PDZK1IP1 (PDZK1 interacting protein 1)

The optimized multi-molecular logistic regression model (Model 2) built on 11 signature genes can effectively predict lymph node metastasis risk in PTC patients, demonstrating robust cross-sex stability, strong compatibility across multiple ML algorithms, and potential clinical utility as a preoperative decision-support tool for lymph node status assessment and personalized treatment planning.

It also highlighted the distinct immune infiltration features between the two diseases. These findings provide novel perspectives on the pathogenesis of IBD and CCA, thereby offering a basis for early screening of CCA in individuals with IBD.

Integrating advanced computational approaches, including Artificial Intelligence and Machine Learning, offers promising avenues to explore inhibitor-induced conformational changes and advance the rational design of selective SGLT1 inhibitors. This review proposes a new framework for selective SGLT1 inhibitor development by aligning computational predictions with experimental validations.

In 2D culture, MAP17-expressing pancreatic cancer cells responded better to gemcitabine and 5-fluorouracil. Our findings suggest that MAP17 expression could enhance the prognostic stratification of pancreatic cancer patients. Moreover, the coadministration of NAMPT inhibitors with current treatments may sensitize tumors with high MAP17 expression to chemotherapy and improve the efficacy of chemotherapy.

The novel molecular classification system and the prognostic prediction model might benefit the management of MESO patients.

Mechanically, PDZK1IP1 silencing blocked CRC progression by inactivating the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of the rapamycin pathway. PDZK1IP1 contributes to the oncogenesis of CRC. This finding provides a basis for the diagnosis, treatment, and prevention of CRC.

MAP17 plays a crucial role in the proliferation and invasion of gastric cancer cells, suggesting its potential as a biomarker and therapeutic target for gastric cancer.

Our findings suggest that MAP17 and the Akt signaling pathway play a crucial role in promoting the progression of PTC. Inhibition of MAP17 suppresses cell viability and induces apoptosis, indicating that MAP17 may be a promising therapeutic target for PTC. The data also highlight the potential for targeting the MAP17-Akt axis in developing future treatments for PTC.

These findings provide insight into the role of MAP17 in quiescence, stemness, and immune evasion, positioning it as a promising therapeutic target.

MAP17 is a novel biomarker linked to macrophage infiltration and immunotherapy responses in NASH patients. The oxidative stress induced by MAP17 activates the p53, PI3K-AKT, and Wnt pathways, all of which contribute to the progression of NASH.

These modified PNA oligomers effectively suppressed PDZK1IP1 gene expression and alleviated interferon γ (IFNγ)-induced inflammatory responses in normal human keratinocytes. These findings suggest the potential application of modified PNAs targeting PDZK1IP1 in the treatment of skin inflammatory diseases.

Our results demonstrate FXR1's oncogenic involvement in ESCA cell lines, suggesting that FXR1 may be implicated in ESCA development by regulating the stability of PDZK1IP1 and ATOH8 mRNAs. For the first time, our findings emphasize the importance of FXR1-PDZK1IP1 and -ATOH8 functional modules in the development of ESCA, which might have potential diagnostic or therapeutic implications.