Detail of "146-72-5"

Reference

Effect of cyclic AMP on catabolite-repressed zoosporangial formation in Phytophthora capsici

Effect of cyclic AMP on catabolite-repressed zoosporangial formation in Phytophthora capsici. Yoshikawa, M.; Masago, H. (Fac. Agric., Kyoto Prefect. Univ., Kyoto, Japan). Can. J. Bot., 55(7), 840-3 (English) 1977. CODEN: CJBOAW. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) Zoosporangial formation in P. capsici was strongly inhibited by glucose [50-99-7] and other catabolites including sugars, citric acid cycle acids, and amino acids, but was only slightly inhibited by 3-O-methylglucose [146-72-5] and 2-deoxyglucose [154-17-6] and by other seemingly weak catabolites. The inhibitions were specifically prevented by cyclic AMP [60-92-4] among the various related nucleotides evaluated. The reversing effect by cyclic AMP was obsd. only on zoosporangial formation that was partially repressed by catabolites, but the completely repressed zoosporangial formation could not be reversed by cyclic AMP. Furthermore, cyclic AMP failed in reversing zoosporangial formation that was inhibited by antibiotics such as antimycin A [1397-94-0] and cycloheximide [66-81-9]. The initiation of zoosporangial formation in the fungus is apparently under the control of catabolite repression that is mediated by cyclic AMP.

Effects of insulin and NSILA on adipocytes of normal and diabetic rats: receptor binding, glucose transport and glucose metabolism

Effects of insulin and NSILA on adipocytes of normal and diabetic rats: receptor binding, glucose transport and glucose metabolism. Schoenle, E.; Zapf, J.; Froesch, E. R. (Dep. Med., Kantonsspital Zurich, Zurich, Switz.). Diabetologia, 13(3), 243-9 (English) 1977. CODEN: DBTGAJ. DOCUMENT TYPE: Journal CA Section: 2 (Hormone Pharmacology) Section cross-reference(s): 14 Isolated fat cells from normal and streptozotocin-diabetic rats were compared with respect to metabolic indices (glucose [50-99-7] uptake, 3-O-methylglucose [146-72-5] efflux) with and without stimulation by insulin [9004-10-8] and nonsuppressible insulin-like activity (NSILA) [61912-98-9]. In addn., binding studies were carried out with these 2 hormones. Basal glucose-14C oxidn. and incorporation into lipids was decreased in diabetic cells and their response to insulin and NSILA was greatly decreased. Basal efflux of 3-O-methylglucose from diabetic cells was somewhat faster than from normal cells. The response to insulin and NSILA was less than in normal cells and it was delayed. The apparent no. of insulin binding sites as well as their affinity for insulin was increased in diabetic cells. In contrast the apparent no. of binding sites for NSILA was decreased in diabetic cells and their affinity for NSILA was increased. In normal cells insulin enhanced binding of NSILA-125I more markedly than in diabetic cells. Apparently, the rate-limiting step of impaired glucose metab. (oxidn. and lipogenesis) in diabetic fat cells is beyond the interaction of the hormone with the receptor. The apparent no. of hormone receptors (insulin, NSILA) on the cell membrane is apparently regulated individually for each binding site.