ASF1B (Anti-Silencing Function 1B Histone Chaperone)

Together these data provide valuable insight into cell-type driven and heterogeneous responses that must be taken into consideration when monitoring molecular perturbations in culture models. We have also built a web interface for the extensive amount of data to allow users to explore the data as a resource for understanding chemical perturbation of diverse cell types.

Silencing APOBEC3B reduced RPA2 and ASF1B levels and suppressed TGF-β signaling. These findings identify APOBEC3B/ASF1B as a central pathway through which HPV infection activates TGF-β signaling and promotes EMT, offering potential biomarkers and therapeutic targets for high-risk HPV-positive OPC.

Additionally, this signaling axis is strongly associated with PD-L1 expression. In conclusion, this study demonstrates ASF1B promotes GC liver metastasis by inhibiting ferroptosis via the ZDHHC9/PCBP1/SLC7A11 axis, providing a potential immunotherapeutic target for GCLM.

Our findings establish SPP1+TNFRSF18+ CD4+ T cells as central regulators of HCC immune suppression, offering novel strategies to enhance HCC immunotherapy.

ASF1B is highly expressed in breast cancer and correlates with poor prognosis and immune cell infiltration. It may serve as a potential prognostic biomarker and therapeutic target in breast cancer.

We identified six biomarkers, namely ARF6, ASF1B, CHD5, FLNA, KDM5B, and SPI1, thereby establishing a theoretical foundation for clinical diagnosis of AML.

This study identified six hub genes (RRM2, HNRNPL, EZH2, METTL1, NHP2L1 and ASF1B) up-regulated in LARC and valuable for predicting patient susceptibility and response to NACR.

Mechanically, our investigation revealed that ASF1B emerged as a promoter of GC progression by downregulating H2A clustered histone 20 (H2AC20), thereby influencing the activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) and extracellular regulated protein kinases (ERK)1/2 signaling pathways. ASF1B, recognized as an oncogene, contributes to the initiation and progression of tumors, positioning it as a prospective target for therapeutic intervention in GC.

Furthermore, we identified physical interactions between H3.5 and histone chaperones Asf1a and Asf1b, HIRA, CAF p150 and DAXX, shedding light on the protein-level regulation of H3.5. These findings provide valuable insights into the molecular mechanisms governing testicular cell differentiation and the potential role of H3.5 in testicular pathologies.

We identified and validated high tissue levels of NCAPH, UBE2C, and ZWINT as novel prognostic risk factors in clinically localized PCa patients. The use of these markers can improve routinely used risk estimation models.

Drug sensitivity analysis suggested higher responsiveness to doxorubicin and etoposide in high-risk patients. This study suggests the potential prognostic value of CRGs in ACC. The CRG_score model provides a robust tool for risk stratification, with implications for treatment strategies.

Furthermore, these genes may affect the recurrence of serous ovarian carcinogenesis. Overall, our analytical study identifies cell cycle-related genes that can potentially be targeted as diagnostic and prognostic markers for serous ovarian cancer.