CV Anja Lührmann
Anja Lührmann studied biology at the University of Leipzig, where she wrote her diploma thesis in the immunobiology section of Prof. Sunna Hauschildt's laboratory. In 2002 she received her PhD from the Julius-Maximilians-University of Würzburg. In her dissertation at the Institute of Microbiology, in the laboratory of Dr. Albert Haas, she studied the maturation of phagosomes containing the intracellular pathogens Rhodococcus equi and Afipia felis. After a short postdoctoral period in the laboratory of Prof. Albert Haas in the Department of Cell Biology at the Rheinische Friedrich-Wilhelms-Universität Bonn, she continued her postdoctoral training in the laboratory of Prof. Craig R. Roy in the field of microbial pathogenicity at Yale University in New Haven, USA. During this time, she investigated the molecular pathogenesis of the obligate intracellular pathogen Coxiella burnetii. This work was supported by a Brown-Coxe fellowship and a DFG research grant.
At the end of 2009, Anja Lührmann returned to Germany and has since been leading an independent research group at the Institute of Microbiology of the Alexander-Friedrich-University Erlangen-Nuremberg, which focuses on molecular and cellular events that enable microbial pathogens to evade host cell defense mechanisms. The particular focus here is on how the obligate intracellular pathogen Coxiella burnetii modulates host cell apoptosis pathways, signal transduction, and vesicular trafficking. This work improves the knowledge of the bacterial pathogenicity of the Q fever pathogen Coxiella burnetii and enables the identification of potential targets for novel therapeutics.
In 2011, Anja Lührmann was awarded the Förderpreis of the German Society for Hygiene and Microbiology. In 2015, she habilitated in Molecular Microbiology and Immunology at the Medical Faculty of the Alexander-Friedrich-University Erlangen-Nuremberg.
- Hayek I, Fischer F, Schulze-Lührmann J, Dettmer K, Sobotta K, Schatz V, Kohl L, Boden K, Lang R, Oefner PJ, Wirtz S, Jantsch J, Lührmann A (2019) Limitation of TCA-cycle intermediates represents an oxygen-independent nutritional antibacterial effector mechanism of macrophages. Cell Reports 26:1-9.
- Schäfer W, Eckart RA, Schmid B, Cagköylü H, Hof K, Muller YA, Amin B, Lührmann A (2017) Nuclear trafficking of the anti-apoptotic Coxiella burnetii effector protein AnkG requires binding to p32 and Importin-a1. Cell Microbiol 19:e12634.
- Schulze-Luehrmann J, Eckart RA, Ölke M, Saftig P, Liebler-Tenorio E, Lührmann A (2016) LAMP proteins account for the maturation delay during the establishment of the Coxiella burnetii-containing vacuole. Cell Microbiol 18:181-194.
- Eckart RA, Schulze-Luehrmann J, Bisle S, Wittmann I, Jantsch J, Schmid B, Berens C, Lührmann A (2014) The anti-apoptotic activity of the Coxiella burnetii effector protein AnkG is controlled by p32-dependent trafficking. Infect Immun 82:2763-2771.
- Klingenbeck L, Eckart RA, Berens C, Lührmann A (2013) The Coxiella burnetii type IV secretion system substrate CaeB inhibits intrinsic apoptosis at the mitochondrial level. Cell Microbiol 15:675-687.
- Carey KL, Newton HJ, Lührmann A, Roy CR (2011) The Coxiella burnetii Dot/Icm system delivers a unique repertoire of type IV effectors into host cells and is required for intracellular replication. PLoS Pathog 7: e1002056.
- Lührmann A, Nogueira C, Carey KL, Roy CR (2010) Inhibition of pathogen-induced apoptosis by a Coxiella burnetii type IV effector protein. Proc Natl Acad Sci U S A 107:18997-19001.
- Pan X, Lührmann A, Satoh A, Laskowski-Arce MA, Roy CR (2008) Ankyrin repeat proteins comprise a diverse family of bacteria type IV effectors. Science 320:1651-1654.
- Lührmann A, Roy CR (2007) Coxiella burnetii inhibits activation of host cell apoptosis through a mechanism that involves preventing cytochrome C release from mitochondria. Infect Immun 75:5282-5289.
- Lührmann A, Streker K, Schüttfort A, Daniels JJ, Haas A (2001) Afipia felis induces uptake by macrophages directly into a nonendocytic compartment. Proc Natl Acad Sci U S A 98:7271-7276.