B
Bhaswati Pandit
Researcher at Saha Institute of Nuclear Physics
Publications - 24
Citations - 1863
Bhaswati Pandit is an academic researcher from Saha Institute of Nuclear Physics. The author has contributed to research in topics: Chinese hamster & Noonan syndrome. The author has an hindex of 11, co-authored 23 publications receiving 1736 citations. Previous affiliations of Bhaswati Pandit include Medical University of South Carolina & Icahn School of Medicine at Mount Sinai.
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Journal ArticleDOI
Gain-of-function RAF1 mutations cause Noonan and LEOPARD syndromes with hypertrophic cardiomyopathy
Bhaswati Pandit,Anna Sarkozy,Len A. Pennacchio,Claudio Carta,Kimihiko Oishi,Simone Martinelli,Edgar A. Pogna,Wendy Schackwitz,Anna Ustaszewska,Andrew P. Landstrom,J. Martijn Bos,Steve R. Ommen,Giorgia Esposito,Francesca Romana Lepri,Christian Faul,Peter Mundel,Juan Pedro López Siguero,Romano Tenconi,Angelo Selicorni,Cesare Rossi,Laura Mazzanti,Isabella Torrente,Bruno Marino,Maria Cristina Digilio,Giuseppe Zampino,Michael J. Ackerman,Bruno Dallapiccola,Marco Tartaglia,Marco Tartaglia,Bruce D. Gelb +29 more
TL;DR: Ectopically expressed RAF1 mutants from the two HCM hotspots had increased kinase activity and enhanced ERK activation, whereas non–HCM-associated mutants were kinase impaired, which implicate increased RAS signaling in pathological cardiomyocyte hypertrophy.
Journal ArticleDOI
Gain-of-function SOS1 mutations cause a distinctive form of Noonan syndrome
Marco Tartaglia,Len A. Pennacchio,Len A. Pennacchio,Chen Zhao,Kamlesh K Yadav,Valentina Fodale,Anna Sarkozy,Anna Sarkozy,Bhaswati Pandit,Kimihiko Oishi,Simone Martinelli,Wendy Schackwitz,Wendy Schackwitz,Anna Ustaszewska,Joel Martin,Joel Martin,James Bristow,James Bristow,Claudio Carta,Francesca Romana Lepri,Francesca Romana Lepri,Cinzia Neri,Cinzia Neri,Isabella Vasta,Kate Gibson,Cynthia J. Curry,Juan Pedro López Siguero,Maria Cristina Digilio,Giuseppe Zampino,Bruno Dallapiccola,Bruno Dallapiccola,Dafna Bar-Sagi,Bruce D. Gelb +32 more
TL;DR: In this paper, the authors reported that 22 of 129 NoNoonan syndrome (NS) patients without PTPN11 or KRAS mutation (17 percent) have missense mutations in SOS1, which encodesa RAS-specific guanine nucleotide exchange factor (GEF).
Journal Article
Gain-of-function SOS1 mutations cause a distinctive form of noonan syndrome
Marco Tartaglia,Len A. Pennacchio,Len A. Pennacchio,Chen Zhao,Kamlesh K Yadav,Valentina Fodale,Anna Sarkozy,Anna Sarkozy,Bhaswati Pandit,Kimihiko Oishi,Simone Martinelli,Wendy Schackwitz,Wendy Schackwitz,Anna Ustaszewska,Joel Martin,Joel Martin,James Bristow,James Bristow,Claudio Carta,Francesca Romana Lepri,Francesca Romana Lepri,Cinzia Neri,Cinzia Neri,Isabella Vasta,Kate Gibson,Cynthia J. Curry,Juan Pedro López Siguero,Maria Cristina Digilio,Giuseppe Zampino,Bruno Dallapiccola,Bruno Dallapiccola,Dafna Bar-Sagi,Bruce D. Gelb +32 more
TL;DR: It is reported that 22 of 129 individuals with Noonan syndrome without PTPN11 or KRAS mutation have missense mutations in SOS1, which encodes a RAS-specific guanine nucleotide exchange factor, and this finding defines a new mechanism by which upregulation of the RAS pathway can profoundly change human development.
Journal ArticleDOI
Deregulated tyrosine-phenylalanine metabolism in pulmonary tuberculosis patients.
Mrinal Kumar Das,Subasa Chandra Bishwal,Aleena Das,Deepti Dabral,Vinod Kumar Badireddy,Bhaswati Pandit,George M. Varghese,Ranjan Kumar Nanda +7 more
TL;DR: A treatment-dependent trend in the urine metabolome of follow-up samples is observed, and subjects declared as clinically cured showed similar metabolic profile as those of asymptomatic healthy subjects, and the deregulated tyrosine-phenylalanine axis reveals a potential target for diagnostics and intervention in TB.
Journal ArticleDOI
The rat STSL locus: characterization, chromosomal assignment, and genetic variations in sitosterolemic hypertensive rats
Hongwei Yu,Bhaswati Pandit,Eric L. Klett,Mi Hye Lee,Kangmo Lu,Khalil Helou,Ikuo Ikeda,Nami Egashira,Masao Sato,Richard L. Klein,Ashok K. Batta,Gerald Salen,Shailendra B. Patel +12 more
TL;DR: A non-synonymous mutation in Abcg5, Gly583Cys, results in sitosterolemia in rat strains that are also hypertensive (WKY, SHR and SHRSP), which may allow us to study the pathophysiological mechanisms involved in the human disease of sitosterolesmia.