Results 181 to 190 of about 101,843 (265)

Mechanical Interactions Impact the Functions of Immune Cells and Their Application in Immunoengineering

open access: yesAdvanced Therapeutics, EarlyView.
This review covers the mechanical forces experienced by immune cells through cell–cell and cell–extracellular matrix interactions and how these forces influence their receptors and functions. These relationships between forces and cellular functions can be exploited using engineering techniques to modify the physical properties of materials for novel ...
Yu‐Chang Chen   +2 more
wiley   +1 more source

Rewiring Neuroimmunity: Nanoplatform Innovations for CNS Disease Therapy

open access: yesAdvanced Therapeutics, EarlyView.
This review explores emerging nanoplatform strategies designed to modulate neuroimmune responses for treating central nervous system (CNS) disorders. It examines structural and microenvironmental barriers, advances in multifunctional and targeted nanotechnologies, and highlights clinical progress and translational challenges, offering insights into the
Muhammad Usman Akbar   +7 more
wiley   +1 more source

Loss of NR2F6 Protects from Salmonella Typhimurium Infection

open access: yesAdvanced Science, EarlyView.
Loss of nuclear receptor NR2F6 reduces tissue‐resident macrophage populations. Nr2f6‐deficient mice are protected from weight loss and bacterial load during infection with Salmonella Typhimurium. Pro‐inflammatory cytokines and iron levels are altered in infected Nr2f6‐deficient mice.
Johannes Woelk   +8 more
wiley   +1 more source

Fibronectin Fibers Progressively Lose Their Tension in Invasive Human Breast Carcinoma while Being Tensed in DCIS and Healthy Breast Tissue

open access: yesAdvanced Science, EarlyView.
Extracellular matrix remodeling is crucial in cancer progression. Using a peptide to probe the tension of ECM fibers, it was found that Fibronectin fibers gradually lose tension as human breast carcinoma progresses, while their tension is maintained in ductal carcinoma in situ (DCIS), the non‐invasive precursor of breast cancer. This loss of tension is
Arnaud Miéville   +6 more
wiley   +1 more source

RONIN/HCF1‐TFEB Axis Protects Against D‐Galactose‐Induced Cochlear Hair Cell Senescence Through Autophagy Activation

open access: yesAdvanced Science, EarlyView.
D‐galactose (D‐gal) induced inner ear hair cell senescence by inhibiting TFEB transcription. RONIN/HCF1 promotes TFEB transcription to prevent cochlear HCs from D‐gal‐induced senescence through autophagy activation. Abstract Age‐related hearing loss is characterized by senescent inner ear hair cells (HCs) and reduced autophagy.
Yongjie Wei   +18 more
wiley   +1 more source

NOX2 Contributes to High‐Frequency Outer Hair Cell Vulnerability in the Cochlea

open access: yesAdvanced Science, EarlyView.
This study first identifies NOX2 as a differentially expressed gene related to oxidative damage in the apical and basal turns through single‐cell RNA sequencing. NOX2 gene knockout mitigates OHCs damage caused by neomycin and noise and enhances Nrf2 expression and nuclear translocation.
Meihao Qi   +16 more
wiley   +1 more source

AAVR Expression is Essential for AAV Vector Transduction in Sensory Hair Cells

open access: yesAdvanced Science, EarlyView.
Decreased sensitivity to AAV vector transduction in the outer hair cells (OHCs) of adult mice is primarily attributed to reduction of AAVR (Kiaa0319l; Au040320). Knockout of AAVR reduces AAV vector transduction efficiency in both inner hair cells (IHCs) and OHCs in neonatal mice.
Fan Wu   +8 more
wiley   +1 more source

Topoisomerase I Inhibition in ETV4‐overexpressed Non‐Small Cell Lung Cancer Promotes Replication and Transcription Mediated R‐Loop Accumulation and DNA Damage

open access: yesAdvanced Science, EarlyView.
The oncogenic ETS factor ETV4 exerts a pleiotropic control over DNA replication both in a transcription‐dependent and ‐independent fashion in NSCLC cells. High‐ETV4 expression leads to R‐loop formation and DNA damage in response to TOP1 inhibition.
Jiaxi Zhang   +14 more
wiley   +1 more source

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