Figure 6 The locationof the SNPs1&2 in EHI_080100 and EHI_065250

Figure 6 The locationof the SNPs1&2 in EHI_080100 and EHI_065250 genes. Mapping of the informative SNPs within the coding sequences. A) EHI_065250 and B) EHI_080100 genes. Nucleotide

position of the amplicon 5’ and 3’ bases are shown and approximate location of the 5’ (green) and 3’ (red) and the positions and number of the targeted SNPs indicated by vertical lines. The bases involved are bracketed in the nucleotide sequence at this region (shown above). The amino acid sequence with changed residues in red is also shown. Discussion E. histolytica SNPs were identified in amebic DNA isolated from a Bangladesh population by amplicon sequencing. Non-Reference SNPs in the EHI_080100 cylicin-2 gene were significantly associated with the virulence phenotype

(amebic this website liver abscess > asymptomatic > diarrhea or dysentery). We initially analyzed the genetic diversity among 12 sequenced E. histolytica genomes that represented different geographical origins and disease manifestations, and selected a set of 21 polymorphic sites in coding regions where SNPs change the encoded amino acid. The distribution of these 21 non-synonymous SNPs in field isolates and cultured strains of E. histolytica were examined in samples collected from an endemic area in Bangladesh by multilocus sequence typing (MLST). Of 16 loci that passed quality control five were invariantor very infrequent in Bangladesh. Our results are inconsistent with a model of clonality in E. histolytica populations. In a clonal population Dichloromethane dehalogenase we would expect to see strong linkage QNZ disequilibrium between markers, since linkage would not be eroded Compound C manufacturer by recombination and sexual reassortment. In fact, we saw only two identical genotypes in our sample, suggesting a considerable amount of recombination and/or reassortment. Our results support previous observations, based on short tandem repeat DNA sequences, of high diversity among genotypes even within limited geographical areas [18, 21, 24]. Due to this complexity, the

number of whole genomes sequenced in the pilot studies, were not sufficient to predict accurately the SNPs associated with disease. However, 2 out of the 16 loci examined,(EHI_065250 and EHI_080100), were significantly associated with disease in isolates collected in Rajshahi and Dhaka, Bangladesh. One caveat to this study was that the amebic liver abscess samples were collected in Rajshahi but the stools samples were collected at a different location (Mirpur, Dhaka); the differences in the grouping of liver abscess and stool E. histolytica could reflect geographical differentiation [24]. Ali et al. have however previously described different genotypes in liver abscess and enteric samples from the same patients [28]. This suggests a possible genetic selection for parasites with invasive capabilities. Based on our data we suggest a divergent rather than sequential model of the potential to cause severe disease [46].

0 6, supplemented with 100 μM of [14C]-glucose After different t

0.6, supplemented with 100 μM of [14C]-glucose. After different times of incubation at 37°C, the Crizotinib mouse glucose remaining in the supernatant (S) and cytoplasmatic SB273005 solutes synthesized from ectoine,

present in the ethanol insoluble (EIF) and soluble (ESF) fractions, respectively, were determined as described in Methods. The data are the averages of three different replicates ± SD (standard deviation). Mutant CHR95 possesses a deregulated ectoine uptake As mutant CHR95, but not the wild type strain, could use ectoines as nutrients at low salinities, we investigated the transport and metabolism of ectoine in both strains in response to increasing osmolarity. As previously reported by Vargas et al [25], the wild type strain showed its maximal ectoine transport rate at the optimal salinity for growth (1.5 M NaCl), which was 3- and 1.5-fold higher than those observed at 0.75 and 2.5 M NaCl, respectively (Figure 3). Notably, the ectoine transport rates of strain CHR95 were 8-, 2.3-, and 2.5-fold higher at 0.75, 1.5, and 2.5 M NaCl, respectively, than those of the wild type grown at the same salt concentrations (Figure 3). Figure 3 C. salexigens CHR95 shows a deregulated ectoine uptake. The wild-type strain and the mutant

CHR95 (ΔacseupRmntR::Tn1732) were grown in glucose M63 minimal medium containing the Trk receptor inhibitor indicated concentration of NaCl. The measurement of 40 [14C]-ectoine uptake rates (vi, expressed as nmol min-1 OD-1 units) was performed as described in Methods. Experiments were repeated twice, and the data correspond to mean values. To test if the metabolism of ectoine was affected in CHR95, the fate of radioactive ectoine was analysed in the presence

or absence of 20 mM glucose as described in Methods, and compared to that of the wild type strain. According to previous studies [25], CO2 production due to ectoine catabolism in the wild type strain was lower (40-fold) in the presence of glucose, suggesting that ectoine utilization is partially repressed by glucose. No significant differences were found between CO2 production from ectoine by CHR95 and the wild type strain, neither with nor without glucose addition (Figure 4a). In both strains, most of the carbon backbone of ectoine (ca. 70% of the total radioactivity added) was found in the ethanol soluble fraction (ESF), whereas only about 3.82% of the total selleck products radioactivity added was found in the ethanol insoluble fraction (EIF). No significative differences were found in the radioactivity present in the ESF and EIF fractions of the wild type and mutant strain. Glucose did not influence the biosynthesis of molecules from ectoine in any of these fractions (Figure 4b). These results suggested that whereas ectoine transport is deregulated in mutant CHR95 at any salinity, ectoine metabolism is not affected in this strain. Figure 4 C. salexigens CHR95 is not affected in the metabolism of ectoine. Cells grown in M63 with 1.

The susceptibility and tolerance to β-lactams of nonpolar

The susceptibility and tolerance to β-lactams of nonpolar

deletion mutants in the three selected genes was examined. It was revealed that Fri is a mediator of tolerance SB202190 in vitro to penicillin G and ampicillin, as well as of resistance to some cephalosporins, including cefalotin and cephradine. The identification of a locus that contributes to tolerance to β-lactams used in the treatment of listeriosis and that is relevant to the innate resistance of L. monocytogenes to cephalosporins is notable in light of the clinical use of these antibiotics. Results Screening of L. monocytogenes genomic libraries for penicillin G-Ro 61-8048 inducible promoters Genomic DNA of L. monocytogenes was fragmented using four different procedures and the obtained chromosomal fragments were cloned upstream of the promoterless hly gene in vector pAT28-hly. This vector has previously been used to identify constitutive as well as inducible promoters of L. monocytogenes[14]. It was chosen for the identification of penicillin

G-inducible promoters because the plasmid is present in L. monocytogenes at high copy number, which permits the selection of even relatively weak promoters driving hly expression. Penicillin G was selected for this study because it is widely used as the antibiotic of choice for the treatment of listerial infections [2]. The four genomic libraries were introduced into L. monocytogenes this website EGDΔhly by electroporation and transformed strains in which putative promoters Protein kinase N1 were trapped upstream of hly, were identified by the creation of hemolytic zones on blood agar plates. To determine whether expression was induced by penicillin G, the strains were replica plated on blood agar plates with or without this antibiotic. Penicillin G was used at a concentration (0.03 μg/ml) that permitted the growth of L. monocytogenes EGD even under prolonged incubation, but which exerted a deleterious effect on the bacteria, as evidenced by a reduced growth rate and lower cell number compared with cultures without the antibiotic. Strains producing larger hemolytic zones on blood agar plates supplemented with penicillin G were identified.

Inducible expression of the promoter-hly fusions in the selected strains in response to the addition of penicillin G was further quantified using a hemolytic activity assay. In the presence of penicillin G a significant increase in hemolytic activity produced by nine of the selected strains was observed (Table 1). Table 1 Expression of promoter- hly fusions in response to the addition of penicillin G as determined by a hemolytic activity assay Hemolytic activity a Strain 15 b 18 b 37 c 41 b 195 d 198 c 199 c 201 c 203 d K 10.2 ± 2.6 8.7 ± 1.6 13.2 ± 3.8 20.7 ± 2.5 30.8 ± 1.2 20.3 ± 1.4 12.2 ± 0.6 21.5 ± 1.3 19.6 ± 1.1 PenG 20.4 ± 1.9** 13.3 ± 0.3* 32.5 ± 4.5** 36.1 ± 1.9** 54.8 ± 1.8 ** 29.5 ± 1.7* 33.9 ± 1.6** 28.5 ± 1.7** 55.5 ± 3.

First, upstream and downstream regions (about 1 kbp) of cbbLS c w

First, upstream and downstream regions (about 1 kbp) of cbbLS c were individually amplified by PCR with genomic DNA of R. eutropha H16 as a template and primer sets of cbbLSc-up5’/cbbLSc-up3’ and cbbLSc-down5’/cbbLSc-down3’, respectively. The second PCR with the amplified fragments

using cbbLSc-up5’/cbbLSc-down3’ primers gave a fused fragment of the upstream and downstream regions of cbbLS c . The resulting fragment was digested by EcoRI and HindIII and then ligated with pK18mobsacB [50] PLX4032 chemical structure at the corresponding sites to obtain pK18ms∆cbbLSc. pK18ms∆cbbLSp for deletion of cbbLS p from megaplasmid pHG1 was constructed in the same way using primer sets of cbbLSp-up5’/cbbLSp-up3’ and cbbLSp-down5’/cbbLSp-down3’. Transconjugation of mobilizable plasmids from E. coli S17-1 to R. eutropha and isolation of this website strains generated by pop in-pop out recombination using the pK18mobsacB-based

suicide plasmids were performed as described previously [13, 14]. The strains H16∆cbbLS c , H16∆cbbLS p , and H16∆∆cbbLS were obtained by single deletion of cbbLS c and cbbLS p , and double deletion of the genes in R. eutropha H16, respectively. Determination of the abundance of 13C in P(3HB) Cultivation of R. eutropha strains H16, H16∆cbbLS c , H16∆cbbLS p , and H16∆∆cbbLS were done in a 500 ml flask on a reciprocal shaker (115 strokes/min) at 30°C. Firstly, the strains were cultivated in 100 ml of a nutrient rich medium composed of 10 g/l tryptone, 2 g/l yeast extract, and 1 g/l meat extract in tap water for 12 h. The grown cells in 50 ml of the culture broth were harvested, washed with a salt solution (9 g/l Na2HPO4 · 12H2O, 1.5 g/l KH2PO4 in deionized water), and then transferred into 100 ml of a nitrogen-free MB medium (pH6.5 adjusted

with KH2PO4) containing 0.5% (w/v) fructose. The cells were further incubated for 24 h to promote P(3HB) biosynthesis. NaH12CO3 (1.08% 13C (natural abundance)) or NaH13CO3 (98% 13C) (Taiyo Nippon Sanso, Tokyo, Japan) 4-Aminobutyrate aminotransferase was added to a final concentration of 5 mM periodically every 2.5 h during the second stage, taking into consideration loss of dissolved CO2 to the atmosphere. The cells after the second stage cultivation were harvested, washed, and lyophilized as described above. The dried cells were subjected to methanolysis, and analyzed by GCMS-QC2010 system (Shimadzu, Kyoto, Japan) equipped with an Caspase Inhibitor VI ic50 InertCap 1 capillary column (ϕ0.25 mm, 30 m) (GL Science, Tokyo, Japan). 13C/12C ratios in the fragments of CH3–CH=OH+ (m/z 45), CH3–C(OH)H–CH3–C=O+ (m/z 87), and CH3–O–CO–CH2–CH=OH+ (m/z 103) derived from 3HB methyl ester were calculated from the respective isotopomer abundances, and the mean was referred as a abundance of 13C in the P(3HB) fraction. RNA-seq data accession number The RNA-seq data used in this study have been deposited in the NCBI Gene Expression Omnibus (GEO) under the accession number of GSE47759. Acknowledgement We thank Prof. K.

Our study provides the first empirical evidence for this hypothes

Our study provides the first empirical evidence for this hypothesis. There have been three major arguments in favor of the pathogenicity-hypothesis for fungi associated with esca and young vine decline, the first of which concerns the worldwide increase of the incidence of esca and young vine decline since the ban of sodium arsenite. It is true that before the ban of sodium arsenite, esca and young vine decline were considered to be negligible diseases (Bertsch et al. 2009; Mugnai et al. 1999; Graniti et al.

2000). However, even if sodium arsenite can reduce the severity of esca symptoms, it does not contribute significantly towards esca incidence and plant mortality (Fussler et al. 2008). This fungicide has never been registered and therefore has never been used in Switzerland, nor in see more Germany. Yet, the emergence of the esca A-1155463 supplier disease followed a very similar pattern in these two countries compared to the other European countries (Fischer and Kassemeyer 2003; Viret et al. 2004). Also, when a restricted

use of sodium arsenite was still allowed in France, Portugal learn more and Spain, esca was nevertheless already widespread in these countries (Mugnai et al. 1999). The causal link between the ban of sodium arsenite and esca emergence appears therefore entirely circumstantial. The two other arguments in favor of a presumed pathogenicity of the esca-associated fungi are the repeated isolation of the same fungal groups from grapevine wood necroses

and, finally, the ability of some of these fungi to decompose grapevine wood in vitro and to generate necroses in vivo. Many past and present studies on esca have presented lists of fungi that were repeatedly isolated from necrotic wood. Consequently, these fungi were thought to be involved in the esca disease (Armengol et al. 2001; Bertsch et al. 2009; Gramaje and Armengol 2011; Larignon and Dubos 1997; Surico et al. 2006), even though one could also argue that all these studies have essentially shown that esca-related fungi are frequently associated with dead wood in V. vinifera. Pathogenicity tests inoculating sterilized wood pieces of grapevine plants with one or several of the esca- or Histamine H2 receptor young vine decline-associated fungi showed that some of these were able to colonize dead wood (Chiarappa 1997; Larignon and Dubos 1997; Mugnai et al. 1996; Úrbez-Torres et al. 2009), without demonstrating that these fungi were able to generate wood necroses in vivo. However, field inoculation experiments showed that wood-streaking and vessel discoloration were induced months after the inoculation with P. chlamydospora and P. aleophilum and that these species could then be isolated back from the margin of the extending necroses (Eskalen et al. 2007).

2002) Table 1 Stable isotopes that are important for isotope rat

2002). Table 1 Stable isotopes that are important for isotope ratio MS and their levels of natural SP600125 in vitro abundance Element check details Symbol Mass of atom (u) Abundance (%) Hydrogen 1H 1.007825 99.9885 Deuterium 2H 2.014102 0.115 Carbon 12C 12.000000 98.93 13C 13.003355 1.07 Nitrogen 14N 14.003074 99.632 15N 15.000109 0.368 Oxygen 16O 15.994915 99.757 17O 16.999132 0.038 18O 17.999160 0.205 Argon 36Ar 35.967546 0.3365 38Ar 37.962732 0.0632 40Ar 39.962383 99.6003 The level of isotopic enrichment (ε) is a measure of the abundance between 0 and 100%. The lower limit

in practice is given by Earth’s natural abundance of isotopes and these ratios provide an incisive tool for examining cycling of elements in biochemical or geochemical reactions. For mono-atomic species, or molecules where only one atom varies in weight, the enrichment level is simply

the ratio between the abundance of the various isotopic species. For diatomic molecules, which effectively represent most of the atmospheric gases, the level is given by the binomial expansion. For oxygen4 this is: $$ \left( m/z \right) 32: 3 4: 3 6= ( 1- \varepsilon )^ 2 : 2\varepsilon ( 1- \varepsilon ) \, :\varepsilon^ 2 $$ (4)and the total 32 + 34 + 36 given as 100%. The relationship between the relative concentration (abundance) and the enrichment is shown in Fig. 3. A practical aspect of this relationship is that at low enrichment levels Berzosertib purchase the concentrations of doubly labeled species are significantly lower than their Cyclin-dependent kinase 3 enrichment ε, for example, the natural abundance of 18O is 0.2039%, but the abundance of the m/z = 36 species is only 0.00042%. Fig. 3 Isotopic enrichment for di-atomic molecules follows a binomial distribution. The figure depicts the changing relative

concentrations for molecular oxygen species with changing 18O enrichment (ε) Another term that is often introduced for changing levels of enrichment is the mole fraction. An example of this is shown below for 13CO2, where the 18O mole fraction, which is typically expressed as 18α, gives an instantaneous measure of enrichment. $$ \, {}^ 1 8\alpha = \frac [ 4 7 ] + 2[49]2 \, ([45] + [47] + [49]) \, $$ (5)Where for example [45] corresponds to the relative concentration of 13C16O16O. Thus, the concentrations of 13C species at m/z = 45, 47 and 49 are used to derive the mole fraction. This enrichment expression is particularly useful for tracking the overall speed of the reaction relative to the background (Mills and Urey 1940; Silverman 1982). Practical applications of MIMS Whole leaf photosynthesis and respiration Photosynthesis and respiration are important biological processes which involve the flux of O2 and CO2 species into and out of biological tissues, particularly leaves.

Protein levels of

Protein levels of nitric oxide synthase (NOS2) were also inhibited in cells treated with the GTA+ve fraction (particularly 20 and 40 ug/ml), but not in cells treated with the GTA-ve fraction (Figure 5). Figure 5 Western analysis of NFκB, IκBα and NOS2 in SW620 cells treated with three concentrations of GTA+ve and GTA-ve extracts and doxorubicin (DOX). Representative

Western blots showing protein levels of NFκB, IκBα and NOS2 in SW620 cells treated with GTA+ve and GTA-ve extracts (see methods). To explore further the effect of GTAs on modulating inflammation, we employed the RAW264.7 mouse macrophage line in which a pro-inflammatory state can be induced by treatment with lipopolysaccharide (LPS). RAW264.7 cells were treated for 4 hours with GTA+ve and GTA-ve fractions prior to the JIB04 mw addition of LPS, and the effects on various proinflammatory markers evaluated. We observed no affect on RAW264.7 cell growth or proliferation rates during the 20 hours post-GTA treatment. RAW264.7 Histone Methyltransferase inhibitor cells treated with GTA+ve fractions prior to LPS stimulation showed a significant dose-dependent reduction (p < 0.05) in the generation of nitric oxide as assessed through the production of nitrite using the Griess reagent system (Figure 6A), which was mirrored by low levels of NOS2 mRNA VX-770 chemical structure transcripts (Figure 6B) and protein levels (Figure 6C). For comparison (and as controls), cells were also

treated with various combinations of free fatty acids including EPA, DHA and equimolar mixtures of 18:1, 18:2 and 18:3 (FA mix), of which only 100 uM DHA showed any protective effect on NOS2 protein induction (Figure 6C). Figure 6 Determination of nitric oxide status in RAW264.7 cells treated with GTA+ve and GTA-ve extracts. RAW264.7 cells were pre-treated for 4 hours with GTA+ve or GTA-ve extracts followed by the addition of LPS (1 ug/ml) for 20 hours. (A) Nitric oxide levels in cells were determined using Griess reagent, (B) NOS2 mRNA transcript levels were determined by real-time rtPCR, and (C) NOS protein (treatment with

80 ug/ml) assessed by Western blot (NS, non-specific). Asterisks indicate p < 0.05 relative to LPS treatment alone, and FA mix in (C) represents a 100 uM equal mixture of 18:1, 18:2 and 18:3 fatty acids. Data are expressed as the average of three duplicate experiments ± 1S.D. Similar effects were observed with TNFα upon treatment with PD184352 (CI-1040) GTA+ve extract, which showed significantly reduced mRNA transcript levels (p < 0.05, Figure 7A) as well as protein levels in cell lysates and conditioned media (Figures 7B and 7C, respectively). Consistent with the above findings, transcript levels of COX2 and IL-1β (Figures 8A and 8B), as well as IL-1β protein levels (Figure 8C), were also significantly reduced (p < 0.05) with GTA+ve treatment. The results indicate that human blood extracts containing GTAs have anti-proliferative and anti-inflammatory properties that GTA-ve extracts lack. Figure 7 TNFα response in RAW264.7 cells treated with GTA+ve and GTA-ve extracts.

Figure 3 Map of Spain showing sampling sites, type of samples and

Figure 3 Map of Spain showing sampling sites, type of samples and results. Among livestock samples, those from sheep (15 samples from 8 provinces) were found belonging to GG I, II, III, IV and VIII; goats (7 samples from 4 provinces) were infected with GG III, IV and VIII; cattle (7 samples from 4 provinces) were all infected by GG III; rats (3 samples selleck kinase inhibitor from 1 province) and a wild boar showed GG IV; finally, 33 ticks of 3 species, from 4 areas

of 2 adjacent regions, carried always GG VII, except for one that carried GG VI. In summary, samples from GG I, II, III, IV, VI, VII and VIII were identified (Additional file 1: Table S1; Table 2, Figures 2 and 3). adaA detection Samples from GG I, II and III were always adaA positive; all GG IV were adaA negative, except for a sheep placenta

that was adaA positive; GG VII samples were adaA negative, except for a tick specimen; GG VIII samples were positive, except for a human sample of acute hepatitis; finally, the this website only sample available from GG VI (one H. AR-13324 supplier lusitanicum tick) was adaA negative (Additional file 1: Table S1, Table 2, Figure 2). All the samples from cases of acute FID with liver involvement (10 samples ifenprodil from 3 distant regions; Figure 3) were adaA negative and the only sample available from a patient with pneumonia was adaA positive. In summary, from the theoretically possible 16 GT (8 GG positive or negative for adaA), 10 were identified in the samples studied (Table 2).

Discussion A multiplex PCR coupled with hybridization by RLB for the characterization of C. burnetii was designed, allowing for its classification into the previously known 8 GG [15] and into up to 16 genotypes, depending on adaA presence/absence. For validation, 15 reference strains characterized in previous studies were used (Additional file 1: Table S1). All of them fell in the same GGs as previously described, when data was available, or grouped in the same clade as described [8–10, 12, 13]. Consequently, an excellent correlation with some previously published schemes and, specifically, with the microarray-based whole genome typing of Beare et al. [15] was observed: the 4 isolates studied by Beare et al. that were also analyzed in this study (NMI, GG I; Henzerling, GG II; Priscilla, GG IV; and Scurry Q217, GG V) were classified with this method into the same GG as described. Also, the analysis of the results by InfoQuest disclosed a tree whose topology was similar to that of Beare et al.

Science 324:268–272PubMedCrossRef Zerges W, Hauser C (2009) Prote

Science 324:268–272PubMedCrossRef Zerges W, Hauser C (2009) Protein mTOR inhibitor synthesis in the chloroplast. In: Stern D, Witman GB, Harris EH (eds) The Chlamydomonas sourcebook, vol 2. Elsevier, Amsterdam, pp 967–1026 Zhao T, Wang W, Bai X, Qi Y (2009) Gene silencing by artificial microRNAs in Chlamydomonas. Plant J 58:157–164CrossRef Zhu J, Fu X, Koo YD, Zhu JK, Jenney FE Jr, Adams MW et al (2007) An enhancer mutant of Arabidopsis salt overly sensitive 3 mediates both ion homeostasis and the oxidative stress response. Mol Cell Biol 27:5214–5224PubMedCrossRef Zimmer SL, Schein A, Zipor G, Stern DB, Schuster G (2009) Polyadenylation in Arabidopsis and Chlamydomonas organelles: the

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“Beginning

in 1952 and extending well into 1954, Melvin Calvin pursued an apparently brilliant idea that involved a chlorophyll-sensitized photochemical reaction of thioctic (lipoic) acid with water to yield a reducing “–SH” and an oxidizing “–SOH” group which could conceivably provide the reduced pyridine nucleotides and the hydroperoxides leading to oxygen in photosynthesis (see e.g., Barltrop et al. 1954; Calvin 1954). (For Calvin’s biography, see Seaborg and Benson (1998).) Everyone in the laboratory was impressed and excited. In the first public presentation of the theory (American Association of the Advancement of Science (AAAS) Meeting, Berkeley, California, 1954), the world-renowned microbiologist Cornelis B.Van Niel, himself a pioneer in photosynthesis, was Phosphoglycerate kinase so impressed that he jumped from his front row seat to congratulate Calvin (see Benson 1995; Fuller1999). Thioctic acid involvement in the photochemical aspects of the quantum conversion of photosynthesis had

consumed at least 2 years of the laboratory’s time and enthusiasm and that of John Barltrop, who was visiting from the Department of Chemistry of the University of Oxford in England (Barltrop et al. 1954; Calvin 1954). The Laboratory’s interest in sulfur metabolism engendered my experiment with the green alga Chlorella cultured with radioactive S-35 sulfate and chromatography of the products. A major (>99%) S-35 labeled product appeared on the film in the location predicted for thioctic acid. Seeing this, Melvin’s eyes almost fell onto the white tabletop. He urged Clint Fuller to search the area with a sensitive bioassay for thioctic acid (Fuller 1999). Melvin’s interest heightened even further. I had been involved in successful efforts with J. Rodney(Rod) Quayle and R. Clint Fuller in demonstrating the function of a carboxylase enzyme for CO2 uptake in algae and photosynthetic bacteria.

Mol Biol Cell 2008,19(12):5214–5225 PubMedCrossRef 3 Walther TC,

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