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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Transcriptional profiling of HERV-K(HML-2) in amyotrophic lateral sclerosis and potential implications for expression of HML-2 proteins

Fig. 1

Depiction of a canonical HERV-K(HML-2) type 2 provirus and RT-PCR amplicons. Proviral 5′ and 3′ Long Terminal Repeats (LTR), gag, pro, pol and env genes, splice donor (SD) and splice acceptor (SA) sites, splicing patterns of full-length (f-l) proviral transcripts, and three different RT-PCR amplicons for identification of transcribed HML-2 loci within the gag and the env gene regions (gag amplicon, env600nt amplicon) are indicated, with the rec/np9 amplicon spanning an intron within env. Location of PCR primers for amplifcation of rec/np9 transcripts are indicated by arrows. A 292-bp deletion in the env gene 5′ region distinguishes HML-2 type 1 from type 2 proviruses and causes an alternative splicing pattern generating the np9 transcript. Env-SP consisting of the N-terminal 96 aa of full-length Env protein is indicated (see also Fig. 4)

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Molecular Neurodegeneration

ISSN: 1750-1326