High impact information on (3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• ATG blocks PKCiota-dependent signaling to Rac1 and inhibits transformed growth of NSCLC cells [1].
• ATG-mediated inhibition of transformation is relieved by expression of constitutively active Rac1, consistent with a mechanism at the level of the interaction between PKCiota and Par6 [1].
• The mol wt of the affinity-labeled proteins in various liver microsomal preparations ranged between 28-36 kilodaltons (kDa), and the ATG concentrations necessary for the inhibition of affinity labeling of microsomes with [125I]bromoacetyl T3 were comparable to those required for inhibition of the enzyme activity in all species except the pig [2].
• The pig liver microsomes demonstrated a dominant affinity-labeled 36-kDa band, but much higher ATG concentrations (micromolar) were required for inhibition of affinity labeling [2].
• By contrast, GLS mRNA levels in IL-1beta-stimulated FLSs were reduced by treatment with aurothioglucose (AuTG) and dexamethasone (DEX) [3].

Anatomical context of (3R,4S,5R,6R)-2-mercapto-6-methylol-tetrahydropyran-3,4,5-triol

• It was concluded that ATM and ATG inhibited lymphocyte function and lymphocyte-amplification of macrophage function [4].
• Glucose transporter (GLUT 4) was assessed in subcellular membrane fractions of white adipose tissue (WAT) from obese insulin-resistant aurothioglucose (AuTG)- or monosodium glutamate (MSG)-treated mice [5].
• ATM and ATG inhibited PHA-stimulated IL-1 production by mononuclear cells but not spontaneous or LPS-induced IL-1 production by adherent monocytes [4].

References