{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThe provided abstracts do not mention MIR1911; instead, they focus on the ASB1 gene and its regulatory role in both anxiety‐related phenotypes and inflammatory responses. In the first study, an epigenome‐wide association analysis (PMID:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "revealed that increased methylation at a CpG site in the promoter of ASB1 was significantly associated with severe anxiety. This epigenetic modification, observed in both a population cohort and a clinical sample—and recapitulated in a murine model of acute stress—suggests that ASB1 may be a stress‐responsive gene that links cytokine signaling to anxiety phenotypes.\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the second study (PMID:"}, {"type": "fg", "children": [{"type": "fg_f", "ref": "2"}]}, {"type": "t", "text": ", ASB1 was shown to positively regulate inflammatory responses. Rather than marking its targets for degradation as typical of its protein family, ASB1 stabilizes TAB2 by preventing K48-linked polyubiquitination. This mechanism enhances downstream NF-κB and MAPK signaling, and functional studies in Asb1-deficient mice demonstrated increased survival in models of septic shock and reduced severity in colitis, thereby underscoring its critical role in modulating the immune response.\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nCollectively, the findings indicate that ASB1 serves as a key mediator linking neuroimmune functions: its epigenetic regulation is associated with stress-induced anxiety symptoms, while its post-translational action supports the stability of inflammatory signaling components. Although the abstracts do not address MIR1911, insights into ASB1’s dual role in neuropsychological stress and inflammation may offer a framework for understanding broader regulatory networks in immune and psychiatric disorders."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Rebecca T Emeny, Jens Baumert, Anthony S Zannas, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Anxiety Associated Increased CpG Methylation in the Promoter of Asb1: A Translational Approach Evidenced by Epidemiological and Clinical Studies and a Murine Model."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Neuropsychopharmacology (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1038/npp.2017.102"}], "href": "https://doi.org/10.1038/npp.2017.102"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "28540928"}], "href": "https://pubmed.ncbi.nlm.nih.gov/28540928"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Panpan Hou, Penghui Jia, Kongxiang Yang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "An unconventional role of an ASB family protein in NF-κB activation and inflammatory response during microbial infection and colitis."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Proc Natl Acad Sci U S A (2021)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1073/pnas.2015416118"}], "href": "https://doi.org/10.1073/pnas.2015416118"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "33431678"}], "href": "https://pubmed.ncbi.nlm.nih.gov/33431678"}]}]}]}