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Biomedical subjects

Y Kuang

Publications and source records attributed to Y Kuang.

At least 55 records · Page 3Linked to original sources
PubMed1997

alpha-Latrotoxin stimulates exocytosis by the interaction with a neuronal G-protein-coupled receptor.

alpha-Latrotoxin is a potent stimulator of neurosecretion. Its action requires extracellular binding to high affinity presynaptic receptors. Neurexin I alpha was previously described as a high affinity alpha-latrotoxin receptor that binds the toxin only in the presence of calcium ions. Therefore, the interaction of alpha-latrotoxin with neurexin I alpha cannot explain how alpha-latrotoxin stimulates neurotransmitter release in the absence of calcium. We describe molecular cloning and functional expression of the calcium-independent receptor of alpha-latrotoxin (CIRL), which is a second high affinity alpha-latrotoxin receptor that may be the major mediator of alpha-latrotoxin's effects. CIRL appears to be a novel orphan G-protein-coupled receptor, a member of the secretin receptor family. In contrast with other known serpentine receptors, CIRL has two subunits of the 120 and 85 kDa that are the result of endogenous proteolytic cleavage of a precursor polypeptide. CIRL is found in brain where it is enriched in the striatum and cortex. Expression of CIRL in chromaffin cells increases the sensitivity of the cells to the effects of alpha-latrotoxin, demonstrating that this protein is functional in coupling to secretion. Syntaxin, a component of the fusion complex, copurifies with CIRL on an alpha-latrotoxin affinity column and forms stable complexes with this receptor in vitro. Interaction of CIRL with a specific presynaptic neurotoxin and with a component of the docking-fusion machinery suggests its role in regulation of neurosecretion.

Amino Acid Sequence↗
PubMed1996

Pertussis toxin-sensitive activation of phospholipase C by the C5a and fMet-Leu-Phe receptors.

Signal transduction pathways that mediate C5a and fMet-Leu-Phe (fMLP)-induced pertussis toxin (PTx)-sensitive activation of phospholipase C (PLC) have been investigated using a cotransfection assay system in COS-7 cells. The abilities of the receptors for C5a and fMLP to activate PLC beta2 and PLC beta3 through the Gbetagamma subunits of endogenous Gi proteins in COS-7 cells were tested because both PLC beta2 and PLC beta3 were shown to be activated by the betagamma subunits of G proteins in in vitro reconstitution assays. Neither of the receptors can activate endogenous PLC beta3 or recombinant PLC beta3 in transfected COS-7 cells. However, both receptors can clearly activate PLC beta2 in a PTx-sensitive manner, suggesting that the receptors may interact with endogenous PTx-sensitive G proteins and activate PLC beta2 probably through the Gbetagamma subunits. These findings were further corroborated by the results that PLC beta3 could only be slightly activated by Gbeta1gamma1 or Gbeta1gamma5 in the cotransfection assay, whereas the Gbetagamma subunits strongly activated PLC beta2 under the same conditions. PLC beta3 can be activated by Galphaq, Galpha11, and Galpha16 in the cotransfection assay. In addition, the Ggamma2 and Ggamma3 mutants with substitution of the C-terminal Cys residue by a Ser residue, which can inhibit wild type Gbetagamma-mediated activation of PLC beta2, were able to inhibit C5a or fMLP-mediated activation of PLC beta2. These Ggamma mutants, however, showed little effect on m1-muscarinic receptor-mediated PLC activation, which is mediated by the Gq class of G proteins. These results all confirm that the Gbetagamma subunits are involved in PLC beta2 activation by the two chemoattractant receptors and suggest that in COS-7 cells activation of PLC beta3 by Gbetagamma may not be the primary pathway for the receptors.

Amino Acid Sequence↗
PubMed1996

Identification of a phospholipase C beta2 region that interacts with Gbeta-gamma.

To delineate the phospholipase C (PLC; EC 3.1.4.3) beta2 sequences involved in interactions with the beta-gamma subunits of G proteins, we prepared a number of mammalian expression plasmids encoding a series of PLC beta2 segments that span the region from the beginning of the X box to the end of the Y box. We found the sequence extending from residue Glu-435 to residue Val-641 inhibited Gbeta-gamma-mediated activation of PLC beta2 in transfected COS-7 cells. This PLC beta2 sequence also inhibited ligand-induced activation of PLC in COS-7 cells cotransfected with cDNAs encoding the complement component C5a receptor and PLC beta2 but not in cells transfected with the alpha1B-adrenergic receptor, suggesting that the PLC beta2 residues (Glu-435 to Val-641) inhibit the Gbeta-gamma-mediated but not the Galpha-mediated effect. The inhibitory effect on Gbeta-gamma-mediated activation of PLC beta2 may be the result of the interaction between Gbeta-gamma and the PLC beta2 fragment. This idea was confirmed by the observation that a fusion protein comprising these residues (Glu-435 to Val-641) of PLC beta2 and glutathione S-transferase (GST) bound to Gbeta-gamma in an in vitro binding assay. The Gbeta-gamma-binding region was further narrowed down to 62 amino acids (residues Leu-580 to Val-641) by testing fusion proteins comprising various PLC beta2 sequences and GST in the in vitro binding assay.

Amino Acid Sequence↗
PubMed1996

Selective G protein coupling by C-C chemokine receptors.

The C-C chemokines are major mediators of chemotaxis of monocytes and some T cells in inflammatory reactions. The pathways by which the C-C chemokine receptors activate phospholipase C (PLC) were investigated in cotransfected COS-7 cells. The C-C chemokine receptor-1 (CKR-1), the MCP-1 receptor-A (MCP-1Ra), and MCP-1Rb can reconstitute ligand-induced accumulation of inositol phosphates with PLC beta2 in a pertussis toxin-sensitive manner, presumably through G beta gamma released from the Gi proteins. However, these three receptors demonstrated different specificity in coupling to the alpha subunits of the Gq class. While none of the receptors can couple to Galphaq/11, MCP-1Rb can couple to both Galpha14 and Galpha16, but its splicing variant, MCP-1Rb, cannot. Since MCP-1Ra and -b differ only in their C-terminal intracellular domains, the C-terminal ends of MCP-1Rs determine G protein coupling specificity. CKR-1 can couple to Galpha14 but not to Galpha16, suggesting some of the C-C chemokine receptors, unlike the C-X-C chemokine receptors, discriminate against Galpha16, a hematopoietic-specific Galpha subunit. The intriguing specificity in coupling of the Gq class of G proteins implies that the chemokines may be involved in some distinct functions in vivo. The commonality of the chemokine receptors in coupling to the Gi-Gbetagamma-PLC beta2 pathway provides a potential target for developing broad spectrum anti-inflammatory drugs.

Animals↗
PubMed1996

[SMC proliferation and its distribution in autologous vein grafts].

SMC proliferation in intimal hyperplasia is a major cause of graft failure. We induced experimental jugular vein to aortic autograft in 120 Wistar rats, and analyzed the SMC proliferation and its distribution in the graft by flow cytometry (FCM) and immunohistochemistry of proliferating cellular nuclear antigen (PCNA) from 2 hours, 6 hours, 24 hours to 1 week, 2 weeks and 4 weeks. Although the number was not apparently increased in autologous vein graft at early stage, SMC proliferation had started. At 1 week after transplantation, the activity of SMC proliferation increased to a maximum, and returned to baseline level 4 weeks. At early stage, the distribution of SMC proliferation located in the media, but at middle stage, both intima and media all presented a relatively higher proliferative activity. The intima formation occurred by the migration of a large population and the proliferation of a relatively small subpopulation of SMC. Therefore, control of SMC proliferation, and migration of autologous vein grafts must be within two weeks after transplantation.

Animals↗
PubMed1995

Selective coupling of beta 2-adrenergic receptor to hematopoietic-specific G proteins.

The coupling of the beta 2-adrenergic receptor (AR) to the alpha subunits of the Gq class of G proteins was investigated in a cotransfection system. COS-7 cells cotransfected with the beta 2-AR cDNA and the G alpha 15 or G alpha 16 cDNA showed marked norepinephrine-induced increases in accumulation of inositol phosphates in a concentration-dependent manner. However, cells cotransfected with the cDNA encoding G alpha q, G alpha 11, or G alpha 14 instead of G alpha 16 gave no ligand-dependent activation of phospholipase C (PLC). The facts that the beta-AR agonist isoprenaline can also induce activation of PLC in cells coexpressing beta 2-AR and G alpha 16 and that the beta 2-AR-specific antagonist propranolol can block norepinephrine-induced activation of PLC in these cotransfected cells further indicate that it is the beta 2-AR that mediates the activation of phospholipase C in these cotransfected cells. To test the possibility of involvement of G beta gamma, a G beta gamma antagonist, G gamma 3 mutant with substitution of a Ser residue for the C-terminal Cys residue, was used because this protein, when expressed in COS-7 cells, can inhibit only G beta gamma-mediated but not G alpha-mediated activation of PLC. The result that the G gamma 3 mutant could not inhibit beta 2-adrenergic receptor-mediated activation of PLC in cells cotransfected with the G alpha 16 cDNA suggests that G beta gamma is unlikely to be a major mediator of beta 2-adrenergic receptor-induced activation of PLC. Thus, we conclude that the beta 2-adrenergic receptor can specifically couple to G alpha 15 and G alpha 16, but not to G alpha q, G alpha 11, or G alpha 14 to activate PLC.

Animals↗
PubMed1995

Encircling suture method in the treatment of femoral venous valvular incompetency.

Many patients with chronic venous insufficiency syndrome caused by the "relative valvular incompetency" with venous dilatation. Eighty-six per cent of the cases can be cured by reducing the femoral venous diameter by simply using the encircling suture method just distal to the first femoral valvular sinus. Our preliminary results suggest that such a method of surgical treatment is simple and efficient.

Adult↗
PubMed1994

Predator-prey dynamics in models of prey dispersal in two-patch environments.

Models are presented for a single species that disperses between two patches of a heterogeneous environment with barriers between patches and a predator for which the dispersal between patches does not involve a barrier. Conditions are established for the existence, uniform persistence, and local and global stability of positive steady states. In particular, an example that demonstrates both the stabilizing and destabilizing effects of dispersion is presented. This example indicates that a stable migrating predator-prey system can be made unstable by changing the amount of migration in both directions.

Animals↗
PubMed1992

[Historical and herbalogical studies on coloring crude drug (Part 1): "Langbacao"].

The name of Langbacao was described for the first time in Kai Bao Ben Cao in 10th century, in which Langbacao was introduced as an herb medicine for scours. While, as the name of Qu, Wujie, it was first described in Er Ya and as the name of Langyecao, it was first described in Ben Cao Shi Yi. Many investigators have confirmed that the original plant of Langbacao is to be Bidens tripartita L. In Japan, Langbacao is generally recognized as ta-u-ko-gi, while some investigators suggested that it is unlikely that ta-u-ko-gi is identical to Langbacao. In the old Chinese literature, Langbacao had been mentioned as a dye which could make hair dark. But in modern Chinese and Japanese literature, few papers reported the use of Bidens tripartita L. as a dye. The characteristics of the shapes of Langbacao between old and modern literature seem not to be consistent. Other names of Langbacao are confused even in the modern literature. It seems that Langbacao in the old literature includes species of the genus Bidens other than B. tripartita.

History, Medieval↗