@article{mbs:/content/journal/jgv/10.1099/vir.0.82744-0, author = "Okada, Tsukasa and Takagi, Michihiro and Murata, Shiro and Onuma, Misao and Ohashi, Kazuhiko", title = "Identification and characterization of a novel spliced form of the meq transcript in lymphoblastoid cell lines derived from Marek's disease tumours", journal= "Journal of General Virology", year = "2007", volume = "88", number = "8", pages = "2111-2120", doi = "https://doi.org/10.1099/vir.0.82744-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.82744-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", abstract = "In tumour cell lines established from Marek's disease (MD) lymphomas L-meq is consistently expressed. It contains a 180 bp insertion encoding additional copies of the proline-rich repeat in the meq open reading frame and its product may contribute to the maintenance of MD virus (MDV) latency. In this study, we identified a novel spliced form of the meq transcript in MD-derived lymphoblastoid cell lines and in MDV-infected cells. This transcript, termed Δmeq, encodes an N-terminal 98 aa of the Meq protein and lacks part of the basic leucine zipper (bZIP) and transactivation domains. In MD cell lines, transcription of L-meq was significantly downregulated, while that of the Δmeq transcript was upregulated during apoptosis. These observations were also confirmed at the protein expression level. Reporter assays using meq- and interleukin-2 (IL-2)-promoter-driven luciferase vectors revealed that ΔMeq suppressed transactivation by L-Meq or Meq in a dose-dependent manner. Immunoprecipitation confirmed that ΔMeq was associated with L-Meq or Meq physically. These results suggest that ΔMeq could be involved in apoptosis in MD cell lines as it works as a negative regulator of L-Meq and Meq by direct interaction.", }