{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T17:45:15Z","timestamp":1773251115235,"version":"3.50.1"},"reference-count":32,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T00:00:00Z","timestamp":1773187200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Genet."],"abstract":"<jats:p>\n                    Huntington\u2019s disease (HD) is caused by a CAG repeat expansion mutation in the\n                    <jats:italic>Huntingtin<\/jats:italic>\n                    (\n                    <jats:italic>HTT<\/jats:italic>\n                    ) gene that transcribes into mRNA and translates into a polyglutamine tract. The mutant\n                    <jats:italic>HTT<\/jats:italic>\n                    gene products drive pathological changes that result in neurodegeneration. The mutant CAG repeat RNA contributes to cellular dysfunction by aberrantly recruiting RNA-binding proteins. For example, the mutant\n                    <jats:italic>HTT<\/jats:italic>\n                    transcript associates with a protein complex containing the MID1 protein. This aberrant recruitment of the MID1 protein complex results in an increased translation of mutant\n                    <jats:italic>HTT<\/jats:italic>\n                    . MID1 expression is abnormally high in both the brains of HD mouse models and HD patients. However, the cell type in which MID1 is overexpressed in HD brains remains obscure. Here, we investigated the MID1 expression in different brain cell types of an HD mouse model. Therefore, we separated neurons, astrocytes and microglia via magnetic sorting and show that MID1 is overexpressed in neurons of an HD mouse model. Moreover, we stained MID1 in brain sections of HD mice via immunohistochemistry and observed MID1 overexpressing cells in cortex. This finding shows that MID1 is highly expressed in neurons\u2013the most vulnerable cell type in HD\u2013underlining its important role in the neurodegenerative process. This supports the concept of blocking the interaction between MID1 and mutant\n                    <jats:italic>HTT<\/jats:italic>\n                    mRNA to counteract mutant HTT translation as a promising therapeutic approach.\n                  <\/jats:p>","DOI":"10.3389\/fgene.2026.1753495","type":"journal-article","created":{"date-parts":[[2026,3,10]],"date-time":"2026-03-10T22:10:25Z","timestamp":1773180625000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Aberrant expression of the MID1 protein in neurons of Huntington\u2019s disease brain"],"prefix":"10.3389","volume":"17","author":[{"given":"Adriana","family":"Geraci","sequence":"first","affiliation":[{"name":"Human- and Neurobiology, Institute of Biology, Department Chemistry and Biology, University of Siegen","place":["Siegen, Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Annika","family":"Reisbitzer","sequence":"additional","affiliation":[{"name":"Human- and Neurobiology, Institute of Biology, Department Chemistry and Biology, University of Siegen","place":["Siegen, Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Janina","family":"Gerhard","sequence":"additional","affiliation":[{"name":"Human- and Neurobiology, Institute of Biology, Department Chemistry and Biology, University of Siegen","place":["Siegen, Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sybille","family":"Krau\u00df","sequence":"additional","affiliation":[{"name":"Human- and Neurobiology, Institute of Biology, Department Chemistry and Biology, University of Siegen","place":["Siegen, Germany"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1965","published-online":{"date-parts":[[2026,3,11]]},"reference":[{"key":"B2","doi-asserted-by":"publisher","first-page":"7655","DOI":"10.1093\/nar\/gkac532","article-title":"Molecular insights into the interaction of CAG trinucleotide RNA repeats with nucleolin and its implication in polyglutamine diseases","volume":"50","author":"An","year":"2022","journal-title":"Nucleic Acids Res."},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.7554\/eLife.38744","article-title":"Metformin reverses early cortical network dysfunction and behavior changes in huntington's disease","volume":"7","author":"Arnoux","year":"2018","journal-title":"Elife"},{"key":"B4","doi-asserted-by":"publisher","first-page":"232","DOI":"10.1038\/nm.3049","article-title":"The E3 ubiquitin ligase midline 1 promotes allergen and rhinovirus-induced asthma by inhibiting protein phosphatase 2A activity","volume":"19","author":"Collison","year":"2013","journal-title":"Nat. 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