SRRM4 (Serine/Arginine Repetitive Matrix 4)

Moreover, site-directed mutation of the rs11067228 non-risk G to the risk A allele enabled binding of the transcription factor SOX4, activating candidate target gene expression. Taken together, our findings indicated that the rs11067228-associated enhancer modulates expression of SRRM4 via allele-specific long-range chromatin interactions, thereby governing PCa drug resistance and neuroendocrine differentiation.

SRRM4 KO is a newly defined factor of UE7T-9 cell penetrating into DCB. SRRM4 KO UE7T-9 cells may be used to analyze hematological diseases such as myelodysplastic neoplasms.

Our findings highlight the potential clinical utility of C1orf112 as a diagnostic and prognostic biomarker in EC, and provide new insights into its regulatory molecular network. This study proposes a conceptual framework for understanding EC pathogenesis and guiding the development of targeted therapies. Nonetheless, further prospective clinical studies and mechanistic investigations are warranted to validate these findings.

It also explores the potential for therapeutic interventions, including pharmacological modulation, on microexon splicing and splicing regulators like SRRM3 and SRRM4, offering perspectives on targeting diseases related to microexon misregulation. More research is needed to better understand similarities and differences between microexon functions across tissues, pathologies, and species.

Similar homeostatic cross-regulation is often observed across paralogous RNA binding proteins. Here we find this concept likewise applies across evolutionarily unrelated but functionally and physically coupled spliceosomal components.

Finally, we show that PRPF40A knockdown causes an increase in productive splicing of its spliceosomal binding partner Luc7l by skipping of a small "poison exon." Similar homeostatic cross-regulation is often observed across paralogous RNA binding proteins. Here we find this concept likewise applies across evolutionarily unrelated but functionally and physically coupled spliceosomal components.

Moreover, the higher risk score of the prognostic risk model predicted poor overall survival in TNBC patients, and nomogram and calibration curve confirmed the potent prediction ability of this model. To sum up, six TIL-related biomarkers (SLITRK3, PCDHGB3, NELL2, SRRM4, ASIC2 and B4GALNT2) were identified and used for the construction of the prognostic risk model, which might provide novel insight for the clinical decisions.

It can be used for diagnosis, classification and targeted treatment strategies comparable to current standards in precision medicine. It provides a rationale for elucidation of the role of RNA editing genes and their clinical significance in colon cancer as prognostic markers.

This study nominates SMARCA4 as a key regulator of the NE state plasticity and defines a novel therapeutic strategy for SCLC.

One of these compounds rescues the splicing of several analyzed microexons in the cerebral cortex of an autism mouse model haploinsufficient for Srrm4, a major activator of brain microexons. We thus describe a broadly applicable high-throughput screening system for identifying candidate splicing therapeutics, and a resource of small molecule modulators of microexons with potential for further development in correcting aberrant splicing patterns linked to human disorders and disease.

Pharmacologic inhibition of OC2 suppresses lineage plasticity reprogramming induced by the AR signaling inhibitor enzalutamide. These results demonstrate that OC2 activation promotes a range of drug resistance mechanisms associated with treatment-emergent lineage variation in PC and support enhanced efforts to therapeutically target OC2 as a means of suppressing treatment-resistant disease.

Collectively, our findings identify SRRM4 as a regulator of brain metastasis colonization, and a potential therapeutic target in breast cancer.