."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nAdditional investigations have linked FKBP8 to processes beyond neural and proteostatic regulation. Several studies demonstrate that FKBP8 modulates gene expression networks that influence tumor invasion, metastasis, and immune cell activity. In these contexts, FKBP8 can regulate anti‐invasive factors and control apoptotic signaling under stress conditions in tissues such as the heart, where its deficiency exacerbates stress-induced apoptosis and inflammation. Furthermore, its functions extend to additional organ systems including auditory and ovarian tissues, highlighting its broad physiological relevance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "10", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Oleg V Bulgakov, Jonathan T Eggenschwiler, Dong-Hyun Hong, et al. 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"}, {"type": "b", "children": [{"type": "t", "text": "Mouse Fkbp8 activity is required to inhibit cell death and establish dorso-ventral patterning in the posterior neural tube."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mol Genet (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/hmg/ddm333"}], "href": "https://doi.org/10.1093/hmg/ddm333"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18003640"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18003640"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Michiko Shirane, Masaharu Ogawa, Jun Motoyama, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Regulation of apoptosis and neurite extension by FKBP38 is required for neural tube formation in the mouse."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genes Cells (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1111/j.1365-2443.2008.01194.x"}], "href": "https://doi.org/10.1111/j.1365-2443.2008.01194.x"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18459960"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18459960"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Shotaro Saita, Michiko Shirane, Tohru Ishitani, et al. 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