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Splice acceptor site

Figure 11. Alternate promoters are used for production of the vertebrate neural and non-neural AADC mRNAs. Non-neural AADC transcription initiates at exon L1, whereas neural transcription initiates at exon N1. The non-neural mRNA splices from exon L1 to 2, since the 5 edge of exon N1 is a site of transcriptional initiation instead of a splice acceptor site. Translation initiates from the same AUG in exon 2 in both mRNAs, producing the same protein product in both tissue types. This scheme holds for both human and rat AADC, although the nomenclature of the exons differs. In rat AADC the exon N1 to 2 splice uses a splice acceptor site 5 bp downstream of the splice acceptor used for the exon L1 to 2 splice (Albert et al., 1992). Figure 11. Alternate promoters are used for production of the vertebrate neural and non-neural AADC mRNAs. Non-neural AADC transcription initiates at exon L1, whereas neural transcription initiates at exon N1. The non-neural mRNA splices from exon L1 to 2, since the 5 edge of exon N1 is a site of transcriptional initiation instead of a splice acceptor site. Translation initiates from the same AUG in exon 2 in both mRNAs, producing the same protein product in both tissue types. This scheme holds for both human and rat AADC, although the nomenclature of the exons differs. In rat AADC the exon N1 to 2 splice uses a splice acceptor site 5 bp downstream of the splice acceptor used for the exon L1 to 2 splice (Albert et al., 1992).
Bonnevie-Nielsen, V., Field, L. L., Lu, S., et al. (2005) Variation in antiviral 2, 5 -oligoade-nylate synthetase (2 5"AS) enzyme activity is controlled by a single-nucleotide polymorphism at a splice-acceptor site in the OASl gene. Am. J. Hum. Genet. 76,623-633. [Pg.392]

A one-year-old male with chronic anemia is found to have (B-thalassemia. Genetic analysis shows that one of his (B-globin genes has a G to A mutation that creates a new splice acceptor site nineteen nucleotides upstream from the normal splice acceptor site of the first intron. Which of the following best describes the new messen ger RNA molecule that can be produced from this mutant gene ... [Pg.428]

Perez-Tur J, Froelich S, Prihar G, et al. 1995. A mutation in Alzheimer s disease destroying a splice acceptor site in the presenilin-1 gene. NeuroReport 7 297-301. [Pg.342]

Clarke LA, Veiga I, Isidro G, Jordtm P, Ramos JS et al (2000) Pathological exon skipping in an HNPCC proband with MLHl splice acceptor site mutation. Genes Chromosomes Cancer 29 367-370... [Pg.412]

I omponio, R. J., Reynolds, T. R Mandel, H., Admoni, O., MeJone, F, Buck, G. A., and Wolf, B, (1997). Profound biotinidase deficiency caused by point mutation that creates a downstream ciyptLc 3 splice acceptor site within an exon of the human biotinidase gene. Huftmts Mol. Genet. 6,739-745. [Pg.674]

Alternative splicing of hPXR (also referred to as hPXR.l) also gives rise to two additional hPXR transcripts in a variety of tissues [16, 25] PXR.2 (splice variant 2, S V2) has a 111 bp deletion at the 5 end of exon 5. This alternative PXR mRNA was originally detected in breast tissue and results in an in-frame deletion of 37 amino acids (174-210) from the LBD of PXR protein [26]. PXR.2 is produced by usage of a cryptic splice acceptor site within exon 5. Human PXR.3 (SV3) was identical to an... [Pg.244]

Although dicistronic and polycistronic mRNAs can be identified in steady-state RNA, two lines of evidence suggest that these molecules probably are not authentic precursors to mature mRNAs. First, in Trypanosoma brucei cells, trans-splicing at three different splice acceptor sites (the a. and P tubulin, and the actin RNA coding regions). [Pg.3]

C. R. Wolf (1990). Alternative splicing in the human cytochrome P450IIB6 gene Use of a cryptic exon within intron 3 and splice acceptor site v/ithin exon 4. Nucleic Acids Res. 18, 189. [Pg.478]

In conclusion, we have synthesized for the first time a-anomeric oligoribonucleotides (a-RNA). This series demonstrates enzymatic stability as compared to 6-RNA, and these anneal in parallel orientation with complementary DNA or RNA strands. However, a 2-a-RNA/l-6-DNA stoichiometry was surprisingly observed at high salt concentration. In addition, when directed on the tat splice acceptor site of HIV, an a-RNA antisense compound unspecifically inhibits de novo HIV infection in MT4 cells. [Pg.309]


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See also in sourсe #XX -- [ Pg.62 ]




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