Ribosomal protein S6 kinase beta-1 gene variants cause hypertrophic cardiomyopathy
J Med Genet.
Times Of India; read the news article here
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 Times Of India; read the news article here |
 Deccan Herald; read the news article here |
 In a collaborative effort with researchers from our lab at inStem and NCBS, a study published in PNAS showed that air pollutants cause irregular heartbeats in bees and mis-expression of cardiac ion channel genes. This is alarming as such an effect might have huge implications on human heart health also. Times Of India; read the news article here |
 Our work on the molecular genetics of cardiomyopathies led to a major discovery as we unraveled an ancient Myosin Binding Protein c3 (MYBPC3) gene deletion as a major risk factor for South Asians. To date, approximately 60 million people carry the heterozygous deletion. This variant, in its homozygous nature, causes severe childhood cardiomyopathies. Of note, this discovery was the subject of a documentary by Dr. Sanjay Gupta of CNN. Please click the youtube video shown below for more details.
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 We discovered the variants in RAF1 (a RAS-MAPK member) as a primary cause of childhood-onset DCM (~10%). This is the first gene causing isolated DCM to be strongly associated with pediatric-onset disease and the first report of DCM principally attributable to altered RAS-MAPK signaling. Implications of these study on public health include various companies across the world use these variants as diagnostic |
 In the current issue of the Journal of Molecular and Cellular Cardiology (July 2011), Dhandapany et al. further explore the ability of Raf1 to regulate hypertrophy of cardiomyocytes. The authors employ three common Raf1 mutations observed in Noonan/LEOPARD syndromes to dissect downstream signaling pathways ultimately impacting myocyte growth control. |
We are a multi-disciplinary team including Geneticists, Clinicians, Bioinformaticians, Engineers, Biochemists, Biophysicists, and Molecular Biologists addressing CVD through a multi-level approach.
Cardiovascular diseases (CVDs) are the leading cause of mortality globally. They are caused by various disorders of the heart and blood vessels. We are interested in understanding three major forms of CVDs including, cardiomyopathies, congenital heart disease and coronary heart disease (heart attacks).
We are a multi-disciplinary team including Geneticists, Clinicians, Bioinformaticians, Engineers, Biochemists, Biophysicists, and Molecular Biologists addressing CVDs through a multi-level approach.
The long-term goals of my group are to explore new genes, mechanisms and relevant drugs that have significant clinical and curative impact on CVDs.
Identifying genes for CVDs
Vinay J Rao
Shashank J
Thiagarajan S
Signaling mechanism of CVDs
Pratul K Jain
Prasanth Chimata
Harshil Chittora
Vinay J Rao
Radhika Agrawal
Shashank J
Lekha Kandasami
Saptashwa Chakrabarti
Saswata Bhattacharyya
Targets for therapies and drug analysis
Pratul K Jain
Prasanth Chimata
Radhika Agrawal
Lekha Kandasami
Saptashwa Chakrabarti
Combatting cardiovascular disease by integrating genetics, basic science and clinical medicine.
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Currently, we are collaborating with various institutes, universities, medical colleges and hospitals as shown below for the patient samples and other reagents. We are also actively looking for new collaborations
If you are interested, please contact us at dhan@instem.res.in or perundur@ohsu.edu
Institute for Stem Cell Science and Regenerative Medicine (InStem),
National Centre for Biological Sciences (NCBS),
GKVK - Post, Bellary Road, Bangalore 560065, India.
Email: dhan@instem.res.in
Department of Molecular and Medical Genetics
Knight Cardiovascular Institute (KCVI), Oregon Health & Sciences University
3181 SW Sam Jackson Park Road L103, Portland, Oregon, U.S.A. 97239-3098
Email: perundur@ohsu.edu