|
|
 |
Name:
Designation:
Areas of Specialization:
E-mail: |
Girish K Radhakrishnan
Scientist-E
Microbial pathogenesis, host-pathogen interaction, immune modulation, negative regulation of innate immunity
girish[at]niab[dot]org[dot]in |
| |
|
|
Education and training:
Dr. Girish K. Radhakrishnan obtained MSc in Microbiology (1999) from School of Biosciences, Mahatma Gandhi University, Kerala and PhD in Biotechnology (2006) from School of Biotechnology, Madurai Kamaraj University, Tamil Nadu. He did his postdoctoral research (2006-2010) at the University of Wisconsin-Madison, USA and worked as Research Assistant Professor at the same university (2010-2012). He joined NIAB on 03 December 2012.
Research experience and interests:
Dr. Radhakrishnan has extensive research experience in the field of microbiology, immunology and protein chemistry. During his tenure at the University of Wisconsin-Madison, Dr. Radhakrishnan worked on the intracellular bacterial pathogen, Brucella melitensis. He studied the mechanisms by which B. melitensis modulates the host immune responses for its chromic persistence in the host. His research work revealed the molecular mechanism of suppression of Toll-like Receptor-2/4 signalling by the Brucella virulence protein, TcpB. At NIAB, he is studying the virulence determinants and immune evasion/suppression strategies of Brucella using various genomics and proteomics approaches with the objectives of developing efficient preventive strategies and diagnostic tools for brucellosis. He is also studying the intrinsic cellular processes that regulate innate immune responses in eukaryotes in the context of host-pathogen interactions.
Selected awards, honours and fellowships:
- Post-doctoral Research Fellowship from University of Wisconsin-Madison, USA (2006-2010)
- CSIR-Junior Research Fellowship-NET in 1999
- Travel grant by USA-Israel Binational Agricultural Research & Development Fund to attend a workshop on ssDNA viruses at Eilat, Israel, 2005
- University Second Rank in MSc
Selected publications:
-
Subathra Murugan, Padmaja Jakka, Swapna Namani, Varadendra Mujumdar and Girish Radhakrishnan (2019). The neurosteroid, pregnenolone promotes degradation of key proteins in the innate immune signalling to suppress inflammation. Journal of Biological Chemistry 294 (12) 4596-4607.
-
Padmaja Jakka, Bindu Bhargavi, Swapna Namani, Subathra Murugan, Gary Splitter and Girish Radhakrishnan (2018). Cytoplasmic Linker Protein CLIP170 Negatively Regulates TLR4 Signaling by Targeting the TLR Adaptor Protein TIRAP. Journal of Immunology 200 (2) 704-714.
-
Padmaja Jakka, Swapna Namani, Subathra Murugan, Nivedita Rai and Girish Radhakrishnan (2017). The Brucella effector protein TcpB induces degradation of inflammatory caspases and thereby subverts non-canonical inflammasome activation in macrophages. Journal of Biological Chemistry 292 (50), 20613-20627.
-
S Azam, SB Rao, P Jakka, VN Rao, B Bhargavi, VK Gupta, G Radhakrishnan. 2016. Genetic characterization and comparative genome analysis of Brucella melitensis isolates from India. International Journal of Genomics 2016:3034756.
-
SB Rao, VK Gupta, M Kumar, NR Hegde, GA Splitter, P Reddanna, GK Radhakrishnan. 2014. Draft genome sequence of the field isolate Brucella melitensis strain Bm IND1 from India. Genome Announcements 2(3):e00497-14.
-
JA Simth, D Magnani, M Kahn, J Harms, M Durward, G Radhakrishnan, Y-P Liu, GA Splitter. 2013. Brucella induces an unfolded protein response via TcpB that supports intracellular replication in macrophages. PLoS Pathogen 9(12): e1003785.
-
GA Splitter, J Harms, E Patersen, D Magnani, M Durward, G Rajashekara, G Radhakrishnan. 2014. Studying host-pathogen interaction events in living mice visualized in real time using biophotonic imaging. Methods in Molecular Biology 1197:67-85.
-
G Radhakrishnan, GA Splitter. 2012. Modulation of host
microtubule dynamics by pathogenic bacteria. Biomolecular Concepts 3(6):571–80.
-
VK Gupta, G Radhakrishnan, J Harms, GA Splitter. 2012. Invasive Escherichia coli vaccines expressing Brucella melitensis outer membrane proteins 31 or 16 or periplasmic protein BP26 confer protection in mice challenged with B. melitensis. Vaccine 30:4017-22.
-
M Durward, G Radhakrishnan, J Harms, C Bareiss, D Magnani, GA Splitter. 2012. Active evasion of CTL-mediated killing and low quality responding CD8+ T Cells contribute to persistence of brucellosis. PLoS ONE 7(4):e34925.
Detailed Profile
|
|
|
|