Results 191 to 200 of about 746,766 (283)

Atrophic Skeletal Muscle‐Derived Extracellular Vesicles Transfer miR‐125a‐5p to Inhibit Bone Formation in Osteoporosis during Aging

open access: yesAdvanced Science, EarlyView.
A muscle‐bone endocrine pathway in aging is revealed in which extracellular vesicles released from atrophic skeletal muscle (Aged‐SKM‐EVs) inhibit bone formation. These EVs deliver miR‐125a‐5p to osteoblasts, thereby suppressing the SIRT7‐Sp7 signaling axis and osteogenic differentiation.
Xiaoyan Shao   +22 more
wiley   +1 more source

Cuproptosis and Disulfidptosis Converge to Empower PD‐L1 Checkpoint Therapy via Cadict‐Induced PD‐L1 Translation

open access: yesAdvanced Science, EarlyView.
This study introduces Cadict, an EGFR‐targeted nanodrug that co‐delivers cuproptosis and disulfidptosis inducers to overcome immune resistance. Cadict synergistically enhances tumor cytotoxicity and sensitizes cancers to ICIs by upregulating PD‐L1 via an Eif5b‐dependent translation mechanism, fostering a potent antitumor immune response and ...
Shaoqing Huang   +12 more
wiley   +1 more source

Assigning cancer stage to patients using administrative claims data: an example for colon and rectal cancers. [PDF]

open access: yesBMC Health Serv Res
Smith RA   +8 more
europepmc   +1 more source

Lipid‐Facilitated Opening of the ADAM10 Sheddase Revealed by Enhanced Sampling Simulations

open access: yesAdvanced Science, EarlyView.
Phosphatidylserine acts as a lipid trigger to enhance activation of the sheddase ADAM10. By integrating fluorescence spectroscopy assays with enhanced sampling molecular dynamics simulations, this study shows that phosphatidylserine promotes ADAM10 catalytic activity along with expansion of its extracellular domains, enhancing accessibility to scaffold
Adrien Schahl   +7 more
wiley   +1 more source

Connexin43 Deficiency Leads to Ventricular Arrhythmias by Reprogramming Proline Metabolism

open access: yesAdvanced Science, EarlyView.
The study demonstrated that connexin43 (Cx43) knockout caused arrhythmic phenotype and decreased proline content in vitro and in vivo. Mechanistically, Cx43 interacts with the amino acid transporter SNAT2 (sodium‐dependent neutral amino acid transporter), and its deficiency disrupts proline transport and metabolism.
Hangying Ying   +8 more
wiley   +1 more source

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