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)

The immature kidney appears to be less responsive to atrial natriuretic peptide (ANP) than the mature kidney. It has been proposed that this difference accounts for the limited ability of the young animal to excrete a sodium load. To delineate the effects of age on the renal response to exogenous ANP, Sprague-Dawley rats were anesthetized for study at 31-32 days of age, 35-41 days of age, and adulthood. Synthetic rat ANP was infused intravenously for 20 min at increasing doses ranging from 0.1 to 0.8 microgram/kg/min, and mean arterial pressure, glomerular filtration rate, plasma ANP concentration, urine flow rate, and urine sodium excretion were measured at each dose. Since cyclic GMP acts as a second messenger for ANP action, urinary cyclic GMP excretion also was measured. Increasing doses of ANP caused a similar decrease in MAP at all ages studied, and increased glomerular filtration rate in adult but not young rats. Increasing the dose of ANP from 0.1 to 0.4 microgram/kg/min caused a greater rise in urine flow and urinary cyclic GMP excretion in adult than young rats, and urine sodium excretion increased more in adults at all doses (p less than 0.05). However, the rise in plasma ANP concentration also was greater in adults than in young rats (p less than 0.05), indicative of greater systemic clearance of ANP in young animals. Increasing levels of plasma ANP concentration were correlated with a greater rise in urine flow in adult than young (31-32 day old) rats (p less than 0.05), but there was no differential effect on urinary cyclic GMP excretion.(ABSTRACT TRUNCATED AT 250 WORDS)
Pediatr Res 1988 Sep
PMID:Renal effects of atrial natriuretic peptide infusion in young and adult rats. 285 May 23

We recently found that the brain cytosolic microtubule-associated protein 1C (MAP 1C) is a microtubule-activated ATPase, capable of translocating microtubules in vitro in the direction corresponding to retrograde transport. (Paschal, B. M., H. S. Shpetner, and R. B. Vallee. 1987b. J. Cell Biol. 105:1273-1282; Paschal, B. M., and R. B. Vallee. 1987. Nature [Lond.]. 330:181-183.). Biochemical analysis of this protein (op. cit.) as well as scanning transmission electron microscopy revealed that MAP 1C is a brain cytoplasmic form of the ciliary and flagellar ATPase dynein (Vallee, R. B., J. S. Wall, B. M. Paschal, and H. S. Shpetner. 1988. Nature [Lond.]. 332:561-563). We have now characterized the ATPase activity of the brain enzyme in detail. We found that microtubule activation required polymeric tubulin and saturated with increasing tubulin concentration. The maximum activity at saturating tubulin (Vmax) varied from 186 to 239 nmol/min per mg. At low ionic strength, the Km for microtubules was 0.16 mg/ml tubulin, substantially lower than that previously reported for axonemal dynein. The microtubule-stimulated activity was extremely sensitive to changes in ionic strength and sulfhydryl oxidation state, both of which primarily affected the microtubule concentrations required for half-maximal activation. In a number of respects the brain dynein was enzymatically similar to both axonemal and egg dyneins. Thus, the ATPase required divalent cations, calcium stimulating activity less effectively than magnesium. The MgATPase was inhibited by metavandate (Ki = 5-10 microM for the microtubule-stimulated activity), 1 mM NEM, and 1 mM EHNA. In contrast to other dyneins, the brain enzyme hydrolyzed CTP, TTP, and GTP at higher rates than ATP. Thus, the enzymological properties of the brain cytoplasmic dynein are clearly related to those of other dyneins, though the brain enzyme is unique in its substrate specificity and in its high sensitivity to stimulation by microtubules.
J Cell Biol 1988 Sep
PMID:Characterization of the microtubule-activated ATPase of brain cytoplasmic dynein (MAP 1C). 297 Oct 69

Vasodilators have demonstrated efficacy in neonates with depressed myocardial function. The magnitude of benefit depends on the preexisting hemodynamic state and concurrent treatment modalities. In patients with increased filling pressures, vasodilators increase cardiac output with negligible effect on MAP, with volume resuscitation to restore pretreatment filling pressures offering additional benefit. The rationale for use in neonatal respiratory disease remains less clear, with no vasoactive drug showing selective pulmonary vasodilatation. Benefit no doubt accrues from the improved coronary perfusion that occurs with reduction in filling pressures. In addition, reduced interventricular diastolic dependence and thereby improved ventricular compliance, as well as the afterload-reducing effect of decreased chamber size, may significantly reduce the effect of the lung disease on myocardial functioning.
Clin Perinatol 1988 Sep
PMID:The use of inotropic and afterload-reducing agents in neonates. 306 49

Axoplasmic vesicles were purified and observed to translocate on isolated microtubules in an ATP-dependent, trypsin-sensitive manner, implying that ATP-binding polypeptides essential for force generation were present on the vesicle surface. To identify these proteins [alpha 32P]8-azidoadenosine 5'-triphosphate ([alpha 32P]8-N3ATP), a photoaffinity analogue of ATP, was used. The results presented here identify and characterize a vesicle-associated polypeptide having a relative molecular mass of 292 kD that bound [alpha 32P]8-N3ATP. The incorporation of label is ultraviolet light-dependent and ATP-sensitive. Moreover, the 292-kD polypeptide could be isolated in association with vesicles or microtubules, depending on the conditions used, and the data indicate that the 292-kD polypeptide is similar to mammalian brain microtubule-associated protein 2 (MAP 2) for the following reasons: The 292-kD polypeptide isolated from either squid axoplasm or optic lobe cross-reacts with antiserum to porcine brain MAP 2. Furthermore, it purifies with taxol-stabilized microtubules and is released with salt. Based on these characteristics, the 292-kD polypeptide is distinct from the known force-generating molecules myosin and flagellar dynein, as well as the 110-130-kD kinesin-like polypeptides that have recently been described (Brady, S. T., 1985, Nature (Lond.), 317:73-75; Vale, R. D., T. S. Reese, and M. P. Sheetz, 1985b, Cell, 42:39-50; Scholey, J. M., M. E. Porter, P. M. Grissom, and J. R. McIntosh, 1985, Nature (Lond.), 318:483-486). Because the 292-kD polypeptide binds ATP and is associated with vesicles that translocate on purified MAP-free microtubules in an ATP-dependent fashion, it is therefore believed to be involved in vesicle-microtubule interactions that promote organelle motility.
J Cell Biol 1986 Sep
PMID:Identification of a MAP 2-like ATP-binding protein associated with axoplasmic vesicles that translocate on isolated microtubules. 309 8

The effectiveness of three different ventilator rates of artificial ventilation (30, 60 and 120/min) was studied in 32 preterm infants, all of whom were suffering from the Respiratory Distress Syndrome (16 were paralysed). Ventilator pressures, I:E ratio and MAP were kept constant at each rate. Increase in rate from 30 to 60 and to 120/min was well tolerated and not associated with episodes of hypotension. The only significant improvement in oxygenation was amongst the non-paralysed infants and at a rate of 120/min (p less than 0.01) this was associated with synchronous respiration. Two different ventilators were used in the study and a significant change in PaCO2 (reduction) occurred only in non-paralysed infants ventilated at a rate of 120/min by Sechrist ventilators (p less than 0.05). This difference may be a direct reflection of differences in ventilator performance at fast rates.
Acta Paediatr Scand 1987 Sep
PMID:Comparison of different rates of artificial ventilation in preterm neonates with respiratory distress syndrome. 331 May 13

Regional blood flow was measured simultaneously in rat sciatic nerves (NBF), truncal skin (SBF), and biceps femoris muscles (MBF) after graded hemorrhages. A modified 14C-butanol "indicator-fractionation" technique was used. In controls NBF was 11.4 +/- 1.38 ml X min-1 X 100 gm-1 and did not differ significantly between limbs. After hypotension, NBF was: 101 mm Hg, 7.7 +/- 1.3; 83 mm Hg, 5.3 +/- 0.6; 62 mm Hg, 4.1 +/- 0.6; 38 mm Hg, 3.1 +/- 0.3. The relationship between NBF and MAP was linear: (r = 0.56; p less than 0.001). SBF also declined linearly in hypotension (r = 0.54; p less than 0.01), but MBF did not change significantly. No significant change in nerve vascular resistance occurred with hypotension but muscle vascular resistance declined progressively. The data indicate a striking absence of autoregulation of NBF, but MBF, as expected, displayed close autoregulation. The vascular mechanisms which regulate resting NBF following hemorrhage differ from those in both muscle and skin: during hypotension, the calculated neurovascular resistance was unchanged, while the resistance in muscle fell and that in the skin increased.
J Trauma 1987 Sep
PMID:Regional blood flow in sciatic nerve, biceps femoris muscle, and truncal skin in response to hemorrhagic hypotension. 365 65

The influence of laryngoscopy and intubation with or without topical lidocaine anesthesia on the endocrine stress response was investigated in six groups of 40 orthopedic surgery patients differing in premedication and technique of lidocaine application (one- or two-step method). Controls were included without lidocaine application. Plasma levels of catecholamines (by HPLC) were measured before induction and 1, 5, and 10 min after intubation, ADH-levels (by RIA) before induction and 5 and 10 min after intubation. In addition, mean arterial pressure (MAP, MAP), HR, and the incidence of coughing and cardiac arrhythmias were observed. The statistical evaluation (analysis of variance with repeated measures on one factor) considered P values of less than 0.05 significant. There was no influence of laryngoscopy and intubation on plasma catecholamine levels during the observation period. A continuous decrease in both levels of epinephrine and norepinephrine was significant. ADH levels showed no significant changes. Lidocaine had no influence on these endocrine parameters. MAP and HR increased after intubation in all groups studied. The increase in HR was less pronounced after lidocaine treatment. Coughing (4 patients) and ventricular dysrhythmia (2 patients) were observed only in patients without lidocaine treatment. In conclusion, no influence of different modes of treatment on the endocrine stress response during intubation became obvious. There was no indication that the cardiovascular symptoms during laryngoscopy and intubation are caused by systemic stress. An explanation may be a direct neural impulse via sympathetic efferents to the heart. On the other hand, topical application of lidocaine did prevent coughing and cardiac irritation, and the increase in HR was attenuated.(ABSTRACT TRUNCATED AT 250 WORDS)
Anaesthesist 1987 Sep
PMID:[The endocrine stress-reaction to orotracheal intubation and topical anesthesia with lidocaine]. 368 17

Rabbit antibodies raised against microtubule-associated protein 1 (MAP-1) from hog brain were found to crossreact with extracellular matrix components of mouse BALB/c 3T3 cell cultures. As shown by immunofluorescence microscopy of confluent cell cultures, the extracellular MAP-related antigen was located on dense fibrillar network arrays underlying and surrounding the cells. The immunoreactive material was sensitive to trypsin but resistant to collagenase. The microtubule-disrupting drug colcemid had no visible effect on the morphology of the anti-MAP-stained network, whereas treatment with cytochalasin B provoked its abolishment. Simian virus 40-transformed BALB/c 3T3 cells expressed considerably less extracellular antigen than did the nontransformed cells. After in vivo radiolabeling of BALB/c 3T3 cells, a secreted polypeptide of Mr 205,000 was isolated by immuno-precipitation from culture media as well as from cell-free extracellular matrices. This antigen was identified as a sulfoglycoprotein, noncollageneous in nature, that undergoes intermolecular disulfide bonding. Anti-MAP-1 antibodies affinity-purified on the extracellular Mr 205,000 protein were immunoreactive with MAP-1 and MAP-2 from brain and decorated cytoplasmic microtubules as demonstrated by immunoblotting and immunofluorescence microscopy. Thus, a structural relationship between cytoskeletal and extracellular polypeptides is demonstrated.
Proc Natl Acad Sci U S A 1985 Sep
PMID:Mr 205,000 sulfoglycoprotein in extracellular matrix of mouse fibroblast cells is immunologically related to high molecular weight microtubule-associated proteins. 389 71

Rats received once daily injections of methamphetamine (MAP; 4 mg/kg/day) intraperitoneally, at most 100 times. Enhanced ambulatory activity by MAP reduced during the long-term administration of MAP. The mean rating score of MAP-induced abnormal behavior, including locomotion, stereotyped behavior, motor inhibition and the response to acoustic stimulation, increased until 56th injection of MAP. But after that, the score tended to decrease mainly because the injected MAP failed to keep the movement of rats reduced under acoustic stimulation. Neither the time course of these rating score nor the decrease in [3H] spiperone binding sites, examined after the injection of MAP 100 times, seemed to develop along with the repeated MAP administration. Thus, the changes in both behavior and [3H] spiperone binding sites produced by repeated MAP would not necessarily indicate the symptoms of MAP-induced psychosis in man, because the susceptibility to psychosis in man increases along with the time of MAP injection. It is presumed that the animal model of psychosis produced by administration of MAP is important not as a model of psychotic symptoms, but as a model of increased susceptibility to psychosis induced by MAP.
Yakubutsu Seishin Kodo 1985 Sep
PMID:[Chronological change in abnormal behavior produced by long-term methamphetamine administration in the rat]. 407 36

The major acute-phase protein (alpha 1-MAP) of rat serum is induced in response to inflammation. This induction may be attributed to a corresponding increase in the level of translatable mRNA for the protein. Using in vitro and in vivo systems, various biosynthetic processing intermediates of this glycoprotein have been isolated. alpha 1-MAP is translated in a rabbit reticulocyte system as a preprotein with an amino-terminal signal peptide and an apparent molecular weight of 51,000. Translation of rough microsomes yields a product with a mass of 57,000 Da, representing the core glycosylated form of alpha 1-MAP. Cotranslational glycosylation appears to occur in a stepwise fashion, since three glycosylated forms of alpha 1-MAP (51,000, 54,000, and 57,000 Da) were detected in polysome translations; these products were digested by endoglycosidase H to a 48,000-Da protein. Two intracellular forms of alpha 1-MAP were observed in vivo, a 57,000-Da (core carbohydrate sidechains) and a 66,000-Da protein (mature complex carbohydrate side-chains); the latter was the only component secreted into the culture medium. To extend our studies on this protein, a cDNA clone specific for alpha 1-MAP was isolated. The recombinant was positively identified by hybrid selection procedures and contains a 1.55-kb insert. Partial radiosequence analysis of the primary translation product indicated the distribution of Leu, Ile, Cys, and Met in the amino-terminal region of this protein. To relate the location of these amino acids with the nucleotide sequence, cDNA was analyzed by the method of Maxam and Gilbert. These results indicate that the cDNA insert contains the 3' poly(A) tail, and alignment of the 5' end of the cDNA with the available amino acid sequence of the primary translation product corroborated that the insert encodes the entire alpha 1-MAP protein except for the first four amino acids of the signal peptide.
Arch Biochem Biophys 1984 Sep
PMID:Rat major acute-phase protein: biosynthesis and characterization of cDNA clone. 620 75


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