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A targeted mutation in mice expressing an N-terminally truncated STAT1 protein (STAT1-\u0394N) typically develops splenomegaly in animals older than 6 months due to the formation of splenic non-Hodgkin lymphomas. The expression of the STAT1-\u0394N variant resulted in the disruption of normal spleen architecture by malignant CD3- and CD20-negative tumor cells, which stained positively for both tyrosine-phosphorylated STAT1 and STAT3. Immunoblotting of lysates from isolated tumor cells revealed the cytokine-independent hyperphosphorylation of both STAT proteins, whereas the expression level of NF-\u03baB was significantly reduced. Gel-shift assays showed that the DNA-binding activity of STAT1-\u0394N was increased compared to the wild-type protein. This elevated level of tyrosine-phosphorylated STAT1-\u0394N did not further increase upon stimulation of isolated tumor cells with either interferon-\u03b3 (IFN\u03b3), lipopolysaccharide (LPS), or the combination of both. Since the truncation mutant was unable to accumulate in the nucleus upon cytokine stimulation, real-time PCR data from tumor tissue as well as from isolated, IFN\u03b3\/LPS-treated lymphoma cells demonstrated significantly reduced STAT1-regulated target gene expression despite its observed hyperphosphorylation. The nuclear import defect of tyrosine-phosphorylated STAT1-\u0394N was associated with an elevated tyrosine-phosphorylation level of its antagonistic homolog STAT3, which is a known oncogene. These data demonstrate that the lack of STAT1 nuclear accumulation interferes with the functional balance between the two STAT proteins and, thereby, promotes the formation of phospho-STAT3-expressing CD3<jats:sup>-\/-<\/jats:sup> CD20<jats:sup>-\/-<\/jats:sup> non-Hodgkin lymphomas in the spleens of the diseased animals.<\/jats:p>","DOI":"10.1186\/s12964-025-02183-2","type":"journal-article","created":{"date-parts":[[2025,4,26]],"date-time":"2025-04-26T16:05:39Z","timestamp":1745683539000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["N-terminal truncation of STAT1 transcription factor causes CD3- and CD20-negative non-Hodgkin lymphoma through upregulation of STAT3-mediated oncogenic functions"],"prefix":"10.1186","volume":"23","author":[{"given":"Sana Mumtaz","family":"Sheikh","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Julia","family":"Staab","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martina","family":"Bleyer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Aleksandar","family":"Ivetic","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fred","family":"L\u00fchder","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Oliver","family":"Wirths","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Meyer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2025,4,26]]},"reference":[{"issue":"2","key":"2183_CR1","first-page":"65","volume":"1","author":"L Avalle","year":"2012","unstructured":"Avalle L, Pensa S, Regis G, Novelli F, Poli V. 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