Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UNIPROT:P00790 (
PGA
)
2,475
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Micellar inhibition effect of gangliosides on a degradation of drug was investigated, where ganglioside G(M1) (
GM1
), G(D1a) (GD1a) and G(T1b) (GTlb) whose sialic acid residue is one, two and three, respectively, were used. The base-catalyzed isomerization of prostaglandin A(2) (
PGA
(2)) to prostaglandin B(2) (PGB(2)) was chosen as a model experiment. The rate for the isomerization of
PGA
(2) was determined by measuring the concentration of
PGA
(2) (and PGB(2)) with a high-performance liquid chromatography. Gangliosides micelles inhibited the isomerization of
PGA
(2). The inhibition effect of GT1b micelles was larger than that of GD1a micelles. This result would be due to the larger absolute value of surface potential of GT1b micelles, which brings about a larger electrostatic repulsion between micellar surface and OH(-). The terminal sialic acid residue of ganglioside was effective to inhibit the isomerization of
PGA
(2).
GM1
micelles without terminal sialic acid residue but with large aggregation number exhibited a superior steric shielding effect rather than an electrostatically repulsive effect. The inhibition effect of
GM1
micelles was enhanced by the mixed micellization with the other ganglioside with a terminal sialic acid residue.
GM1
-GD1a or
GM1
-GT1b mixed micelles remarkably inhibited the isomerization of
PGA
(2). The physiological activity of PGs in the biological membranes containing gangliosides was also discussed.
...
PMID:Inhibition effects of gangliosides G(M1), G(D1a) and G(T1b) on base-catalyzed isomerization of prostaglandin A(2). 1116 47
We analyzed the in vivo tumor regression activity of high molecular mass poly-gamma-glutamate (gamma-
PGA
) from Bacillus subtilis sups. chungkookjang. C57BL/6 mice were orally administered 10-, 100-, or 2000-kDa gamma-
PGA
or beta-glucan (positive control), and antitumor immunity was examined. Our results revealed higher levels of NK cell-mediated cytotoxicity and IFN-gamma secretion in mice treated with higher molecular mass gamma-
PGA
(2000 kDa) vs those treated with lower molecular mass gamma-
PGA
(10 or 100 kDa) or beta-glucan. We then examined the effect of oral administration of 10- or 2000-kDa gamma-
PGA
on protection against B16 tumor challenge in C57BL/6 mice. Mice receiving high molecular mass gamma-
PGA
(2000 kDa) showed significantly smaller tumor sizes following challenge with the MHC class I-down-regulated tumor cell lines, B16 and TC-1 P3 (A15), but not with TC-1 cells, which have normal MHC class I expression. Lastly, we found that gamma-
PGA
-induced antitumor effect was decreased by in vivo depletion of NK cells using mAb PK136 or anti-asialo
GM1
Ab, and that was completely blocked in NK cell-deficient B6 beige mice or IFN-gamma knockout mice. Taken together, we demonstrated that oral administration of high molecular mass gamma-
PGA
(2000 kDa) generated significant NK cell-mediated antitumor activity in mice bearing MHC class I-deficient tumors.
...
PMID:Oral administration of high molecular mass poly-gamma-glutamate induces NK cell-mediated antitumor immunity. 1761 66