Biomedical subjects

L Liao

Publications and source records attributed to L Liao.

75 records · Page 5Linked to original sources

PubMed1988

Monoclonal anti-idiotypic antibodies to an I-J interacting molecule inhibit suppression in an H-2 restricted way.

We have obtained 10 mAb from two independent fusions that are anti-idiotypic to the combining site of an anti-I-Jk antibody. These mAb block Ts cell function isn a genetically restricted manner in vitro and in vivo and recognize a determinant on macrophage membranes. In addition, they do not affect the I-Ek-restricted activation of a Th cell line specific for pigeon heart cytochrome c. We conclude that these mAb may recognize a molecule other than conventional I-Ek on cells interacting with Ts cells that is involved in mediating Ts activity. The molecule recognized may be a modified I-Ek molecule or a molecule not encoded by the genes encoding I-Ek.

Animals↗

PubMedDate not supplied

Determinants of species- and placenta-specific expression of p100 GAP.

This study was based on the hypothesis that both primary sequence and methylation status of the GTPase activating protein (GAP) gene limits expression of p100 GAP to primate placenta. Due to alternate splicing, a 65-bp insert appears between the first and second coding exons of p100 GAP mRNA, and translation of p100 GAP initiates within this insert. Examination of the sequence surrounding the 65-bp insert revealed that the monkey GAP gene contained both the 3' splice donor site and the internal start codon, whereas the mouse GAP gene contained neither. To address p100 GAP tissue specificity, the methylation status of the GAP gene was examined. Site-specific demethylation was found to correlate with synthesis of p100 GAP, suggesting that methylation regulates the expression of different GAP isoforms. The results of this study provide a mechanistic basis for the observation that p100 GAP is synthesized only in primate placenta and suggest that its expression is regulated, in part, by gene methylation.

Adult↗

PubMedDate not supplied

Inheritance and allelism of resistance to soybean mosaic virus in Zao18 soybean from China.

Soybean mosaic disease caused by soybean mosaic virus (SMV) occurs wherever soybean [Glycine max (L.) Merr.] is grown and is considered one of the most important soybean diseases in many areas of the world. Use of soybean cultivars with resistance to SMV is a very effective way of controlling the disease. China has rich soybean germplasm, but there is very limited information on genetics of SMV resistance in Chinese soybean germplasm and reaction of the resistance genes to SMV strains G1-G7. There also is no report on allelic relationships of resistance genes in Chinese soybeans with other named genes at the three identified loci Rsv1, Rsv3, and Rsv4. The objectives of this study were to examine reactions of Chinese soybean cultivar Zao18 to SMV strains G1-G3 and G5-G7, to reveal the inheritance of SMV resistance in Zao18 and to determine the allelic relationship of resistance genes in Zao18 with previously reported resistance genes. Zao18 was crossed with the SMV-susceptible cultivar Lee 68 to study the inheritance of resistance. Zao18 was also crossed with the resistant lines PI96983, L29, and V94-5152, which possess Rsv1, Rsv3, and Rsv4, respectively, to examine the allelic relationship between the genes in Zao18 and genes at these three loci. Our research results indicated that Zao18 possesses two independent dominant genes for SMV resistance, one of which is allelic to the Rsv3 locus; the other is allelic with Rsv1. The presence of both genes (Rsv1 and Rsv3) in Zao18 confers resistance to SMV strains G1-G7.

Alleles↗