SRC (SRC Proto-Oncogene)

KI95 represents the shortest active U94 fragment that preserves biological function, with critical residues likely located within the β-sheet region. These findings highlight the importance of structural integrity in U94 functionality and suggest KI95 as a potential therapeutic agent for cancer treatment.

We therefore conclude that IL-1β exerts significant effects on cell death and proliferation in leukaemic lymphoblasts through the PI3K/AKT/NF-κB pathway, with the study's findings indicating that an inflammatory environment may promote such lymphoblasts to acquire neoplastic characteristics. As such, the proteins involved in the effects evaluated in this work could be considered as potential therapeutic targets for the treatment of Acute Lymphoblastic Leukaemia (ALL).

An 18-month HFD successfully established a translational M. fascicularis model replicating key metabolic disorders (MASH, diabetes, cardiac hypertrophy). BAAT, CS/MDH1/H6PD, and SRC/MAPK14/EMD/ITGB1 were identified as mechanistic biomarkers for these conditions.

Compared with those of the Liuwei Dihuang Pills group, the expression level of p62, FcγRⅡB, SHP-1, and c-Src in the Liuwei Dihuang Pills + LV-shGPNMB group was significantly increased, and the level of LC3Ⅱ/LC3Ⅰ was significantly decreased. These results indicate that Liuwei Dihuang Pills can inhibit the FcγRⅡB/c-Src pathway by up-regulating the GPNMB expression, thereby increasing autophagy levels, enhancing neuroprotective ability, and alleviating Alzheimer's disease.

Our experimental results further confirmed that the compound possesses activities in inhibiting cell proliferation and promoting apoptosis. CAZ-AVI can correct cellular dysfunction and optimize immune responses, thereby providing new strategies and insights for the treatment of pneumonia.

In this study, OATP1B1 uptake function was found to be significantly suppressed by SRC proto-oncogene, non-receptor tyrosine kinase family kinase inhibitors, with SU6656 demonstrating the most potent inhibitory effect...Abrogation of Caveolin-1 exhibited no effect on the interaction between YES-1 and OATP1B1 but reduced the phosphorylation level of the transporter. Taken together, inhibitors of YES-1 may alter the uptake function of OATP1B1, potentially leading to drug-drug interactions related to post-translational modification.

This study demonstrates that although all four methods can isolate GELNs, UC is recommended for fundamental research due to its high protein yield, excellent stability, and potent in vitro anti-lung cancer activity. Furthermore, the anti-lung cancer activity of GELNs may be attributed to the regulation of GSK3B, PGR, and SRC by 10-Gingerol, Hexahydrocurcumin, and [6]-Dehydrogingerdione.

Molecular docking of 5 active ingredients with HIF1A and inosine-5'-monophosphate dehydrogenase 2 showed strong binding affinity. This study reveals the multicomponent, multi-target, and multi-pathway mechanism of GTD in the treatment of OA, providing a foundation for further experimental validation and suggesting new research directions.

FN1 and C3 dysregulation directly contributes to OLP pathogenesis via immune-stromal crosstalk. Core proteins such as FN1 and C3 may serve as promising non-invasive diagnostic biomarkers and therapeutic targets, warranting further validation.

Pae overcomes CRPC resistance by targeting SRC-mediated pathways, presenting a promising therapeutic strategy. Our findings underscore the utility of network pharmacology-guided drug discovery and advocate for further clinical exploration of Pae in precision oncology.

This study comprehensively illustrates the potential targets and molecular mechanism of Lut in alleviating the GPS-induced increase in vascular endothelial permeability. The CD44 pathway and Lut may be an effective target and antibiotic alternative, respectively, to prevent the increased vascular endothelial permeability caused by GPS.

RIV exerts a protective effect against SU-induced cardiomyocyte injury by inhibiting the MAPK signaling pathway. RIV therapy may be a promising strategy to inhibit SU's cardiotoxicity in cancer patients.