MAPRE1

CLASP2 decreased the sensitivity of BC to CDDP in vivo. Our results imply that CLASP2 contributes to tumorigenesis and cisplatin resistance in BC via targeting MAPRE1, thereby promoting BC progression and providing a new therapeutic target for BC treatment.

Nocodazole treatment, a microtubule-depolymerizing agent, reduces Rac1 activity, restoring cranial NC cell morphology, actin distribution, and overall migration. Our findings highlight Gαi2 crucial role in cranial NC cell migration by modulating microtubule dynamics through EB1 and Rac1 activity.

Using high-throughput transcriptomic data, we identified hub LRGs and highlighted the role of lactate-mediated lactylation in UC. MSN and MAPRE1 were confirmed to be upregulated in an inflammatory environment, underscoring their potential for personalized UC diagnosis and treatment.

These cases demonstrate that KMT2A rearrangements can be found in primary CTCLs rather than solely acute leukemias, illustrating the importance of correlating molecular findings with clinical and histologic features in diagnosis. Additionally, this finding suggests that the subset of CTCLs driven by aberrancy of the KMT2A pathway may be responsive to therapy with hypomethylating agents or menin inhibitors, as seen in acute leukemias.

In addition, TRPC1 could promote the development of liver cancer by up-regulating the expression of ABI2, MAPRE1, YEATS2, MTA3, TMEM237, MTMR2, CCDC6, AC069544.2, and NCBP2 genes. These results illustrate that TRPC1 is very valuable in the study of liver cancer.

Together we present the method for tubulin tyrosination profiling in living cells. Our results show that detyrosination-tyrosination is not restricted to α-tubulins with coded C-terminal tyrosine and is thus involved in fine-tuning of the  tubulin  and non-tubulin proteins during neuronal differentiation.

Restoration of MAPKE1 levels reversed miR-526b-3p effects on the glioma process and resistance to ADR. These results suggest that miR-526b-3p acts as a diagnostic marker in glioma development and therapeutic target of the glioma resistance to ADR.

Among these proteins, the levels of 4 mRNAs including MAPRE1, CCT7, TKT, and HSPA8 in CRC tissues showed a statistically significant increase compared to noncancerous tissues from patients using the NCBI microarray datasets. Our results indicate that the method shown here is useful in identifying arginine-methylated proteins, and significance of arginine modification in the proteins identified here should be further identified during CRC development.

To conclude, this work clarified the carcinogenic impact of circSOX13-miR-3194-3p-MAPRE1 axis on NSCLC and DDP resistance. CircSOX13 can be a potential diagnostic marker and therapeutic target for NSCLC, thus providing a new insight for clinically reversing its acquired resistance.

AIM2 can play a driver role in epithelial carcinogenesis by linking cytokine-STAT3 signalling, innate immunity and epithelial cell migration, independent of inflammasome activation.