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Name: Bhaswati Pandit

Email:

Position: Assistant Professor

Highest Educational Qualification: Ph.D

Past Appointments:

Awards & Honours: Best publication of the year 2007, Mount Sinai School of Medicine

Fellowships & Memberships of Professional Societies: American Heart Association

Orations & Special Lectures:

Dept. of Human Genetics, University of Michigan, Ann Arbor, USA, 2004

Dept. of Biotechnology, Heritage Institute of Technology, Calcutta, India, 2004.

Research Interests:

My major research interest is human genetics and genetic diseases in particular. I am particularly interested about cardiovascular, neurological and immune dysfunction. My focus is on disease gene identification, mutation detection, epigenetic control and regulation of gene expression under normal and disease condition in a genome wide manner. Besides, biological role of disease genes will also be studied to understand the underlying pathogenesis.

Current Projects:

Genetic and Epigenetic study of Systemic Lupus Erythematosus(SLE)

The major goal of this project is to understand the molecular basis of SLE among Indians with renal involvement as a major phenotype. SLE is a heterogeneous autoimmune complex disease characterized by immune dysfunction. The hall mark of SLE is generation of auto antibodies. Till date no definite gene responsible for SLE has been identified, but several association studies and expression analysis in a genome wide manner have revealed role of interferon, cytokines triggering many signaling pathways in the immune system. I am interested in identifying and mapping regulators of pathways involved in SLE along with role of microRNA, copy number variation etc. in development of SLE.

Molecular mechanism of hypertrophic cardiomyopathy development

The overall aim of this project is to investigate the molecular interaction between RAF1 and DSCR1.4 an inhibitor of Calcineurin to provide insights into the molecular mechanism for developing cardiac hypertrophy in Noonan syndrome patients. Noonan syndrome (NS) is characterized by several developmental defects including short stature, webbed neck, skeletal abnormalities and cardiac features like pulmonic stenosis and hypertrophic cardiomyopathy (HCM). The causal genes for NS are the members of RAS-MAPK family. Among them RAF1 mutation was predominant in NS patients having HCM phenotype. Mutation in RAF1 gene is present in three distinct regions of the gene. Two mutation clusters around the phosphorylated serine residues 259 and 621 are associated with HCM whereas the third cluster in the activation domain is not. This urges us to investigate how hypertrophy is correlated with RAF1 gene function. Our aim is to identify the pathway how RAF1 or the RAS-MAPK collaborates with other signaling network associated with cardiac hypertrophy development.

Past Major Projects:

List of Publications

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