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Mutation sites conferring picolinate auxin resistance in AFB5.

Mutation spectrum of the p53 protein in tumors. The linear strnctnre is shown of p53 and the frequency of mutations found in tumors. The black bars indicate the approximate position and the relative frequency of the p53 mutations. The frequency of mutations in the region of the DNA binding domain is of note. The sites of the most frequent mutations coincide with positions of the p53 protein that are directly involved in interactions with the DNA sequence see

Mutation spectrum of the p53 protein in tumors. The linear structure is shown of p53 and the frequency of mutations found in tumors. The black bars indicate the approximate position and the relative frequency of the p53 mutations. The fre-

Mutational analysis of the CDTF-1 binding site. Electrophoretic mobflity shift assays were performed on the SPRR3 28-mer in the presence of 1 mM CaCb. For efficient DNA binding, a long oligonucleotide was required

Mutational analysis of the SPRR3 proximal promoter region

Mutational mechanisms.

Mutational surf.

Mutations in DNA caused by nitrosamines. Nitrosamines are consumed in many natural products and are produced in the stomach from nitrites used as preservatives and secondary amines found in foods such as fish. They are believed to be responsible for the high incidence of gastric cancer found in Japan and Iceland, where salt-preserved fish was a major dietary item. Nitrosamine metabolites methylate guanine .

Mutations in E. coli signal sequence that result in export-defective proteins. From Silhavy et al. .

Mutations in glucose phosphate isomerase gene.

Mutations in glucose-6-phosphate dehydrogenase deficiency. shows the references.

Mutations in human PrP associated with familial TSE and disease susceptibility. The structure of human PrP is shown . The legend is the same as for

Mutations in L-type pyruvate kinase gene. shows the references, ins insertion, del deletion.

Mutations in the have been identified and are indicated. In some regions, many mutations have been found. These are indicated by the brackets.

Mutations in the human Cav1.4

Mutations in the human Cav2.1 and rocker phenotypes

Mutations in the human Cav3.2

Mutations in the human Cavl.l and Cay 1.2 , respectively. Also shown is the nucleotide deletion in the mouse Cay 1.1 homolog associated with Muscular Dysgenesis

Mutations in the retinoblastoma gene. A. Sporadic retinoblastoma. B. Familial retinoblastoma.

Mutations in the RUNXl gene precede the onset of a clinical symptoms of acute leukemia. Strikingly, the translocation or point mutations are detectably before birth in cases of pediatric acute leukemia, and at a incidence 100-fold that of the leukemia incidence. The accumulation of secondary mutations are probably necessary for the overt disease - but for the most part the critical mutations are unknown. Adapted from .

Mutations of a model inhibitor to a model substrate

Mutations of gene sequences that may affect protein function and cause disease.

Mutations of P450 -a leadingto altered substrate specificities. WT

Mutations of PMCA2. Mutations are named as referred to in the text and shown on the structural schematic from

Mutations on MAPT exon 10 cause excessive skipping of exon 10

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