Figure 7 Phylogenetic tree showing the evolutive distances amongs

Figure 7 Phylogenetic tree showing the evolutive distances amongst IATs and putatives IALs from

several ascomycetes. The IAT of P. chrysogenum (GenBank: P15802), the IAT of A. nidulans (GenBank: P21133) and a hypothetical protein of A. oryzae which shares 84% identity with the P. chrysogenum IAT (GenBank: XP_001825449), were compared to the P. chrysogenum IAL and putative homologues of this protein that are present in different PLX4032 clinical trial ascomycetes, such as A. oryzae (GenBank: BAE55742), A. clavatus (GenBank: XP_001271254), A. niger (GenBank: XP_001399990), A. terreus (GenBank: XP_001213312 and XP_001216532), N. fischeri (GenBank: XP_001263202), A. fumigatus (GenBank: XP_754359) and A. nidulans (aatB-encoded protein GenBank: XP_664379). Sequences were aligned using the MegAlign program (Lasergene, DNASTAR, Inc.). Intron content of the genes encoding these proteins is indicated in brackets. Genes encoding IATs in P. chrysogenum, A. nidulans and A. oryzae contain three introns, thus differing from those genes encoding IAL and IAL-homologues (Fig. 7). Only the aatB gene encoding the A. nidulans IAL homologue and one of the A. terreus ial gene homologue (GenBank: XP_001213312), contain three introns. This suggests that

alternatively, ial and ial gene homologues might have had a different origin from the IAT-encoding genes (penDE or aatA genes), selleck products thus encoding proteins with a different function as it was confirmed by the lack of penicillin biosynthetic activity of the P. chrysogenum IAL. With this hypothesis, only the aatB gene from A. nidulans would be a real paralogue of the IAT-encoding gene (aatA) formed by gene duplication from a common ancestor. This is supported by the Alanine-glyoxylate transaminase presence of penicillin forming activity of the aatB-encoded IAL homologue and by the presence of the same transcription factors binding to the promoter

regions of these two genes [35]. Conclusion If there was a common ancestor for the ial and penDE genes, most of the Ascomycota fungi initially had the potential capacity to perform the acyltransferase reaction. However, only a few of them, like A. nidulans and P. chrysogenum, were able to develop during evolution, the penDE encoding the highly functional IAT enzyme. The penDE gene was linked to the first two genes (of bacterial origin) of the penicillin pathway, which endowed these microorganisms with an important ecological advantage because of the ability to generate aromatic penicillins. It is likely that the de novo formation of this cluster occurred in a common ancestor of the genera Penicillium and Aspergillus, since the pen cluster is present in several species of those genera [40–42]. However, not all genomes of the aspergilli contain the pen cluster; e.g., A. fumigatus lacks it, although it contains the ial gene.

Curr Sci 102:8 Singh JS, Kushwaha SPS (2008) Forest biodiversity

Curr Sci 102:8 Singh JS, Kushwaha SPS (2008) Forest biodiversity and its conservation in India. Int For Rev 10(2):292–304 Srivastava P, Kumar A, Behera SK, Sharma YK, Singh N (2012) Soil carbon sequestration: an innovative strategy for reducing atmospheric carbon dioxide concentration. Biodivers Conserv. doi:10.​1007/​s10531-012-0229-y”
“Introduction It is now widely accepted that we are in the midst of an

extinction crisis brought about by land conversion, overexploitation, pollution and invasive species (Pimm et al. 2006; Wake and Vredenburg 2008). For well-studied taxa, current extinction rates are two to three orders of magnitude greater than background rates and equally above rates at which new species evolve (Dirzo and Raven 2003). This loss of species has negative economic,

ethical, and aesthetic impacts and is essentially permanent over time scales relevant to humans. Consequently, efforts to prevent extinctions have been extensive, but the efficacy of such efforts is often not evaluated (Sutherland et al. 2004; Ferraro and Pattanayak 2006). Here we report on the accomplishments and resulting biodiversity impacts of an international conservation organization that specializes in the prioritization, planning and implementation of invasive vertebrate eradications from islands. Island Conservation is a US-headquartered non-government conservation organization founded in 1994 whose mission is “to prevent 17DMAG datasheet extinctions”. Island Conservation started as an entirely volunteer organization with offices in the US and Mexico and now has 30 paid employees and learn more programs in North America, South America, the Caribbean and the Tropical Pacific. The Mexican branch of Island Demeclocycline Conservation, Conservación de Islas, has experienced similar growth and in 2009 the two organizations became formally independent. In this paper we examine accomplishments between 1994 and 2009. Methods To quantify Island Conservation’s accomplishments, we compiled a database of plant and vertebrate biodiversity, area and location for all islands

where they attempted to eradicate one or more invasive mammal species. We used the IUCN Redlist (http://​iucnredlist.​org, 2004) to determine if an endemic vertebrate species was threatened (classified as Critically Endangered, Endangered or Vulnerable). We did not determine the threatened status of plants as the IUCN Redlist coverage of plant taxa was not adequate. We did not independently evaluate the success or failure of attempted eradications, but instead relied on the assessments of Island Conservation staff, the organizations that manage the islands, and island users. Two of the authors of this paper (Tershy and Croll) founded Island Conservation but are no longer affiliated with the organization.

05) of the down-regulated miR-200a*, and miR-148b* in SP of HCC

05). of the down-regulated miR-200a*, and miR-148b* in SP of HCC cells had the fold changes 0.1 ± 0.04, and 0.4 ± 0.08, respectively (P < 0.01). Figure 4 Validation of microarray data using real-time RT-PCR. (A) The levels of miR-21, miR-34c-3p, miR-470*, miR-10b and let-7i* are significantly increased, while the levels of miR-200a*, miR-148b are significantly decreased in the SP of HCC cells compared to the fetal liver cells, according to the results of microarray analysis (gray bar). Real-time RT-PCR analysis of these miRNAs Daporinad clinical trial using total

RNA isolated from the SP fractions showed similar results (white bar). (B) Real-time analysis revealed that some known target genes of those partially validated miRNAs are also significantly differentially expressed between the SP sorted from the HCC cells and fetal liver cells (* P < 0.05; ** P < 0.01). The levels of target gene mRNA are inversely correlated with associated microRNA expression in SP cells. To further confirm the differentially expressed miRNA, selleck compound some known target genes expression of those validated miRNAs excluded miR-470* and miR-148b were detected in sorted SP cells and compared by using qRT-PCR between fetal liver cell and HCC cells. These target genes were PTEN (miR-21), P53 (miR-34c),

Rho C (miR-10b), RAS (let-7i), and ZEB1 (miR-200a). As shown in Figure 4B, the relative gene expression of PTEN, P53, RhoC and RAS in SP from HCC cells were Sinomenine significantly lower than in fetal liver cells. On the contrary, the relative expression of ZEB1 gene in SP from HCC cells was higher than in fetal liver cells. Respectively, corresponding specific data were 0.78 ± 0.24 vs 0.33 ± 0.18 (PTEN), 1.79 ± 0.36 vs 0.81 ± 0.29 (P53), 1.16 ± 0.44 vs 0.72 ± 0.34 (RhoC), 3.52 ± 1.13 vs 1.62 ± 0.92 (RAS), and 0.27 ± 0.11 vs 0.48 ± 0.13 (ZEB1). These data were indirectly validated the differentially expressing profile of those miRNAs in SP fractions between HCC cells and fetal liver cells. Discussion There is a growing realization that many cancers may harbor a small population of cancer stem cells (CSCs).

These cells not only exhibit stem cell characteristics, but also, importantly, are tumor-initiating cells and are responsible for cellular heterogeneity of cancer due to aberrant SB203580 cell line differentiation. According to the hierarchical model of cancer, the origin of the cancer stem cells may be long-lived somatic stem cells. Therefore, markers of “”normal”" stem cells are being sought with the expectation that these molecules are also expressed by cancer stem cells, and can be used to identify them. In fact, the specific markers of many somatic stem cells, e.g., HSCs, are still unidentified, and it is difficult to screen putative stem cell markers useful for isolation and characterization of liver cancer stem cells.

This result offered at least a mechanism for the difference in th

This result offered at least a mechanism for the difference in the efficacy of sunitinib between clinical and preclinical trials. It should be considered if sunitinib acts via some of its targets on B16 cells. Previous studies reported that B16 cells did not express VEGFR1, VEGFR2, VEGFR3 [54, 55],

PDGFRα and PDGFRβ [56] but no more than 10% of B16 cells expressed c-Kit [57]. Whether sunitinib acts on B16 cells through the c-Kit target remains to be investigated in the further study. Chronic stress has been demonstrated to promote development and progression of tumors in several human cancer cells in xenografts including prostate cancer, ovarian cancer and MDV3100 solubility dmso breast cancer [9, 13, 15, 46, 58], whereas no date regarding the influence of chronic stress in cancer models under sunitinib in vivo has been reported so far. This study showed that consecutive NE pumped stimulated the growth of primary tumor in a mouse melanoma model and could be blocked by propranolol. This result provided a piece of evidence for the discrepancy in the efficacy of sunitinib between clinical and preclinical

trials and was consistent with the results in the other studies in our laboratory (mouse colon cancer CT26 homograft and human colon cancer SW480 and HT-29 xenografts, unpublished selleck kinase inhibitor date not shown). To further investigate stress-induced angiogenesis in vivo, we analysed the immunoreactivity for VEGF and CD31, counted the MVD and measured the protein levels of VEGF, IL-8 and IL-6 in mouse serums. As expected, in accordance with the results in vivo as mentioned in the previous paragraph, chronic stress promoted angiogenesis and neovascularization in B16F1 tumors, thus withstood Methane monooxygenase the anti-angiogenic treatment of sunitinib. Interestingly, relatively low VEGF expression was found in tumor and endothelial cells while stronger VEGF expression usually found in peri-necrotic tumors cells mainly by reason of hypoxia as reported in the other study [59]. In clinic, the serum levels of VEGF, IL-8 and IL-6 have been suggested as SCH727965 ic50 potentially

predictive markers for survival in cancer patients under sunitinib. Bauerschlag et al. [60] found that 18 cases with a decrease in VEGF serum concentration out of 29 ovarian cancer patients with sunitinib therapy had a longer progression-free survival (PFS) compared to 11 cases with an increase in VEGF serum concentration (10.5 VS 2.9 months). Likewise, the lower serum VEGF level was reported to be associated with longer PFS and objective response rate in patients under sunitinib with bevacizumab-refractory metastatic renal cancer [61]. Bellmunt et al. [62] announced that the low serum IL-8 level was related to long median time to progression in urothelial cancer patients receiving sunitinib as first-line treatment.

For the deletion constructs of pilC and pilQ strain FSC237 was us

For the deletion constructs of pilC and pilQ strain FSC237 was used as template and for the pilT deletion the strain FSC155 buy R406 was used as a template. The sequence for the pilT construct is almost identical between FSC155 and FSC237 except for three substitutions upstream of the deletion in non-coding sequences, and eight substitutions in a downstream pseudogene. The PCR fragments were cloned into the suicide vector pDM4 and the resulting plasmids

pAL12 (pilC), pAL16 (pilQ), and pAL18 (pilT) (Table 2) were introduced into strain FSC237 by conjugal mating as previously described [7]. The in vitro growth rate of the different mutant strains were compared with the wild type strain by measuring OD at different time points, 0 h, 6 h and ON after dilution in Chamberlain medium. RNA isolation find more and RT-PCR Bacteria were grown for 18 h on plates, harvested and suspended in TRIzol reagent (Life Technologies). Total RNA was extracted and treated with

RNase-free DNase I (Roche), phenol extracted, and precipitated by ethanol. An aliquot of the RNA (3 μg) was used to synthesize cDNA using random hexamers (final concentration 25 ng/μl) and Superscript III reverse transcriptase as described by the manufacturer (Life Technologies). In control experiments samples processed without addition of RT enzyme were used. Animal infections F. tularensis strains were grown for 16 h on BCGA before the bacteria were suspended in phosphate buffered saline (PBS) pH 7.4 to an OD540 = 1, which normally corresponds to approximately 2 × 109 bacteria/ml. The bacterial suspension was then diluted in PBS into two doses used for challenge, around 10 and 100 bacteria in a total volume of 100 μl. All bacterial infections were initiated by subcutaneous injections of 6-8 week old C57Black/6 female mice. The study was approved by the Local Ethical Committee on Laboratory Animals in Umeå, Sweden. For competitive index (CI) infections, the mice were infected with a 50:50 mixture of mutant and wild-type strains with around 50 bacteria of each strain. Mice were culled five days post-infection, and the spleens were homogenized in 1 ml of PBS and spread on BCGA.

Individual colonies were analysed by PCR with primers specific for each mutation in order to examine the distribution of each strain. Spleens from at least three animals were click here collected for each pair of strains, Bacterial neuraminidase and at least 200 colonies were analysed by PCR. The CI was calculated for each strain by dividing the ratio of mutant/wt after infection (determined with PCR) with the ratio of mutant/wt before infection (determined by viable count). Statistical analysis was performed with a GraphPad Prism computer software program using a paired Student’s t-test (one-tailed) where P < 0.05 was regarded as significant. Gel electrophoresis and Western blotting Samples were boiled in the presence of SDS and Β-mercaptoethanol for 5 min and then separated on a 12% acrylamide gel by electrophoresis as described by Laemmli [31].

’s (unpublished) ITS analysis Species included Type species: Chr

’s (unpublished) ITS analysis. Species included Type species: Chromosera viola. Comments This new, currently monotypic buy S63845 subgenus in Chromosera is erected for C. viola. It was

originally described in Hygrocybe by Geesink & Bas, then transferred to Cuphophyllus by Bon because of the highly interwoven hyphae in the lateral strands of the lamellar context. Gloioxanthomyces Lodge, Vizzini, Ercole & Boertm., gen. PCI-34051 nov. MycoBank MB804073 Type species: Hygrophorus vitellinus Fr., Monogr. Hymenomyc. Suec. (Upsaliae) 2(2): 312 (1863), ≡ Gloioxanthomyces vitellinus (Fr.) Lodge, Vizzini, Ercole & Boertm. Lectotype here designated for Hygrophorus vitellinus Fr. is an illustration cited in Fries, Monogr. Hymenomyc. Suec. (Upsaliae) 2(2): 312 (1863): Icon. t. 167, f. 3. Pileus and stipe yellow or orangish yellow, viscid; lamellae arcuate-decurrent, yellow, with a gelatinized or subgelatinized edge, edged often darker (translucent). Basidiospores ellipsoid this website or subglobose, Q 1.0—1.6, mean Q 1.2—1.3, guttulate in KOH, with a wide hilar appendix, inamyloid, acyanophilic, hyaline, smooth; basidia usually 4-sterigmate, with basal clamp connection occasionally a moderate medallion type, short, 30—40 μm long, ratio of basidia to basidiospore

length 4–5; pileipellis and stipitipellis an ixotrichodermium or ixocutis; trama not dextrinoid; lamellar trama subregular, central strand not differentiated, elements cylindric to subglobose, some subglobose cells highly inflated to 10—30 μm diam., subhymenium

of tightly interwoven small diameter hyphae, not gelatinized except at the lamellar edge; edge gelatinized or subgelatinized; cheilocystidia clavate, simple or slightly lobed. Clamp connections present throughout, occasionally a modest medallion type, not toruloid. It differs from Chromosera subg. Oreocybe in presence of a gelatinized lamellar edge and cheilocystidia, and basidiospores with smaller Q (1.2–1.3 PRKD3 vs. 1.4–1.8) and never constricted. It differs from Chromosera subg. Chromosera in absence of dextrinoid reactions in the context, absence of pigment globules in the pileipellis and lamellar edge gelatinized with cheilocystidia present. It differs from Chromosera subg. Subomphalia in absence of violaceous pigments, viscid rather than dry surfaces, and absence of a central strand in the lamellar trama. Etymology Gloio — glutinous, xantho —yellow, myces — fungus. Gloioxanthomyces vitellinus (Fr.) Lodge, Vizzini, Ercole & Boertm., comb. nov. MycoBank MB804074 Basionym: Hygrophorus vitellinus Fr., Monogr. Hymenomyc. Suec. (Upsaliae) 2(2): 312 (1863), ≡ Gliophorus vitellinus (Fr.) Kovalenko (1988), [=?Hygrocybe luteolaeta Arnolds]. Lectotype for Hygrophorus vitellinus Fr. is an illustration cited by Fries in Monogr. Hymenomyc. Suec. (Upsaliae) 2(2): 312 (1863): Hym. Eur. p. 417, Icon. T. 167, f. 3.

Acknowledgements Matthew

Acknowledgements Matthew buy BIBW2992 Rhea, PhD, David Turbow, PhD and Angela Hegamin, PhD were dissertation committee members who read, critiqued and approved the final dissertation manuscript. VPX Sports provided the product support. Christopher Taber, Katherine Doberne and Marina Kolomey provided research assistance and data collection. References 1. Kerksick C, Harvey T, Stout J, Campbell B,

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Clin Chem LabMed 2010,48(6):757–767. Full Text 7. Nikolaidis MG, Jamurtas AZ, Paschalis V, Fatouros IG, Koutedakis Y, Kouretas D: The effect of muscle-damaging exercise on blood and skeletal muscle oxidative stress: magnitude and time-course considerations. Sports Med 2008,38(7):579–606. PubMed AbstractPubMedCrossRef 8. Miranda-Vilela AL, Akimoto Non-specific serine/threonine protein kinase AK, Lordelo GS, Pereira LC, Grisolia CK, Klautau-Guimarães MD: Creatine kinase MM TaqI and methylenetetrahydrofolate reductase C677T and A1298C gene polymorphisms influence exercise-induced C-reactive protein levels. Eur J Appl Physiol 2012,112(3):941–950.

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Deletion of an additional 63 bp caused an increase of about 60% m

Deletion of an additional 63 bp caused an increase of about 60% more β-galactosidase activity. To confirm that the RNA polymerase binding regions are located within the sequences spanning up to the selleck products consensus -35 sequences, 3′ Selleckchem Olaparib end deletion constructs lacking sequences up to the -35 region for genes 14 and 19

(65 and 57 bp, respectively) were prepared and assessed for β-galactosidase activity. These deletions led to the complete loss of β-galactosidase activity (Figure 6A–B lane 11 and 6C–D lane 6). Figure 6 Deletion analysis of promoter regions of genes 14 and 19. β-galactosidase activity of extracts prepared from E. coli cultures of bacteria transformed with various deletion constructs was determined. Panels A and C have cartoons depicting deletion constructs and their orientations for genes 14 and 19, respectively. (Solid black boxes represent lacZ gene, and right and left arrowhead

lines show orientation of the promoter regions ligated in front of the lacZ coding sequence. Lengths INCB018424 of the promoter regions in base pairs are indicated on the left. Panels B and D contain the β-galactosidase activity analysis data. (β-galactosidase activity was expressed as percent activity relative to the activity observed for full length promoter segments.) Data are presented with SD values calculated from four independent experiments (P ≤ 0.001). Location of -10 and -35 regions To determine whether the consensus -35 and -10 represented true RNA polymerase binding site regions, constructs lacking either the predicted -35 or -10 alone or the regions spanning from -35 to -10 were generated, and the effect of the loss of these sequences on promoter activity was evaluated by measuring

β-galactosidase activity. Deletion of the predicted -35 regions alone or in combination with the -10 for both the genes resulted in decline of β-galactosidase activity to the background levels observed for negative controls. Deletion of the consensus -10 region alone for both the genes, however, resulted in no significant change to the promoter activity (Figure 7). The impact of the deletions of -35 and -10 are very similar for both genes’ promoters. Figure 7 Deletion analysis spanning the -35 and -10 regions of genes 14 and 19. β-galactosidase activity of extracts prepared from E. coli cultures of bacteria transformed HSP90 with -35 or -10 deletions or deletions spanning from -35 to 10 were determined. Panels A and C have cartoons depicting deletion constructs and their orientations for genes 14 and 19, respectively. Panels B and D contained the β-galactosidase activity analysis data. Data are presented with SD values calculated from four independent experiments (P ≤ 0.001). Discussion Differences in protein expression influenced by vertebrate and tick cell environment are now well documented for E. chaffeensis [18–20] and other tick-transmitted bacteria [12, 13, 15, 16]. We recently reported novel data describing differences in immune response in the murine host against E.

All authors were involved

in at least one of the followin

All authors were involved

in at least one of the following: Selleckchem ARN-509 conception, design, data acquisition, data analysis, statistical analysis, and interpretation of data. All authors drafted the manuscript and/or revised the manuscript for important intellectual Foretinib content, and all authors provided final approval of the version to be published. Organon (now Merck & Co., Inc.) provided the study drug (Org 26576) and financial support for the conduct of the studies. Dr. Nations was employed by Merck Sharp & Dohme Corp. (Whitehouse Station, NJ, USA) at the time of this research. Drs. Bursi and Schipper were employed by Merck Sharp & Dohme Oss BV (Oss, the Netherlands) at the time of this research. Dr. Dogterom is currently an employee of Merck Sharp & Dohme Oss BV. The employers of Drs. Ereshefsky and Gertsik (California Clinical Trials Medical Group, Inc.) and Dr. Mant (Quintiles) were paid by Organon (now Merck & Co., Inc.) for their work on this trial. References 1. Cutler NR, Sramek JJ, Murphy MF, et al. Critical pathways to success in CNS drug development. 1st ed. Oxford: LY2874455 clinical trial Wiley-Blackwell, 2010CrossRef 2. Sramek JJ, Cutler NR. Investigator perspective on MTD: practical application of an MTD definition — has it accelerated development? J Clin Pharmacol 2000; 40: 1184–7.PubMed 3. Ereshefsky L, Jhee

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PubMedCrossRef 4 Lamont RJ, Chan A, Belton CM, Izutsu KT, Vasel

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cells. Infect Immun 1995,63(10):3878–3885.PubMed 5. Zhang W, Ju J, Rigney T, Tribble selleck chemical GD: Fimbriae of Porphyromonas gingivalis are important for initial invasion of osteoblasts, but not for inhibition of their differentiation and mineralization. J Periodontol 2011,82(6):909–916.PubMedCrossRef 6. Zhang W, Swearingen EB, Ju J, Rigney T, Tribble GD: Porphyromonas gingivalis invades osteoblasts and inhibits bone formation. Microbes Infect 2010,12(11):838–845.PubMedCrossRef 7. Ozeri V, Rosenshine I, Ben-Ze’Ev A, Bokoch GM, Jou TS, Hanski E: De novo formation of focal complex-like structures in host cells by invading Streptococci. Mol Microbiol 2001,41(3):561–573.PubMedCrossRef 8. Agerer F, Lux S, Michel A, Rohde M, Ohlsen K, Hauck CR: Cellular invasion by Staphylococcus aureus reveals a functional link between focal adhesion kinase and cortactin in integrin-mediated internalisation. J Cell Sci 2005,118(Pt 10):2189–2200.PubMedCrossRef 9. Plancon L, Du Merle L, Le Friec S, Gounon P, Jouve M, Guignot J, Servin A, Le Bouguenec C: Recognition of the

cellular beta1-chain integrin by the bacterial AfaD invasin is implicated in the internalization of afa-expressing GW786034 solubility dmso pathogenic Escherichia coli strains. Cell Microbiol 2003,5(10):681–693.PubMedCrossRef 10. Amano A: Molecular interaction of Porphyromonas gingivalis with host cells: implication for the microbial pathogenesis of periodontal disease. J Periodontol 2003,74(1):90–96.PubMedCrossRef 11. Tsuda K, Furuta

N, Inaba H, Kawai S, Hanada K, Yoshimori T, Amano A: Functional analysis of alpha5beta1 integrin and lipid rafts in invasion of epithelial cells by Porphyromonas gingivalis using fluorescent beads coated with bacterial membrane vesicles. Cell Struct Funct 2008,33(1):123–132.PubMedCrossRef 12. Yilmaz O, Watanabe K, Lamont RJ: Involvement of integrins in fimbriae-mediated binding and invasion by Porphyromonas gingivalis. Cell Microbiol 2002,4(5):305–314.PubMedCrossRef 13. Schoenwaelder SM, Burridge K: Bidirectional signaling between the cytoskeleton and integrins. Curr Opin Cell Biol 1999,11(2):274–286.PubMedCrossRef Mirabegron 14. Young VB, Falkow S, Schoolnik GK: The invasin protein of Yersinia enterocolitica: internalization of invasin-bearing bacteria by eukaryotic cells is associated with reorganization of the cytoskeleton. J Cell Biol 1992,116(1):197–207.PubMedCrossRef 15. Yilmaz O, Young PA, Lamont RJ, Kenny GE: Gingival epithelial cell signalling and cytoskeletal responses to Porphyromonas gingivalis invasion. Microbiology 2003,149(Pt 9):2417–2426.PubMedCrossRef 16. Maniotis AJ, Chen CS, Ingber DE: Demonstration of mechanical connections between integrins, cytoskeletal filaments, and nucleoplasm that stabilize nuclear structure. Proc Natl Acad Sci U S A 1997,94(3):849–854.PubMedCrossRef 17.