Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.11.18 (MAP)
 7,412 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

5,5'-Bis[8-(phenylamino)-1-naphthalenesulfonate] (bis-ANS), the fluorescent probe which binds to tubulin, inhibits its assembly into microtubules [Horowitz et al. (1984) J. Biol. Chem. 259, 14647-14650]. The results described in this paper demonstrate that bis-ANS is quite distinct from other well-known microtubule inhibitors in its specificity of action. The inhibitory potentials of bis-ANS and its three structural analogues ANS, Prodan [6-propionyl-2-(dimethylamino)naphthalene], and NSA (naphthalenesulfonic acid) have been compared. It is found that they can be arranged in the following order according to their polymerization inhibitory potentials: bis-ANS approximately equal to Prodan much greater than ANS greater than NSA. Interestingly, the naphthalene nucleus is sufficient to cause inhibition of polymerization. Detailed experiments were carried out to examine the mode of assembly inhibition by aminonaphthalenes at the molecular level, using bis-ANS as a representative. It was found that there was little or no effect of bis-ANS on the assembly of tubulin when polymerization was induced by assembly promoters like taxol, DMSO, or glutamate, or on the assembly of subtilisin-digested protein (tubulin S), for all of which half-maximal inhibition could not be achieved even at 120 microM bis-ANS. On the contrary, bis-ANS acts as an inhibitor in the case of MAP- (MAP2 and tau) and poly(L-lysine)-induced assembly of tubulin, with half-maximal inhibitory concentrations ranging from 1.5 to 7.6 microM. Our results place bis-ANS as a novel inhibitor, which seems to specifically inhibit C-termini-mediated assembly. Of all assembly inhibitors known so far, none exhibits such selection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bis-ANS as a specific inhibitor for microtubule-associated protein induced assembly of tubulin. 163 59

The purpose of this study was to observe the effects of opioid receptor and alpha-adrenergic receptors in the lower brain stem on the depressor response to electrical stimulation of renal afferent nerve, using intracisternal injection of blockers of these receptors. Experiments were conducted in sodium pentobarbital-anesthetized rabbits. The intracisternal injection (ict) of artificial cerebrospinal fluid (CSF) did not greatly affect the depressor response to stimulation of renal afferent nerve (RAS) and of aortic nerve (ANS). Ict of 550 nmol naloxone significantly inhibited the depressor response to RAS (P less than 0.05) but enhanced the depressor response to ANS (P less than 0.05). Ict of 335 nmol phentolamine significantly inhibited the depressor response to both RAS and ANS. Ict of naloxone reversed the phentolamine inhibition of the depressor response to ANS but did not affect the phentolamine inhibition of the depressor response to RAS. Ict of both naloxone and phentolamine did not affect the inhibitory interaction between the RAS-induced depressor and aortic baroreflex. Ict of phentolamine significantly decreased MAP, and ict of naloxone did not decrease MAP but reversed the decrease in MAP by ict of phentolamine. These data suggest that the activation of opioid receptors in the lower brain stem enhances the depressor response to RAS and attenuates the depressor response to ANS. Moreover, activation of alpha-adrenergic receptors in the lower brain stem facilitates the depressor response to RAS and ANS.
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PMID:[Effects of intracisternal injection of naloxone on the depressor response to stimulation of renal afferent nerve in rabbits]. 255 72