Results 241 to 250 of about 375,320 (335)

Human Atlas of Tooth Decay Progression: Identification of Cellular Mechanisms Driving the Switch from Dental Pulp Repair Toward Irreversible Pulpitis

open access: yesAdvanced Science, EarlyView.
Tooth decay progression transforms the dental pulp response from repair to fibrosis. At early stages, stromal cells reprogram to repair the extra cellular matrix (ECM), blood vessels, and nerves, remodel and grow, keeping repair possible. In advanced decay, hypoxia, and vessel regression, in complement with an immune switch, fuel nerve degeneration and
Hoang Thai Ha   +12 more
wiley   +1 more source

Ubc9‐Mediated SUMOylation of RPL3, an Unappreciated Mechanism against Hepatocyte Senescence by Repressing the DHX9‐p16 Axis

open access: yesAdvanced Science, EarlyView.
Liver aging is characterized by a decline in the expression of the SUMO‐conjugating enzyme Ubc9, resulting in reduced SUMOylation levels in hepatocytes, particularly in the case of ribosomal protein RPL3. Disruption of RPL3 SUMOylation increases its nuclear translocation. Interestingly, ribosome‐free RPL3 facilitates the recruitment of helicase DHX9 to
Hao Xie   +22 more
wiley   +1 more source

Site‐Specific Mitochondrial RNA N1‐Methyladenosine Demethylation via an Engineered MTS‐PUF‐ALKBH3 Fusion Protein

open access: yesAdvanced Science, EarlyView.
A CRISPR‐free mitochondrial RNA m1A demethylation (MRD) editor combining MTS, PUF proteins, and ALKBH3 enables precise m1A removal from mitochondrial mRNA and tRNA, which influences mitochondrial protein levels, cellular proliferation, ATP production, and mitochondrial respiration. Subsequently, in vivo demethylation of the m1A modification is achieved
Xiangrui Li   +13 more
wiley   +1 more source

Pharmacological CLK inhibition disrupts SR protein function and RNA splicing blocking cell growth and migration in TNBC. [PDF]

open access: yesBreast Cancer Res
Liu N   +8 more
europepmc   +1 more source

CDK4/6 Inhibitor Priming Enhances PD‐1 Blockade via Sellhi Neutrophil‐Induced Stat5a+ Progenitor Exhausted CD8+ T Cell

open access: yesAdvanced Science, EarlyView.
Activated tumor‐intrinsic cyclin D1‐CDK4/6 signaling attenuates lymphocyte infiltration, and consequently, and immunotherapy resistance in HNSCC. It is discovered that brief CDK4/6i priming before anti‐PD‐1 results in enhanced durability of ICB response durability through Stat5a+ progenitor exhausted CD8+ T cells induced by IL15‐secreted Sell(hi ...
Yu Zhang   +13 more
wiley   +1 more source

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