CHD4 (Chromodomain Helicase DNA Binding Protein 4)

Our results also reveal changes in the conformational ensemble of the entire tail, re-positioning it on the nucleosomal DNA and promoting intra-tail interactions. We demonstrate that these changes in the nucleosome, produced by mutations, alter the association of a tandem of plant homeodomain-fingers from CHD4 with the unmodified H3 tails.

These findings demonstrate that Chd4 conditional knockout using BAC-Sprr2f-Cre is not sufficient to alter the structure and function of the endometrial epithelium or drive tumorigenesis. As CHD4 is frequently co-mutated with other cancer driver genes such as TP53, PIK3CA, and PTEN, future mouse modeling efforts emulating patient mutational profiles might provide insight into the role of CHD4 in endometrial carcinoma.

This study identifies NCOA5 and CHD4 as crucial proviral cofactors and NRAS as a potent antiviral factor regulating HBV replication. The findings highlight HBV's profound host dependence, uncover specific molecular mechanisms (involving HNF4A, epigenetic regulation of cccDNA, and cell cycle), and reveal validated host targets for potential therapeutic strategies against HBV infection.

We detected highly frequent genetic alterations in autoantibody-related genes, supporting their role in the CAD pathogenic mechanisms. Moreover, our findings suggest that distinct TCR repertoire and immune signatures between tumoural and nontumoural tissues may underlie divergent cancer and dermatomyositis outcomes.

In particular, the prognostic formula comprising ZHX2, SMPD4, and CHD4 using the Lasso-Cox regression model properly distinguished the BCR-free survival curves, indicating that these genes could be signatures for disulfidptosis. Decoding disulfidptosis-related data in the transcriptome would provide crucial clues for finding novel approaches to personalized cancer medicine in prostate cancer.

Multimodal analysis (PET/CT, biomarkers, pathology) confirmed the case as luminal-A subtype and revealed a significant response to endocrine therapy. We hypothesize that this CHD4 mutation may alter the protein's dual regulatory balance, particularly enhancing its potential gene-activating functions, and propose that impaired chromatin remodeling driven by such mutations is associated with metastatic progression of breast cancer.

Furthermore, similar GEMINI assays revealed induction of C > G mutations in cells treated with decitabine. Taken together, these findings demonstrate that azanucleosides induce C > G mutations both in vitro and in vivo, and are linked to leukemic transformation in murine cells.

Predictive models constructed based on genes related to cellular senescence and disulfide death predict the prognosis of breast cancer patients.

These findings demonstrate that Chd4 conditional loss using BAC-Sprr2f-Cre is not sufficient to alter the structure and function of the endometrial epithelium or drive tumorigenesis. As CHD4 is frequently co-mutated with other cancer driver genes such as TP53, PIK3CA, and PTEN, future mouse modeling efforts emulating patient mutational profiles might provide insight into the role of CHD4 in endometrial carcinoma.

These findings suggest that AFF2-rearranged tumors form a spectrum of carcinomas with diverse morphologies, immunophenotypes, and differentiation patterns. Given the consistent involvement of the AFF2 gene and uniform AFF2 immunohistochemical positivity despite morphological heterogeneity, we propose naming this entity AFF2 carcinoma.

Functionally, suppression of CHD4 expression inhibited GC cell migration, invasion, and metastasis in vivo, while MYH9 restoration reversed these effects. Collectively, these findings establish CHD4 as a key regulator of GC metastasis through the MYH9/GSK3β/β-catenin axis and underscore its potential as a therapeutic target for inhibiting GC progression.