Dr. Khader Valli Rupanagudi
Scientific Officer Grade I

Biosketch
Projects
People
Publications
Contact
Biosketch
Biosketch
Dr. Khader Valli Rupanagudi completed his Ph.D. with Summa cum laude in Autoimmunity in
2013 at the Ludwig Maximilian University of Munich (LMU Munich), Germany. Following his
doctoral studies, he joined the Centre for Neuroscience at the Indian Institute of Science
(IISc) in Bangalore as a Senior Research Scientist, where he worked from June 2013 to
December 2017.
In December 2017, Khader transitioned to the role of Scientific Officer Grade I at the Centre
for Brain Research, IISc. There, he currently leads the Next Generation Sequencing (NGS) Lab
and contributes to the flagship projects of the CBR.
Projects
Role of translation regulation in neurodevelopment:
At CBR, Dr. Khader and his team are involved in Genome Wide Association Studies (GWAS)
and Whole Genome Sequencing (WGS) of human volunteers from ongoing projects at CBR.
In the GenomeIndia project, which is a pan-India project involving 84 ethnic populations,
they performed GWAS and WGS, which led to the cataloguing of Indian-specific variants.
This information is critical for understanding genetic predispositions to diseases and
tailoring precision medicine for the Indian population.
In SANSCOG and TLSA longitudinal projects, which are meant to understand the risk and
protective factors of dementia in the elderly population in India, the team performs GWAS
and WGS, leading to the understanding of risk variants associated with dementia.
In the Young and Late Onset Parkinson’s Disease (YLOPD) project, which is a longitudinal
study on Parkinson’s disease (PD). Dr. Khader and his team perform GWAS and WGS
analyses, leading to the identification of new risk variants associated with PD.
The team was also a part of the INSACOG (Indian SARS-CoV-2 Genomics Consortium) project
and contributed to coronavirus sequencing during the pandemic. Additionally, they conduct
RNA sequencing as per the requirement from the faculty of CBR.
People
Mohammad Hanif Kaba Mujawar,
Senior Technical Assistant.
Vinayak Hosawad
Technical Assistant
Manasvi Vukku
Data Analyst
Alumni
Amrita Mondal
Data Analyst
Hiba Ali
Research Intern
Annapurna Vasagiri
Research Intern
Goutham Kumar
Project Assistant
Disha Awasthy
Project Associate
Ankita Khan
Project Assistant
Publications
Ahmad F, Das D, Kommaddi RP, Diwakar L, Gowaikar R, Rupanagudi KV, Bennett DA, Ravindranath V. “Isoform-specific hyperactivation of calpain-2 occurs presymmptomatically at the sysnapse in Alzheimer’s disease mice and correlates with memory deficits in human
subjects”. Sci Rep. Sep 2018
Ahmad F, Singh K, Das D, Gowaikar R, Shaw E, Ramachandran A, Rupanagudi KV, Kommaddi RP, Bennett DA, Ravindranath V. “Reactive oxygen species-mediated loss of synaptic Akt1 signaling leads to deficient activity-dependent protein translation early in alzheimer’s disease”. Antioxid Redox Signal. April 2017
Devarapu SK, Kumar Vr S, Rupanagudi KV, Kulkarni OP, Eulberg D, Klussmann S, Anders HJ. “Dual blockade of the pro-inflammatory chemokine CCL2 and the homeostatic chemokine CXCL12 is as effective as high dose cyclophosphamide in murine proliferative lupus nephritis”.
Clin Immunol. August 2016.
Wolfgang Neuhofer, Christoph Küper, Julia Lichtnekert, Konstantin Holzapfel, Khader V. Rupanagudi, Maria-Luisa Fraek, Helmut Bartels and Franz-Xaver Beck. “Focal adhesion kinase
regulates the activity of the osmosensitive transcription factor TonEBP/NFAT5 under hypertonic conditions”. Frontiers in Physiology. April 2014.
Khader Valli Rupanagudi, Onkar P. Kulkarni, Julia Lichtnekert, Murthy Narayana Darisipudi, Shrikant R Mulay, Brigitte Schott, Sabine Gruner, Wolfgang Haap, Guido Hartmann, and Hans-
Joachim Anders. “Cathepsin S inhibition suppresses systemic lupus erythematosus and lupus
nephritis because cathepsin S is essential for MHC class II-mediated CD4 T cell and B cell
priming”. Annals of Rheumatic Diseases. Dec 2013.
Shrikant R Mulay, Onkar P. Kulkarni, Khader Valli Rupanagudi, Adriana Migliorini, Murthy Narayana Darisipudi, Akosua Vilaysane, Daniel Muruve, Yan Shi, Fay Munro, Helen Liapis and
Hans-Joachim Anders. “Calcium oxalate crystals induce renal inflammation by NLRP3-mediated
IL-1β secretion”. The journal of clinical investigation. Dec 2012.
Ramanjaneyulu Allam, Christina Rebecca Scherbaum, Murthy Narayana Darisipudi, Shrikant
R. Mulay, Holger Hägele, Julia Lichtnekert, Jan Henrik Hagemann, Khader Valli Rupanagudi, Mi
Ryu, Claudia Schwarzenberger, Bernd Hohenstein, Christian Hugo, Bernd Uhl, Christoph A.
Reichel, Fritz Krombach, Marc Monestier, Helen Liapis,Kristin Moreth, Liliana Schaefer and
Hans-Joachim Anders. “Histones from Dying Renal Cells Aggravate Kidney Injury via TLR2 and TLR4”. Journal of the american society of nephrology. June 2012.
Neha Sehgal, Alok Gupta, Rupanagudi Khader Valli, Shanker Datt Joshi, Jessica T Mills, Edith
Hamel, Pankaj Khanna, Subhash Chand Jain, Suman S Thakur, Vijayalakshmi Ravindranath.
“Withania somnifera reverses Alzheimer's disease pathology by enhancing low-density lipoprotein receptor-related protein”. PNAS Jan 2012.
Lalitha Durgadoss, Prakash Nidadavolu, Rupanagudi Khader Valli, Uzma Saeed, Mamata
Mishra, Pankaj Seth and Vijayalakshmi Ravindranath. “Redox modification of Akt mediated by the dopaminergic neurotoxin, MPTP, in mouse midbrain, leads to downregulation of pAkt”. The
FASEB Journal Dec 2011.
Julia Lichtnekert, Onkar P. Kulkarni, Shrikant R. Mulay, Khader Valli Rupanagudi, Mi Ryu,
Ramanjaneyulu Allam, Volker Vielhauer, Dan Muruve,, Maja T. Lindenmeyer, Clemens D. Cohen
and Hans-Joachim Anders. “Anti-GBM glomerulonephritis involves IL-1 but is independent of
NLRP3/ASC inflammasome-mediated activation of caspase-1”. PLoS ONE Oct 2011.
Julia Lichtnekert*, Khader Valli Rupanagudi*, Onkar P. Kulkarni, Murthy Narayana
Darisipudi, Ramanjaneyulu Allam and Hans-Joachim Anders. “Activated protein C attenuates
systemic lupus erythematosus and lupus nephritis in MRL-Fas(lpr) mice”. Journal of
Immunology Sep 2011. *Equal contribution.
Neha Sehgal, Varsha Agarwal, Rupanagudi Khader Valli, Shanker Dutt Joshi, Leposava Antonovic, Henry W. Strobel and Vijayalakshmi Ravindranath. “Cytochrome P4504f, a potential
therapeutic target for limiting neuroinflammation”. Biochemical Pharmacology July 2011.
Murthy Narayana Darisipudi, Ramanjaneyulu Allam, Khader Valli Rupanagudi, Hans-
Joachim Anders. “Polyene Macrolide Antifungal drugs Trigger Interleukin-1β Secretion by Activating the NLRP3 Inflammasome”. PLoS ONE May 2011.
Ramanjaneyulu Allam, Murthy Narayana Darisipudi, Khader Valli Rupanagudi, Julia
Lichtnekert, Jurg Tschopp, and Hans-Joachim Anders. “Cutting Edge: Cyclic Polypeptide and
Aminoglycoside Antibiotics Trigger IL-1β Secretion by Activating the NLRP3 Inflammasome”.
The Journal of Immunology Jan 2011.
Uzma Saeed, Ajit Ray, Rupanagudi Khader Valli, Madan Ram Kumar and Vijayalakshmi
Ravindranath. “DJ-1 loss by glutaredoxin but not glutathione depletion triggers Daxx
translocation and cell death”. Antioxidants & Redox Signaling July 2010.
Smitha Karunakaran, Uzma Saeed, Mamata Mishra, R. Khader Valli, Shanker Datt Joshi, Durga Praveen Meka, Pankaj Seth, and Vijayalakshmi Ravindranath. “Selective Activation of
p38 Mitogen-Activated Protein Kinase in Dopaminergic Neurons of Substantia Nigra Leads to
Nuclear Translocation of p53 in 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine -Treated Mice”.
The Journal of Neuroscience Nov 2008.
Uzma Saeed, Lalitha Durgadoss, R. Khader Valli, Dinesh C. Joshi, Preeti G. Joshi,
Vijayalakshmi Ravindranath. “Knockdown of Cytosolic Glutaredoxin 1 Leads to Loss of Mitochondrial Membrane Potential: Implication in Neurodegenerative Diseases”. PLoS ONE June 2008.
Varsha Agarwal, Reddy P. Kommaddi, Khader Valli, Daniel Ryder, Thomas M. Hyde, Joel E.
Kleinman, Henry W. Strobel, Vijayalakshmi Ravindranath. “Drug Metabolism in Human Brain:
High Levels of Cytochrome P4503A43 in Brain and Metabolism of Anti-Anxiety Drug Alprazolam
to Its Active Metabolite”. PLoS ONE June 2008.
Contact
-
Centre for Brain Research
Indian Institute of Science Campus
CV Raman Avenue
Bangalore 560012, India. - 080-2293 3588