{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNote that the provided abstracts do not mention ZNF32‑AS3; instead, they describe the functions of Pramel7 in embryonic stem cell (ESC) biology. In the first study, Pramel7 is identified as an essential factor for maintaining pluripotency and sustaining self‐renewal in ESCs. Here, LIF signaling directly upregulates Pramel7 through both STAT3‐mediated transcription and PI3K–GSK3β pathways. Elevated Pramel7 supports long‑term self‑renewal—even in the absence of exogenous LIF—by inactivating ERK phosphorylation and thereby suppressing differentiation. Conversely, the loss of Pramel7 prompts ESC differentiation even when LIF is present."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the second study, Pramel7’s function is further linked to the regulation of DNA methylation dynamics. Here, Pramel7 expression in ESCs leads to a preimplantation epiblast–like gene signature by promoting global DNA hypomethylation. Mechanistically, Pramel7 targets UHRF1—a critical factor required for DNA methylation maintenance—for proteasomal degradation. This regulation is pivotal during blastocyst formation, and forced expression of Pramel7 effectively locks ESCs in a naive pluripotency state, underscoring its role in modulating the epigenetic landscape."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Elisa A Casanova, Olga Shakhova, Sameera S Patel, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Pramel7 mediates LIF/STAT3-dependent self-renewal in embryonic stem cells."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Stem Cells (2011)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/stem.588"}], "href": "https://doi.org/10.1002/stem.588"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "21425410"}], "href": "https://pubmed.ncbi.nlm.nih.gov/21425410"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Urs Graf, Elisa A Casanova, Sarah Wyck, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Pramel7 mediates ground-state pluripotency through proteasomal-epigenetic combined pathways."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Nat Cell Biol (2017)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/ncb3554"}], "href": "https://doi.org/10.1038/ncb3554"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28604677"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28604677"}]}]}]}