Marin Vulic
Affiliations: | Biological Sciences | Northeastern University, Boston, MA, United States |
Area:
Animal Physiology Biology, Microbiology BiologyGoogle:
"Marin Vulic"
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Publications
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| Khanna S, Pardi DS, Kelly CR, et al. (2016) A Novel Microbiome Therapeutic Increases Gut Microbial Diversity and Prevents Recurrent Clostridium difficile Infection. The Journal of Infectious Diseases |
| Schumacher MA, Balani P, Min J, et al. (2015) HipBA-promoter structures reveal the basis of heritable multidrug tolerance. Nature. 524: 59-64 |
| Lombardo M, Vulic M, Ohsumi T, et al. (2015) Vancomycin-Resistant Enterococcal iters Diminish Among Patients With Recurrent Clostridium difficile Infection After Administration of SER-109, A Novel Microbiome Agent Open Forum Infectious Diseases. 2 |
| Theodore A, Lewis K, Vulic M. (2013) Tolerance of Escherichia coli to fluoroquinolone antibiotics depends on specific components of the SOS response pathway. Genetics. 195: 1265-76 |
| Wu Y, Vulić M, Keren I, et al. (2012) Role of oxidative stress in persister tolerance. Antimicrobial Agents and Chemotherapy. 56: 4922-6 |
| Dörr T, Vulić M, Lewis K. (2010) Ciprofloxacin causes persister formation by inducing the TisB toxin in Escherichia coli. Plos Biology. 8: e1000317 |
| Dörr T, Lewis K, Vulić M. (2009) SOS response induces persistence to fluoroquinolones in Escherichia coli. Plos Genetics. 5: e1000760 |
| Hansen S, Lewis K, Vulić M. (2008) Role of global regulators and nucleotide metabolism in antibiotic tolerance in Escherichia coli. Antimicrobial Agents and Chemotherapy. 52: 2718-26 |
| Babic A, Lindner AB, Vulic M, et al. (2008) Direct visualization of horizontal gene transfer. Science (New York, N.Y.). 319: 1533-6 |
| Spoering AL, Vulic M, Lewis K. (2006) GlpD and PlsB participate in persister cell formation in Escherichia coli. Journal of Bacteriology. 188: 5136-44 |