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Nonsense sequence

The number of conceivable synthetic pathways is reduced substantially if we confine the term synthesis to those reasonable sequences of chemical reactions which lead from some readily available starting materials to the desired target compounds without obvious waste of material and labor, and without involving nonsense sequences of operations, i. e., synthetic pathways that contain imnecessary "loops . ) For instance, we should not consider a synthesis of NaCl from strychnine hydrochloride and tri-phenylmethyl sodium i ) a reasonable synthetic of NaCl. [Pg.24]

More direct evidence for the formation of dimers by the tRNA al. embedded homodimeric maxizyme (tRNAVal Mz Fig.3B)was provided by gel-shift analysis in the absence of the substrate. As controls, we also analyzed tRNAVal transcripts that contained a nonsense sequence between the tRNAVal portion and the terminator sequence, as well as transcripts of the gene for the tRNAVal-embedded parental hammerhead ribozyme (tRNAVal.R32). Shifted bands (dimers) were observed only in the case of the tRNAVal-Mz (Fig.3B). [Pg.426]

An analogous pattern of configurations can be seen m the aldopentoses when they are arranged m the order ribose arabinose xylose lyxose (RAXL is an easily remem bered nonsense word that gives the correct sequence) This pattern is discernible even m the aldotetroses erythrose and threose... [Pg.1032]

Carbonic anhydrase (CA) exists in three known soluble forms in humans. All three isozymes (CA I, CA II, and CA III) are monomeric, zinc metalloenzymes with a molecular weight of approximately 29,000. The enzymes catalyze the reaction for the reversible hydration of C02. The CA I deficiency is known to cause renal tubular acidosis and nerve deafness. Deficiency of CA II produces osteopetrosis, renal tubular acidosis, and cerebral calcification. More than 40 CA II-defi-cient patients with a wide variety of ethnic origins have been reported. Both syndromes are autosomal recessive disorders. Enzymatic confirmation can be made by quantitating the CA I and CA II levels in red blood cells. Normally, CA I and CAII each contribute about 50% of the total activity, and the CAI activity is completely abolished by the addition of sodium iodide in the assay system (S22). The cDNA and genomic DNA for human CA I and II have been isolated and sequenced (B34, M33, V9). Structural gene mutations, such as missense mutation, nonsense... [Pg.36]

Ware J., Russell S. R., Vicente V., et al. Nonsense mutation in the glycoprotein Iba coding sequence associated with Bemard-Soulier syndrome. Proc Natl Acad Sci USA 1990 87,2026-30. [Pg.166]

Nonsense mutation A nonsense mutation is also a change in one DNA base pair. Instead of substituting one amino acid for another, however, the altered DNA sequence prematurely signals the cell to stop building a protein. This type of mutation results in a shortened protein that may function improperly or not at all. [Pg.24]

Codon A set of three nucleotides in a protein coding sequence that specifies individual amino acids or a termination signal (codon, terminator). Most codons are universal, but some organisms do not produce the transfer RNAs (RNA, transfer) complementary to all codons. These codons are referred to as unassigned codons (codons, nonsense). [NIH]... [Pg.63]

The stem-loop structure in the noncoding 3 region of selenoprotein mRNAs has also been termed a SECTS element in mammals although it has a different overall structure. ° In silica analysis of the human genome sequence, using this consensus SECTS element along with the presence of the characteristic UGA codon within an exon, has led to the discovery of several new selenoproteins, including a selenium-dependent methionine sulfoxide reductase. It has been shown that a specific complex exists for selenoprotein synthesis that shuttles between the nucleus and the cytosol. This possibly protects the preformed complex for nonsense-mediated decay to allow for more efficient selenoprotein synthesis. The specific tRNA needed for selenocysteine... [Pg.128]

The answer is C. Production of a truncated protein indicates that a mutation has occurred, but this phenomenon may have arisen from a frameshift mutation (insertion or deletion) or by a nonsense mutation. The most likely possibility is a nonsense mutation because sequence analysis of the truncated protein showed that it had normal (wild-type) sequence. Insertion and deletion events often produce a stretch of garbled or abnormal protein sequence at the C-terminal end of the truncated protein arising from out-of-frame translation of the mRNA downstream of the mutation until a stop codon is encountered. [Pg.183]

When ionizing radiation affects just one nucleotide in a sequence, this may produce a point mutation. Most point mutations are of little consequence because the same protein or a functional variation is made anyway. However, some point mutations result in a nonsense message from which a nonfunctional protein is constructed, while other point mutations give a meaningful but changed message leading to a protein with altered properties. [Pg.431]

Termination ("stop" or "nonsense ) codons Three of the codons, UAG, UGA, and UAA, do not code for amino acids, bit rather are termination codons. When one of these codons appears in an mRNA sequence, it signals that synthesis of the peptide chain coded for by that mRNA is completed. [Pg.430]

Codons are composed of three nucleotide bases usually presented in Ihe mRNA language of A, G, C, and U. They are always written 5 —>3. Of the 64 possible three-base combinations, 61 code for the twenty common amino acids and three signal termination of protein synthesis (translation). Altering the nucleotide sequence in a codon can cause sient mutations (the altered codon also codes for the original amino acid), missense mutations (the altered codon codes for a different amino acid), or nonsense mutations (the altered codon is a termination... [Pg.441]

Altering the nucleotide sequence in a codon can cause silent mutations (the altered codon also codes for the original amino acid), missense mutations (the altered codon codes for a different amino acid), or nonsense mutations (the altered codon is a termination codon). [Pg.505]

Nonsense mutation. A change in the base sequence that converts a sense codon (one that specifies an amino acid) to one that specifies a stop (a nonsense codon). There are three nonsense codons. [Pg.914]

Nonsense suppressors are produced by tethering a nonnatural amino acid to a stop (or nonsense ) anticodon in tRNA. As a result, the stop codon in an mRNA sequence is converted from a protein synthesis termination site to a site at which the nonnatural amino acid may specifically be inserted. DNA base substitutions that correspond to the stop anticodon of tRNA may thus be made in order to specifically incorporate nonnatural amino acids into proteins. [Pg.67]


See other pages where Nonsense sequence is mentioned: [Pg.668]    [Pg.714]    [Pg.194]    [Pg.892]    [Pg.835]    [Pg.635]    [Pg.668]    [Pg.714]    [Pg.194]    [Pg.892]    [Pg.835]    [Pg.635]    [Pg.1025]    [Pg.420]    [Pg.325]    [Pg.363]    [Pg.363]    [Pg.19]    [Pg.88]    [Pg.334]    [Pg.78]    [Pg.5]    [Pg.48]    [Pg.88]    [Pg.245]    [Pg.277]    [Pg.56]    [Pg.117]    [Pg.166]    [Pg.69]    [Pg.1479]    [Pg.1039]    [Pg.248]    [Pg.215]    [Pg.150]    [Pg.343]   
See also in sourсe #XX -- [ Pg.226 ]




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