Acts as a thyroid-hormone receptor antagonist. The v-ErbA oncogene cooperates with v-ErbB and other primarily sarcoma-inducing oncogenes in transformation of erythroblasts. It is non transforming by itself and cannot induce self-renewal of erythroblasts. Instead it blocks the residual capacity of the v-ErbB cells to differentiate terminally. Late-budding domains (L domains) are short sequence motifs essential for viral particle budding. They recruit proteins of the host ESCRT machinery (Endosomal Sorting Complex Required for Transport) or ESCRT-associated proteins. Gag contains one L domain: a PPXY motif which potentially interacts with the WW domain 3 of NEDD4 E3 ubiquitin ligase (Potential). Specific enzymatic cleavages in vivo yield mature proteins. THRA, the cellular counterpart of v-ErbA, is a thyroid hormone receptor alpha. This protein is synthesized as a Gag-vErbA-vErbB polyprotein. Belongs to the nuclear hormone receptor family. NR1 subfamily.