Results 151 to 160 of about 87,400 (287)

Targeting KDM3B Elicits Anti‐tumor Immunity by Alleviating SHP1–mediated STING Suppression in Triple–Negative Breast Cancer

open access: yesAdvanced Science, EarlyView.
P3FI–90 treatment targets KDM3B, reshapes the epigenetic landscape, and suppresses SHP1 expression, thereby activating STING–TBK1–IRF3–type I IFN signaling pathway. Consequently, CD8+ T cells are recruited to the tumor site and activated to produce IFN–γ and GZMB, leading to the killing of TNBC cells.
Xiaolong Wang   +8 more
wiley   +1 more source

PDIA6–SCD1 Axis Rewires Lipid Metabolism to Drive Gastric Cancer Progression

open access: yesAdvanced Science, EarlyView.
Protein disulfide isomerase A6 (PDIA6) is identified as an oncogenic driver in gastric cancer. PDIA6 directly binds and stabilizes SCD1 by limiting its ubiquitin–proteasome‐mediated degradation, thereby sustaining monounsaturated fatty acid (MUFA)‐enriched lipid homeostasis and lipid metabolic reprogramming.
Zhen Tian   +13 more
wiley   +1 more source

Single‐Cell RNA Editing Identifies T Cell ADAR1 as a Key Regulator of Immune Exhaustion and Anti‐PD‐1 Resistance in Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
Single‐cell RNA editing analysis identifies ADAR1 as a regulator of dysfunctional T cell states in colorectal cancer. Elevated ADAR1 activity promotes T cell exhaustion and impairs antitumor immunity partly through TGF‐β‐SMAD signaling, contributing to anti‐PD‐1 resistance and highlighting T cell ADAR1 as a potential therapeutic target and biomarker ...
Da Kang   +10 more
wiley   +1 more source

Targeting the HSPA8‐CMA‐ATP6V1A Axis Triggers Lysosomal Hyperacidification and Catastrophic Vacuolation in Prostate Cancer

open access: yesAdvanced Science, EarlyView.
Our experimental evidence supports a model in which ALO targets the HSPA8‐CMA‐ATP6V1A axis to induce lysosomal hyperacidification and initiate osmotic and lipidomic stress. These changes are associated with LMP and loss of lysosomal integrity in prostate cancer cells.
Bingzheng An   +8 more
wiley   +1 more source

Pericentrosomal Redistribution of the Endoplasmic Reticulum Ensures Organelle Symmetric Inheritance and Mitotic Progression

open access: yesAdvanced Science, EarlyView.
Upon mitotic entry, RTN4 relocalizes to the pericentrosomal region, forming a more tubular ER network around centrosomes. CDK1‐mediated phosphorylation of RTN4 increases its interaction with Rab11 GTPase, facilitating dynein‐dependent transport of RTN4 to the pericentrosomal region.
Xiangyu Xu   +9 more
wiley   +1 more source

Microscale characterisation of a manufacturing route for lentiviral vectors

open access: yes, 2015
Lentiviral vectors used in clinical trials are currently produced by transient transfection of adherent human embryonic kidney (HEK)293(T) cells. However, this approach is not scalable and for commercialisation the development of alternative strategies ...
Guy, HM
core  

Neuron‐Derived MIF Engages VCAM1 to Fuel a Self‐Amplifying CXCL8 Loop That Drives Perineural Invasion and Metastasis in Gastric Cancer

open access: yesAdvanced Science, EarlyView.
Neuron‐derived MIF binds VCAM1 on gastric cancer cells and activates ERK/STAT3 signaling, leading to CXCL8 transcription and secretion. Tumor‐derived CXCL8 subsequently stimulates neuronal CXCR2 to enhance MIF production, establishing a self‐amplifying MIF–VCAM1–CXCL8 positive‐feedback loop that promotes perineural invasion, tumor progression, and ...
Xunjun Li   +13 more
wiley   +1 more source

Walsh & Hoyt: Potential Therapeutic Targets in Lentivirus Infections

open access: yes, 2005
The lipid envelope renders the lentiviral virion exquisitely susceptible to environmental insults, such as inactivation by drying or physical agents such as heat, disinfectants (e.g., glutaraldehyde and hypochlorite), or even soap and water.
Lynn K. Gordon, MD
core  

RBM12 Maintains Glioma Stem Cells by Activating Amino Acid‐Dependent mTORC1 Signaling via SLC7A5 mRNA Stabilization

open access: yesAdvanced Science, EarlyView.
This study shows that in glioma stem cells (GSCs), RBM12 recruits ALKBH5 to remove m6A from SLC7A5 transcripts, thereby enhancing mRNA stability, which elevates large neutral amino acid (LNAA) levels and activates mTORC1, promoting GSC proliferation, self‐renewal, and tumor growth.
Hong Lei   +18 more
wiley   +1 more source

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