Disease relevance of CASC3

• Association of the breast cancer protein MLN51 with the exon junction complex via its speckle localizer and RNA binding module [1].
• Human breast carcinomas show MLN51 overexpression in malignant epithelial cells [2].
• Metastatic Lymph Node 51 (MLN51) cDNA was isolated by differential screening of a human breast cancer metastasis cDNA library [2].

High impact information on CASC3

• Most interesting, we have identified a region within MLN51 sufficient to bind RNA, to interact with Magoh and spliced mRNA, and to address the protein to nuclear speckles [1].
• Its fly homolog, named barentsz, as well as the proteins mago nashi and tsunagi have been shown to be required for proper oskar mRNA localization to the posterior pole of the oocyte [1].
• An additional eIF4AIII-specific motif forms part of the binding site for MLN51, another EJC core component [3].
• In MS2 tethering assays Acinus stimulated gene expression at the RNA level, while MLN51, another EJC factor, stimulated mRNA translational efficiency [4].
• Anti-GM-CSF neutralizing antibody blocked the MLN51 expression even though the FLSs were cultured in the presence of SF [5].

Anatomical context of CASC3

• MLN51 expression was significantly enhanced in the FLSs when the growth-retarded FLSs were treated with granulocyte-macrophage colony-stimulating factor (GM-CSF) or synovial fluid (SF) [5].

Regulatory relationships of CASC3

• However, growth-retarded RA FLSs passaged in vitro expressed small quantities of MLN51 [5].

Other interactions of CASC3

• We show that the MLN51-dependent stimulation increases both the affinity of eIF4AIII for ATP and the rate of enzyme turnover; the K(M) is decreased by an order of magnitude and k(cat) increases 30 fold [6].
• We found that the MLN51 (metastatic lymph node 51) gene, identified in breast cancer, is remarkably upregulated in the hyperactive RA FLSs [5].

References