Results 171 to 180 of about 5,085 (284)

The C‐terminal truncated splicing variant of NK1R negatively modulates substance P‐stimulated NK1R signaling

open access: yesFEBS Open Bio, EarlyView.
The neurokinin 1 receptor exists as full‐length (NK1L) and C‐terminally truncated (NK1S) splice variants. We show that NK1S heterodimerizes with NK1L, impairing Gαq coupling and Ca2+ mobilization while enhancing β‐arrestin1 recruitment. NK1S suppresses substance P‐driven gene expression and cell migration, revealing NK1S as an endogenous biased ...
Lan Phuong Nguyen   +8 more
wiley   +1 more source

IGF2 knockout reduces but does not abolish osteosarcoma growth in vitro and in vivo

open access: yesFEBS Open Bio, EarlyView.
To test whether endogenous IGF2 promotes osteosarcoma growth, IGF2 was knocked out in Saos2 cells via CRISPR‐Cas9. KO cells showed reduced proliferation in vitro, and knockout xenografts in mice reached only ~25% of wild‐type tumor volume. Insulin‐like growth factor 2 (IGF2) is implicated in osteosarcoma, but direct functional evidence of its role is ...
Shun Yao, Marco Archetti
wiley   +1 more source

TRPML1 agonist ML‐SA5 attenuates pulmonary fibroblast activation by suppressing mTOR and restoring autophagic flux

open access: yesFEBS Open Bio, EarlyView.
TGF‐β1 stimulation downregulates lysosomal channel TRPML1 in pulmonary fibroblasts. The TRPML1 agonist ML‐SA5 suppressed fibroblast‐to‐myofibroblast activation and collagen production. Mechanistically, ML‐SA5 inhibited mTOR phosphorylation, restored autophagic flux, and its effects were enhanced by rapamycin (mTOR inhibitor) and reversed by MHY1485 ...
Jiatong Yao   +10 more
wiley   +1 more source

Chronobiology of Cancer: How Aging Fuels Oncogenesis at the Molecular Level

open access: yesAging and Cancer, EarlyView.
This graphical abstract illustrates the key biological pathways linking aging with cancer development and progression. In the upper left, cumulative exposure to ultraviolet radiation, toxins, and reactive oxygen species (ROS) causes DNA damage and genomic instability, whereas age‐related decline in repair mechanisms, such as ATM/ATR, BER, and NER ...
Anu Singh, Aroonima Misra, Sufian Zaheer
wiley   +1 more source

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