3 and 25 μl of cell cultures were added to each well The bioassa

3 and 25 μl of cell cultures were added to each well. The bioassay plates were incubated at 28°C for 24 hr. DSF activity was indicated by the presence of a blue halo around the well. To quantify DSF production, blue halo zone widths in the bioassay were converted to DSF units using the formula: DSF(unit ml-1) = 0.134 e(1.9919W), where W is the width in centimeters of the blue halo zone surrounding each well. Relative level of DSF-family signals in one sample was quantified using peak area in HPLC elute. One unit of DSF was defined as 100,000 μV/sec. Purification of DSF, BDSF and CDSF Xoo strain was cultured in YEB

medium for 48 h. Five liters of bacterial supernatant were collected by centrifugation at 3,800 rpm for 30 min

at 4°C MK0683 in vitro (J6-HC Centrifuge, BECKMAN COULTER™). The pH of the supernatants was adjusted to 4.0 by adding hydrochloric acid prior to extraction with an equal volume of ethyl acetate twice. The ethyl acetate fractions were collected and the solvent was removed by rotary evaporation at 40°C to dryness. The residue was dissolved in 20 ml of methanol. The crude extract, divided into four batches, was subjected to flash column chromatography using a silica gel column (12 × 150 mm, Biotage Flash 12 M cartridge), eluted with ethyl acetate-hexane selleck (25:75, v/v, 0.05% acetic acid). The collected active component was then applied to HPLC on a C18 reverse-phase column (4.6 × 250 mm, Phenomenex Luna), eluted with water in methanol (20:80, v/v, 0.1% formic acid) at a flow rate of 1 ml/min in a Waters 2695 system with 996 PDA detector. GSK1904529A manufacturer Structure analysis 1H, 13C, 1H-1H COSY, and heteronuclear multiple

quantum coherence (HMQC) nuclear magnetic resonance (NMR) spectra in CDCl3 solution were obtained using a Bruker DRX500 spectrometer operating at 500 MHz for 1H or 125 MHz for 13C. High-resolution electrospray ionization mass spectrometry was performed on a Finnigan/MAT MAT 95XL-T mass spectrometer. Quantitative determination of extracellular xylanase activity and EPS production The fresh colonies of Xoo strains were inoculated Urease in 50 ml of YEB liquid medium with or without DSF-family signals at a starting OD600 of 0.05. After growth for two days, the bacterial cultures at an OD600 of 2.5 were collected and the supernatants were prepared by centrifugation at 14,000 rpm for 10 min. The extracellular xylanase activity in the culture supernatants of Xoo strains were measured by using 4-O-methyl-D-glucurono-D-xylan-Remazol Brilliant Blue R (RBB-Xylan; Sigma Co.) according to the methods described previously [31, 25]. To determine the production of EPS, potassium chloride was added to 10 ml of the supernatants at a final concentration of 1.0% (w/v). Two volumes of absolute ethanol were added to the supernatants and the mixtures were then kept at -20°C for overnight. The precipitated EPS molecules were spun down and dried at 55°C oven overnight before determination of dry weight.

In contrast to most other bacterial pathogens, cultivation of F

In contrast to most other bacterial pathogens, cultivation of F. tularensis is difficult due to its fastidious nature and its susceptibility to overgrowth by concomitant flora. Additionally, growth may be delayed (up to 12 days) and cultivation of F. tularensis poses a significant threat of laboratory infections. EX 527 in vitro Only recently, conventional and real-time PCR protocols for the detection and identification of F. tularensis have been published, but still none of these techniques is sufficiently evaluated to be routinely used in clinical laboratories [36]. In this study we

evaluated the potential of rRNA gene targeted PCR and sequencing as well as fluorescent in situ hybridization for the detection and differentiation of Francisella species. In- silico analysis of partial and complete 16S rRNA genes available in publicly accessible databases like GenBank confirmed the results of a previous study by showing that 16S rRNA sequences from F. tularensis subspecies are almost identical, and therefore, are only of limited value for the detection and discrimination of F. tularensis on the species or subspecies level [32]. In this

NVP-BGJ398 clinical trial regard, the difficulties to discriminate type A and ACY-1215 order type B strains resembled the situation in the closely related zoonotic pathogens Yersinia (Y.) pseudotuberculosis all and Y. pestis or Burkholderia (B.) pseudomallei and B. mallei [25, 37, 38] In contrast to those studies, comparison of full-length 23S rRNA genes of all

F. tularensis subspecies as well as F. philomiragia revealed several discriminative SNPs. The sequence data obtained from rRNA gene sequences, known to be highly conserved in bacterial phylogeny, could be successfully used for the construction of hybridization probes, allowing a rapid genotype-based detection of Francisella species on different taxonomic levels. A unique 23S rRNA target region suitable for the detection of F. tularensis subsp. holarctica (type B) could be identified. For the discrimination of F. tularensis subsp. tularensis (type A) and subsp. mediasiatica, an identification approach was developed by employing two different probes. Six type A strains, 31 type B strains as well as three F. tularensis subsp. mediasiatica strains were correctly identified by this approach, whereas no false-positive signal was observed with 71 other variably related bacterial species. Similar results were gained employing species-specific probes for F. philomiragia and F. tularensis, which were tested with all mentioned F. tularensis strains as well as four F. philomiragia strains. We also developed an in situ hybridization protocol for F. tularensis subsp. novicida, which allowed the detection of all four available strains of this subspecies.

4 (http://​beast ​bio ​ed ​ac ​uk/​Tracer) No well supported top

4 (http://​beast.​bio.​ed.​ac.​uk/​Tracer). No well supported topological differences were found between the BI and ML trees; the ML tree was used in the subsequent analysis. Divergence in climate envelopes and allopatry Climate envelopes for western and eastern Amazonian Atelopus were modelled, subsequently mapped into geographic space and compared. https://www.selleckchem.com/products/azd2014.html For our approach we used the presence data points listed in the Appendix (30 for all western and 54 for all eastern Amazonian Atelopus; Fig. 2). We created models based on seven macroscale bioclimatic parameters (Table 2) describing the availability of thermal energy and water, widely used in climate envelope models (e.g. Selleckchem Foretinib Carnaval and

Moritz 2008; Rödder and Lötters 2009). Using DIVA-GIS 5.4 (Hijmans et al. 2001), bioclimatic parameters were extracted from the WorldClim

1.4 interpolation model with grid cell resolution 2.5 min for the period 1950–2000 (Hijmans et al. PF-6463922 mw 2005) at (i) the species records as well as (ii) at 1,000 random points within both the MCP of the western and eastern Atelopus presence. For comparison, we computed boxplots with XLSTAT 2009 (Addinsoft). Subsequently, climate envelope models were generated and mapped with MaxEnt 3.2.19 (Phillips et al. 2006) based on the principle of maximum entropy (Jaynes 1957). This approach yields more reliable results than comparable methods (e.g. Elith et al. 2006; Heikkinen et al. 2006; Wisz et al. 2008), especially when data points for species number relatively few (e.g. Hernandez et al. 2006). Using default Metformin settings, 25% of the data points were randomly reserved for model testing (duplicate presence records

in one grid cell were automatically removed). Prediction accuracy was evaluated through threshold-independent receiver operating characteristic (ROC) curves and the calculation of the area under the curve (AUC) method (e.g. Hanley and McNeil 1982). We acknowledge that there is currently some discussion about the suitability of AUC (Lobo et al. 2008). However, for our application AUC is the best possible choice. Elith and Graham (2009) pointed out that none of the frequently applied statistics in AUC are misleading and that appropriate statistics relevant to the application of the model need to be selected. The logistic MaxEnt output was chosen which is continuous and linear scaled (0–1, with 0.1 being the minimum Maxent value at the training records already suggesting suitability to the species under study; Phillips et al. 2006). Table 2 AUC values per model, climate envelope overlap in terms of I and D values and assessment of their similarity and equivalency via randomization tests (see text) Bioclimatic parameter Model fit D I AUCWestern, AUCEastern Overlap Identity Similarity Overlap Identity Similarity Western, Eastern Western, Eastern Annual mean temperature 0.798, 0.750 0.93 ns <0.01, <0.05 0.94 ns <0.01, <0.05 Mean monthly temperature range 0.796, 0.896 0.58 <0.01 <0.01, ns 0.72 <0.05 <0.

J Vasc Interv Radiol 2008, 19:1693–1698 PubMedCrossRef 24 Fava M

J Vasc Interv Radiol 2008, 19:1693–1698.PubMedCrossRef 24. Fava M, Meneses L, Loyola S, Tevah J, Bertoni H, Huete I, Mellado #this website randurls[1|1|,|CHEM1|]# P: Carotid artery dissection: endovascular treatment. Report of 12 patients. Catheter Cardiovasc Interv 2008, 71:694–700.PubMedCrossRef 25. Schulte S, Donas KP, Pitoulias GA, Horsch S: Endovascular treatment of iatrogenic and traumatic carotid artery dissection. Cardiovasc Intervent Radiol 2008, 31:870–874.PubMedCrossRef 26. DuBose J, Recinos G, Teixeira PG, Inaba K, Demetriades D: Endovascular stenting for the treatment of traumatic internal carotid injuries: expanding

experience. J Trauma 2008, 65:1561–1566.PubMedCrossRef 27. Siomin V, Angelov L, Li L, Vogelbaum MA: Results of a survey of neurosurgical practice patterns regarding the prophylactic

use of anti-epilepsy drugs in patients with brain tumors. J Neurooncol 2005, 74:211–215.PubMedCrossRef 28. Kim YJ, Xiao Y, Mackenzie CF, Gardner SD: Availability of trauma specialists in level I and II trauma centers: a national survey. J Trauma 2007, 63:676–683.PubMedCrossRef 29. Berry C, Sandberg DI, Hoh DJ, Krieger MD, McComb JG: Use of cranial fixation pins in pediatric neurosurgery. Neurosurgery 2008, 62:913–918. discussion 918–919PubMedCrossRef 30. Lebude B, Yadla S, Albert T, Anderson DG, Harrop JS, Hilibrand A, Maltenfort M, Sharan A, Vaccaro AR, Ratliff JK: Defining “”Complications”" in Spine Surgery: Neurosurgery and Orthopedic Spine Surgeons’ Survey. selleck kinase inhibitor J Spinal Disord Tech 2010,23(8):493–500.PubMedCrossRef

31. Glotzbecker MP, Bono CM, Harris MB, Brick G, Heary RF, Wood KB: Surgeon practices regarding postoperative thromboembolic prophylaxis after high-risk spinal surgery. Spine (Phila Pa 1976) 2008, 33:2915–2921.CrossRef 32. American College of Surgeons Committee on Trauma: National Trauma Data Bank. Chicago, IL; 2010. 33. Hollingworth W, Nathens AB, Kanne JP, Crandall ML, Crummy TA, Hallam DK, Wang MC, Jarvik JG: The diagnostic accuracy Guanylate cyclase 2C of computed tomography angiography for traumatic or atherosclerotic lesions of the carotid and vertebral arteries: a systematic review. Eur J Radiol 2003, 48:88–102.PubMedCrossRef 34. Hoit DA, Schirmer CM, Weller SJ, Lisbon A, Edlow JA, Malek AM: Angiographic detection of carotid and vertebral arterial injury in the high-energy blunt trauma patient. J Spinal Disord Tech 2008, 21:259–266.PubMedCrossRef 35. Biffl WL, Egglin T, Benedetto B, Gibbs F, Cioffi WG: Sixteen-slice computed tomographic angiography is a reliable noninvasive screening test for clinically significant blunt cerebrovascular injuries. J Trauma 2006, 60:745–751. discussion 751–742PubMedCrossRef 36. Bub LD, Hollingworth W, Jarvik JG, Hallam DK: Screening for blunt cerebrovascular injury: evaluating the accuracy of multidetector computed tomographic angiography. J Trauma 2005, 59:691–697.PubMed 37.

TgCyp18 stimulated IL-12 production in macrophages [13] and DCs [

TgCyp18 stimulated IL-12 production in macrophages [13] and DCs [12]. Therefore, macrophages and DCs both play CAL-101 molecular weight a role in IL-12 production in the present study. Further investigations are required to distinguish the relative contributions made by these cells. These results suggest that CCR5-independent accumulation of inflammatory cells at the site of infection might produce higher levels of pro-inflammatory cytokines in CCR5−/−

mice. The ability of T. gondii to attract, invade, and survive inside immune cells (T cells, DCs and macrophages), along with the migratory properties of DCs and macrophages that allow parasite dissemination around the host click here have been reported previously [7, 24]*[26]. Our results revealed that while T. gondii could infect CD3+, CD11c+, and CD11b+ cells, it exhibited a preference for CD11b+. We observed enhanced recruitment of CD11b+ cells after infection with RH-OE. This chemotactic AMN-107 order effect of TgCyp18 was correlated with the ability of RH-OE to increase CCR5 expression levels. Thus, overproduction of TgCyp18 during RH-OE infection enhanced cellular recruitment. Recruitment of CD11b+ cells in CCR5−/− mice infected with RH-OE was also higher than that in RH-GFP-infected mice.

Additionally, there was no significant difference in the recruitment of CD11b+ cells between WT and CCR5−/− mice that were infected peritoneally with RH-GFP tachyzoites. Recently, our group demonstrated that recombinant TgCyp18 controlled the in vitro migration 4-Aminobutyrate aminotransferase of macrophages and lymphocytes in CCR5-dependent and -independent ways [14]. Therefore, the results presented here suggest that the TgCyp18-induced cell migration occurred in a CCR5-independent way in our in vivo experimental

model. Migration of macrophages and lymphocytes to the site of infection would enhance T. gondii invasion into these cells, after which the parasite-infected cells, such as CD11b+ leukocytes, are transported to other organs [7]. Our quantitative PCR analyses revealed that infection with RH-OE resulted in an increased parasitic load in the liver compared with RH-GFP infection. These results suggest that cells recruited by TgCyp18 are used to shuttle the parasite to other organs. In general, chemokines and their receptors play an important role in the migration of immune cells. A previous study showed that an early burst of CCR5 ligand production occurred in the tissue of WT and CCR5−/− mice by day 5 after oral infection with T. gondii strain 76 k cysts [27]. Our present study showed that recombinant TgCyp18 increased the expression levels of CCL5 in macrophages. In addition, significantly higher levels of CCL5 were detected in the peritoneal fluids of CCR5−/− mice infected RH-OE.

Scidmore M, Hackstadt T:

Scidmore M, selleck kinase inhibitor Hackstadt T: Mammalian 14–3-3beta associates with the Chlamydia trachomatis inclusion membrane via its interaction with IncG. Mol Microbiol 2001, 39:1638–1650.PubMedCrossRef IACS-10759 ic50 15. Hybiske K, Stephens R: Mechanisms of host cell exit by the intracellular bacterium Chlamydia . Proc Natl Acad Sci USA 2007, 104:11430–11435.PubMedCrossRef 16. Stone C, Johnson D, Bulir D, Mahony J: Characterization of the putative type III secretion ATPase CdsN (Cpn0707) of Chlamydophila pneumoniae. J Bacteriol 2008, 190:6580–6588.PubMedCrossRef 17. Blaylock B, Riordan K, Missiakas D, Schneewind O: Characterization of the Yersinia enterocolitica type III secretion ATPase YscN and its

regulator, YscL. J. Bacteriol 2006, 188:3525–3534.PubMedCrossRef 18. Fields K, Hackstadt T: Evidence for the secretion of Chlamydia trachomatis CopN by a type III secretion mechanism. Mol. Microbiol 2000, 38:1048–1060.PubMedCrossRef 19. selleck chemicals llc Riordan K, Schneewind O: YscU cleavage and the assembly of Yersinia type III secretion machine complexes. Mol Microbiol 2008, 68:1485–1501.PubMedCrossRef 20. Johnson D, Stone C, Mahony J: Interactions between CdsD, CdsQ, and CdsL, three putative Chlamydophila

pneumoniae type III secretion proteins. J Bacteriol 2008, 190:2972–2980.PubMedCrossRef 21. Aizawa S: Bacterial flagella and type III secretion systems. FEMS Microbiol Lett 2001, 202:157–164.PubMedCrossRef 22. Kalman S, Michell W, Marathe R, Lammel C, Fan J, Hyman R, Olinger L, Grimwood J, Davis R, Stephens R: Comparative genomes of Chlamydia pneumoniae and C. trachomatis. Nat Genet 1999, 21:385–389.PubMedCrossRef 23. Peters J, Wilson J, Myers G, Timms P, Bavoil P: Type III secretion a la Chlamydia . Trends Microbiol 2007, 15:241–251.PubMedCrossRef 24. Ghelardi E, Celandroni F, Salvetti S, Beecher D, Gominet M, Lereclus D, Wong A, Senesi S: Requirement of flhA for swarming differentiation, flagellin export, and secretion

of virulence-associated proteins in Bacillus thuringiensis . J Bacteriol 2002, 184:6424–6433.PubMedCrossRef 25. McMurry J, Arnam J, Kihara M, Macnab R: Analysis of Paclitaxel the cytoplasmic domains of Salmonella FlhA and interactions with components of the flagellar export machinery. J Bacteriol 2004, 186:7586–7592.PubMedCrossRef 26. Bigot A, Pagniez H, Botton E, Frehel C, Dubail I, Jacquet C, Charbit A, Raynaud C: Role of FliF and FliI of Listeria monocytogenes in flagellar assembly and pathogenicity. Infect Immune 2005, 73:5530–5539.CrossRef 27. Akeda Y, Galan J: Chaperone release and unfolding of substrates in type III secretion. Nature 2005, 437:911–915.PubMedCrossRef 28. Paul K, Erhardt M, Hirano T, Blair D, Hughes K: Energy source of flagellar type III secretion. Nature 2008, 451:489–492.PubMedCrossRef 29. Kubori T, Shimamoto N, Yamaguchi A, Namba K, Aizawa S: Morphological pathway of flagellar assembly in Salmonella typhimurium . J Mol Biol 1992, 226:433–446.PubMedCrossRef 30.

aeruginosa, isogenic ampG and ampP insertional inactivation mutan

aeruginosa, isogenic ampG and ampP insertional inactivation Verubecestat price mutants were constructed in the prototypic P. aeruginosa strain PAO1, referred to as PAOampG {Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleck Anti-infection Compound Library|Selleck Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Selleckchem Anti-infection Compound Library|Selleckchem Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|Anti-infection Compound Library|Antiinfection Compound Library|buy Anti-infection Compound Library|Anti-infection Compound Library ic50|Anti-infection Compound Library price|Anti-infection Compound Library cost|Anti-infection Compound Library solubility dmso|Anti-infection Compound Library purchase|Anti-infection Compound Library manufacturer|Anti-infection Compound Library research buy|Anti-infection Compound Library order|Anti-infection Compound Library mouse|Anti-infection Compound Library chemical structure|Anti-infection Compound Library mw|Anti-infection Compound Library molecular weight|Anti-infection Compound Library datasheet|Anti-infection Compound Library supplier|Anti-infection Compound Library in vitro|Anti-infection Compound Library cell line|Anti-infection Compound Library concentration|Anti-infection Compound Library nmr|Anti-infection Compound Library in vivo|Anti-infection Compound Library clinical trial|Anti-infection Compound Library cell assay|Anti-infection Compound Library screening|Anti-infection Compound Library high throughput|buy Antiinfection Compound Library|Antiinfection Compound Library ic50|Antiinfection Compound Library price|Antiinfection Compound Library cost|Antiinfection Compound Library solubility dmso|Antiinfection Compound Library purchase|Antiinfection Compound Library manufacturer|Antiinfection Compound Library research buy|Antiinfection Compound Library order|Antiinfection Compound Library chemical structure|Antiinfection Compound Library datasheet|Antiinfection Compound Library supplier|Antiinfection Compound Library in vitro|Antiinfection Compound Library cell line|Antiinfection Compound Library concentration|Antiinfection Compound Library clinical trial|Antiinfection Compound Library cell assay|Antiinfection Compound Library screening|Antiinfection Compound Library high throughput|Anti-infection Compound high throughput screening| and PAOampP, respectively. The β-lactamase activity in the two isogenic mutants, PAOampG and PAOampP, was

compared to PAO1. In the absence of β-lactam antibiotics, all strains showed a basal level of β-lactamase activity (Table 1). Upon challenge with 500 μg/ml of benzyl-penicillin, this level was elevated 10-fold (p < 0.05) in PAO1 (Table 1). However, the β-lactamase activities of PAOampP and PAOampG remained low in the presence of β-lactam antibiotic, indicating a loss of β-lactamase induction (Table 1). The loss of inducibility in PAOampG could be partially restored by expressing ampG in trans, whereas the β-lactamase inducibility of PAOampP was completely recovered when ampP was supplied in trans (Table 1). Both PAOampP and PAOampG mutants had the other copy selleck chemical of the permease gene intact. These observations suggest that ampG and ampP are individually important members of the β-lactamase induction system.

To confirm that ampG and ampP play independent roles, cross-complementation of PAOampP with pAmpG, and PAOampG with pAmpP was performed. Similar to the mutants, the cross-complemented strains did not show inducible β-lactamase activity (Table 1). Table 1 β-lactamase activity of P. aeruginosa PAO1, PAOampG and PAOampP in the absence Oxymatrine and presence of β-lactam Strain and plasmid Relevant genotypes (supplement in trans) β-lactamase activitya     Uninduced Induced b PAO1 ampG + ampP + 22.2 ± 9.7 221.4c ± 9.2 PAOampG ampG – ampP + 20.4 ± 6.2 28.8d ± 3.3 PAOampP ampG + ampP – 4.2 ± 6.2 32.2d ± 3.3 PAOampG/pKKF69 ampG – ampP + (ampG + ) 8.4 ± 1.4 87.6 ± 14.4 PAOampP/pKKF73 ampG + ampP – (ampP + ) 8.8 ± 1.8 217.9 ± 35.5 PAOampG/pKKF73 ampG – ampP + (ampP + ) 2.1 ± 2.0 14.4 ± 1.9

PAOampP/pKKF69 ampG + ampP – (ampG + ) 5.3 ± 1.9 10.6 ± 2.7 a Cultures at OD600 of 0.6-0.8 were divided in two. One set was induced with 500 μg/ml benzyl-penicillin for three hours before harvesting. Assays were performed on sonicated lysate using nitrocefin as a chromogenic substrate. One milliunit of β-lactamase is defined as 1 nanomole of nitrocefin hydrolyzed per minute per microgram of protein. Assays were performed in triplicate. b Induction was carried out using 500 μg/ml benzyl-penicillin c p < 0.05 compared to uninduced PAO1 d p < 0.05 compared to induced PAO1 To further understand the role of ampG and ampP in β-lactamase induction, β-lactamase activity was assayed at different concentrations of benzyl-penicillin in PAO1, PAOampG and PAOampP (Figure 5). Upon encounter with the inducer (25 μg/ml), there was approximately 38% induction (Figure 5). For strain PAO1, this increase in β-lactamase activity continued in a dose-dependent manner until the maximum level of β-lactamase activity was reached when 100 μg/ml of benzyl-penicillin was added (Figure 5).

Proc Natl Acad Sci USA 106(29):11857–11861 doi:10 ​1073/​pnas ​0

Proc Natl Acad Sci USA 106(29):11857–11861. doi:10.​1073/​pnas.​0903586106 PubMed Busch A, Hippler M (2011) The structure and function of eukaryotic XMU-MP-1 in vitro photosystem I. Biochim Biophys Acta 1807(8):864–877. doi:10.​1016/​j.​bbabio.​2010.​09.​009 www.selleckchem.com/products/c646.html PubMed Byrdin M, Jordan P, Krauss N, Fromme P, Stehlik D, Schlodder E (2002) Light harvesting

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42(14):4226–4234PubMed Croce R, Zucchelli G, Garlaschi FM, Bassi R, Jennings RC (1996) Excited state equilibration in the photosystem I-light-harvesting I complex: p700 is almost isoenergetic with its antenna. Biochemistry 35:8572–8579PubMed Croce R, Zucchelli G, Garlaschi FM, Jennings RC (1998) A thermal broadening study of the antenna chlorophylls in PSI-200, LHCI, and PSI core. Biochemistry 37:17355–17360PubMed Croce R, Dorra D, Angiogenesis inhibitor Holzwarth AR, Jennings RC (2000) Fluorescence decay and spectral evolution in intact photosystem I of higher plants. Biochemistry 39:6341–6348PubMed Croce R, Morosinotto T, Castelletti S, Breton J, Bassi R (2002) The Lhca antenna complexes of higher plants photosystem I. Biochim Biophys Acta Bioenerg 1556(1):29–40 Croce R, Morosinotto T, Ihalainen

JA, Chojnicka A, Breton J, Dekker JP, van Grondelle R, Bassi R (2004) Origin of the 701-nm fluorescence emission of the Lhca2 subunit of higher plant photosystem I. J Biol Chem 279(47):48543–48549PubMed Croce R, Chojnicka A, Morosinotto T, Ihalainen JA, van Mourik F, Dekker JP, Bassi R, van Grondelle R (2007) The low-energy forms of photosystem I light-harvesting complexes: spectroscopic properties and pigment–pigment interaction characteristics. Biophys J 93(7):2418–2428PubMed Damjanovic A, Vaswani HM, Fromme P, Fleming GR (2002) Chlorophyll excitations in photosystem I of Synechococcus elongatus. J Phys Chem B 106(39):10251–10262 Urocanase Drop B, Webber-Birungi M, Fusetti F, Kouril R, Redding KE, Boekema EJ, Croce R (2011) Photosystem I of Chlamydomonas reinhardtii contains nine light-harvesting complexes (Lhca) located on one side of the core. J Biol Chem 286(52):44878–44887. doi:10.​1074/​jbc.​M111.​301101 PubMed Du M, Xie XL, Jia YW, Mets L, Fleming GR (1993) Direct observation of ultrafast energy transfer in psi core antenna. Chem Phys Lett 201:535–542 Elrad D, Grossman AR (2004) A genome’s-eye view of the light-harvesting polypeptides of Chlamydomonas reinhardtii.


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