Results 141 to 150 of about 34,272 (251)

Chemoproteomic Identification of AKT2 as a Paclitaxel‐Binding Protein via C─C Bond‐Linked Probe PTX‐4 in Paclitaxel‐Resistant Breast Cancer

open access: yesAdvanced Science, EarlyView.
ABSTRACT Breast cancer remains one of the most prevalent malignancies among women, and taxane‐based chemotherapies such as paclitaxel and docetaxel are central to standard treatment regimens. However, drug resistance in breast cancer limits therapeutic efficacy and contributes to recurrence and metastasis.
Kai Wang   +7 more
wiley   +1 more source

Mitigating Cancer Therapy–Related Cognitive Impairment by Targeted Activation of Undruggable Phosphatase

open access: yesAdvanced Science, EarlyView.
An RVG‑engineered exosomal saRNA delivery system (RVG‑EVs‑saPtpro) effectively targets and activates hippocampal PTPRO, functioning as a “molecular brake” to alleviate cancer therapy‑related cognitive impairment (CTRCI) by enhancing neuronal survival, neurogenesis, and synaptic plasticity.
Zhimeng Yao   +18 more
wiley   +1 more source

HNRNPU K181 Lactylation Drives Cervical Cancer Growth by Upregulating PHGDH and Reprogramming Serine Metabolism

open access: yesAdvanced Science, EarlyView.
Lactate in cervical cancer induces HNRNPU K181 lactylation, opposed by NAA50‐mediated acetylation and suppressed by Pazopanib. This lactylation enhances HNRNPU binding to PHGDH pre‐mRNA exon 1, maintaining exon 1‐containing transcripts and mRNA stability, thereby activating serine metabolism.
Chang Zhang   +6 more
wiley   +1 more source

TSPYL5 Promotes Triple‐Negative Breast Cancer Metastasis by Antagonizing USP10‐Mediated PTEN Stabilization to Unleash a ZEB1‐Dependent EMT Program

open access: yesAdvanced Science, EarlyView.
The hyperactivation of PI3K/AKT signaling in PTEN wild‐type triple‐negative breast cancer represents a clinical paradox. We delineate a novel post‐translational regulatory axis wherein the oncogene TSPYL5 competitively antagonizes the deubiquitinase USP10.
Jiaying Shi   +8 more
wiley   +1 more source

Mitochondrial Dysfunction Unravels the Potential Molecular Link Between Night Shift Work‐Related Circadian Disruption and Elevated Blood Pressure in Human and Mouse Models

open access: yesAdvanced Science, EarlyView.
This diagram illustrates that night shift work disrupts circadian clock genes (like CLOCK, BMAL1) in both humans and mice. This disruption leads to mitochondrial dysfunction (imbalanced fusion/fission proteins) and increased oxidative stress, which is identified as the primary mechanism ultimately causing elevated blood pressure.
Zhaoqiang Jiang   +16 more
wiley   +1 more source

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