The T2 relaxivity of the SiO2-coated MNPs made from group C was 1

The T2 relaxivity of the SiO2-coated MNPs made from group C was 130 ± 2 mM−1s−1 (Figure 5b), which was approximately 27% lower than that of the original core particles. Group C was selected for SiO2 coating in order to get final SiO2-coated SPIO MNPs with a diameter of 50 to 100 nm and with a moderate T2 relaxivity value. The SiO2 coating would facilitate the addition of therapeutic Staurosporine datasheet and targeting functions such as drugs and antibodies

to the MNPs, enabling them to serve as both imaging agents and a therapeutic carrier species. Figure 4 Calculated T 2 relaxation rates and relaxivity and representative MR image for the four groups. Concentration-dependent T2 relaxation rates (1/T2) (a), calculated T2 relaxivity r 2 (b) for the four groups at 4.7 T (200 MHz for protons), and representative MR image (c) for the four groups depending on the Co/Fe concentration. The slopes of the fitted lines provide the T2 relaxivity (r 2) at the concentration of 1 mM for each group; the values are 302 ± 9, 268 ± 8, 179 ± 5, and 66 ± 4 mM−1s−1 for groups

A, B, C, and D, respectively. A representative T2-weighted MR image (TE/TR = 10/10,000 ms, slice thickness = 2 mm, number of scans = 2), obtained by a conventional spin-echo pulse sequence on a 4.7-T MRI system, from the samples with four different Co/Fe concentrations (0.25, 0.5, 0.75, and 1.0 mM) for the groups A to D is shown (c). The signal decrease due to T2 negative contrast is higher with increasing JAK cancer particle size and increasing Co/Fe concentration, especially for group A, which is in accordance with the result shown in (a). Figure 5 TEM images (a) and T 2 property measurement (b) of the SiO 2 -coated MNPs. The TEM images show that the particles consisted of core CoFe2O4 nanoparticles and a SiO2 coating with

a shell thickness of approximately 25 nm, providing a total particle diameter of 70.8 ± 4.3 nm (note the inset for the particle shape in detail). The measured r 2 was 130 ± 2 mM−1s−1, which was 27% smaller than that of the MNP group C core alone. There have been several reports on Fe3O4-based MNPs with a narrow size distribution made by the coprecipitation method. Lee et al. used a piezoelectric nozzle [20], which, despite effectively controlling the particle next size, requires specialized equipment and many steps. Jiang et al. employed a coprecipitation methodology using urea, which provided SPIO MNPs with a narrow size distribution [27]. The average diameter of these MNPs could be adjusted from 8 to 50 nm depending on the decomposition of urea in the ferrite solution; however, they required additional dextran coating in order to make them water soluble. In the present study, the use of centrifugation in combination with the coprecipitation method enabled effective regulation of the size of the MNPs without the requirement for a specialist. A large quantity of each size of particles could be produced, overcoming many of the shortcomings of the coprecipitation method.

The Onecut transcription factor HNF6, not expressed in the immedi

The Onecut transcription factor HNF6, not expressed in the immediate periportal hepatoblasts inhibits TGFβ signaling in the parenchyma, and this allows normal hepatocyte differentiation. In the present study, an induction of TGFβ1 was observed in the hepatocytes the area surrounding the repairing biliary ductules, reminiscent of the changes seen in embryonic development. However, HNF6 immunohistochemistry did not reveal significant changes after

DAPM treatment in both the models under study. TGFβ1 induction was also observed in the in vitro hepatocyte organoid cultures undergoing biliary transdifferentiation [4]. Recently, TGFβ1-treated fetal hepatocytes were found to behave as liver progenitors and also gain GDC-0994 expression of CK19 [24]. The data from our study suggest that TGFβ1 signaling can lead to transdifferentiation without any changes in the HNF6 expression in the adult liver upon need. It is possible that other transcription factors like OC-2

known to have overlapping target genes of HNF6 [32] may be responsible for the TGFβ1 increase in the periportal hepatocytes. The periportal hepatocytes expressed CK19 after DAPM challenge with or without BDL pointing to the source of the likely pool of hepatocytes capable of undergoing transdifferentiation. These results are also consistent with our previous findings indicating that subpopulation of periportal hepatocytes represents the progenitor pool from which biliary cells may emerge in situations of compromised learn more biliary proliferation [1]. Taken together

the findings from this study indicate that the hepatocytes constitute facultative stem cells for the biliary cells capable of repairing liver histology when the classic biliary regeneration fails. The findings also suggest that subpopulations of hepatocytes in periportal region may have a higher tendency to function as facultative stem cells compared to other cells of their kind, even though they function as hepatocytes ADAM7 under normal circumstances. The exact molecular mechanisms that govern interchange in expression of cell-specific HNFs remain to be elucidated. Our earlier study with hepatocyte organoid cultures point to the role of HGF and EGF in hepatobiliary transdifferentiation [4]. Via AKT independent PI3 kinase pathway, HGF and EGF promote hepatocyte to BEC transdifferentiation [4]. It is also known that Foxo transcription factors are regulated by the PI3 kinase/AKT pathway [33]. It is possible that similar signaling occurs through HGF and/or EGF via PI3 kinase regulating expression of HNF transcription factors that in turn lead to transdifferentiation. Overall, understanding of transdifferentiation of native hepatocytes and BECs may prove to be pivotal in cellular therapy against liver diseases. Conclusions Under compromised biliary regeneration, transdifferentiation of hepatocytes into biliary cells provides a rescue mechanism.

Table 5 Relative energy and food craving analyses of METABO and p

* indicates statistically significant difference (P < 0.05) between groups at the post time point via ANCOVA. Table 5 Relative energy and food craving analyses of METABO and placebo groups from week 0 through week 8   METABO Placebo P n = 27 n = 18 Value1   Baseline Mid point End of study Baseline Mid point End of study    

(Week 0) (Week 4) (Week 8) (Week 0) (Week 4) (Week 8)   Energy 3.04 ± 0.9 3.7 ± 0.67 3.93 ± 0.62 3.33 ± 0.69 3.67 ± 0.84 3.5 ± 0.92 0.22, 0.02* Sweet 2.36 ± 0.8 2.05 ± 0.84 1.92 ± 0.91 2.48 ± 0.81 2.02 ± 0.84 2.12 ± 0.71 0.58, 0.30 FFF 2.85 ± 0.87 2.56 ± 0.94 2.35 ± 0.92 2.9 ± 0.54 2.28 ± 0.83 2.53 ± 0.68 0.48, https://www.selleckchem.com/products/bmn-673.html 0.48 Fats 2.16 ± 0.85 1.92 ± 0.77 1.86 ± 0.8 2.04 ± 0.49 1.97 ± 0.46 2.02 ± 0.56 0.12, 0.03* Carbs 2.26 ± 0.81 2.07 ± 0.74 2.01 ± 0.8 2.52 ± 0.64 2.1 ± 0.7 2.21 ± 0.61 0.86, 0.92 Healthy 2.44 ± 0.77 2.41 ± 0.72 2.38 ± 0.73 2.56 ± 0.49 2.21 ± 0.78 2.43 ± 0.51 0.42, 0.92 Values are mean ± SD. 1P values are for the differences between the two groups, METABO versus placebo at week 4 and week 8, respectively. *Significant result via ANCOVA (i.e. week 8 time points are significantly different from each other after using the week 0 time point as the covariate). FFF, selleck compound fast food fats; Fats: total fats; Carbs: carbohydrates. Safety No serious adverse events occurred during this study and analyses of standard clinical chemistry panels of serum and plasma revealed no statistically significant abnormalities of clinical importance.

There were no significant between group effects for any cardiovascular variable during the 8-week trial, and the changes

Chlormezanone within groups were modest and non-significant. For resting systolic blood pressure, the placebo group went from 119.3 + 11.5 mmHg to 121.2 + 10.6 mmHg while the METABO™ group changed from 119.8 + 10.0 to 118.1 + 10.3 mmHg. Similarly, for resting diastolic blood pressure the placebo group dropped from 80.3 + 5.2 to 76.1 + 6.3 mmHg while the METABO™ group fell from 77.8 + 8.7 to 76.9 + 9.1 mmHg. For resting heart rate, the placebo group went from 69.4 + 8.4 to 69.9 + 7.9 beats/min while the METABO™ group did not experience a mean change (70.1 + 8.2 to 70.1 + 8.4 beats/min). The incidence of non-serious adverse events (e.g., stomach upset, etc.) were transient and similar, with no significant differences between placebo and METABO. Discussion The results from this study demonstrate that as an adjunct to an 8-week diet and weight loss program, administration of METABO significantly decreases body weight, body fat mass, waist and hip girth, while increasing lean mass compared to the placebo.

Nat Commun 2013, 4:1335 CrossRef 20 Link JR, Sailor MJ: Smart du

Nat Commun 2013, 4:1335.CrossRef 20. Link JR, Sailor MJ: Smart dust: self-assembling, self-orienting photonic crystals of porous Si. Proc Natl Acad Sci U S A 2003, 100:10607–10610.CrossRef 21. Theiss M: Hard and Software Dr Bernhard Klein Str 110 D-52078 Aachen. Germany; http://​www.​wtheiss.​com/​ 22. Anglin EJ, Cheng L, Freeman WR, Sailor MJ: Porous silicon in drug delivery devices and materialsÅô. Adv Drug Deliv Rev 2008,

60:1266–1277.CrossRef 23. Meiliana S, Brian SH, Sébastien P: RAFT polymerization: a powerful tool for the synthesis and study of oligomers. In Progress in Controlled Radical Polymerization: Materials and Applications, Volume 1101. Washington, DC: American Chemical Society; 2012:13–25. selleck products ACS Symposium Series 24. Pacholski C, Sartor M, Sailor MJ, Cunin F, Miskelly GM: Biosensing using porous silicon double-layer interferometers: reflective interferometric Fourier transform spectroscopy. J Am Chem Soc 2005, 127:11636–11645.CrossRef 25. Pace S, Seantier B, Belamie E, Lautredou N, Sailor MJ, Milhiet P-E, Cunin F: Characterization of phospholipid bilayer formation on a thin film of porous SiO2 by reflective interferometric Fourier transform spectroscopy (RIFTS). Langmuir 2012, 28:6960–6969.CrossRef 26.

Moore R: Method of making a plastic optical element. In Selleckchem NU7026 Book method of making a plastic optical element. City: Eastman Kodak Company (Rochester, NY); 1974. 27. Martin TP, Sedransk KL, Chan K, Baxamusa SH, Gleason KK: Solventless surface photoinitiated polymerization: grafting chemical vapor deposition (gCVD). Macromolecules 2007, 40:4586–4591.CrossRef 28. Marmur A: Soft contact: measurement and interpretation of contact angles. Soft Matter 2006, 2:12–17.CrossRef

29. Pace S, Gonzalez P, Devoisselle JM, Milhiet PE, Brunela D: F. C: Grafting of monoglyceride molecules for the design of hydrophilic and stable porous silicon surfacesw. New J Chem 2010, 34:29–33.CrossRef 30. Vasani Roflumilast RB, Cole MA, Ellis AV, Voelcker NH: Stimulus-responsive polymers at nona-inferfaces. In Nanomaterials for life Sciences: Polymeric Nanomaterials, Volume 10 Edited by: Wiley-VCH, Challa SSRK. 2010. Competing interests The authors declare that they have no competing interests. Authors’ contributions SPa and WZ carried out the polymer synthesis and the polymer characterization. SPa carried out the porous silicon synthesis and the characterization and drafted the manuscript. RV participated in the samples characterization. SPa, SPe, and NV conceived of the study, and participated in its design and coordination. NV helped to draft the manuscript. All authors read and approved the final manuscript.

Furthermore, by virtue of the step-and-repeat mechanism, the NIL

Furthermore, by virtue of the step-and-repeat mechanism, the NIL process can be extended for up to 8″ wafers. Figure 3 Photograph of nanoimprinted 4″ Si wafer (a) and SEM image showing long-range order of corresponding nanostructures (b). The wafer in (a), produced by SRNIL, was deliberately tilted at an angle to bring out the violet-blue tinge arising from the optical diffraction caused by the highly ordered nanoimprinted hexagonal studs of 300-nm periodicity. Metal-catalyzed electroless etching The mechanism of MCEE is well discussed in literature and will not be described at length here [28]. Briefly, in a solution of HF and an oxidative agent, e.g., H2O2, of appropriate concentrations, regions of Si that are in

contact with a noble metal, such as Au or Ag, are etched MX69 much faster than those regions without metal coverage. This phenomenon arises because the noble metal acts as a catalyst facilitating the local injection of holes into Si, resulting in its oxidation and subsequent removal by HF. The reaction is redox in nature and 4SC-202 clinical trial the metal ‘sinks’ into Si, creating an etched path. Therefore, by pre-patterning a noble metal layer on Si prior to immersion in HF/H2O2,

patterned etched structures can be generated. The steps leading up to MCEE for the stud-patterned wafers are described as follows and schematically shown in Figure 4. After the removal of the residual material at the recessed regions by RIE, a thin layer of Au (approximately 20-nm thick) acting as the catalyst was deposited by electron beam evaporation at a pressure of approximately 10-6 Torr. The wafer was then immersed in a solution of 4.6 M HF and 0.44 M H2O2 for the required period of time, after which the reaction was halted by rapid removal of the wafer from the chemical solution and subsequent immersion in deionized water. Next, the Au layer was removed in aqua regia at 70°C, and the NIL mask was stripped in boiling piranha solution to reveal the Si nanostructures. Figure 4 The generation of wafer scale, highly ordered

Si nanostructures from a SRNIL nanoimprinted Si wafer via MCEE. Results and discussion Figure 5a shows a 4″ Si wafer bearing 32 fields (each 10 Inositol monophosphatase 1 mm × 10 mm) of hexagonal Si nanopillars in a hexagonal arrangement generated by the aforementioned approach. The near-perfect ordering of the Si nanopillars can be deduced from the optically diffracted violet-blue light when the wafer was tilted at an angle against a diffused white light source. The near-perfect long-range ordering is also observed in the SEM image of Figure 5b. Figure 5c shows the closed-up SEM plan view of the hexagonal Si nanopillars. The period of the nanopillars is 300 nm (corresponding to an area density of 1.28 × 107 pillars/mm2) as defined by the nanoimprinting mould, while the lateral facet-to-facet dimensions is approximately 160 nm, a reduction from the approximately 180-nm pores in the NIL mould.

coli results indicate that ebb tides enable domestic wastewater t

coli results indicate that ebb tides enable domestic wastewater to flow through groundwater into the coastal waters. This is also supported by sediment analysis. Fig. 8 Quantification of Escherichia

coli at high tide and low tide in the reef-flat seawater at site 2-2 As shown in Fig. 9, relatively high numbers of E. coli were detected during the ebb tide on 7 August 2010 and 29 August 2011. However, the maximum number of E. coli during the ebb tide on 7 August 2010 was 2.5 × 104 MPN/100 mL, while it was 1.1 × 103 MPN/100 mL on 29 August 2011. The transition period from neap tide to spring tide would gradually increase the amount of sea water flowing into the septic tank from the bottom and the amount of domestic this website wastewater leaking and subsequently flowing into the coastal waters, due to the gradual RG7420 cost increase in water-level difference between high tide and low tide. On the other hand, just after a spring tide, domestic wastewater inside the septic tanks would mostly have leaked out, because of the maximum water-level difference. Thus, high numbers of E. coli as observed on 7 August 2010 would not be found. These runoff mechanisms give the explanation of the differences in the numbers of E. coli on 7 August 2010 and 29 August 2011. Fig. 9 Temporal variation in E. coli in the reef-flat seawater on 7 August 2010 and 29 August 2011 at site 2-2 Surficial sediments at sites 2-1, 2-2, 2-3 and 2-4 were grey sand with a hydrogen sulfide

odour. AVS concentrations ranged from 0.024 to 0.133 mg/g. This corresponds to the sediment quinone analysis that detected MK-7, which occurs in sulfate-reducing bacteria. Digging in the sandy beach between the households and the coast revealed similar grey sand. However, no grey sand was found at the other sites and AVS concentrations were less than the detection limit (0.002 mg/g). Therefore, sulfate reduction occurs in sediments from sites 2-1, 2-2, 2-3 and 2-4. This further lends support to the hypothesis

that domestic wastewater runoff migrates to the coast through the groundwater. There is a strong possibility that the coastal water pollution in the lagoon due to poorly constructed sanitary facilities is connected Tau-protein kinase to the decrease in sand supply as observed in other atolls (Ebrahim 2000; Fujita et al. 2009; Hirshfield et al. 1968), because the coastal environments are chronically damaged. In other words, the results from this study demonstrate an urgent need for the development and implementation of effective water quality control strategies. To consider such strategies, we should pay attention to both hard and soft infrastructures. The former in order to improve the purification capability of existing sanitary facilities for wastewater treatment. Improved sanitary facilities should be suitable for the geophysical and social surroundings specific to atolls. The latter in order to establish a policy for the water quality improvement and to develop local capacity building.

The placement of a block below the center axis indicates inverted

The placement of a block below the center axis indicates inverted regions. Comparisons between WORiC and WOCauB2 reveal a single block of homologous sequences spanning the structural and packaging regions (figure 3a). There are three separate areas of dissimilarity between WORiC and WOCauB2. These include two transposable elements and an uncharacterized phage protein [WRi_007190]. Notable areas of dissimilarity between WOVitA1 Selleckchem HMPL-504 and WORiC (white areas; figure 3b) include two transposable elements [WRi_006820] interrupting an ankyrin repeat protein gene [WRi_006810, WRi_p06840]. Genome alignments were also used to assign possible functions to

previously annotated hypothetical ORFs. A hypothetical gene, [WRi_p07030], shares 74.7% pairwise identity to the virulence protein gene VrlC.1 of WOVitA1 and is

pseudonized by the transposon insertion [WRi_007040]. The annotated hypothetical protein [WRi _007070] is homologous to tail protein I from WOVitA1 (96%, 3e-143). The major region of dissimilarity between WOVitA1 and WORiC could be a result of horizontal gene transfer into WOVitA1 or gene loss in WORiC. These ORFs in WOVitA1 encode MutL and three transcriptional regulators [ADW80184.1, ADW80182.1 to ADW80179.1]. Although WOVitA1 and WORiC share 36 homologs compared to 33 shared between WORiC and WOCauB2, WORiC is more similar to WOCauB2 (92.4%). The WORiB genome shares only the ORFs found within the packaging region

[WRi_005460 to WRi_005610] with WORiC (figure 3c). However, when the pyocin sequences, containing the viral structural genes, PLX3397 purchase are included in the WOMelB genome and aligned with WORiC, the structural and packaging regions are conserved, but rearranged in WOMelB compared to WORiC (figure 3d). The evolutionary relationships of the tail morphogenesis module and head assembly and DNA packaging module were examined by phylogenetic analysis. Phylogenetic trees based on baseplate assembly protein W and the large terminase subunit showed different evolutionary relationships for related phages, with the exception of the WOMelB, WORiB1 and WORiB2 clade (figure 4). WORiC shows the greatest phylogenetic relatedness Molecular motor to WOCauB2 and WOCauB3 for baseplate assembly protein W (figure 4a), which is reflected by the degree of nucleotide similarity in the alignment (figure 3a). In contrast, the large terminase subunit of WORiC is most closely related to the wMel and wRi B-type phages (figure 4b). Figure 4 Phylogeny of terminase and baseplate assembly protein W amino acid sequences. Maximum-likelihood phylogeny based on translated amino-acid sequences of A) baseplate assembly gene W (tail morphogenesis module) and B) large terminase subunit gene (DNA packaging and head assembly module) of Wolbachia WO phages from published genomes. Bootstrap values for each node are based on 1000 resamplings.

It was reported that PhaP3 was a major phasin in the phaP1-defici

It was reported that PhaP3 was a major phasin in the phaP1-deficient MCC950 manufacturer mutant of R. eutropha[40]; therefore, the release of PhaR from the phaP3 region may occur only in the absence of PhaP1. A previous observation suggested that PhaP2 (PHG202) was not present on the granule surface in vivo, whereas the expression level of phaP2 was very high in the growth and PHA production phases. Another study suggested that PhaP2 may have indirectly participated

in the formation of P(3HB) granule by interacting with other phasins [41]. In our study, phaP4 (H16_B2021) was expressed during cultivation with the lower level than phaP1 and phaP2. PhaP5 (H16_B1934) [41], PhaP6 (H16_B1988) and PhaP7 (H16_B2326) [42], and PhaM (H16_A0141) [43] were recently identified as HDAC inhibitors list new granule-associated proteins, although the expression levels of their corresponding genes were observed to be very low. The weak expression level of phaP5 in F26 markedly contradicted with a previous microarray analysis [22]; hence, further validation will be necessary.

R. eutropha possesses 5 PHA depolymerases with a DepA domain (phaZ1-Z5), 2 additional depolymerases with an LpqC domain (phaZ6 and phaZ7) and 2 hydroxybutyrate oligomer hydrolases (phaY1 and phaY2) that are considered to be involved in mobilization of P(3HB). Despite the cellular phases examined in the present study were not the PHA utilization phase, the expression levels of phaZ4 (PHG178) and phaY2 (H16_A1335) in the growth phase; and phaZ1 (H16_A1150) and phaZ6 (H16_B2073) in the

PHA production phase were rather higher than those of others. Transporters Kaddor et al. demonstrated that PD184352 (CI-1040) the fructose-specific ABC-type transporter FrcACB, which is encoded within the sugar degradation gene cluster 1, was essential for the growth of R. eutropha H16 on fructose [44]. We observed significant down-regulation of these genes in the PHA production phase compared with the growth phase, as described above (Figure 2 and Additional 1: Table S3). The weak expression level of frcACB may be sufficient to support an adequate carbon flux for PHA biosynthesis, or other transporters may have roles in this process. However, the resent microarray analysis reported up-regulation of the fructose transporter genes during nitrogen starvation [22]. copP2 (H16_A3668), which encodes a putative copper uptake P-type ATPase; and nosFD (PHG249-PHG250), which encodes putative copper-specific ABC transporter subunits, were highly up-regulated in the growth phase along with copDCBA (H16_B2182-B2185) and copZ (H16_A3669) (Additional file 1: Table S3), which confer resistance to copper. The up-regulation of these genes was estimated to be due to formation of active copper-containing enzymes, such as cytochrome c oxidase, in an aerobic respiratory chain [45]. 13CO2 Fixation into P(3HB) synthesized from fructose in the presence of NaH13CO3 by R.

albicans strains was present mainly in the fraction precipitated

albicans strains was present mainly in the fraction precipitated with 85% ammonium sulfate (Figure 1b). Fractions precipitated with 30% and 50% ammonium sulfate exhibited weak inhibition. The supernatant obtained after 85% ammonium sulfate precipitation clearly did not exhibit any antifungal activity. The GW-572016 ic50 antifungal substance present in the 85% cut-off also inhibited germ tube formation in C albicans NCIM 3471 (data not shown). As is clear from Table 3,

ammonium sulfate precipitation resulted in an approximate 2-fold increase in specific activity. After ion- exchange chromatography using DEAE Sepharose, the adjacent fractions 31–35 in the chromatogram, showed biological activity (Figure 3), and the specific activity increased 17-fold. After gel filtration, the recovery was

approximately 22-fold. Based on the purification steps summarised in Table 3, it was concluded that the total active antimycotic protein recovered was 0.45% only. Table 3 Summarised Purification steps of ACP Purification stage Volume (mL) Activity (AU mL-1) Protein (mg mL-1) Specific activity (AUmg-1protein) Purification factor Recovery (%) Culture Supernatant 400 1600 0.4025 39751 1 100 Ammonium sulfate selleck screening library and dialysis 10 3200 0.0444 72072 1.8 11 Ion Exchange Chromatography 6 1600 0.0023 695652 17.5 0.57 Gel Filtration 2 1600 0.0018 888888 22.4 0.45 Figure 3 Chromatogram of antimycotic protein ACP produced by E. faecalis on DEAE Sepharose, absorbance of fractions taken at 280 nm. Fractions (31–35) showing biological activity. Direct detection of activity on PAGE After gel filtration, partially purified active pooled fractions (30 μL), were loaded onto Tricine gel containing 10% resolving and 5.0% stacking gel. A clear zone of inhibition on the C. albicans MTCC 3958 overlaid gel was shown in a Petri dish (Figure 4), wherein a simultaneously silver stained gel showed a corresponding band that 3-oxoacyl-(acyl-carrier-protein) reductase was responsible for the biological activity. Based on the polypeptide molecular weight marker, the molecular mass of the active peptide was estimated to be approximately 43 kDa (Figure 4). We did not observe any biological activity of the bands using glycine Native PAGE. Figure 4 Tricine-PAGE

of ACP purification fractions and gel overlay with C. albicans (MTCC 183). Lane 1, molecular weight marker. Lane 2, dialyzed concentrate after 85% ammonium sulfate fractionation. Lane 3, pooled active fractions collected through DEAE Sepharose matrix. Lane 4, silver stained fractions after gel filtration using Sephadex-G 75. Lane 5, Inhibition zone by antimycotic protein (ACP) on the overlay gel. Amino acid sequencing The first 12 amino acid residues of the N-terminal were determined by Edman degradation. The minor sequence obtained from the twice repeated N-terminal sequencing was GPGGPG, and the same partial sequence was matched for homology. Complete homology was not found in the NCBI BLAST result. However, the GPGG sequence matched a known ABC transporter, i.e.

Trifonov T, Rodriguez A, Servera F, Marsal LF, Pallares J, Alcubi

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