FOS (Fos Proto-Oncogene AP-1 Transcription Factor Subunit 2)

This case underscores the importance of molecular diagnostics in identifying rare genetic alterations and highlights the need for further research into targeted therapies for BRAF fusion-driven cancers. The discovery of this novel fusion expands our understanding of the molecular landscape of PTC and provides a foundation for future therapeutic development.

In a murine model of MDA-MB-231-induced osteolytic lesions, oral administration of 10 mg/kg SHP099 reduces osteoclasts and prevents the trabecular bone loss. Our study identifies SHP2 as a druggable target for inhibiting breast cancer-induced osteoclast differentiation, positioning the specific inhibitors of SHP2 as potential drugs developed to treat tumour-induced osteolysis in the future.

Glutamate probe analysis showed excessive glutamate release in the BLA, which was reduced by the chemical inhibition of the PrL-BLA circuit. This study identifies a PrLGlu-BLAGlu circuit controlling CIBP, offering new therapeutic insights.

When animals were challenged with TNFα after receiving minocycline, fewer c-Fos-positive cells were induced in the DVC and selectively in the rostral VLM. These findings highlight the spatial selectivity of cells in the brainstem to increased peripheral pro-inflammatory signaling, as well as the impact of resident microglia on autonomic circuitry responses.

Furthermore, gene reporter assay confirmed that TUDCA inhibited the transcriptional activity of NF-κB and AP1. These results suggest that TUDCA could exert a potent anti-metastatic activity in PMA-stimulated HT-1080 cells through modulation of MMPs, MAPKs signaling pathway, and NF-κB and AP1 transcription factors.

HQGZWWT significantly ameliorated CINP by increasing sciatic nerve conduction velocity, reducing oxidative stress and inflammatory responses, and inhibiting ferroptosis. Both HQGZWWT and its active monomeric component paeoniflorin protect neurons by suppressing ferroptosis, thereby exerting preventive and therapeutic effects against CINP. These findings provide new insights into the clinical treatment of CINP with HQGZWWT. Inhibiting ferroptosis by regulating the p38/c-FOS/NF-κB pathway through HQGZWWT and its primary monomeric component paeoniflorin represents a promising therapeutic strategy for preventing and treating oxaliplatin-induced CINP.

NPM1 acts as an oncogenic driver in colorectal cancer by activating the AKT/mTOR signaling pathway. Elevated NPM1 expression highlights its potential as a diagnostic, prognostic, and therapeutic biomarker in CRC.

Following enzalutamide (ENZ) treatment, GSTA1 expression is inhibited...TNFRSF13B induces c-Fos expression, forming a transcriptional complex with c-Jun, thereby regulating chromogranin A (CHGA) and promoting the neuroendocrine phenotype. Our study suggested that GSTA1 deficiency leads to elevated ROS levels and activation of TNFRSF13B and c-FOS, which subsequently transcriptionally regulate CHGA and ultimately drive neuroendocrine differentiation in PCa.

R. intestinalis may be a promising candidate for microbiota-based strategies against PD.

Our findings demonstrate that γ-Mag inhibits osteoclastogenesis and bone resorption by targeting the PI3K/AKT/NF-κB pathway, thereby blunting the C-FOS/NFATc1 transcriptional program. This study establishes γ-Mag as a promising natural lead compound for the treatment of postmenopausal osteoporosis.

These findings demonstrate the dose-dependent inhibitory effect of L-quebrachitol on osteoclastogenesis through the modulation of RANK-mediated signaling pathways and prevention of bone loss in an animal model. However, further exploration of the potential of L-quebrachitol as an effective approach for osteoporosis is required.

PAE200-Cd significantly increased the expression of cytochrome P450 family 1 subfamily A (CYP1A1) and downregulated the expression of metallothionein (MT) and cysteine-aspartic proteases-9 (Caspase-9). The optimal PAE dose for counteracting waterborne Cd-induced growth impairment and hepatic oxidative stress was 173.37-173.90 mg/kg for largemouth bass.