PubMed 39 Savina A, Jancic C, Hugues S, Guermonprez P, Vargas P,

PubMed 39. Savina A, Jancic C, Hugues S, Guermonprez P, Vargas P, Moura IC, Lennon-Dumenil AM, Seabra MC, Raposo G, Amigorena S: NOX2 controls phagosomal pH to regulate antigen processing during crosspresentation by dendritic cells. Cell 2006,126(1):205–218.PubMedCrossRef Authors’ contributions AB, KV and HA designed and performed experiments and analyzed data. VB analyzed the data and wrote the manuscript. All authors approve the final

manuscript.”
“Background LRR (leucine rich repeat) domains are present in over 60, 000 proteins listed in PFAM, PRINTS, SMART, InterPro and PANTHER databases [1]. LRR-containing proteins have been BMN 673 price identified in viruses, bacteria, archae, and eukaryotes. Most LRR proteins are involved in protein, ligand and in protein, protein interactions; these include plant immune response and the mammalian innate immune response [2–6]. All LRR units can be divided into a HCS (highly C646 research buy conserved segment) and a VS (variable

segment). The HCS part consists of an eleven residue stretch, LxxLxLxxNxL, or a twelve residue stretch, LxxLxLxxCxxL, in which “”L”" is Leu, Ile, Val, or Phe, “”N”" is Asn, Thr, Ser, or Cys, and “”C”" is Cys, Ser or Asn. Three residues at positions 3 to 5 in the highly conserved segments form a short β-strand. The β-strands stack parallel and the multiple LRRs then form an arc. The concave face consists of a parallel β-sheet and the convex face is made of a variety of secondary structures including the a-helix, 310-helix, polyproline II helix, and an extended structure or a tandem arrangement of β-turns. In most LRR proteins the β-strands Rutecarpine on the concave surface and (mostly) helical elements on the convex surface are connected by short loops or β-turns. Seven classes of LRRs have been recognized, characterized by different lengths and consensus sequences of the VS part of the repeats [7, 8]. They are “”RI-like”", “”CC”", “”Bacterial”", “”SDS22-like”", “”plant specific”", “”typical”", and “”TpLRR”"[3]. The seven classes of LRR domains adopt a variety of structures. “”Typical”" LRRs are the most abundant LRR class. The

consensus sequence is LxxLxLxxNxLxxLpxxoFxxLxx. The repeat length is 20-27 residues. Bold uppercase letters indicate more than 70% occurrence of a given residue in a certain position; normal letters indicate 40-70% occurrence and lowercase letters indicate 30-40% occurrence; “”o”" indicates a non-polar residue, and “”x”" indicates nonconserved residues. Their variable segments adopt mainly polyproline II plus β-turn, consecutive β-turns or β-turn plus polyproline II in the convex faces; the structural units may be represented by β – (βt + PPII). “”RI-like”" LRRs are contained in proteins such as ribonuclease inhibitor and Ran GTPase learn more activating protein. The consensus sequence is LxxLxLxxNx(L/C)xxxgoxxLxxoLxxxxx. The repeat length is 28-29. Their VSs mainly adopt α-helix (β – α structural units). Cysteine-containing (CC) LRR proteins include GRR1 proteins from Saccharomyces cerevisiae.

Mol

Mol Cancer Ther 2012, 11:2301–2305.PubMedCrossRef 32. Jang MH, Kim EJ, Choi Y, Lee HE, Kim YJ, Kim JH, Kang E, Kim SW, Kim IA, Park SY: FGFR1 is amplified during the progression see more of in situ to invasive breast carcinoma. Breast Cancer Res 2012, 14:R115.PubMedCrossRef 33. Moelans CB, de Wegers RA,

Monsuurs HN, Maess AH, van Diest PJ: Molecular differences between ductal carcinoma in situ and adjacent invasive breast carcinoma: a multiplex ligation-dependent probe amplification study. Cell Oncol (Dordr) 2011, 34:475–482.CrossRef Competing interests The authors declare that they have no competing interests. Authors’ contribution EB drafted the manuscript, MB interpreted the molecular analyses

and drafted the manuscript, GB set up the database, AC interpreted the molecular analysis, EM participated in the sequence alignment, AN recruited tissue samples, MC recruited tissue samples, AM reviewed the criticisms, EB recruited the clinical information, FM recruited the clinical information, GT recruited the clinical information, SC recruited the clinical information, SP performed the technical experiments, MC interpreted the immunophenotypical analysis, GZ recruited tissue samples, KM verified the distribution of HER2 analysis, GM participated in the sequence alignment, FB approved, followed and managed all processing steps of research. All the authors read and approved the final manuscript.”
“Background AZD0156 cell line Breast cancer is one of the most common malignant cancers among women worldwide. In 2012, an estimated 220,000 individuals were diagnosed with breast cancer and the mortality associated with breast cancer is nearly 40,000 in the United States [1]. Radiotherapy plays an

important role in the treatment of breast cancer. Several randomized clinical trials have shown that improved disease-free and overall survival rates were improved by the addition of radiotherapy in the treatment of women with breast cancer [2–5]. However, tumor radioresistance remains a fundamental barrier to attaining maximal efficacy with radiotherapy for the treatment of breast cancer. Radioresistance may be present at the beginning of therapy, causing the patients to fail to respond buy 5-FU to treatment (intrinsic radioresistance), or it may emerge over time during radiotherapy treatment (acquired radioresistance). Fractionated radiation (FR) is often used in radiotherapy to facilitate the Copanlisib ic50 recovery of normal tissues. Cancer cells may acquire radioresistance during fractionated radiotherapy, which results in treatment failure. Overcoming the acquired radioresistance of breast cancer could improve the outcome of breast cancer patients who receive radiotherapy. Apoptosis, or programmed cell death, is the mechanism of radiation-induced cancer cell death [6, 7].

41) Post-traumatic stress disorder (PTSD) Impact of event scale (

41) Post-traumatic stress disorder (PTSD) Impact of event scale (van der Ploeg and Kleber 2003; ≥26) Anxiety Brief symptom inventory for anxiety (de Beurs and Zitman 2005; >0.41) Physical health www.selleckchem.com/products/bay-57-1293.html requirements Cardio-respiratory, musculoskeletal, relevant strength, balance, coordination, carrying capacity Fire-fighting simulation test,

test I (Plat et al. 2010a; not passing all parts, selleck compound completion >24 min and 35 s or not passing the stair-climb test within one hour)   Fire-fighting stair-climb test, test II (Plat et al. 2010b) (not finishing the test) OR ((not reaching >85% of theoretical max. heart rate at the end of the test or not within 2 min) OR (not within 1 min)) Airways Signalling question complaints airways/lungs after exposure (yes) Sense-related

requirements Vision Landolt C test (NOG 2004; best eye < 0.8 and least eye <0.5) 5, 0.6 and 0.4 m Colour vision Ishihara colour test (NOG 2004; >3 errors) Hearing Whisper test (Eekhof et al. 2002; >4 errors at one ear) Skin Signalling question complaints skin after exposure (yes) Cardiovascular risk factors Cardiovascular diseases Body mass index (>25.0) (Graham et al. 2007) Waist circumference (men > 1.02 m; women > 0.88 m)   Systolic blood pressure (≥140 mmHg)   Diastolic blood pressure (≥90 mmHg)   Smoking Obatoclax Mesylate (GX15-070) (yes)   Diabetes mellitus (yes) Psychological selleck chemical health requirements Psychological health was assessed using information about sleepiness, work-related fatigue, depression, post-traumatic stress disorder and anxiety. The measurement scales and applied limits are shown in Table 1. Physical health requirements Two physical job-specific tests were used to measure physical health: the fire-fighting simulation test and the fire-fighting stair-climb test. These two physical, job-specific tests

reflect the necessary physical capacity for satisfactory job performance, both in the cardio-respiratory system and in the musculoskeletal system, i.e. strength, balance, coordination and carrying capacity. The two tests are described in detail by Plat et al. (2010a, b). In addition to these tests, fire fighters reported whether they experienced airway problems after incidental or recurrent exposure to a high concentration of inhaled gas in the previous 6 months (Table 1). Sense-related requirements Eye sight and proper hearing as well as skin problems of the hands/arms were tested. Proper eye sight was tested at several distances (5.0, 0.6, 0.4 m), and colour vision was also tested. Proper hearing was tested using the whisper test, which is a test used by Dutch general practitioners (Eekhof et al. 2002).

BCC has also been shown to colonise natural habitats including ag

BCC has also been shown to colonise natural habitats including agricultural soils, plant rhizospheres, and river waters [4–7]. The maize rhizosphere is a favourable niche for BCC bacteria, probably due to their ability to metabolise at high rates maize root exudates [8] and has

also been suggested to represent a natural reservoir of bacterial strains that may exhibit this website pathogenic traits [9–13]. A close association between maize roots and BCC has been observed in a number of different locations worldwide [6, 14–17]. Studies on BCC populations recovered from Italian maize rhizosphere have shown the presence of several BCC species such as B. cepacia, B. cenocepacia (recA lineage IIIB), B. ambifaria, B. pyrrocinia, and BCC groups such as BCC5 and

BCC6 suggesting YH25448 possible novel plant associated species within the complex [14, 18–20]. In Mexico, where maize has traditionally been cultivated for thousands of years, B. cenocepacia (recA lineage IIIB) and B. vietnamiensis were isolated with other Burkholderia species from the rhizosphere of local and commercial varieties of maize plants cultivated in distant geographical regions [[21, 22], our unpublished data]. The maize rhizosphere is a dynamic and active environment in which many factors may affect the diversity and activity of microbial communities [23, 24]. The distribution of identical clones among BCC populations recovered from geographically disparate Italian maize rhizospheres suggested that bacterial flow may occur among BCC populations of different geographic areas [20]. Therefore, assessing the diversity of maize-rhizosphere associated BCC species in different and distant Angiogenesis inhibitor countries may provide critical insight into the population structure, evolution and ecology of such BCC populations. Indexing allelic variation in sets of housekeeping genes provides a good basis for estimating overall levels of genotypic

variation in microbial populations [25, 26]. Methods based on this principle, such as multilocus restriction typing (MLRT), multilocus enzyme electrophoresis (MLEE), and multilocus sequence typing (MLST), provide good insights into the genetic relationships among strains [27–30]. During the last decade, MLST has emerged as a powerful tool until in studies of BCC epidemiology and population structure [31]. MLRT has a lower discrimination power than MLST, but acceptable turnaround time and lower cost make it really advantageous, especially for an ‘in-house’ initial genotype screening of isolates collected in large-scale [32–34]. Furthermore, MLRT has been used to study the global epidemiology and the population structure of B. cenocepacia [26, 32], Streptococcus pneumoniae [28] and Helicobacter pylori [35], as well as to determine the genetic relationships among strains of Neisseria meningitidis [25, 36], Staphylococcus aureus [37], Escherichia coli [38] and Yersinia enterocolitica biovar 1A [30].

in the ultra-runners in a 161-km ultra-marathon [7] The lowest Δ

in the ultra-runners in a 161-km ultra-marathon [7]. The lowest Δ body mass in R3 might be also due to a colder temperature than in other races, because

of a wind chill and heavy NSC23766 purchase raining during the race, there was probably less sweat loss. R1 and R4 were held in favorable weather conditions in contrast with the colder ambient temperatures in R2 and R3, moreover accompanied with rain during the whole race. The highest number of dehydrated athletes was in R4 (the multi-stage race), on the contrary, the least number of overhydrated finishers was in R1 (the 24-hour MTB race) with no case of EAH. Higher Δ body mass were seen in R1 and R4 compared to races held under colder conditions (R2,R3). Although there PND-1186 were large differences in ambient temperatures during the day and night,

EAH did not occur in R1 in very high ambient temperature. Therefore we concluded that like in Hoffman Sotrastaurin et al. [11] and Knechtle et al. [15] the environmental conditions probably had an influence on race performance, but not on the prevalence of EAH in our subjects in these concrete races. The present work is also in agreement with previous studies [11, 38] showing that while a greater ambient temperature was associated with the number of dehydrated finishers, it was not associated with a larger number of overhydrated finishers. The hypothesis that body mass losses would have no influence on race performance [11] was supported in R2 (the 24-hour MTB race). Δ body mass was negatively

related to race performance, finishers with the greatest body mass losses tended to have a better race performance such as a higher number of achieved kilometers. The significant relationship medroxyprogesterone between percentage Δ body mass and race time showed that the fastest runners tended to lose more body mass as observed by Hoffman et al. [11] in a 161-km ultra-marathon and Kao et al. [32] in a 24-hour running race. Also, in Zouhal et al. [47] a loss in body mass did not affect performance, and in Knechtle et al. [15] faster runners in a 100-km ultra-marathon lost more body mass than slower runners. These data support the finding that Δ body mass during exercise may not reflect exact changes in hydration status [20, 60], and a loss in body mass did not impair race performance. Presumably, the decrease in body mass in the present athletes in R2 could also be due to dehydration [60], or changes in body mass representing a balance of fluid and energy intake and fluid and energy losses from external and internal sources with significant fat mass losses during the race [26, 37]. We assume that the loss in body mass could be also due to a substrate losses as well as fluid losses. The additional finding that in any race post-race body mass or Δ body mass was negatively related to post-race plasma [Na+] warrants further investigation.

But according to http://​www ​indexfungorum ​org (June 2011), W

But according to http://​www.​indexfungorum.​org (June 2011), W. gigantospora is the generic type of Wettsteinina. Both W. gigantospora and W. gigaspora were treated as the synonyms of W. mirabilis (Niessl) Höhn. http://​www.​indexfungorum.​org (June, 2011, Synonymy Contributor: CBS (2010)). We tentatively described the generic type of W. gigantospora as a representing of the type of W. gigaspora here. New family names, i.e. Pseudosphaeriaceae

and Wettsteininaceae (as Wettsteiniaceae) and a new order, Pseudosphaeriales had been introduced to accommodate Wettsteinina and its synonym Pseudosphaeria (Höhnel 1907; Locquin 1972). After a systematic study, Wettsteinina was included in Pleosporaceae based on its “Pleospora-type” p38 MAPK inhibitor centrum, and Pseudosphaeriaceae and Wettsteininaceae are treated as synonyms of Pleosporaceae (Shoemaker and Babcock 1987). Phylogenetic study Wettsteinina macrotheca (Rostr.)

E. Müll., W. pachyasca (Niessl) Petr. and W. dryadis (Rostr.) Petr. were reported to be closely related to Pleomassaria siparia (Melanommataceae) (Kodsueb et al. 2006a), and W. lacustris (Fuckel) Shoemaker & C.E. Babc. nested within Lentitheciaceae (Schoch et al. 2009). The generic type has not been sequenced. Concluding remarks The most striking character for find more Wettsteinina is its asymmetrical ascospores, thick-walled obpyriform asci and lack of Fedratinib mouse pseudoparaphyses at maturity. These characters are comparable with genera in the Capnodiales and Venturiales. The phylogenetic significance of these characters are not fully understood, while the hemibiotrophic or saprobic

life style may indicate its polyphyletic nature (Shoemaker and Babcock 1987). Strains from the genus, in particular the generic type require DNA sequence data so that the phylogenetic placement can be investigated. Wilmia Dianese, Inácio & Dorn. -Silva, Mycologia C-X-C chemokine receptor type 7 (CXCR-7) 93: 1014 (2001). (Phaeosphaeriaceae) Generic description Habitat terrestrial, hemibiotrophic or biotrophic. Ascomata small, scattered, immersed, globose to subglobose, papillate. Peridium thin, composed of a few layers of brown, thick-walled cells of textura angularis to prismatica. Hamathecium comprising filliform, septate, rarely branching, evanescent, cellular pseudoparaphyses embedded in mucilage. Asci bitunicate, fissitunicate, cylindrical to clavate, with a short, furcate pedicel and ocular chamber. Ascospores fusoid, pale brown, 1-septate. Anamorphs reported for genus: see below. Literature: Dianese et al. 2001. Type species Wilmia brasiliensis Dianese, Inácio & Dorn.-Silva, Mycologia 93: 1014 (2001). (Fig. 96) Fig. 96 Wilmia brasiliensis (from UB Col. Microl 8438, holotype). a Section of an ascoma. Note the setae in the ostiole. b Conidioma of the coelomycetous anamorphic stage. c, d Clavate asci with short furcate pedicels. e, f Released 1-septate pale brown ascospores. Scale bars: a, b = 100 μm, c, d = 20 μm, e, f = 10 μm Ascomata 175–240 μm high × 95–145 μm diam.

We confirmed that large quantities of cytotoxic NK cells can be e

We confirmed that large quantities of cytotoxic NK cells can be expanded from PBMC in the presence of K562 cells expressing membrane-bound IL-15 and 4-1BBLigand from normal individuals p38 MAP Kinase pathway and patients with various solid tumors. Ex-vivo expansion tended to alter the balance of NK cell receptor expression towards those that activate

and mediate cytotoxicity. This activity resulted in cytotoxicity against various allogeneic tumor targets and more importantly, against autologous-derived gastric tumor targets. Blocking studies identified multiple activating receptor-ligand interactions that would be predicted to mediate NK cell cytotoxicity. Moreover, these activating receptor-ligand interactions were operative in antibody-dependent cellular cytotoxicity (ADCC) in an allogeneic and autologous setting. Importantly, as a mean for future clinical translation, GMP compliant cytolytic NK cells could efficiently be expanded from lymphocyte-enriched cell fractions obtained

from PBMC by counter current elutriation. Our studies demonstrate that human NK cells VS-4718 mw acquire cytolytic activity against autologous gastric tumor cells after ex-vivo expansion and suggest a therapeutic potential for autologous expanded NK cells, both directly and in combination with monoclonal antibodies in future cell-based immunotherapy. Methods Cells and Cell Fractions Human blood samples were GDC-0994 purchased (BRT Laboratories, Baltimore, MD) and whole peripheral blood mononuclear cells (PBMC) were isolated using density-gradient centrifugation. Using leukapheresis products 17-DMAG (Alvespimycin) HCl purchased from the same source, the constitutive cell populations were fractionated

by continuous-counterflow elutriation following protocols established by the manufacturer of cell separator (Elutra, Gambro BCT). This instrument uses continuous counter-flow elutriation technology to separate cells fractions based primarily by size and secondarily by specific gravity. In brief, the leukapheresis product was loaded via an inlet pump into a constantly rotating (2400 rpm) elutriation chamber. Based on centrifuge speed and cell density, five elutriated cell fractions were collected. PBMC and various elutriated cell fractions were viably frozen in RPMI-1640 (Invitrogen Corp., Grand Island, NY) supplemented with 20% human AB serum (Gemini Bio-Products, Woodland, CA) and 10% Dimethylsulfoxide (Sigma, St. Louis, MO) using an automated cell freezer (Gordinier Electronics, Roseville, MI) and stored in the vapor phase of liquid nitrogen until used. The myeloid cell line K562, prostate cancer cell lines LNCaP, PC-3 and DU-145 and breast cancer cell line MCF-7 were available in our laboratory. The lung cancer cell line H358 was kindly provided by Dr. S. Ostrand-Rosenberg (Department of Biological Sciences, University of Maryland Baltimore County, Catonsville, MD) and the Head and Neck cancer cell line TU-167 was kindly provided by Dr. S.

albicans genomic DNA (American Type Culture Collection, Manassas,

albicans genomic DNA (American Type Culture Collection, Manassas, VA, USA), the normalized plasmid standards in triplicate reactions. Laboratory analysis of click here assay performance using diverse bacterial genomic DNA To assess our assay performance against diverse bacteria,

we tested our assay against a diverse collection of bacterial genomic DNA to determine the assay efficiency and correlation coefficients. The details are as follows: Bacterial strains Arsenophonus nasoniae ATCC 49151 , Budvicia aquatica ATCC 51341, Buttiauxella gaviniae ATCC 51604, Cedecea davisae ATCC 33431 , Cellvibrio gilvus ATCC13127, Citrobacter freundii ATCC 8090, Clostridium difficile ATCC 9689, Cronobacter aerogenes ATCC 13048, Ewingella americana ATCC 33852 , Edwardsiella tarda ATCC 15947, Escherichia vulneris ATCC 33821, Hafnia

alvei ATCC 29926, Ewingella americana ATCC 33852 , Klebsiella oxytoca ATCC 49131, Kluyvera ascorbata this website ATCC 33433, Leclericia adecarboxylata ATCC 700325, Leminorella richardii ATCC 33998, Moellerella wisconsensis ATCC 35621, Morganella morganii ATCC 25830, Obesumbacterium proteus ATCC 12841, Pantoea agglomerans ATCC 27155, Photorhabdus asymbiotica ATCC 43950, Plesiomonas shigelloides ATCC 14029, Pragia fontium ATCC 49100, Proteus mirabilis ATCC 29906 , Providencia rustigianii ATCC 33673, Pseudomonas aeruginosa ATCC 27853, Pseudomonas andersonii ATCC BAA-267, Pseudomonas anguilliseptica ATCC 33660, Pseudomonas heptaminol azotofixans ATCC BAA-1049, Pseudomonas fragi ATCC 4973, Pseudomonas lundensis ATCC 49968, Pseudomonas luteola ATCC 43273, Pseudomonas mendocina ATCC 25411, Pseudomonas monteilii ATCC 700476, Pseudomonas mosselii ATCC BAA-99, Pseudomonas otitidis ATCC BAA-1130, Pseudomonas pseudoalcaligenes ATCC 17440, Psuedomonas putida ATCC 12633, Pseudomonas stutzeri ATCC 17588, Pseudomonas taetrolens ATCC 4683, Rahnella aquatilus ATCC 33071, Raoultella ornithinolytica ATCC 31898 , Shigella dysenteriae ATCC 13313, Salmonella

enterica ATCC 13076, Serratia liquefaciens ATCC 27592, Tatumella ptyseos ATCC 33301, Trabulsiella guamensis ATCC 49492, Yersinia enterocolitica ATCC 9610, and Yokenella regensburgei ATCC 43001 were obtained from the American Type Culture Collection (Manassas, VA, USA). Bacterial propagation and enrichment were Doramapimod nmr performed under the appropriate condition for each bacterial strain following ATCC recommendations. Extraction of bacterial genomic DNA Extraction using the enriched broth was performed using ZR Fungal/Bacterial DNA MiniPrepTM (Zymo Research, Irvine, CA, USA) following the manufacturer’s instruction. Elution of the purified genomic DNA was performed using 100 μl of 1X TE buffer.

Importantly, the LPS array can be remodeled in response to

Importantly, the LPS array can be remodeled in response to environmental conditions such as external pH [68, JQEZ5 supplier 69]. How then might cholesterol modulate LPS biogenesis and modification? The lipid compositions of the inner and outer membranes of gram negative bacteria are specific and distinct [70], but little is known about the subcellular compartmentation of cholesterol in H. pylori or other prokaryotes. We propose that the presence of cholesterol is needed to establish the proper membrane

composition and structure that permit the orderly building of nascent LPS as it transits across the inner membrane/periplasmic/outer membrane compartments. In this model, altered membrane composition may influence the activity of LPS biosynthetic enzymes embedded in the membrane, leading to improper LPS modification. Alternatively, cholesterol

depletion may result in dysregulation of LPS transporter function due to alterations in membrane structure and composition. The dysregulated movement of LPS among inner membrane, periplasmic, and outer membrane compartments would then result in aberrant modifications to its structure. This scenario would be consistent with the observed discrepancy between whole cell Lewis antigen levels measured by immunoblot and cell surface levels measured by ELISA. That is, it is possible that under cholesterol-depletion the Lewis antigen-bearing LPS may learn more be less effectively transported to the cell surface. Preliminary

evidence indicates that membrane cholesterol may also influence certain ABC transporters and the ComB DNA transporter in H. pylori (Hildebrandt, Trainor and McGee, unpublished results). Thus, cholesterol may support a wider range of physiological processes in the bacterial membrane than is currently appreciated. Conclusions We have demonstrated for the first Janus kinase (JAK) time that cholesterol, though nonessential to growth of H. pylori, is nevertheless essential for gastric colonization in an animal model. We have further shown that cholesterol plays important roles in determining LPS structure as well as Lewis antigen expression, and that these biological effects are highly specific for cholesterol. LPS profiles of mutant strains lacking the O-chain retain responses to cholesterol availability, providing evidence for structural changes to the oligosaccharide core/lipid A moieties. Disruption of the lipid A 1-phosphatase gene, lpxE, eliminated the effect of cholesterol on LPS profiles, suggesting that aberrant forms of LPS that appear upon cholesterol depletion are dependent upon 1-dephosphorylation of lipid A. The roles of cholesterol in LPS structural modification and in Lewis antigen expression do not require α-glucosylation of cholesterol. Thus, cholesterol imparts these benefits independently of its Dorsomorphin ic50 previously reported role in resistance to host phagocytosis and T-cell responses, which require the alpha-glycoside metabolite of cholesterol [35].

PubMed 5 Tamagnini P, Troshina O, Oxelfelt F, Salema R, Lindblad

PubMed 5. Tamagnini P, Troshina O, Oxelfelt F, Salema R, Lindblad P: Hydrogenases in Nostoc sp. Strain PCC 73102, a strain lacking a bidirectional enzyme. Appl Environ Microbiol 1997,63(5):1801–1807.PubMed 6. Forzi L, Sawers RG: Maturation of [NiFe]-hydrogenases selleck kinase inhibitor in Escherichia coli. Biometals 2007. 7. Bock A, King PW, Blokesch M, Posewitz MC: Maturation of hydrogenases. Adv Microb Physiol 2006, 51:1–71.CrossRefPubMed 8. Jacobi A, Rossmann R, Bock A: The hyp operon gene products are required for the maturation of catalytically active hydrogenase

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Thiamet G 3 from Escherichia coli taking place after nickel incorporation. FEBS Lett 2000,473(2):254–258.CrossRefPubMed 15. Thiemermann S, Dernedde J, Bernhard M, Schroeder W, Massanz C, Friedrich B: Carboxyl-terminal processing of the cytoplasmic NAD-reducing hydrogenase of INCB28060 supplier Alcaligenes eutrophus requires the hoxW gene product. J Bacteriol 1996,178(8):2368–2374.PubMed 16. Wünschiers R, Batur M, Lindblad P: Presence and expression of hydrogenase specific C-terminal endopeptidases in cyanobacteria. BMC Microbiol 2003,3(8):8.CrossRefPubMed 17. Fritsche E, Paschos A, Beisel H-G, Böck A, Huber R: Crystal Structure of the Hydrogenase Maturationing Endopeptidase HYBD from Escherichia coli. J Mol Biol 1999,288(5):989–998.CrossRefPubMed 18. Maier T, Bock A: Generation of Active [NiFe] Hydrogenase in Vitro from a Nickel-Free Precursor Form. Biochemistry 1996,35(31):10089–10093.CrossRefPubMed 19. Theodoratou E, Paschos A, Magalon A, Fritsche E, Huber R, Böck A: Nickel serves as a substrate recognition motif for the endopeptidase involved in hydrogenase maturation. Eur J Biochem 2000, 267:1995–1999.CrossRefPubMed 20. Axelsson R, Oxelfelt F, Lindblad P: Transcriptional regulation of Nostoc uptake hydrogenase.