Disease relevance of Psmd7

• Animals homozygous for proviral integrations were derived for all strains with the exception of Mov 24, where the provirus is inserted on the Y chromosome, and Mov 34 [1].
• Retroviruses and insertional mutagenesis in mice: proviral integration at the Mov 34 locus leads to early embryonic death [1].
• Mov34 protein from mouse brain interacts with the 3' noncoding region of Japanese encephalitis virus [2].
• Competition experiments using the RNA extracted from JEV virions established that the 36-kDa Mov34 protein indeed bound to the JEV genome [2].
• Overlapping phage lambda clones containing the entire Mov-34 gene have been isolated [3].

High impact information on Psmd7

• Similar to the previously derived Mov 13 mutation, proviral integration at the Mov 34 locus interferes with the expression of the adjacent gene [1].
• Embryos homozygous at the Mov 34 locus develop normally to the blastocyst stage and die shortly after implantation, indicating that virus integration resulted in a recessive lethal mutation [1].
• Screening of the neonatal mouse brain cDNA library with the JEV 3'-SL structure RNA identified a 36-kDa Mov34 protein interacting with it [2].
• The cDNA contains an open reading frame that encodes a 36.6 kDA protein 96% identical to mouse Mov-34 and 67% identical to its Drosophila melanogaster homolog [4].
• The 5' flanking region of the Mov-34 gene contains neither "TATA" nor "CAAT" box sequences, and 5' end mapping by primer extension and ribonuclease protection reveal multiple transcription initiation sites [3].

Biological context of Psmd7

• The Mov-34 gene spans just over 8 kb and contains seven exons [3].

Other interactions of Psmd7

• The Mov-34 mutation is a recessive embryonic lethal mutation caused by experimental introduction of a recombinant Moloney murine leukemia provirus into the mouse germline [3].

References