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DynaPURLS: Dynamic Refinement of Part-Aware Representations for Skeleton-Based Zero-Shot Action Recognition

arXiv:2512.11941v2 Announce Type: replace-cross Abstract: Zero-shot skeleton-based action recognition (ZS-SAR) is fundamentally constrained by prevailing approaches that rely on aligning skeleton features with static, class-level semantics. This coarse-grained alignment fails to bridge the domain shift between seen and unseen classes, thereby impeding the effective transfer of fine-grained visual knowledge. To address these limitations, we introduce \textbf{DynaPURLS}, a unified framework that establishes robust, multi-scale visual-semantic correspondences and dynamically refines them at inference time to enhance generalization. Our framework leverages a large language model to generate hierarchical textual descriptions that encompass both global movements and local body-part dynamics. Concurrently, an adaptive partitioning module produces fine-grained visual representations by semantically grouping skeleton joints. To fortify this fine-grained alignment against the train-test domain shift, DynaPURLS incorporates a dynamic refinement module. During inference, this module adapts textual features to the incoming visual stream via a lightweight learnable projection. This refinement process is stabilized by a confidence-aware, class-balanced memory bank, which mitigates error propagation from noisy pseudo-labels. Extensive experiments on three large-scale benchmark datasets, including NTU RGB+D 60/120 and PKU-MMD, demonstrate that DynaPURLS significantly outperforms prior art, setting new state-of-the-art records. The source code is made publicly available at https://github.com/Alchemist0754/DynaPURLS
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ANP32E drives lung adenocarcinoma progression via GSK3beta-mediated glycolytic reprogramming

Cell Death Dis. 2026 Apr 14. doi: 10.1038/s41419-026-08712-2. Online ahead of print.

ABSTRACT

Lung adenocarcinoma (LUAD), a leading cause of cancer mortality, involves incompletely understood epigenetic-metabolic crosstalk. We identified ANP32E as a key regulator through multi-omics (TCGA, scRNA-seq) and clinical analyses, finding its overexpression correlates with poor prognosis. Functionally, ANP32E knockdown suppressed proliferation, migration, and glycolysis in LUAD cells (A549/H1975) and attenuated xenograft growth, while overexpression promoted tumorigenesis. Mechanistically, ANP32E transcriptionally upregulates histone demethylase KDM3B, reducing repressive H3K9me2 marks at the EGFR promoter to enhance EGFR transcription. This activates PI3K/AKT signaling, inducing inhibitory GSK3Ξ² phosphorylation. Combined with ANP32E-mediated GSK3Ξ² suppression, this dual inactivation liberates oncogenic glycolysis. Crucially, KDM3B silencing or EGFR inhibition (Cetuximab) abrogated ANP32E-driven phenotypes. High-throughput screening identified Penta-O-galloyl-Ξ²-D-glucose (PGG) as an ANP32E-targeting compound, with molecular dynamics confirming binding. PGG dose-dependently inhibited the ANP32E/KDM3B/EGFR axis in vitro and suppressed tumor growth in vivo. Thus, ANP32E drives LUAD progression via KDM3B/EGFR-mediated GSK3Ξ² inactivation, representing a prognostic biomarker and therapeutic target validated by PGG.

PMID:41980942 | DOI:10.1038/s41419-026-08712-2

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