ASAP1 (ArfGAP With SH3 Domain)

Although no adjuvant therapy was required following complete resection, documentation of this fusion provides a rational framework for future molecularly guided treatment should disease recurrence occur. This case expands the spectrum of oncogenic BRAF fusion partners in LGG and underscores the importance of integrated RNA-based diagnostics and computational validation in precision neuro-oncology.

At a physiologically relevant Vm of -30 mV, the voltage sensitivity of rEstus-NI (6.6 ps/mV) is 3.6 and 1.4 times greater than that of ASAP1 and rEstus, respectively. As a proof of concept, we successfully used rEstus-NI to estimate absolute resting Vm in HEK293T, A375 melanoma, and MCF7 breast cancer cells and quantified spontaneous Vm fluctuations in A375 cells.

We identify key residues on the PH domain and Arf that drive this allosteric mechanism, which mathematical modeling shows contributes as much to GTPase activation as membrane recruitment. The finding that PH domains directly modulate small GTPases has broad implications for the Ras and Rho oncoprotein families.

Our study revealed that SCAFs were strongly correlated with cancer stemness in HCC. A novel machine learning model based on senescent CAF-related genes was constructed to accurately predict prognosis in HCC patients. Furthermore, CTHRC1 was identified as a novel prognostic and therapeutic biomarker to predict poor prognosis in HCC and promote cancer stemness and metastasis through the Notch signaling pathway, with its expression being transcriptionally regulated by SOX4.

In summary, we describe a third subtype of PLAG family-altered pediatric CNS embryonal tumor characterized by PLAG1 gene fusion, which leads to upregulation of PLAG1 and downstream genes. We therefore propose to rename ET, PLAGL to ET, PLAG (CNS embryonal tumor with PLAG family gene alteration) together with a specification of the respective subtype.

These findings suggest that targeting ASAP1 may offer a novel therapeutic strategy to limit PTC metastasis by suppressing EMT and attenuating the TGFβ pathway.

It also reflects the biomarker potential of exosomal circRNAs as diagnostics and prognostics, allowing their dynamic application in liquid biopsies to monitor the progression of GBM over time. This review tries to develop an understanding of the complex nature of mechanisms conferring resistance to TMZ, with a particular focus on new insights regarding the potential roles of exosomal circular RNAs.

Further, through mathematical modeling, we quantified the contribution of this newly discovered allosteric mechanism to ASAP1 GTPase-activating protein activity and found that it contributes equally to GTPase activation as membrane recruitment. The discovery that PH domains can directly affect nucleotide hydrolysis by a small GTPase has ramifications for the larger group of small GTPases, that include Ras and Rho proteins, that are regulated by proteins with PH domains, control diverse cellular functions and are oncoproteins.

In xenograft experiments, ASAP1 promoted tumor growth and angiogenesis. miR-let-7a-5p can affect the migration, invasion and F-actin bundle formation of gastric cancer cells by targeting ASAP1.

This study clarifies AHR's role in regulating gene expression and metabolism in HCC, revealing novel lncRNA biomarkers and potential therapeutic targets that could aid HCC. Further research is needed to explore AHR's effects on the regulation of glucose-lipid metabolism in HCC.

Our results support a new conceptual model in which the PH domain contributes to efficient catalysis not only by membrane recruitment but by acting as a critical component of the catalytic interface, binding Arf·GTP and allosterically driving it towards the catalytic transition state. We discuss the biological implications of these results and how they may apply more broadly to poorly understood membrane-dependent regulatory mechanisms controlling catalysis of the ArfGAP superfamily as well as other peripheral membrane enzymes.

AMAP1 and NF-kB expression were reduced by conventional siRNA methods, and osimertinib was used as an epithelial growth factor receptor (EGFR) inhibitor...Subsequently, NF-κB knockdown downregulated PD-L1 levels, while double knockdown of AMAP1 and NF-κB, restored PD-L1 expression. AMAP1 may inversely regulate PD-L1 through negative feedback of pEGFR and activation of NF-κB in NSCLC cell lines.