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C Xia

Publications and source records attributed to C Xia.

59 records · Page 4Linked to original sources

Chemical modification of GSH transferase P1-1 confirms the presence of Arg-13, Lys-44 and one carboxylate group in the GSH-binding domain of the active site.

GSH transferase P1-1 (GSTP1-1) was modified with group-specific reagents. Kinetic experiments demonstrated that inactivation of GSTP1-1 occurred upon reaction of one arginine residue per subunit with diacetyl, one lysine residue per subunit with 2,4,6-trinitrobenzene sulphonate, or one carboxylate group per subunit with 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide. All three inactivation reactions were inhibited by compounds known to bind at the GSH site of the enzyme but were unaffected by the electrophile 1-chloro-2,4-dinitrobenzene. N-terminal sequence analysis showed that Arg-13 was modified by diacetyl and that this modification was inhibited by GSH. Arg-11 was not modified. The lysine residue modified by 2,4,6-trinitrobenzene sulphonate and protected by S-octylglutathione was identified as Lys-44 by sequencing of tryptic peptides. The findings are in agreement with the involvement of Arg-13 and Lys-44 in binding of GSH, as determined from the crystal structure [Reinemer, Dirr, Ladenstein, Huber, Lo Bello, Frederici and Parker (1992) J. Mol. Biol. 227, 214-226]. The present data also implicate a single carboxylate in GSH binding, consistent with the involvement of Asp-98 of subunit B determined from the crystallographic study. The GSH-binding determinants of GSTP1-1 are compared using sequence similarity with those of GSTs of Alpha, Mu and Theta classes.

Amino Acid Sequence↗

The human glutathione S-transferase P1-1 gene: modulation of expression by retinoic acid and insulin.

Glutathione S-transferases (GSTs) are a group of enzymes which play an important role in the detoxication of xenobiotics. It is shown that the expression of human glutathione S-transferase P1-1 (GSTP1-1) is suppressed by retinoic acid (RA) as the result of decreased transcription from its gene, GSTP1. Chloramphenicol acetyltransferase (CAT) assays indicate that the effect of RA on the transcription of a GSTP1 promoter-CAT fusion gene is mediated by the region -99 to +72 of GSTP1. A consensus activator protein 1-binding site, located at nucleotide position -59 to -65 of GSTP1, is suggested to be responsible for RA repression. This effect of RA on GSTP1 expression is mediated by the human beta-type RA receptor, hRAR beta, but not the chicken retinoid X receptor, cRXR. The retinoid X receptor does not augment the action of hRAR beta on GSTP1. In addition, it is shown that GSTP1-1 expression is enhanced by insulin as a result of increased transcription of GSTP1. Assay of CAT activity indicates that the effect of insulin on the transcription of GSTP1 is also mediated by the region -99 to +72 of GSTP1. Comparison with sequences of other insulin-responsive genes, suggests that insulin enhancement of GSTP1 expression is effected by an eight-base-pair sequence, 'CCCGCGTC', located at +48 to +55 in intron 1 of the gene. These results are discussed in relation to the increased expression of GSTP1-1 in many tumour cells.

Animals↗

Six-year progression of destructive periodontal disease in 2 subgroups of elderly Chinese.

Two groups of elderly chinese were selected from a large epidemiological sample on the basis of a low ("best" group) or a high ("worst" group) number of sites with attachment loss levels > or = 6 mm and/or pocket depth > or = 4 mm and at least 16 teeth present. Six years later the patients were clinically reexamined and the subgingival microflora was assessed. This paper presents the clinical characteristics of destructive periodontal disease progression among the two subgroups. The "best" group lost an average of 1.8 teeth, contrasting the average loss of 5.3 teeth among the "worst" group. Virtually all teeth lost among the "worst" group had a baseline attachment loss level > or = 4 mm, in contrast to 48% among the "best" group. While dental caries could be identified as a cause of tooth loss in both groups, the excess tooth loss among the "worst" group seems attributable to periodontal destruction. The average of 1.21 mm attachment/site lost among the "best" group was not statistically significantly different from the 1.36 mm/site lost among the "worst" group during the 6 years. Individual mean losses of attachment ranged from a gain of 0.03 mm to a loss of 3.19 mm. An attachment loss > or = 2 mm at a site was highly positively associated with a high initial attachment loss level (> or = 4 mm) at that site among the "best" group, whereas a highly negative association was seen among the "worst" group.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

[The distribution of normal oral flora in 49 healthy children and juvenile].

The frequencies and proportions of predominant cultiv ableoral bacteria associated with 49 healthy children and juvenile (6-25 yr old) were studied. A total of 72 bacterial species belonging to 28 genus were detected in 195 samples of saliva, fissure plaque, supragingival plaque, and subgingival plaque. The predominant bacteria were Oral streptococci, Neisseria, Actinomyces, Capnocytophaga, Bacteroides and Fusobacterium in the normal oral cavity of healthy children and juvenile. There were differences in the distribution of the predominant flora, e.g. Fusobacterium and Bacteroides had higher incidence and proportion in the subgingival plaque than in the fissure plaque.

Adolescent↗

Tooth mortality and periodontal conditions in 60-80-year-old Chinese.

The study comprised 544 persons aged 60 yr or more from two urban Residential Areas and one rural village (including a nursing home) of Beijing area. Overall, the sample accounted for 81% of the total population of elderly aged 60 yr or more in the village/areas so defined. Each person was examined for dental status, plaque, calculus, gingivitis, loss of attachment, pocket depth and tooth mobility. Edentulousness was seen in 0-29% of the persons examined, depending on age and sex. The mean number of teeth present ranged from 6.9 to 23.9, depending on age and sex, and area. The oral hygiene was poor; approximately 50% of all surfaces had immediately visible plaque deposits and calculus. About 50% of the surfaces had a loss of attachment greater than or equal to 4 mm, while less than 15% presented pockets greater than or equal to 4 mm. More than 50% of the individuals had loss of attachment greater than or equal to 4 mm on more than 40% of their surfaces. The proportion of surfaces per person with loss of attachment greater than or equal to 7 mm; and pockets greater than or equal to 4 mm, respectively, showed a pronounced skewed distribution. These findings indicate that a subfraction of individuals is responsible for a substantial proportion of the severe periodontal breakdown leading to loss of teeth. This, in turn, raises important questions as to the most appropriate strategies for the prevention and control of periodontal diseases for the Chinese population.

Aged↗