Journal articles: 'Host-Pathogen interface'

1

Wilson, Van G. "Sumoylation at the Host-Pathogen Interface." Biomolecules 2, no. 2 (April 5, 2012): 203–27. http://dx.doi.org/10.3390/biom2020203.

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Kuehne, Sarah A. "Communication at the host-pathogen interface." Journal of Oral Microbiology 9, sup1 (May 30, 2017): 1325269. http://dx.doi.org/10.1080/20002297.2017.1325269.

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3

Liles, W. Conrad. "The dynamic pathogen–host response interface." Drug Discovery Today: Disease Mechanisms 4, no. 4 (December 2007): 205–6. http://dx.doi.org/10.1016/j.ddmec.2008.02.005.

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4

Kaye, Paul, and Phillip Scott. "Leishmaniasis: complexity at the host–pathogen interface." Nature Reviews Microbiology 9, no. 8 (July 11, 2011): 604–15. http://dx.doi.org/10.1038/nrmicro2608.

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Lonergan, Zachery R., and Eric P. Skaar. "Nutrient Zinc at the Host–Pathogen Interface." Trends in Biochemical Sciences 44, no. 12 (December 2019): 1041–56. http://dx.doi.org/10.1016/j.tibs.2019.06.010.

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Nosanchuk, Joshua D., and Attila Gacser. "Histoplasma capsulatum at the host–pathogen interface." Microbes and Infection 10, no. 9 (July 2008): 973–77. http://dx.doi.org/10.1016/j.micinf.2008.07.011.

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Stebbins, C. Erec. "Structural microbiology at the pathogen-host interface." Cellular Microbiology 7, no. 9 (July 5, 2005): 1227–36. http://dx.doi.org/10.1111/j.1462-5822.2005.00564.x.

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8

Coombes, Brian K. "Regulatory evolution at the host–pathogen interface." Canadian Journal of Microbiology 59, no. 6 (June 2013): 365–67. http://dx.doi.org/10.1139/cjm-2013-0300.

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Horizontal gene transfer plays a major role in microbial evolution by innovating the bacterial genome with new genetic blueprints to adapt to previously unexploited niches. However, to benefit from these genetic acquisitions, the bacterium must integrate the expression of these new genes into existing regulatory nodes and deploy them at the right time. There is much to gain from uncovering the genetic diversity in noncoding DNA that is selective during host infection because of the beneficial effect it has on bacterial gene expression. By identifying genes that have undergone regulatory evolution, a deeper understanding of the arms race between host and pathogen is gained.

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Colonna, Marco, Bali Pulendran, and Akiko Iwasaki. "Dendritic cells at the host-pathogen interface." Nature Immunology 7, no. 2 (February 2006): 117–20. http://dx.doi.org/10.1038/ni0206-117.

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Kelsall, Brian L., Christine A. Biron, Opendra Sharma, and Paul M. Kaye. "Dendritic cells at the host-pathogen interface." Nature Immunology 3, no. 8 (August 2002): 699–702. http://dx.doi.org/10.1038/ni0802-699.

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Grohmann, Christoph, Danushka S. Marapana, and Gregor Ebert. "Targeted protein degradation at the host–pathogen interface." Molecular Microbiology 117, no. 3 (December 2, 2021): 670–81. http://dx.doi.org/10.1111/mmi.14849.

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Schumann, Ralf R. "Host cell–pathogen interface: molecular mechanisms and genetics." Vaccine 22 (December 2004): S21—S24. http://dx.doi.org/10.1016/j.vaccine.2004.08.012.

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13

Wanford, Joseph J., and Charlotte Odendall. "Ca2+-calmodulin signalling at the host-pathogen interface." Current Opinion in Microbiology 72 (April 2023): 102267. http://dx.doi.org/10.1016/j.mib.2023.102267.

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14

Hood, M. Indriati, and Eric P. Skaar. "Nutritional immunity: transition metals at the pathogen–host interface." Nature Reviews Microbiology 10, no. 8 (July 16, 2012): 525–37. http://dx.doi.org/10.1038/nrmicro2836.

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15

Beutler, B. "Sepsis begins at the interface of pathogen and host." Biochemical Society Transactions 29, no. 6 (November 1, 2001): 853–59. http://dx.doi.org/10.1042/bst0290853.

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To the modern mind, the term ‘sepsis’ conjures up images of microbes. It is easy to forget that the word predates any understanding of the microbial origins of infectious disease. Derived from the Greek ‘sepsios’ (rotten), sepsis denotes decay: a phenomenon that humans once regarded as a mysterious though inevitable natural process. A living organism does not accept decay passively. Virtually all multicellular life forms are capable of resisting infection through the generation of a vigorous immune response. In mammals, the response is so stereotypic that it has come to define sepsis itself: it is often called the ‘septic syndrome’. Our current understanding of the innate immune system is deeply rooted in the study of sepsis. The chain of events linking infection to tissue injury and cardiovascular collapse is not obvious, and affirmation of the concept required three major discoveries. First, the septic syndrome was found to be caused by toxic products of microbes. Secondly, these toxic substances were found to be toxic because of their propensity to activate cells of the innate immune system, prompting cytokine production. Thirdly, the activating events initiated by microbial toxins were traced to members of an ancient family of defensive molecules, versions of which operate in virtually all multicellular life forms. In mammals, proteins of this family are now known as Toll-like receptors. They represent a point of direct contact, and first contact, between a pathogen and the host immune system.

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16

Sampson, Samantha L. "Mycobacterial PE/PPE Proteins at the Host-Pathogen Interface." Clinical and Developmental Immunology 2011 (2011): 1–11. http://dx.doi.org/10.1155/2011/497203.

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The mycobacterial PE/PPE proteins have attracted much interest since their formal identification just over a decade ago. It has been widely speculated that these proteins may play a role in evasion of host immune responses, possibly via antigenic variation. Although a cohesive understanding of their function(s) has yet to be established, emerging data increasingly supports a role for the PE/PPE proteins at multiple levels of the infectious process. This paper will delineate salient features of the families revealed by comparative genomics, bioinformatic analyses and genome-wide screening approaches and will summarise existing knowledge of subcellular localization, secretion pathways, and protein structure. These characteristics will be considered in light of findings on innate and adaptive host responses to PE/PPE proteins, and we will review the increasing body of data on B and T cell recognition of these proteins. Finally, we will consider how current knowledge and future explorations may contribute to a more comprehensive understanding of these intriguing proteins and their involvement in host pathogen interactions. Ultimately this information could underpin future intervention strategies, for example, in the area of new and improved diagnostic tools and vaccine candidates.

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17

Sansonetti, P. "Bacterial infertion: close encounters at the host-pathogen interface." Research in Microbiology 149, no. 4 (April 1998): 301. http://dx.doi.org/10.1016/s0923-2508(98)80305-7.

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18

Hodgkinson, Victoria, and Michael J. Petris. "Copper Homeostasis at the Host-Pathogen Interface: FIGURE 1." Journal of Biological Chemistry 287, no. 17 (March 2, 2012): 13549–55. http://dx.doi.org/10.1074/jbc.r111.316406.

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19

Koh, Eun-Ik, and Jeffrey P. Henderson. "Microbial Copper-binding Siderophores at the Host-Pathogen Interface." Journal of Biological Chemistry 290, no. 31 (June 8, 2015): 18967–74. http://dx.doi.org/10.1074/jbc.r115.644328.

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20

Zackular, Joseph P., Walter J. Chazin, and Eric P. Skaar. "Nutritional Immunity: S100 Proteins at the Host-Pathogen Interface." Journal of Biological Chemistry 290, no. 31 (June 8, 2015): 18991–98. http://dx.doi.org/10.1074/jbc.r115.645085.

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21

Manning, Jessica E., and Tineke Cantaert. "Time to Micromanage the Pathogen-Host-Vector Interface: Considerations for Vaccine Development." Vaccines 7, no. 1 (January 21, 2019): 10. http://dx.doi.org/10.3390/vaccines7010010.

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The current increase in vector-borne disease worldwide necessitates novel approaches to vaccine development targeted to pathogens delivered by blood-feeding arthropod vectors into the host skin. A concept that is gaining traction in recent years is the contribution of the vector or vector-derived components, like salivary proteins, to host-pathogen interactions. Indeed, the triad of vector-host-pathogen interactions in the skin microenvironment can influence host innate and adaptive responses alike, providing an advantage to the pathogen to establish infection. A better understanding of this “bite site” microenvironment, along with how host and vector local microbiomes immunomodulate responses to pathogens, is required for future vaccines for vector-borne diseases. Microneedle administration of such vaccines may more closely mimic vector deposition of pathogen and saliva into the skin with the added benefit of near painless vaccine delivery. Focusing on the ‘micro’–from microenvironments to microbiomes to microneedles–may yield an improved generation of vector-borne disease vaccines in today’s increasingly complex world.

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22

Wu, Qian, Qingdian Mu, Zhidan Xia, Junxia Min, and Fudi Wang. "Manganese homeostasis at the host-pathogen interface and in the host immune system." Seminars in Cell & Developmental Biology 115 (July 2021): 45–53. http://dx.doi.org/10.1016/j.semcdb.2020.12.006.

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23

Huyvaert, Kathryn, Robin Russell, Kelly Patyk, Meggan Craft, Paul Cross, M. Garner, Michael Martin, Pauline Nol, and Daniel Walsh. "Challenges and Opportunities Developing Mathematical Models of Shared Pathogens of Domestic and Wild Animals." Veterinary Sciences 5, no. 4 (October 30, 2018): 92. http://dx.doi.org/10.3390/vetsci5040092.

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Diseases that affect both wild and domestic animals can be particularly difficult to prevent, predict, mitigate, and control. Such multi-host diseases can have devastating economic impacts on domestic animal producers and can present significant challenges to wildlife populations, particularly for populations of conservation concern. Few mathematical models exist that capture the complexities of these multi-host pathogens, yet the development of such models would allow us to estimate and compare the potential effectiveness of management actions for mitigating or suppressing disease in wildlife and/or livestock host populations. We conducted a workshop in March 2014 to identify the challenges associated with developing models of pathogen transmission across the wildlife-livestock interface. The development of mathematical models of pathogen transmission at this interface is hampered by the difficulties associated with describing the host-pathogen systems, including: (1) the identity of wildlife hosts, their distributions, and movement patterns; (2) the pathogen transmission pathways between wildlife and domestic animals; (3) the effects of the disease and concomitant mitigation efforts on wild and domestic animal populations; and (4) barriers to communication between sectors. To promote the development of mathematical models of transmission at this interface, we recommend further integration of modern quantitative techniques and improvement of communication among wildlife biologists, mathematical modelers, veterinary medicine professionals, producers, and other stakeholders concerned with the consequences of pathogen transmission at this important, yet poorly understood, interface.

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24

Zhang, C., O. Crasta, S. Cammer, R. Will, R. Kenyon, D. Sullivan, Q. Yu, et al. "An emerging cyberinfrastructure for biodefense pathogen and pathogen–host data." Nucleic Acids Research 36, Supplement_1 (November 4, 2007): D884—D891. http://dx.doi.org/10.1093/nar/gkm903.

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Abstract The NIAID-funded Biodefense Proteomics Resource Center (RC) provides storage, dissemination, visualization and analysis capabilities for the experimental data deposited by seven Proteomics Research Centers (PRCs). The data and its publication is to support researchers working to discover candidates for the next generation of vaccines, therapeutics and diagnostics against NIAID's Category A, B and C priority pathogens. The data includes transcriptional profiles, protein profiles, protein structural data and host–pathogen protein interactions, in the context of the pathogen life cycle in vivo and in vitro. The database has stored and supported host or pathogen data derived from Bacillus, Brucella, Cryptosporidium, Salmonella, SARS, Toxoplasma, Vibrio and Yersinia, human tissue libraries, and mouse macrophages. These publicly available data cover diverse data types such as mass spectrometry, yeast two-hybrid (Y2H), gene expression profiles, X-ray and NMR determined protein structures and protein expression clones. The growing database covers over 23 000 unique genes/proteins from different experiments and organisms. All of the genes/proteins are annotated and integrated across experiments using UniProt Knowledgebase (UniProtKB) accession numbers. The web-interface for the database enables searching, querying and downloading at the level of experiment, group and individual gene(s)/protein(s) via UniProtKB accession numbers or protein function keywords. The system is accessible at http://www.proteomicsresource.org/.

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25

DAY, B., and T. GRAHAM. "The Plant Host Pathogen Interface: Cell Wall and Membrane Dynamics of Pathogen-Induced Responses." Annals of the New York Academy of Sciences 1113, no. 1 (May 18, 2007): 123–34. http://dx.doi.org/10.1196/annals.1391.029.

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26

Zoued, Abdelrahim, Hailong Zhang, Ting Zhang, Rachel T. Giorgio, Carole J. Kuehl, Bolutife Fakoya, Brandon Sit, and Matthew K. Waldor. "Proteomic analysis of the host–pathogen interface in experimental cholera." Nature Chemical Biology 17, no. 11 (October 21, 2021): 1199–208. http://dx.doi.org/10.1038/s41589-021-00894-4.

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27

Zückert, Wolfram R. "A call to order at the spirochaetal host-pathogen interface." Molecular Microbiology 89, no. 2 (June 19, 2013): 207–11. http://dx.doi.org/10.1111/mmi.12286.

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28

Eledge, Michael R., and Laxmi Yeruva. "Host and pathogen interface: microRNAs are modulators of disease outcome." Microbes and Infection 20, no. 7-8 (August 2018): 410–15. http://dx.doi.org/10.1016/j.micinf.2017.08.002.

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29

Fu, Yue, Feng-Ming James Chang, and David P. Giedroc. "Copper Transport and Trafficking at the Host–Bacterial Pathogen Interface." Accounts of Chemical Research 47, no. 12 (October 13, 2014): 3605–13. http://dx.doi.org/10.1021/ar500300n.

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30

Iyer, Namrata, and Shipra Vaishnava. "Vitamin A at the interface of host–commensal–pathogen interactions." PLOS Pathogens 15, no. 6 (June 6, 2019): e1007750. http://dx.doi.org/10.1371/journal.ppat.1007750.

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31

Rumbaugh, Kendra P. "Convergence of hormones and autoinducers at the host/pathogen interface." Analytical and Bioanalytical Chemistry 387, no. 2 (August 16, 2006): 425–35. http://dx.doi.org/10.1007/s00216-006-0694-9.

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32

Casanova, James E. "Bacterial Autophagy: Offense and Defense at the Host–Pathogen Interface." Cellular and Molecular Gastroenterology and Hepatology 4, no. 2 (September 2017): 237–43. http://dx.doi.org/10.1016/j.jcmgh.2017.05.002.

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33

Miao, Yansong, Xiangfu Guo, Kexin Zhu, and Wenting Zhao. "Biomolecular condensates tunes immune signaling at the Host–Pathogen interface." Current Opinion in Plant Biology 74 (August 2023): 102374. http://dx.doi.org/10.1016/j.pbi.2023.102374.

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34

Joyce, Luke R., and Kelly S. Doran. "Gram-positive bacterial membrane lipids at the host–pathogen interface." PLOS Pathogens 19, no. 1 (January 5, 2023): e1011026. http://dx.doi.org/10.1371/journal.ppat.1011026.

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35

SAHA, B., A. M. D. J. TONKAL, S. CROFT, and S. ROY. "Mast cells at the host-pathogen interface: host-protection versus immune evasion in leishmaniasis." Clinical & Experimental Immunology 137, no. 1 (June 8, 2004): 19–23. http://dx.doi.org/10.1111/j.1365-2249.2004.02505.x.

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36

Daly, James L. "Endosomes, receptors, and viruses." Science 378, no. 6622 (November 25, 2022): 845. http://dx.doi.org/10.1126/science.adf4469.

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37

Wang, Yifan, Lamba Omar Sangaré, Tatiana C. Paredes-Santos, and Jeroen P. J. Saeij. "Toxoplasma Mechanisms for Delivery of Proteins and Uptake of Nutrients Across the Host-Pathogen Interface." Annual Review of Microbiology 74, no. 1 (September 8, 2020): 567–86. http://dx.doi.org/10.1146/annurev-micro-011720-122318.

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Many intracellular pathogens, including the protozoan parasite Toxoplasma gondii, live inside a vacuole that resides in the host cytosol. Vacuolar residence provides these pathogens with a defined niche for replication and protection from detection by host cytosolic pattern recognition receptors. However, the limiting membrane of the vacuole, which constitutes the host-pathogen interface, is also a barrier for pathogen effectors to reach the host cytosol and for the acquisition of host-derived nutrients. This review provides an update on the specialized secretion and trafficking systems used by Toxoplasma to overcome the barrier of the parasitophorous vacuole membrane and thereby allow the delivery of proteins into the host cell and the acquisition of host-derived nutrients.

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38

Ross-Davis, A. L., J. E. Stewart, J. W. Hanna, M. S. Kim, B. J. Knaus, R. Cronn, H. Rai, B. A. Richardson, G. I. McDonald, and N. B. Klopfenstein. "Transcriptome of an Armillaria root disease pathogen reveals candidate genes involved in host substrate utilization at the host-pathogen interface." Forest Pathology 43, no. 6 (June 15, 2013): 468–77. http://dx.doi.org/10.1111/efp.12056.

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39

Walsh, Brenna J. C., and David P. Giedroc. "H2S and reactive sulfur signaling at the host-bacterial pathogen interface." Journal of Biological Chemistry 295, no. 38 (July 22, 2020): 13150–68. http://dx.doi.org/10.1074/jbc.rev120.011304.

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Bacterial pathogens that cause invasive disease in the vertebrate host must adapt to host efforts to cripple their viability. Major host insults are reactive oxygen and reactive nitrogen species as well as cellular stress induced by antibiotics. Hydrogen sulfide (H2S) is emerging as an important player in cytoprotection against these stressors, which may well be attributed to downstream more oxidized sulfur species termed reactive sulfur species (RSS). In this review, we summarize recent work that suggests that H2S/RSS impacts bacterial survival in infected cells and animals. We discuss the mechanisms of biogenesis and clearance of RSS in the context of a bacterial H2S/RSS homeostasis model and the bacterial transcriptional regulatory proteins that act as “sensors” of cellular RSS that maintain H2S/RSS homeostasis. In addition, we cover fluorescence imaging– and MS–based approaches used to detect and quantify RSS in bacterial cells. Last, we discuss proteome persulfidation (S-sulfuration) as a potential mediator of H2S/RSS signaling in bacteria in the context of the writer-reader-eraser paradigm, and progress toward ascribing regulatory significance to this widespread post-translational modification.

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40

Weiner, Allon, and Jost Enninga. "The Pathogen–Host Interface in Three Dimensions: Correlative FIB/SEM Applications." Trends in Microbiology 27, no. 5 (May 2019): 426–39. http://dx.doi.org/10.1016/j.tim.2018.11.011.

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41

Manzano-Román, Raúl, Noelia Dasilva, Paula Díez, Verónica Díaz-Martín, Ricardo Pérez-Sánchez, Alberto Orfao, and Manuel Fuentes. "Protein arrays as tool for studies at the host–pathogen interface." Journal of Proteomics 94 (December 2013): 387–400. http://dx.doi.org/10.1016/j.jprot.2013.10.010.

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42

Emmersen, Jeppe, Stephen Rudd, Hans-Werner Mewes, and Igor V. Tetko. "Separation of sequences from host–pathogen interface using triplet nucleotide frequencies." Fungal Genetics and Biology 44, no. 4 (April 2007): 231–41. http://dx.doi.org/10.1016/j.fgb.2006.11.010.

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43

Park, Bonggoo, and George Y. Liu. "Targeting the host–pathogen interface for treatment of Staphylococcus aureus infection." Seminars in Immunopathology 34, no. 2 (November 17, 2011): 299–315. http://dx.doi.org/10.1007/s00281-011-0297-1.

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44

Nairz, Manfred, Andrea Schroll, Thomas Sonnweber, and Günter Weiss. "The struggle for iron - a metal at the host-pathogen interface." Cellular Microbiology 12, no. 12 (October 21, 2010): 1691–702. http://dx.doi.org/10.1111/j.1462-5822.2010.01529.x.

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45

Rana, Jyoti, R. Sreejith, Sahil Gulati, Isha Bharti, Surangna Jain, and Sanjay Gupta. "Deciphering the host-pathogen protein interface in chikungunya virus-mediated sickness." Archives of Virology 158, no. 6 (January 20, 2013): 1159–72. http://dx.doi.org/10.1007/s00705-013-1602-1.

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46

Becker, Kyle W., and Eric P. Skaar. "Metal limitation and toxicity at the interface between host and pathogen." FEMS Microbiology Reviews 38, no. 6 (November 2014): 1235–49. http://dx.doi.org/10.1111/1574-6976.12087.

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47

Capdevila, Daiana A., Jiefei Wang, and David P. Giedroc. "Bacterial Strategies to Maintain Zinc Metallostasis at the Host-Pathogen Interface." Journal of Biological Chemistry 291, no. 40 (July 26, 2016): 20858–68. http://dx.doi.org/10.1074/jbc.r116.742023.

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48

Smith, Kelly D. "Iron metabolism at the host pathogen interface: Lipocalin 2 and the pathogen-associated iroA gene cluster." International Journal of Biochemistry & Cell Biology 39, no. 10 (2007): 1776–80. http://dx.doi.org/10.1016/j.biocel.2007.07.003.

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49

Amos, Beatrice, Cristina Aurrecoechea, Matthieu Barba, Ana Barreto, Evelina Y. Basenko, Wojciech Bażant, Robert Belnap, et al. "VEuPathDB: the eukaryotic pathogen, vector and host bioinformatics resource center." Nucleic Acids Research 50, no. D1 (October 28, 2021): D898—D911. http://dx.doi.org/10.1093/nar/gkab929.

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Abstract The Eukaryotic Pathogen, Vector and Host Informatics Resource (VEuPathDB, https://veupathdb.org) represents the 2019 merger of VectorBase with the EuPathDB projects. As a Bioinformatics Resource Center funded by the National Institutes of Health, with additional support from the Welllcome Trust, VEuPathDB supports >500 organisms comprising invertebrate vectors, eukaryotic pathogens (protists and fungi) and relevant free-living or non-pathogenic species or hosts. Designed to empower researchers with access to Omics data and bioinformatic analyses, VEuPathDB projects integrate >1700 pre-analysed datasets (and associated metadata) with advanced search capabilities, visualizations, and analysis tools in a graphic interface. Diverse data types are analysed with standardized workflows including an in-house OrthoMCL algorithm for predicting orthology. Comparisons are easily made across datasets, data types and organisms in this unique data mining platform. A new site-wide search facilitates access for both experienced and novice users. Upgraded infrastructure and workflows support numerous updates to the web interface, tools, searches and strategies, and Galaxy workspace where users can privately analyse their own data. Forthcoming upgrades include cloud-ready application architecture, expanded support for the Galaxy workspace, tools for interrogating host-pathogen interactions, and improved interactions with affiliated databases (ClinEpiDB, MicrobiomeDB) and other scientific resources, and increased interoperability with the Bacterial & Viral BRC.

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50

Manners, JM. "The Host-Haustorium Interface in Powdery Mildews." Functional Plant Biology 16, no. 1 (1989): 45. http://dx.doi.org/10.1071/pp9890045.

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The powdery mildew fungi have proven to be a useful model system for studies of the host-parasite interface in biotrophic parasitism. Investigation of the interface has requrred the development of novel experimental approaches, for example the isolation of populations of haustoria in association with other interface components and the chemical and physical manipulation of living isolated epidermal strips infected wth powdery mildew fungi. These experimental approaches have provided information on the nature of metabolites transferred from host to pathogen at the interface and on the underlymg mechanisms. Studies of incompatible interactions with powdery mildew fungi have indicated that the establishment of a functional host-haustorial interface is critical for successful infection. In future, the application of recombinant DNA and monoclonal antibody technologies to the host-haustorium interface of powdery mildews should lead to a more detailed molecular analysis of the interface, and thus provide new insights into its structure and function.

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Journal articles on the topic 'Host-Pathogen interface'

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