ROCK2 (Rho Associated Coiled-Coil Containing Protein Kinase 2)

These findings indicate that ROCK2 promotes EMT process and tumor progression in PC-3 cells. Targeting ROCK2 may represent a promising therapeutic strategy for androgen-independent prostate cancer.

GRc treatment effectively reduced ROCK2 expression and suppressed the secretion of inflammatory cytokines. These findings elucidate the pathological role of the ROCK2/NF-κBp65 signaling axis in SE and provide compelling evidence that GRc mitigates SE, at least in part, by directly binding to ROCK2 and inhibiting NF-κBp65 phosphorylation.

Targeted inhibition of ROCK2 by screening for J059-0149 increases the sensitivity of osteosarcoma to MPPa-PDT. In conclusion, our study establishes a novel mechanism to reverse MPPa-PDT resistance in osteosarcoma by targeting ROCK2-mediated autophagy, providing new targets and research ideas for the clinical treatment of osteosarcoma MPPa-PDT resistance.

In conclusion, the ROCK2/UBA52/Drp1 axis is a pivotal driver of Pemigatinib resistance in CCA cells. These results provide novel insights into Pemigatinib resistance in CCA cells, suggesting that ROCK2 is a promising therapeutic target for the treatment of CCA.

We also identified the underlying mechanism by which USP35 promotes ROCK2 expression through binding to gene amplified in squamous cell carcinoma 1 (GASC1) and diminishing GASC1 ubiquitination and degradation. Overall, our findings identified a critical function of USP35 in HCC proliferation, suggesting USP35 may be a potential therapeutic target for HCC oncogenicity.

Elevated ROCK2 protein levels could serve as a promising biomarker for ICIs-associated myocarditis. ROCK2 detection, combined with traditional markers, may enhance diagnostic accuracy. Further studies are warranted to explore ROCK2 inhibition as a potential therapeutic strategy for managing ICIs-associated myocarditis.

Furthermore, the results showed that the GAS and GA combination could elevate the level of S1PR1 and inhibit the expression of ROCK2 and the phosphorylation of NF-κB, which are key targets involved in sphingolipid pathways. Our study revealed that the combination of GAS and GA could suppress inflammation and apoptosis, which are highly correlated with sphingolipid signaling pathways, making it a potential candidate for the treatment of HTN.

Additionally, ROCK2 expression was elevated in the doxorubicin-resistant leukemia cell line HL-60/ADM when compared to their individual parent cells...Finally, we discovered that TRIM26, a specific E3 ligase, is capable of ubiquitylating ROCK2, and the upregulation of TRIM26 within HL-60/ADM cells resulted in heightened sensitivity to the drug and reduced resistance. Thus, our study presents a new strategy for overcoming drug resistance in AML through targeting ROCK2/AKT/MAPK signaling pathway.

The functional suppression of CCAT1 holds promise in enhancing the sensitivity to erlotinib by reversing EMT through the miR-181a-5p/ROCK2 signaling pathway. These findings provide valuable insights into the mechanisms underlying erlotinib resistance in CCA and the potential strategies for its treatment.

CIMT might overcome RhoA/ROCK2 signaling by upregulating the transcription of Sox2 to Fyn in the brain to induce maturation and differentiation of oligodendrocytes, thereby promoting myelin remodeling and improving motor function in rats with HCP.Impact. The pathway mediated by Sox2/Fyn could be a promising therapeutic target for HCP.

Co-immunoprecipitation confirmed the interaction between HUWE1 and ROCK2, and we examined the levels of ROCK2 ubiquitination following MG132 treatment. Inhibition of HUWE1 or overexpression of ROCK2 counteracted the sensitization effect of si-KDM4A on TMZ responsiveness in T98G cells. Our findings highlight KDM4A's role in enhancing TMZ resistance in glioma cells by modulating ROCK2 and HUWE1 transcription and expression through H3K9me3 and H3K36me3 removal.

Conclusion Knock-down of ROCK2 gene can significantly improve the cognitive function and inhibit the apoptosis of nerve cells of APP/PS1 mice. The mechanism may be related to promoting mitochondrial fusion and inhibiting its division.