Vestigial Like 4 (Drosophila) Proteins (VGLL4)

Human Vestigial Like 4 (Drosophila) (VGLL4) interaction partners

1. Results identify VGLL4 as a direct target gene of miR (show MLXIP Proteins)-130b in Bladder cancer (BCa (show BLNK Proteins)) cells. Its suppression is crucial for miR (show MLXIP Proteins)-130b-induced BCa (show BLNK Proteins) cell proliferation, migration and invasion.

2. The Vgll4 is phosphorylated in vitro and in vivo by cyclin-dependent kinase 1 (CDK1 (show CDK1 Proteins)) during antimitotic drug-induced mitotic arrest and also in normal mitosis.

3. VGLL4 - novel candidate genes validated in a large case-control sample of schizophrenia.

4. The expression level of VGLL4 protein was down-regulated in gastric cancer tissues.VGLL4 inhibits epithelial-mesenchymal transition in part through suppressing Wnt (show WNT2 Proteins)-beta-catenin (show CTNNB1 Proteins) signaling pathway in gastric cancer.

5. our study suggested that downregulation of VGLL4 was very important in the progression of ESCC, and restoring the function of VGLL4 might be a promising therapeutic strategy for ESCC.

6. VGLL4 directly competes with YAP (show YAP1 Proteins) in binding to TEADs and executes its growth-inhibitory function through two TDU (show VGLL1 Proteins) domains.

7. rs2616551 in VGLL4 was found to be nominally associated with anorexia nervosa.

8. This study introduces a novel gain-of-function approach for studying hESC maintenance and presents VGLL4 as a previously undescribed regulator of this process.

9. Loss of VGLL4 expression is associated with gastric cancer.

10. Vgl-4 may play a role in the apoptotic pathways by regulating translocation of IAPs between different cell compartments.

Mouse (Murine) Vestigial Like 4 (Drosophila) (VGLL4) interaction partners

1. VGLL4 inhibits cardiomyocyte proliferation by inhibiting TEAD1 (show TEAD1 Proteins)-YAP (show YAP1 Proteins) interaction and by targeting TEAD1 (show TEAD1 Proteins) for degradation.

2. Vgl-4 modulates the activity of TEF-1 (show TEAD1 Proteins) factors and counteracts alpha1-adrenergic activation of gene expression in cardiac myocytes