RUVBL1 (RuvB Like AAA ATPase 1)

EpCAM and RUVBL1 are promising diagnostic biomarkers for EC, linking sEV-mediated pathways to disease progression. These findings provide insights into EC pathogenesis and highlight potential therapeutic targets.

RUVB-like 1 (RUVBL1), a protein that regulates the essential mechanism of carcinogenesis, including chromatin remodeling, DNA repair, and transcriptional control, was discovered as an intriguing CAU target. These results were corroborated via in silico and biological investigations that elucidated CAU role in the regulation of RUVBL1 activity, highlighting its promising therapeutic relevance.

Our findings highlight the potential of RUVBL1 as a prognostic biomarker and therapeutic target to enhance treatment efficacy.

The mechanistic basis of substrate recognition, the phosphorylation-independent interactions, and the functional contribution of alternative PAQosome assemblies remain limited. This review highlights PIH1D1 and RPAP3 as dynamic proteins at the crossroads of protein homeostasis, signaling pathways, and diseases.

Notably, small-molecule inhibitors of RUVBL1/2 ATPase activity, which have anti-PDAC activity in vivo, suppress KLF5-dependent transcription. These findings define a previously unrecognized mechanism of ATP hydrolysis-dependent transcriptional coactivation and highlight a potential therapeutic strategy for modulating aberrant lineage programs in cancer.

Mechanistically, the targeting of LIC1 by DAA markedly disrupts the interactions between LIC1 and stress-sensing effector RuvB-like AAA ATPase 1, which in turn elevates downstream GCN2-eIF2α-ATF4 axis-mediated integrated stress response, ultimately promoting autophagic cell death. Our findings define LIC1 as a novel therapeutic target for NSCLC and highlight the potential of DAA as a promising autophagy inducer for treatment of this disease.

This model guides lymphadenectomy decisions, reduces overtreatment, and enhances patient survival. Our work bridges molecular insights with clinical practice and provides a foundation for further research into the management of CC.

The simulations revealed key binding residues, including Ile56, Lys59, Leu87, Pro296, and Ile326 in RUVBL1 and Asp88, Ile89, Pro93, Phe354, and Ala92 in MAPK1 that mediate stable interactions with doxorubicin. This study presents a comprehensive analytical approach for investigating the interactions between doxorubicin and multiple protein targets, providing a reference framework for understanding the molecular mechanisms of anticancer drugs and for future analyses of similar data sets.

In vivo, CLNS1A overexpression accelerated tumor growth and reduced survival, whereas CLNS1A knockdown sensitized tumors to cisplatin, enhancing therapeutic efficacy. These findings suggest that CLNS1A is a potential biomarker and therapeutic target, and its inhibition offers a strategy to overcome drug resistance and limit the metastatic progression of lung cancer.

The nomogram could accurately predict shrinkage modes after NAT, and may help guide the individualized selection of breast conserving surgery candidates after NAT. RUVBL1-AS1 might be a promising therapeutic target of paclitaxel-based chemotherapy inHER2 + breast cancer.

In this study, utilizing a genome-wide CRISPR activation screen with olaparib, we identified ARL11 as a potential modulator of PARPi treatment response in BRCA-wild-type MDA-MB-231 cells...Clinical sample analysis reveals that the expression levels of ARL11 and RUVBL1/2 are significantly elevated in breast cancer patients compared to healthy controls. Collectively, our findings suggested that ARL11 and RUVBL1/2 may be promising therapeutic targets to sensitize breast cancer cells to PARPi therapy.