After 30 min of labeling, cells were transferred to fresh phospha

After 30 min of labeling, cells were transferred to fresh phosphate-free MOPS medium containing 1 mM BSA and 150 μg/ml spectinomycin and allowed to incubate

further for 3 hr without CCCP. At 0 and 3 hr of chasing, equal volume of cell aliquot was withdrawn on ice, centrifuged and subjected to isolation of aggregated proteins. The isolated aggregates were immunoprecipitated with anti-AP antibody. The immunocomplex was run on 12% Gemcitabine concentration SDS-polyacrylamide gel, the gel was dried and subsequently set to autoradiography. The autoradiograph (Fig. 6B) of the electrophoresed immunoprecipitates indicated that the amount of AP-aggregate, after 3 hr of chasing (lane b), was about 66% INCB28060 in vivo less than its initial amount at 0 hr of chasing (lane a). This signified that the AP-aggregate had been degraded finally with time. It seemed that the degradation of AP-aggregate had been possibly caused by some induced heat-shock protease(s). When the degradation of the CCCP-mediated AP-aggregate

was checked, by the same ‘pulse-chase and immunoprecipitation’ experiment in two different E. coli mutants for the heat-shock proteases Lon (JT4000) and ClpP (SG22159), it was observed that in the clpP mutant, no degradation of the AP-aggregate took place (lanes c and d, Fig. 6B); whereas in the lon mutant, degradation occurred (lanes e and f, Fig. 6B). This result clearly implied that not the major heat-shock protease Lon, rather a minor protease ClpP was responsible for the degradation P505-15 nmr phenomenon. Such degradation removed the translocation-incompetent,

non-functional AP and thus was essential for cell survival; this was supplemented from the fact that the clpP mutant (SG22159) was more sensitive to CCCP than wild type strain SG20250. In the presence of 25 μM CCCP, where the wild type cells had some growth, the mutant cells became bacteriostatic, and by the treatment of 50 μM CCCP for 90 min, where there was no killing of E. coli SG20250 cells, about 90% cell-killing occurred in case of E. coli SG22159 strain (data not shown). When the cell extract of AP-induced culture was subjected to two-step immunoprecipitation study using anti-DnaK and anti-AP antibodies serially, the final immunoprecipitate of the CCCP-treated cells, in contrast to that of the control cells, had contained AP in addition to the DnaK protein (fig. 7A). This clearly signified that the first immunoprecipitate with anti-DnaK antibody had certainly contained AP i.e., the non-translocated AP in the CCCP-treated cells was present in cell cytosol as a binary complex form with DnaK. This result justified the fact of sigma-32 stabilization in the protonophores-treated cells as – the non-translocated proteins had signaled DnaK/J to bind with them, finally freeing and so stabilizing sigma-32.

Recent studies on laryngeal, esophageal, and uterine cervical car

Recent studies on laryngeal, esophageal, and uterine cervical carcinoma also found that the EGFR status of the primary tumor was retained in the metastases [21–23]. There are few reports in the literature concerning the stability of EGFR protein expression between paired samples of NSCLC primary tumors and the corresponding metastases. In the studies by Italiano et al [26] and

Gomez-Roca et al [27], analyzed by immunohistochemistry, 33% of the cases with NSCLC showed discordance in EGFR status between primary tumor and metastases, suggesting that EGFR expression might not be stable during metastasis progression. However, according to the recent report by Badalian et al, the expression status of EGFR protein was reported to be highly similar in the bone metastasis compared to that in primary NSCLC, without positive to negative or negative to positive EGFR conversions occur in their small cohort of NSCLC [28]. Individual comparison of corresponding primary and metastatic tissues indicated that downregulation of EGFR was a rare event (2/11 cases) while upregulation was observed more frequently (4/11 cases), however, the expression level was maintained in about half of the analyzed cases. This observation suggests that EGFR expression status is relatively well-preserved Everolimus cell line during metastatic progression of NSCLC to the bone. In another study, Milas et al [18] reported on analysis of EGFR expression in 29 cases NSCLC with brain metastases.

Nine out of the 29 cases were studied regarding EGFR expression in the lymph node metastases. Immunostaining was present in 84% (21/25) of the primary tumors, in 56% (5/9) of the lymph nodes metastases, and in 59% (17/29) of the brain metastases. However, comparisons of paired samples from primary tumors and corresponding metastases were not made. There are conflicting results regarding the stability of EGFR protein

expression between paired samples of NSCLC primary tumors and the corresponding Palbociclib metastases, and our research add to the body of data on the PLX3397 research buy subject. Conclusions The EGFR is commonly expressed in NSCLC, its expression in the primary tumor and the corresponding lymph node metastasis is discordant in about 10% of the patients. When overexpression is considered, the discordance is observed in about 20% of the cases. However, concerning EGFR overexpression in the primary tumors, similar expression in the metastases could be predicted with a reasonably high probability, which is encouraging for testing of EGFR targeted nuclide radiotherapy. Acknowledgements The authors thank Min Lin for help with the immunohistochemical stainings and Qi Dong for help with the photos in Figure 1. The authors acknowledge economical support from grants from Science and Technology Project of Zhejiang (No. 2009C34018), National Natural Science Foundation of China to Q Wei (No. 30970863). References 1. Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ: Cancer statistics 2009.

Here we showed that, like THP1 cells, normal monocytes promote Wn

Here we showed that, like THP1 cells, normal monocytes promote Wnt signaling in tumor cells through an NF-κB (Fig. 2B) and AKT (Fig. 5B) dependent pathway. Abnormal activation of AKT is found in a variety of human tumors, including colorectal cancer, as a result of activating mutations of PIK3CA, overexpression of AKT,

the loss of PTEN, or constitutive signaling by Ras [49]. However, it was demonstrated that in epithelial cells mutant Ras is not sufficient for full activation of the PI3K kinase, induction of AKT or inactivation of GSK3β [50] and that co-expression of Ras with selleck chemicals llc PIK3CA is required for AKT activation and full transformation. Consistently,

colorectal tumors often co-express kRas and PI3KCA mutations [51]. However, despite the fact that HCT116 cells carry both kRas mutation and the PI3KCA mutation [52], the level of activated AKT in these cells is rather low (Fig. 3). We showed that tumor associated macrophages, or IL-1, significantly increase AKT signaling in HCT116 cells and inactivate GSK3β, suggesting that inflammatory signals may substitute for the cooperative mutations during tumor progression. A number of studies have established that inflammation contributes to many types of malignancies, including colorectal cancer. Consistently, learn more IBD patients have elevated risk

for colorectal cancer, and anti-inflammatory Blasticidin S agents exert chemopreventive activity. Mutations in NOD2 that have been linked to Crohn’s disease, and therefore to increased risk of colorectal cancer, are associated with increased production of IL-1β and increased colonic inflammation [53]. The role of NF-κB, which is a major signaling pathway utilized by proinflammatory cytokines, including IL-1β, in ulcerative colitis and colon cancer has been established [22]. In this report we present data which demonstrate that IL-1β-induced NF-κB activation is coupled to Wnt signaling, a major oncogenic pathway which regulates differentiation and proliferation of tetracosactide intestinal epithelial cells. Our findings established a direct link between inflammation and tumor progression, and suggest a model whereby Wnt driven tumorigenesis is modulated by IL-1β-dependent signaling from the macrophages present in the tumor microenvironment. Colon cancer development/progression can be controlled by chemopreventive agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs) and vitamin D. NSAIDs act through inhibition of COX-2 activity [54] and inhibition of peroxisome proliferator-activated receptor δ (PPARδ) [55]. Several NSAIDs, such as sulindac and aspirin, are also potent inhibitors of NF-κB activity in tumor cells [56,57].

Rahim R, Ochsner UA, Olvera

C, Graninger M, Messner P, La

Rahim R, Ochsner UA, Olvera

C, Graninger M, Messner P, Lam JS, Soberon-Chavez G: Cloning and functional characterization of the Pseudomonas aeruginosa rhlC gene that encodes rhamnosyltransferase 2, an enzyme responsible for di-rhamnolipid biosynthesis. Mol Microbiol 2001,40(3):708–718.CrossRefPubMed 20. Sim SH, Yu Y, Lin CH, Karuturi RK, Wuthiekanun V, Tuanyok A, Chua HH, Ong C, Paramalingam SS, Tan G, et al.: The core and accessory genomes of Burkholderia pseudomallei : implications for human melioidosis. PLoS Pathog 2008,4(10):e1000178.CrossRefPubMed 21. Mahenthiralingam E, Urban TA, Goldberg JB: The multifarious, multireplicon Burkholderia cepacia complex. Nat Rev Microbiol 2005,3(2):144–156.CrossRefPubMed 22. Andrä J, Rademann J, Howe J, Koch MH, Heine H, Zähringer

U, Brandenburg K: Endotoxin-like properties of a rhamnolipid exotoxin from Burkholderia ( Pseudomonas ) plantarii : immune cell stimulation and selleckchem biophysical characterization. Biol Chem 2006,387(3):301–310.CrossRefPubMed 23. Häußler S, Nimtz M, Domke T, Wray V, Steinmetz I: Purification and characterization of a cytotoxic exolipid of Burkholderia pseudomallei. Infect Immun 1998,66(4):1588–1593.PubMed 24. Brett PJ, DeShazer D, Woods DE:Burkholderia thailandensis sp. nov., a Burkholderia pseudomallei -like species. Int J Syst Bacteriol 1998,48(Pt 1):317–320.CrossRefPubMed 25. Kim HS, Schell MA, Yu Y, Ulrich RL, Sarria SH, Nierman WC, DeShazer D: Bacterial genome adaptation to niches: divergence of the potential virulence genes in three Burkholderia species of different survival Temozolomide purchase strategies. BMC Genomics 2005, learn more 6:174.CrossRefPubMed 26. Yu Y, Kim HS, Chua HH, Lin CH, Sim SH, Lin D, Derr Cediranib (AZD2171) A, Engels R, DeShazer D, Birren B, et al.: Genomic patterns of pathogen evolution revealed by comparison of Burkholderia pseudomallei , the causative agent of melioidosis, to avirulent Burkholderia thailandensis. BMC Microbiol 2006, 6:46.CrossRefPubMed 27. Häußler S, Rohde M, von Neuhoff N, Nimtz M, Steinmetz I: Structural and Functional Cellular Changes

Induced by Burkholderia pseudomallei Rhamnolipid. Infect Immun 2003,71(5):2970–2975.CrossRefPubMed 28. Rahman KS, Rahman TJ, McClean S, Marchant R, Banat IM: Rhamnolipid biosurfactant production by strains of Pseudomonas aeruginosa using low-cost raw materials. Biotechnol Prog 2002,18(6):1277–1281.CrossRefPubMed 29. Robert M, Mercadé ME, Bosch MP, Parra JL, Espuny MJ, Manresa MA, Guinea J: Effect of the carbon source on biosurfactant production by Pseudomonas aeruginosa 44T1. Biotechnol Lett 1989, 11:871–874.CrossRef 30. Trummler K, Effenberger F, Syldatk C: An integrated microbial/enzymatic process for production of rhamnolipids and L-(+)-rhamnose from rapeseed oil with Pseudomonas sp DSM 2874. Eur J Lipid Sci Technol 2003, 105:563–571.CrossRef 31. Henrichsen J: Bacterial surface translocation: a survey and a classification. Bacteriol Rev 1972,36(4):478–503.PubMed 32.

Among quinolones, moxifloxacin appears to also be effective again

Among quinolones, moxifloxacin appears to also be effective against Bacterioides fragilis, suggesting that the drug may be equally effective without co-administered Alvocidib antianaerobic agents [230–232]. However, in recent years, the ever-increasing incidence of drug resistance

among Enterobacteriaceae and non-fermentative gram-negative bacilli has discouraged the drug’s use in empirical regimens. Aminoglycosides are particularly active against aerobic gram-negative bacteria and act synergistically against certain gram-positive organisms. They are effective against Pseudomonas aeruginosa but are ineffective against anaerobic bacteria. Aminoglycosides may be suboptimal for treatment of abscesses or PI3K inhibitor intra-abdominal infections due

to their low penetration in acidic environments [233]. Tigecycline is a parenteral glycylcycline antibiotic derived from minocycline. It is the first representative of the glycylcycline class of antibacterial agents to be marketed for clinical use [234, 235]. While tigecycline does not feature in vitro activity against P. aeruginosa or P. mirabilis, it remains a viable treatment option for complicated IAIs due to its favorable in vitro activity against anaerobic organisms, Enterococci, several ESBL- and carbapenemase-producing Enterobacteriaceae, Acinetobacter species, and Stenotrophomonas maltophilia[236–238]. The use of tigecycline

to treat IAIs is particularly useful in light of its unique pharmacokinetic properties; the drug is eliminated by active biliary secretion and is therefore able to establish high biliary and fecal concentrations [239]. Cultures from Sunitinib in vivo the site of infection are always recommended for patients with healthcare-associated infections or with community-acquired infections at risk for resistant pathogens. In these patients, the causative pathogens and the related resistance patterns are not readily predictable and therefore require further analysis (Recommendation 1C). The results of microbiological analysis are helpful in designing therapeutic strategies for individual patients to customize antibiotic treatments and ensure adequate antimicrobial coverage. Although it has been documented that bacteriological cultures have little impact on the course of treatment of common conditions like appendicitis [240], in this era of prevalent drug-resistant microorganisms involved in both nosocomial and community-acquired infections, the threat of resistance is a source of major concern that cannot be ignored. In 2010, a review was published investigating the value of peritoneal fluid cultures in cases of appendicitis [241].

Patients who present with an advanced stage of HCC (Patients with

Patients who present with an advanced stage of HCC (Patients with BCLC stage C) will currently be treated, among other modalities, with transarterial chemoembolisation (TACE) or the multi-thyrosin-kinase inhibitor sorafenib [6]. selleck compound This treatment aims to prolong survival while maintaining the best possible quality of life. Other patients with advanced hepatocellular carcinoma may participate in clinical studies for new treatment modalities or substances, respectively. One substance which has been

discussed controversially in the last years is octreotide. Somatostatin and its synthetic analogues, octreotide and lanreotide are potentially active against HCC due to their antiproliferative and apoptosis-inducing activity; in addition HCC has been shown to overexpress somatostatin receptors on the cell surface [7–10]. Several years ago Kouroumalis et al [11] published a randomized controlled trial which showed a significantly improved survival in patients with inoperable hepatocellular carcinoma treated with octreotide as compared to placebo (13.0 versus 4.0 months). In addition,

a second randomized placebo-controlled trial [12] showed an improved survival (49.0 versus 28.0 weeks) and quality of life in patients with advanced hepatocellular carcinoma treated with long-acting octreotide. In contrast, Yuen et al [13] did not find a survival benefit of octreotide-monotherapy in patients with advanced hepatocellular

carcinoma. Similarly, a large German study [14] reported an equally poor median survival in the treatment group (4.7 months) and the Selleck TSA HDAC control group (5.3 months), respectively. It is interesting to note that in the two negative studies [13, 14] the median survival of octreotide treated patients and the control group was extremely poor making it difficult to show any possible influence Cyclin-dependent kinase 3 of octreotide treatment on survival. In contrast, in the two positive studies [11, 12] survival even in the placebo arms was considerably longer suggesting differences in patient selection. Due to these divergent study results concerning the influence of octreotide on survival we decided to analyze retrospectively the survival of our patients with hepatocellular carcinoma and octreotide monotherapy and compared it to stage-matched patients who received either TACE, multimodal therapy or palliative care. Patients and methods Patient characteristics The charts of all patients with hepatocellular carcinoma (HCC) seen at the department of Gastroenterology and Hepatology, Medical A-1210477 University of Vienna from 1992 to 2004 were reviewed for this retrospective study. At the time of diagnosis 95 of these patients were in BCLC [2] stage A or B and received either TACE, multimodal therapy, long-acting octreotide [Sandostatin LAR] or palliative care.

2007;9(Suppl 5):15–22 27 Bramlage P Fixed combination of irbes

2007;9(Suppl 5):15–22. 27. Bramlage P. Fixed combination of irbesartan and hydrochlorothiazide in the management of Ruxolitinib clinical trial hypertension. Vasc Health Risk Manag. 2009;5:213–24.PubMedCrossRef 28. Croxtall JD, Keating GM. Irbesartan/Hydrochlorothiazide: in moderate to severe hypertension. Drugs. 2008;68:1465–72.PubMedCrossRef”
“1 Introduction Acute sore throat (pharyngitis) is one of the most common illnesses for which children and

their parents visit selleck kinase inhibitor primary care physicians [1]. For example, in the ambulatory setting, acute pharyngitis accounts for around 1 % of primary care visits [2]. Most cases (up to 80 %) are caused by viruses and are benign and self-limiting [3]. However, bacteria (e.g. group A beta-hemolytic streptococci) are another common cause, particularly among children [4]. The diagnosis of pharyngitis must distinguish children

with viral buy MK-0518 pharyngitis, who would not benefit from antibiotic therapy, from those children with group A beta-hemolytic streptococcal pharyngitis, for whom antibiotics are appropriate [1]. Making this distinction is crucial in attempting to minimize the unnecessary use of antimicrobial agents in children and providing suitable symptomatic relief. The absence of fever or the presence of clinical features such as conjunctivitis, cough, or hoarseness, suggest a viral etiology [1]. The clinical manifestations of acute sore throat are related to inflammation of the pharynx and/or tonsils, and include pain, redness, heat, and swelling [5, 6]. Despite the fact that antibiotics are still often requested and prescribed for acute sore throat, many patients (adults and children) consult their primary care physician to establish the cause of the symptoms, to obtain pain relief, and for information on the course of the disease [7, 8]. Furthermore, because the majority of sore throats are caused by viruses and buy Gefitinib not bacteria, antibiotics are generally ineffective and not recommended by clinical bodies for primary treatment of sore throat [9]. Instead, clinically proven over-the-counter (OTC) medications, which provide

rapid and effective relief of symptoms of acute sore throat, regardless of cause, are increasingly important in the self-management of this condition. Throat lozenges containing amylmetacresol (AMC) and 2,4-dichlorobenzyl alcohol (DCBA), which possess antibacterial, antiviral, and local anesthetic properties, provide symptomatic relief of sore throat [6, 10]. They are licensed for OTC use in the UK and around the world for adults and children for the symptomatic relief of mouth and throat infections [11]. Safety profiles are well established, and in some countries the lozenges have been used for over 50 years. Lozenges containing AMC/DCBA have been studied in several clinical trials conducted in adults and have demonstrated significant analgesic, functional, sensorial, and psychological effects from as early as 1–5 minutes and lasting up to 2 h post-dose [5, 12, 13].

Such an approach requires that goals and plans for evaluations ar

Such an approach requires that goals and plans for evaluations are incorporated into the construction schedule. Step 5: Determine sampling scheme Several key questions Afatinib mouse related to data collection should now be addressed: (1) How long should sites be monitored before and after road mitigation? (2) How often should sites be monitored? (3) How many replicates are needed? As these decisions are unlikely to be independent, we recommend conducting model-based power analyses to optimize the sampling design (see, e.g., van der Grift et al. 2009b). For example, Fig. 2 illustrates the relationship between mitigation

effectiveness (the expected effect size) on the degree of temporal replication needed for adequate statistical power. Similar graphs can be produced for other design variables such as sampling frequency and the number of replicate sites. Note that either pilot studies or pre-existing data on anticipated effect sizes are needed to conduct this type of analysis. Fig. 2 Hypothetical Selleckchem LY2606368 relation between the probability of detecting an effect of road selleck chemicals llc mitigation and the duration of monitoring after the mitigation measures are put in place. The three scenarios illustrate variations in the expected effectiveness of mitigation, e.g. road mitigation is expected to reduce the

road effect by 100, 75 or 50 %. The figure shows that if we want to achieve statistical power of 80 % we should measure the response variable for 3, 6 and 12 years in scenarios 1, 2, and 3, respectively. This figure assumes that the effect of the mitigation measure on the population is

immediate. However, response Low-density-lipoprotein receptor kinase times of the population to both the road and the mitigation measures also have to be considered The sampling scheme is related to the chosen measurement endpoint and the characteristics of the studied species. For example, for a highly mobile species with a long lifespan, monitoring over a longer period would be required to assess a change in population density than that required to detect a change in movement. Similarly, a shorter monitoring period would be required to assess a change in road-kill numbers for a species that crosses roads frequently than for a species that crosses roads infrequently. For some measurement endpoints, such as changes in population size/density, higher levels of replication will allow a quicker evaluation of effectiveness. A study with three replicates will need to be continued for longer than a study with ten replicates, because with more replication the uncertainty in effect size will be reduced, thus allowing a reliable decision to be reached sooner. The rate of use of wildlife crossing structures often increases over time (e.g., Clevenger and Waltho 2003; Ford et al. 2010) due to habituation or gradual improvement in the quality of the crossing structure (e.g., vegetation succession on wildlife overpasses).

J Bacteriol 2001,183(8):2454–2462 PubMedCrossRef 47 Law RJ, Haml

J Bacteriol 2001,183(8):2454–2462.PubMedCrossRef 47. Law RJ, Hamlin JN, Sivro A, McCorrister SJ, Cardama GA, Cardona ST: A functional phenylacetic acid catabolic pathway is required for full pathogenicity of Burkholderia cenocepacia in the Caenorhabditis elegans

host model. J Bacteriol 2008,190(21):7209–7218.PubMedCrossRef 48. Bae T, Banger AK, Wallace A, Glass EM, Aslund F, Schneewind O, Missiakas DM: this website Staphylococcus aureus virulence genes identified by bursa aurealis mutagenesis and nematode killing. check details Proc Natl Acad Sci U S A 2004,101(33):12312–12317.PubMedCrossRef 49. Lee H, Yoon H, Ji Y, Kim H, Park H, Lee J, Shin H, Holzapfel W: Functional properties of Lactobacillus strains isolated from Acadesine concentration kimchi. Int J Food Microbiol 2011,145(1):155–161.PubMedCrossRef 50. Tarmy EM, Kaplan NO: Chemical characterization of D-lactate dehydrogenase from Escherichia coli B. J Biol Chem 1968,243(10):2579–2586.PubMed 51. Tsoi SC, Li SS: The nucleotide and deduced amino-acid sequences of a cDNA encoding lactate dehydrogenase from Caenorhabditis elegans: the evolutionary relationships of lactate dehydrogenases from mammals, birds, amphibian, fish, nematode,

plants, bacteria, mycoplasma, and plasmodium. Biochem Biophys Res Commun 1994,205(1):558–564.PubMedCrossRef 52. Mshvildadze M, Neu J: Probiotics and prevention of necrotizing enterocolitis. Early Hum Dev 2009,85(10 Suppl):S71-S74.PubMedCrossRef 53. Brady LJ, Gallaher DD, Busta FF: The role of probiotic cultures in the prevention of colon cancer. J Nutr 2000,130(2S Suppl):410S-414S.PubMed 54. Shin SC, Kim SH, You

H, Kim B, Kim AC, Lee KA, Yoon JH, Ryu JH, Lee WJ: Drosophila microbiome modulates host developmental and metabolic homeostasis via insulin signaling. Science 2011,334(6056):670–674.PubMedCrossRef 55. Virk B, Correia G, Dixon DP, Feyst I, Jia J, Oberleitner N, Briggs Z, Hodge E, Edwards R, Ward J, et al.: Excessive folate synthesis limits lifespan in the C. elegans: E. coli aging model. BMC Biol Galeterone 2012, 10:67.PubMedCrossRef 56. Brenner S: The genetics of Caenorhabditis elegans. Genetics 1974,77(1):71–94.PubMed 57. Hsu AY, Poon WW, Shepherd JA, Myles DC, Clarke CF: Complementation of coq3 mutant yeast by mitochondrial targeting of the Escherichia coli UbiG polypeptide: evidence that UbiG catalyzes both O-methylation steps in ubiquinone biosynthesis. Biochemistry 1996,35(30):9797–9806.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions FG and GM designed, planned, and conducted experiments, data/statistical analyses, data interpretation, and manuscript preparation. RS designed, planned, and conducted experiments, data/statistical analyses, and data interpretation. VT, EW, and LL conducted experiments. CS provided experimental design and data interpretation.

The Table of Additional File 2 lists all significant spot abundan

+Fe conditions). Comprehensive MS and MS2 datasets are provided in the Table of Additional File 3. The concise protein lists in the Tables 1, 2 and 3 are of particular interest in the context of iron homeostasis. Only if protein abundance ratios differed substantially comparing the -Fe vs. +Fe datasets at 26°C and 37°C, the temperature dependency was pointed out in the following paragraphs. Table 1 Abundance differences of Y. TSA HDAC pestis proteins profiled in periplasmic fractions of iron-rich vs. iron-starved cells Spot No a) Gene locus b) gene name c) Protein description c) Subc. Loc. d) Fur/RyhB

e) Mascot Score f) exp Mr (Da) exp pI 26°C, Vs (-Fe) g) 26°C, Vs (+Fe) h) 26-ratio -Fe/+Fe i) 26°C P-value j) 37-ratio -Fe/+Fe k) 53 y0028 malE CB-839 concentration periplasmic maltose-binding protein PP   2150 43937 5.53 0.72 5.98 0.121 0.000 0.760 54 y0137 degQ serine endoprotease PP   1077 55588 6.43 0.39 0.11 2.41 0.0177 0.900 55 y0291 – putative tospovirus resistance protein D U   486 18721 5.44 2.05 0.47 4.320 0.000 N.D. 56 y0541 hmuT hemin-binding periplasmic protein PP Fur 228 27164 5.85 0.46 0.11 4.328 0.000 > 20 57 y0542 hmuS hemin uptake system component U Fur 989 38188 5.56 0.53 0.19 2.780 0.000 2.091 58 y0869 Selleckchem BVD-523 cybC cytochrome b(562) PP Fur 626 5035 5.64 0.13 0.03 4.746 N.D. 3.160 59 y0964 frsA fermentation/respiration switch protein U   586 51326 5.98 0.15 0.07 2.208 0.000 1.875 60 y1128 bglX putative beta-glucosidase PP   2324 81506 5.43 3.01 0.52 5.822 0.000 1.740 61 y1189 gltI solute-binding periplasmic protein of glutamate/aspartate ABC transporter PP   2512 35927 7.20 0.41 2.91 0.141 0.005 HSP90 N.D. 62 y1223 nrdE ribonucleoside-diphosphate reductase 2, alpha subunit U Fur 198 79914 6.32 0.03 – > 20 N.D. N.D. 63 y1222 nrdF ribonucleoside-diphosphate reductase 2,

beta chain U Fur 561 39335 5.11 0.77 – > 20 N.D. > 20 64 y1430 – putative putative periplasmic iron-binding signal peptide protein U   3359 41211 6.09 – 0.57 < 0.05 N.D. < 0.05 65 y1526 yfuA putative solute-binding protein for iron ABC transporter PP Fur 1979 39620 6.65 2.36 1.46 1.618 0.061 N.D. 66 y1607 hisJ histidine-binding periplasmic protein of high-affinity histidine transport system PP   1494 31529 5.01 0.29 0.93 0.309 0.000 0.350 67 y1744 - hypothetical protein y1744 CY   324 5183 5.92 0.38 - > 20 N.D. 4.510 68 y1897 yfeA periplasmic-binding protein for iron and manganese ABC transporter CM Fur 1201 31395 5.80 2.87 0.63 4.576 0.000 4.780 69 y1936 sufC iron-sulfur cluster assembly protein SufC, ATPase component ML Fur 726 28460 5.10 0.16 0.02 7.514 0.000 > 20 70 y1937 sufD cysteine desulfurase activator complex subunit SufD U Fur 369 60476 6.76 0.06 – > 20 N.D.