Subrata Banerjee
Saha Institute of Nuclear Physics
27 Papers
243 Citations
Subrata Banerjee is an academic researcher from Saha Institute of Nuclear Physics. The author has contributed to research in topics: Notch signaling pathway & Human leukocyte antigen. The author has an hindex of 13, co-authored 27 publications.
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Papers
Epstein-Barr virus latent membrane protein-2A alters mitochondrial dynamics promoting cellular migration mediated by Notch signaling pathway.
TL;DR: The data indicate that viral LMP2A causes an elevated mitochondrial fission in gastric and breast cancer cells, which is manifested by elevated fission protein dynamin-related protein 1 (Drp1) and LMP1-mediated Notch pathway is responsible for this enhanced fission.
p27 and Leukemia: Cell Cycle and Beyond
Anita Roy,Subrata Banerjee +1 more
TL;DR: The functions of p27 are summarized while highlighting its emerging roles in leukemia and its role in cell cycle progression is highlighted.
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Epstein–Barr virus-encoded small non-coding RNAs induce cancer cell chemoresistance and migration
TL;DR: A novel role of EBERs is revealed in the coordination of IL-6-STAT3 signaling pathway to chemoresistance and cellular migration in gastric cancer cells in vitro.
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Analysis of human lymphocyte antigen class I expression in gastric cancer by reverse transcriptase-polymerase chain reaction.
TL;DR: Selective locus-specific losses of HLA class I along with impaired expression of accessory molecules may explain the complex phenomena by which gastric tumors escape both cytotoxic T-lymphocyte- as well as natural killer cell-mediated immune defense.
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Down-regulation of locus-specific human lymphocyte antigen class I expression in Epstein-Barr virus-associated gastric cancer: implication for viral-induced immune evasion.
TL;DR: To understand whether the association between Epstein–Barr Virus (EBV) and gastric cancer (GC) has any role in loss of surface expression of human lymphocyte antigen (HLA) class I, the authors analyzed locus‐specific transcriptional expression of HLA‐A,HLA‐B, HLAC, and Hla‐E in EBV‐associated andEBV‐negative GC tissues.
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