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PubMed2002

Contribution of body surface mapping to clinical outcome after surgical ablation of postinfarction ventricular tachycardia.

This article investigates the influence of body surface mapping on outcome of ventricular antiarrhythmic surgery. Preoperative mapping is advocated to optimize map-guided antiarrhythmic surgery of postinfarction ventricular tachycardia. We sequentially analyzed the results of catheter activation sequence mapping, body surface mapping, and intraoperative multielectrode mapping in 54 patients and made a comparison with 30 control patients (group B) in whom catheter activation sequence mapping was omitted. Endpoints were actuarial survival, freedom of arrhythmia, and comparability of the localisation of sites of ventricular tachycardia origin. A total of 128 morphologically different monomorphic sustained ventricular tachycardias were mapped in group A. In group A, 87 ventricular tachycardias were mapped preoperatively with body surface mapping and 30 ventricular tachycardias with catheter activation sequence mapping. In 19 of 24 ventricular tachycardias (79%) that were localized with both mapping methods the ventricular tachycardia exit site was similar. In-hospital death was 1 of 85 (1.2%). Actuarial freedom from ventricular arrhythmias at 4-year follow-up was 74.1 +/- 6.0% in group A vs. 90.0+/-5.5% in group B (P =.10). In group A 14 of 54 patients died (29.6%), whereas 4 of 30 patients (13.3%) died in group B (P =.09). Arrhythmia freedom and survival is as good in patients mapped with body surface mapping only as in patients mapped with body surface mapping and catheter activation sequence mapping.

Aged↗
PubMed2001

An enhanced linkage map of the sheep genome comprising more than 1000 loci.

A medium-density linkage map of the ovine genome has been developed. Marker data for 550 new loci were generated and merged with the previous sheep linkage map. The new map comprises 1093 markers representing 1062 unique loci (941 anonymous loci, 121 genes) and spans 3500 cM (sex-averaged) for the autosomes and 132 cM (female) on the X chromosome. There is an average spacing of 3.4 cM between autosomal loci and 8.3 cM between highly polymorphic [polymorphic information content (PIC) > or = 0.7] autosomal loci. The largest gap between markers is 32.5 cM, and the number of gaps of > 20 cM between loci, or regions where loci are missing from chromosome ends, has been reduced from 40 in the previous map to 6. Five hundred and seventy-three of the loci can be ordered on a framework map with odds of > 1000 : 1. The sheep linkage map contains strong links to both the cattle and goat maps. Five hundred and seventy-two of the loci positioned on the sheep linkage map have also been mapped by linkage analysis in cattle, and 209 of the loci mapped on the sheep linkage map have also been placed on the goat linkage map. Inspection of ruminant linkage maps indicates that the genomic coverage by the current sheep linkage map is comparable to that of the available cattle maps. The sheep map provides a valuable resource to the international sheep, cattle, and goat gene mapping community.

Animals↗
PubMed1989

Multiple electrosensory maps in the medulla of weakly electric gymnotiform fish. II. Anatomical differences.

Both wave- and pulse-type species of weakly electric gymnotiform fish have 3 topographic maps of electroreceptive information in the electrosensory lateral line lobe (ELL). These maps receive identical input from trifurcating axons of phase- and amplitude-coding primary afferents (Carr et al., 1982; Heiligenberg and Dye, 1982). Physiological experiments in the ELL of the wave-type fish Eigenmannia show that the amplitude-coding pyramidal cells differ among maps with respect to receptive field size, sensitivity, rate of adaptation, and temporal-frequency response (Shumway, 1989). This study investigated morphological correlates of the physiological differences among maps. Estimates of primary afferent convergence in Eigenmannia, based on map size, cell counts, and areas of terminal fields from intracellularly filled P-type primary afferents, suggest a 2-fold increase in convergence in the lateral map relative to the centromedial map. Similar differences in convergence between maps are found in the wave-type species Apteronotus leptorhynchus and the pulse-type fish Hypopomus occidentalis. The lateral and centrolateral maps in Hypopomus, however, show an even greater difference in convergence. Comparison of the efferent projections of pyramidal cells among the different maps of Eigenmannia indicates that cells from the 3 maps terminate in the same laminae of the torus semicircularis, but the maps differ in the strength of projection to particular laminae. In both wave-type species, the abundance of a class of interneurons which receives descending input and inhibits pyramidal cells (interneurons of the ventral molecular layer) differs among maps; the centromedial map has 10 times fewer neurons of this type than the other 2 maps. Cytochrome oxidase studies in all 3 species demonstrated increased levels of activity in the lateral map, within the region receiving descending input from the cerebellum. These results suggest that the primary anatomical bases of the physiological differences among maps are differences in the amount of primary afferent convergence, coupled with differences in descending input.

Animals↗
PubMed1982

A taxol-dependent procedure for the isolation of microtubules and microtubule-associated proteins (MAPs).

The effect of the antimitotic drug taxol on the association of MAPs (microtubule-associated proteins) with microtubules was investigated. Extensive microtubule assembly occurred in the presence of Taxol at 37 degrees C. at 0 degrees C, and at 37 degrees C in the presence of 0.35 M NaCl, overcoming the inhibition of assembly normally observed under the latter two conditions. At 37 degrees C and at 0 degrees C, complete assembly of both tubulin and the MAPs was observed in the presence of Taxol. However, at elevated ionic strength, only tubulin assembled, forming microtubules devoid of MAPs. The MAPs could also be released from the surface of preformed microtubules by exposure to elevated ionic strength. These properties provided the basis for a rapid new procedure for isolating microtubules and MAPs of high purity from small amounts of biological material. The MAPs could be recovered by exposure of the microtubules to elevated ionic strength and subjected to further analysis. Microtubules and MAPs were prepared from bovine cerebral cortex (gray matter) and from HeLa cells. MAP 1, MAP2, and the tau MAPs, as well as species of Mr = 28,000 and 30,000 (LMW, or low molecular weight, MAPs) and a species of Mr = 70,000 were isolated from gray matter. Species identified as the 210,000 and 125,000 mol wt HeLa MAPs were isolated from HeLa cells. Microtubules were also prepared for the first time from white matter. All of the MAPs identified in gray matter preparations were identified in white matter, but the amounts of individual MAP species differed. The most striking difference in the two preparations was a fivefold lower level of MAP 2 relative to tubulin in white matter than in gray. The high molecular weigh MAP, MAP1, was present in equal ratio to tubulin in white and gray matter. These results indicate that MAP 1 and MAP2, as well as other MAP species, may have a different cellular or subcellular distribution.

Alkaloids↗
PubMed1998

The distribution of murine 115-kDa epithelial microtubule-associated protein (E-MAP-115) during embryogenesis and in adult organs suggests a role in epithelial polarization and differentiation.

In interphase cells microtubules play fundamental roles in the intracellular distribution and movement of organelles and vesicles and thereby contribute to cellular polarization and differentiation. The organization of microtubules varies with the cell type and is presumably controlled by tissue-specific microtubule-associated proteins (MAPs). The 115-kDa epithelial MAP (E-MAP-115) has been identified as a microtubule-stabilizing protein predominantly expressed in cell lines of epithelial origin. To assess a putative function of E-MAP-115 in epithelial morphogenesis in vivo, we have cloned the cDNA encoding the murine protein and studied the cellular distribution of E-MAP-115 mRNA and protein during murine embryogenesis and in adult organs. Analysis of the predicted amino acid sequence of murine E-MAP-115 revealed 81% sequence identity with its human homolog, the best-conserved part of the protein being the microtubule-binding site. Our data indicate that E-MAP-115 is expressed in several epithelia from 9.5 days of embryogenesis onwards and that its expression levels increase during development. From 14.5 days onwards, E-MAP-115 mRNA is found in some neuronal cells as well. In adult organs, E-MAP-115 is most abundant in epithelial cells of kidney tubules, in absorptive cells of the intestine and is widely distributed in the testis. E-MAP-115 expression correlates with the differentiation of certain epithelial cell types: in the adult intestine, for example, E-MAP-115 mRNA and protein are more abundant in the differentiating than in the proliferative cell compartment. Moreover, E-MAP-115 expression clearly correlates with the degree of cellular apicobasal polarity. In the developing kidney, E-MAP-115 mRNA is detected in the cuboidal cells of S-shaped bodies, of primitive tubules and glomerula, whereas, E-MAP-115 mRNA and protein are absent from mature podocytes which have lost their initial apico-basal polarity. The pattern of distribution of E-MAP-115 in vivo is so far unique for a MAP. Taken together, our results provide support for a role of E-MAP-115 in reorganizing the microtubule cytoskeleton during epithelial cell polarization and differentiation.

Aging↗
PubMed1991

Electrocardiographic markers of ischemia during mental stress testing in postinfarction patients. Role of body surface mapping.

In patients with coronary artery disease, radionuclide investigations have documented a high incidence of mental stress-induced myocardial ischemia in the absence of significant electrocardiographic changes and/or angina. To investigate the causes of the low electrocardiographic sensitivity, we recorded body surface maps during mental arithmetic in 22 normal volunteers and 37 postinfarction patients with residual exercise ischemia. Myocardial perfusion was studied with thallium-201 or technetium-99 (SESTAMIBI) planar scans. In 14 patients, body surface maps were also recorded during atrial pacing at the heart rate values achieved during mental stress. While taking the body surface maps, the area from J point to 80 msec after this point (ST-80) was analyzed by integral maps, difference maps, and departure maps (the difference between each patient's difference map and the mean difference map for normal subjects). The body surface mapping criteria for ischemia were a new negative area on the integral maps, a negative potential of more than 2 SD from mean normal values on the difference maps, and a negative departure index of more than 2. Scintigraphy showed asymptomatic myocardial hypoperfusion in 33 patients. Eight patients had significant ST segment depression. The ST-80 integral and difference maps identified 17 ischemic patients. Twenty-four patients presented abnormal departure maps. One patient presented ST depression and abnormal body surface maps without reversible tracer defect. In 14 of 14 patients, atrial pacing did not reproduce the body surface map abnormalities. The analyses of the other electrocardiographic variables showed that in patients with mental stress-induced perfusion defects, only changes of T apex-T offset (aT-eT) interval in Frank leads and changes of maximum negative potential value of aT-eT integral maps significantly differed from those of normal subjects. Our results confirm the low electrocardiographic sensitivity for detecting mental stress-induced myocardial hypoperfusion in postinfarction patients. ST analysis in the body surface map increases the information content of the electrocardiographic signal. T wave analysis appears to offer fewer diagnostic advantages.

Cardiac Pacing, Artificial↗
PubMed1993

[Assessment of myocardial viability by exercise stress-redistribution myocardial scintigraphy with thallium-201: the usefulness of C-map].

Standard exercise (Ex)-redistribution (RD) myocardial imaging with thallium-201 (201Tl) may not differentiate viable myocardium from necrosis. This study was intended to clarify whether 201Tl washout rate (WOR) abnormality after Ex can detect myocardial viability in the myocardium with perfusion defect using routine RD image. We performed Ex-RD (three hours after) myocardial tomography with 201Tl in 29 patients with coronary artery disease. From myocardial tomography, 201Tl distribution Bull's-eye maps (Ex and RD) and WOR Bull's-eye map were made. At RD image before PTCA, by referring to the original image, the activity of the myocardial region below 40% to 55% of the maximal 201Tl activity was considered as perfusion defect (RD-Map). Then we constructed a new image (C-Map) by adding the location of WOR abnormality (< or = 30%) to the RD-Map and each map was divided into 17 segments. If the defect-segment in the RD-Map corresponded to WOR abnormality, the segment in the C-Map was judged as viable (no defect). The C-Map and myocardial imaging after PTCA (Post-Map) were compared. In the RD-Map before PTCA, defect was found in 152 segments but in the C-Map they decreased to 59 segments, while defect was found in 62 segments in the Post-Map. In 23 patients the number of defect-segments in the C-Map decreased as compared with those in the RD-Map. And in 22 of them, the Post-Map showed the reduction of defect-segments in comparison with the RD-Map, but in one of them defect did not change.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Comparison of Z and multivariate statistical brain electromagnetic maps for the localization of brain lesions.

Conventional Z maps provide probability statements about the deviation of observed values from the norm. Galán et al. (1994) introduced Simultaneous Significance Probability Scales to detect abnormalities over the whole map, making use of the information provided by the topographic structure of dependencies. They also described multivariate brain electromagnetic (MBE) maps for compact presentation of complex spatio-temporal information. In this paper, using the distance-based localization receiver operating characteristic curves (DL-ROC curves), we compare the localization provided by computed tomography with that provided by Z and MBE maps in 61 patients with brain lesions. Maps were calculated for absolute power and relative power in delta, theta, alpha and beta bands for voltage and current source densities (CSD). In each patient, all maps were compared and the map with the highest value of the area of the DL-ROC curve was considered to be the "best map." Z maps of CSD were the "best maps" in 24 patients. In the voltage montage, we observed that multivariate maps add some information not contained in the Z maps. However, for CSD, Z maps were more accurate than multivariate maps. A very consistent finding was the observation that lesions were better detected by maps analyzing the delta band, while edema was better represented by maps in the theta range.

Brain Damage, Chronic↗
PubMed2002

The role of mitogen-activated protein (MAP) kinase in breast cancer.

Mitogen-activated protein kinase (MAP kinase) cascades transmit and amplify signals involved in cell proliferation as well as cell death. These signal transduction pathways serve as an indicators of the intensity of trafficking induced by various growth factor, steroid hormone, and G protein receptor mediated ligands. Three major MAP kinase pathways exist in human tissues, but the one involving ERK-1 and -2 is most relevant to breast cancer. Peptide growth factors acting through tyrosine kinase containing receptors are the major regulators of ERK-1 and -2. Estradiol, progesterone, and testosterone can act non-genomically via membrane associated receptors to activate MAP kinase as can various other ligands acting through heterotrimeric G protein receptors. Recent studies demonstrate that breast cancers frequently contain an increased proportion of cells with the activated form of MAP kinase. In estrogen receptor positive breast tumors, MAP kinase pathways can exert "cross talk" effects at the level of ER induced transcription as well as at the level of the cell cycle. Estradiol stimulates cell proliferation by mechanisms which involve activation of MAP kinase, either through rapid, non-transcription effects or by increasing growth factor production and consequently MAP kinase. Progesterone and androgens also stimulate MAP kinase through both of these two mechanisms. Strategies used to treat hormone dependent breast cancer appear to result in upregulation of MAP kinase activation. Direct experimental data demonstrate that the pressure of estradiol deprivation results in the upregulation of MAP kinase in breast cancer cells growing in tissue culture and as xenografts. A number of investigators have now studied the expression of activated MAP kinase in human breast cancer tissues by enzymatic assay and by immunohistochemical techniques. Approximately half of breast tumors express more activated MAP kinase than does the surrounding benign tissue. Studies show a trend toward higher MAP kinase activity in primary tumors of node positive than in node negative patients. However, larger numbers of patients must be studied for these results to achieve statistical significance. The up-regulation of MAP kinase activity does not represent mutations of Ras, but appears to result from enhancement of growth factor pathway activation. No data are yet available on the relationship between MAP kinase activation and apoptosis. Additional studies are now needed to determine the precise relationship between MAP kinase activation and tumor proliferation, apoptosis, and degree of invasiveness as well as on disease free and overall survival.

Breast Neoplasms↗
PubMed2000

High-resolution EEG mappings: a spherical harmonic spectra theory and simulation results.

Shown first is the equivalence between the multiple expansion (ME) of the brain electrical generator and the spherical harmonic spectra (SHS) of the potential generated by the electrical generator in an infinite volume conductor. Based on the equivalence, the SHS and the spatial filters which connect the SHS with the ME are deduced, in a concentric 3 sphere conductor and for the 5 EEG source mappings. They are cortical potential mapping (CPM), scalp Laplacian mapping (LM), pseudo-cortical potential mapping (PCPM), equivalent dipole layer mapping (EDM) and equivalent charge layer mapping (ECM). The theoretical simulation study of the spatial filters and mappings indicate that all 5 mappings provide higher resolution imaging maps of brain electrical activity than the scalp potential map. In the inverse problem, a spherical spline fit algorithm is provided to reconstruct the SHS of the scalp recording potential, and then the SHS and maps of the 5 mappings are reconstructed by utilizing the spatial filters and the SHS of the scalp potential. The results indicate that the correlativity order between a reconstructed map and the actual cortical potential map is CPM > or = EDM > PCPM > LM > ECM. An empirical VEP data study shows that any one of the 5 mappings also provides higher spatial resolution than the scalp potential map.

Brain↗
PubMed1997

MAP kinase is required for the spindle assembly checkpoint but is dispensable for the normal M phase entry and exit in Xenopus egg cell cycle extracts.

In Xenopus laevis egg cell cycle extracts that mimic early embryonic cell cycles, activation of MAP kinase and MAP kinase kinase occurs in M phase, slightly behind that of maturation promoting factor. To examine the possible role of MAP kinase in the in vitro cell cycle, we depleted the extracts of MAP kinase by using anti-Xenopus MAP kinase antibody. Like in the mock-treated extracts, the periodic activation and deactivation of MPF occurred normally in the MAP kinase-depleted extracts, suggesting that MAP kinase is dispensable for the normal M phase entry and exit in vitro. It has recently been reported that microtubule depolymerization by nocodazole treatment can block exit from mitosis in the extracts if enough sperm nuclei are present, and that the addition of MAP kinase-specific phosphatase MKP-1 overcomes this spindle assembly checkpoint, suggesting the involvement of MAP kinase in the checkpoint signal transduction. We show here that the spindle assembly checkpoint mechanism cannot operate in the MAP kinase-depleted extracts. But, adding recombinant Xenopus MAP kinase to the MAP kinase-depleted extracts restored the spindle assembly checkpoint. These results indicate unambiguously that classical MAP kinase is required for the spindle assembly checkpoint in the cell cycle extracts. In addition, we show that strong activation of MAP kinase by the addition of a constitutively active MAP kinase kinase kinase in the absence of sperm nuclei and nocodazole, induced mitotic arrest in the extracts. Therefore, activation of MAP kinase alone is sufficient for inducing the mitotic arrest in vitro.

Animals↗
PubMed2004

Magnetoelectroanatomic mapping of arrhythmias in structural heart disease using a novel multielectrode catheter:.

Electroanatomic mapping with CARTO requires point-by-point acquisition using the mapping catheter's bipolar tip electrode. This study evaluates the utility of a novel 26-electrode catheter (Qwikstar) for electroanatomic mapping of arrhythmias in patients with structural heart disease. The multielectrode catheter acquires activation times and anatomic data simultaneously from its tip and shaft electrodes. Eight patients (6 men, 2 women, age 47 years [37, 65]) with atrial tachycardia (n = 6) and ventricular tachycardia (n = 2) due to congenital heart disease (n = 4) and cardiomyopathy (n = 4) were studied. Using the multielectrode catheter, the electroanatomic map was constructed in two stages: (1) a scout map using the minimum number of tip and shaft electrode data points that covered > 70% of the tachycardia cycle length and/or the majority of the chamber volume, and (2) a complete map using additional tip electrode data points. A total of 36 (28, 510) tip electrode and 38 (34, 42) shaft electrode electroanatomic data points comprised the scout map. The complete map was constructed with a total of 102 (73, 134) tip electrode electroanatomic data points. In three patients, the scout map suggested a cavotricuspid isthmus dependent atrial flutter that was confirmed with the complete map. In another four patients, the scout map identified the earliest site of focal activation, which was also confirmed with the complete map. In comparison, activation mapping using the bipolar catheter (Navistar) in a group of arrhythmia-matched control subjects required 210 (180, 320) electroanatomic data points (P = 0.012 vs multielectrode catheter complete map). In conclusion, for large macroreentrant or focal arrhythmias in patients with structural heart disease, the multielectrode catheter can generate a scout map that accurately guides complete electroanatomic mapping using fewer point-by-point acquisitions than the bipolar catheter.

Adult↗
PubMed1999

A high-density integrated genetic linkage and radiation hybrid map of the laboratory rat.

The laboratory rat (Rattus norvegicus) is a key animal model for biomedical research. However, the genetic infrastructure required for connecting phenotype and genotype in the rat is currently incomplete. Here, we report the construction and integration of two genomic maps: a dense genetic linkage map of the rat and the first radiation hybrid (RH) map of the rat. The genetic map was constructed in two F2 intercrosses (SHRSP x BN and FHH x ACI), containing a total of 4736 simple sequence length polymorphism (SSLP) markers. Allele sizes for 4328 of the genetic markers were characterized in 48 of the most commonly used inbred strains. The RH map is a lod >/= 3 framework map, including 983 SSLPs, thereby allowing integration with markers on various genetic maps and with markers mapped on the RH panel. Together, the maps provide an integrated reference to >3000 genes and ESTs and >8500 genetic markers (5211 of our SSLPs and >3500 SSLPs developed by other groups). [Bihoreau et al. (1997); James and Tanigami, RHdb (http:www.ebi.ac.uk/RHdb/index.html); Wilder (http://www.nih.gov/niams/scientific/ratgbase); Serikawa et al. (1992); RATMAP server (http://ratmap.gen.gu.se)] RH maps (v. 2.0) have been posted on our web sites at http://goliath.ifrc.mcw.edu/LGR/index.html or http://curatools.curagen.com/ratmap. Both web sites provide an RH mapping server where investigators can localize their own RH vectors relative to this map. The raw data have been deposited in the RHdb database. Taken together, these maps provide the basic tools for rat genomics. The RH map provides the means to rapidly localize genetic markers, genes, and ESTs within the rat genome. These maps provide the basic tools for rat genomics. They will facilitate studies of multifactorial disease and functional genomics, allow construction of physical maps, and provide a scaffold for both directed and large-scale sequencing efforts and comparative genomics in this important experimental organism.

Alleles↗
PubMed1989

Multiple electrosensory maps in the medulla of weakly electric gymnotiform fish. I. Physiological differences.

The electrosensory lateral line lobe in the weakly electric gymnotiform fish Eigenmannia contains 3 topographic maps of high-frequency (tuberous) electroreceptive information from the body surface. The maps receive identical primary afferent input since axonal collaterals of both amplitude- and phase-coding afferents project to all 3 maps (Heiligenberg and Dye, 1982). Response properties of the amplitude-coding pyramidal neurons in the multiple maps were investigated in order to determine whether the maps differ physiologically. Units in the lateral map have larger receptive fields and are more sensitive than units in the centromedial map. The former units respond more phasically and with shorter latencies to step changes in stimulus amplitude (measured from the stimulus onset to the maximum response). Although 75% of pyramidal cells in all maps show a center-surround receptive-field organization, the strength of the inhibitory surround varies among maps, tending to be weakest for units in the lateral map and strongest for units in the centromedial map. Pyramidal neurons also differ in their responses with respect to the temporal frequency of amplitude modulations; the majority of units in the lateral map prefer high temporal frequencies, while those in the centromedial map prefer low frequencies. These results suggest that the multiple electrosensory maps could provide the initial separation of spatial and temporal processing of sensory information, much as has been suggested for X and Y ganglion cells in the cat retina (Shapley and Perry, 1986). The centromedial map could provide high spatial contrast with correspondingly poor temporal resolution, while the more sensitive units in the lateral map could best provide information about temporal changes in stimulus amplitude.

Adaptation, Physiological↗
PubMed1995

Transcriptional regulation by MAP kinases.

Tyrosine kinase growth factor receptors activate MAP kinase by a complex mechanism involving the SH2/3 protein Grb2, the exchange protein Sos, and Ras. The GTP-bound Ras protein binds to the Raf kinase and initiates a protein kinase cascade that leads to MAP kinase activation. Three MAP kinase kinase kinases have been described--c-Raf, c-Mos, and Mekk--that phosphorylate and activate Mek, the MAP kinase kinase. Activated Mek phosphorylates and activates MAP kinase. Subsequently, the activated MAP kinase translocates into the nucleus where many of the physiological targets of the MAP kinase signal transduction pathway are located. These substrates include transcription factors that are regulated by MAP kinase phosphorylation (e.g., Elk-1, c-Myc, c-Jun, c-Fos, and C/EBP beta). Thus the MAP kinase pathway represents a significant mechanism of signal transduction by growth factor receptors from the cell surface to the nucleus that results in the regulation of gene expression. Three MAP kinase homologs have been identified in the rat: Erk1, Erk2, and Erk3. Human MAP kinases that are similar to the rat Erk kinases have also been identified by molecular cloning. The human Erk1 protein kinase has been shown to be widely expressed as a 44-kDa protein in many tissues. The human Erk2 protein kinase is a 41-kDa protein that is expressed ubiquitously. In contrast, a human Erk3-related protein kinase has been found to be expressed at a high level only in heart muscle and brain. The loci of these MAP kinase genes are widely distributed within the human genome: erk2 at 22q11.2; erk1 at 16p11.2; and ek3-related at 18q12-21. In the yeast Saccharomyces cerevisiae, five MAP kinase gene homologs have been described: smkl, mpk1, hog1, fus3, and kss1. Together, these kinases are a more diverse group than the human erks that have been identified. Thus the erks are likely to represent only one subgroup of a larger human MAP kinase gene family. A candidate for this extended family of MAP kinases is the c-Jun NH2-terminal kinase (Jnk), which binds to and phosphorylates the transcription factor c-Jun at the activating sites Ser-63 and Ser-73. Evidence is presented here to demonstrate that Jnk is a distant relative of the MAP kinase group that is activated by dual phosphorylation at Tyr and Thr.

Amino Acid Sequence↗
PubMed2004

Ice mapping during cryothermal ablation of accessory pathways in WPW: the role of the temperature time constant.

AIM: Cryothermal energy has the ability reversibly to demonstrate loss of function with cooling, ice mapping, at less deep temperatures. The purpose of this study was to investigate the time course of the temperature during ice mapping of accessory pathways. METHODS AND RESULTS: Thirteen patients with the Wolff-Parkinson-White (WPW) syndrome underwent cryoablation. After identification of a prospective ablation site, ice mapping was performed by cooling the tip to a minimum of -30 degrees C. Successful ice mapping was defined by loss of accessory pathway (AP) conduction. A total of 104 ice maps were analyzed. Successful ice mapping was demonstrated in 17 attempts. There was no significant difference in mapping temperature between successful and unsuccessful ice mapping (-29.4+/-3.2 degrees Celsius vs -30.4+/-1.7 degrees Celsius). The temperature time constant tau during successful ice mapping was significantly shorter compared with unsuccessful ice mapping (7.0+/-1.1 s vs 10.1+/-1.3 s; P<0.0001). The response time (RT) to mapping temperature of -30 degrees C was significantly prolonged in unsuccessful ice mapping attempts (35.8+/-4.5 s vs 53.5+/-11.0 s; P<0.0001). Significant correlations were found between successful ice mapping and the temperature time constant, and between RT and the temperature time constant (P<0.001). CONCLUSION: The ability to identify prospective ablation sites by ice mapping was demonstrated. Successful ice mapping attempts were characterized by a short temperature time constant and a short response time to mapping temperature with a sudden disappearance of pathway conduction.

Adult↗
PubMed1990

Peptides corresponding to the second repeated sequence in MAP-2 inhibit binding of microtubule-associated proteins to microtubules.

Bovine brain high molecular weight microtubule-associated proteins (MAPs) can be displaced from assembled tubules by peptides corresponding to the second of three nonidentical repeated sequences in mouse MAP-2. The octadecapeptide m2 (VTSKCGSLKNIRHRPGGG) can release MAP-1b from MAP-containing microtubules, and the extended second-sequence peptide m2' (VTSKCGSLKNIRHRPGGGRVK) displaces MAP-1a and MAP-1b as well as MAP-2a and MAP-2b. Peptides m2 and m2' stimulate tubulin polymerization in the absence of MAPs or microtubule-stabilizing agents, and m2' acts as a competitive inhibitor of radiolabeled MAP-2 binding. The dissociation constant for MAP-2 binding to taxol-stabilized tubules was 3.4 microM in the absence of m2' and 14 microM in the presence of 1.5 mM of the m2' peptide. We estimate that the inhibition constant for peptide m2' is about 0.5 mM, about 100 times lower than for the Km of MAP-2. These observations suggest that the second repeated sequence in MAP-2 may represent an important recognition site for MAP binding to microtubules and that other structural features within MAP-2 may reinforce the strength of MAP-microtubule interactions.

Amino Acid Sequence↗
PubMed2001

Binding of Fyn to MAP-2c through an SH3 binding domain. Regulation of the interaction by ERK2.

Microtubule-associated protein 2 (MAP-2) isoforms are developmentally expressed in the nervous system and contain a number of functional domains. Adjacent to the first repeat of the microtubule-binding domain is an RTPPKSP motif for binding SH3 domains. To identify SH3-containing proteins that interact with MAP-2, transfections, filter overlay assays, glutathione S-transferase (GST)-mediated binding assays, co-immunoprecipitations and enzyme-linked immunosorbent assays were performed. Transfections of MAP-2a, MAP-2b, and MAP-2c constructs into COS7 cells, followed by incubation of the cell lysates with SH3-GST fusion proteins, determined that the strongest interaction was between MAP-2c and the non-receptor tyrosine kinase Fyn; however, MAP-2b and MAP-2c also bound to Grb2. Co-immunoprecipitation of Fyn and MAP-2c from human fetal homogenates confirmed the interaction in vivo. MAP-2 synthetic peptides spanning the RTPPKSP motif bound to Fyn, and the interaction was regulated by phosphorylation. Co-transfections with MAP-2c and the extracellular signal-regulated kinase 2 (ERK2) demonstrated that MAP-2c is threonine/serine-phosphorylated on its RTPPKSP motif and that threonine phosphorylation abolished the MAP-2c/Fyn binding. Kinase assays and co-transfection of MAP-2c and Fyn confirmed that Fyn tyrosine kinase phosphorylates MAP-2c. Thus, the activation of signaling pathways may regulate cytoskeletal dynamics by altering the state of phosphorylation of MAP-2 by both ERK2 and Fyn kinase.

Adaptor Proteins, Signal Transducing↗