Epithelial Splicing Regulatory Protein 1 Proteins (ESRP1)

Xenopus laevis Epithelial Splicing Regulatory Protein 1 (ESRP1) interaction partners

1. Ptbp1 abundance is controlled in Xenopus epidermis via alternate splicing: skipping of exon 11 is the default splicing pattern, but Esrp1 stimulates ptbp1 expression by favoring the inclusion of exon 11 up to a level that is limited by Ptbp1 itself.

Human Epithelial Splicing Regulatory Protein 1 (ESRP1) interaction partners

1. Low ESRP1 expression is associated with Invasion and Metastasis of Lung Adenocarcinoma.

2. study defines a Snail-ESRP1 cancer axis that is crucial for human lung carcinogenesis, with implications for new intervention strategies and translational opportunities

3. Results show that ESRP1 regulates CD44 splice isoform switching and EMT in ovarian cancer cells.

4. In humans, ESRP1 is downregulated in inflamed biopsies from inflammatory bowel disease patients. ESRP1 loss is an adverse prognostic factor in colorectal cancer. Furthermore, generation of ESRP1-dependent GPR137 isoforms is altered in colorectal cancer and expression of a specific GPR137 isoform predicts colorectal cancer patient survival.

5. Our study supports the role of ESRP1 as tumor suppressor and strongly suggests that ESRPs are candidate markers for early detection, diagnosis, and prognosis of CRC.

6. High ESRP1 expression may thus stimulate growth of cancer epithelial cells and promote colorectal cancer progression.

7. Results showed that the expression patterns of these genes were indicative of the onset of EMT in in-vitro models, but not in tissue samples. However, the ratio between ESRP1 or ESRP2 and RBFOX2 significantly decreased during EMT and positively correlated with the EMT-specific phenotype in cell models. Low ESRP1/RBFOX2 ratio value was associated with a higher risk of metastasis in early breast cancer patients.

8. Downregulated ESRP1 by sirna resulted in an isoform switching from CD44v to CD44s, which modulated epithelial-mesenchymal transition.

9. ALK oncogenic activity is involved in the regulation of an epithelial mesenchymal transition phenotype in a subset of non-small cell lung carcinomas by repression of the epithelial splicing regulatory protein 1.

10. ZEB1-induced epithelial-to-mesenchymal transition and associated molecular changes in ESRP1 and CD44 contribute to early pathogenesis and metastatic potential in established lung cancer

11. The molecular mechanisms by which ESRP1 and ESPR2 exert positive as well as negative effects on cancer progression have been summarized. (Review)

12. Recombinant human ESRP1-RRM3 was subjected to biomolecular NMR and its chemical shifts and structural coordinates were determined and deposited in the BioMagResBank and Protein Data Bank respectively. Its interaction with RBPMS2 was mapped.

13. Altered Expression and Splicing of ESRP1 in Malignant Melanoma Correlates with Epithelial-Mesenchymal Status and Tumor-Associated Immune Cytolytic Activity.

14. Data show that both rab G-Protein RAB25 and RNA-binding protein ESRP1 were suppressed by transcription factor ZEB1, which was in turn regulated via epigenetic mechanisms.

15. MCL1 with the deletion of 801G and 802A sites could not be correctly spliced by ESRP1 and no significant difference was seen in the expressions of isoform 1 and 3 in mutant MCL1

16. ESRP1 and ESRP2 suppress cancer cell motility via different mechanisms.

17. Results show that ESRP1 regulates the expression pattern of FGFR-2 isoforms, attenuates cell growth, migration, invasion and metastasis, and is a favorable prognostic factor in pancreatic ductal adenocarcinoma.

18. Data suggest that alternative splicing in ESRP1 transcripts in somatotroph adenomas is essential in epithelial-mesenchymal transition progression and in response to somatostatin analog antineoplastic treatment.

19. ESRP1 and PNN modulate alternative splicing of a specific subset of target genes, but not general splicing events, in HCET cells to maintain or enhance epithelial characteristics.

20. the transcription repressor Snail binds to E-boxes in the ESRP1 promoter, causing repression of the ESRP1 gene.

Mouse (Murine) Epithelial Splicing Regulatory Protein 1 (ESRP1) interaction partners

1. bleomycin (BLM) inhibited the expression of epithelial splicing regulatory protein 1 (ESRP1), resulting in enhanced alternative splicing of FGFR2 to the mesenchymal isoform IIIc. BLM-induced lung fibrosis was also associated with the activation of TGF-b/Smad signaling.

2. Study documented the expression of Esrp1 during gonadal development and in differentiating cells of the adult gonads: in mouse fetal gonads, Esrp1 mRNA was specifically detected in germ cells of either sex and absent from somatic gonadal cells. Esrp1 mRNA was present in a gonocyte-enriched cell fraction and in all germ cells examined in postnatal testis.

3. Findings reveal that Esrp1-regulated splicing in ureteric epithelial cells plays an important role in renal development. Defects in Esrp1 KO kidneys likely reflect reduced and/or absent ureteric branching, leading to decreased nephron induction secondary to incorrect Fgfr2 splicing and other splicing alterations

4. implicate mutations in Epithelial Splicing-Regulatory Protein 1 as a cause of SNHL and demonstrate the complex interplay between alternative splicing

5. Loss of both Esrp1 and its paralog Esrp2 results in widespread developmental defects with broad implications to human disease.

6. The expression levels of three splicing factors, ESRP1, PTB and SF2/ASF, are significantly altered during cardiac hypertrophy in mice.

7. ESRP1 thus acts as a physiological regulator of the finely-tuned balance between self-renewal and commitment to a restricted developmental fate.

8. Esrp1 could play an important role in the morphological changes underlying embryogenesis of the placenta and embryo.

9. Alternative splicing of CD44 mRNA by ESRP1 enhances lung colonization of metastatic cancer cell.

10. Epithelial splicing regulatory proteins 1/2 (ESRP1/2) are epithelial cell-type-specific regulators of FGFR2 splicing.