Siddhartha Kundu
All India Institute of Medical Sciences
20 Papers
43 Citations
Siddhartha Kundu is an academic researcher from All India Institute of Medical Sciences. The author has contributed to research in topics: Biology & Chemistry. The author has an hindex of 5, co-authored 15 publications. Previous affiliations of Siddhartha Kundu include Jawaharlal Nehru University.
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Papers
Insights into the molecular mechanism of apoptosis induced by TNF-α in mouse epidermal JB6-derived RT-101 cells
TL;DR: The results show that ERKs decreased transiently or remain unchanged, JNK decreased robustly, whereas c-Jun increased transiently, thereby indicating that members of MAPK family are differentially regulated in response to TNF-alpha induced apoptosis, whereas NF-kappaB protein expression decreased transientably and activity decreased at 24 h post-treatment.
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Unity in diversity, a systems approach to regulating plant cell physiology by 2-oxoglutarate-dependent dioxygenases
TL;DR: It is surmised that the alpha-ketoglutarate dependent superfamily of non-haem iron (II) dioxygenases could influence cell physiology as a cohesive unit, and that the broad spectra of substrates transformed is an absolute necessity to this portrayal.
In silico Identification and Taxonomic Distribution of Plant Class C GH9 Endoglucanases.
Siddhartha Kundu,Rita Sharma +1 more
TL;DR: This work utilized non redundant plant GH9 enzymes with characterized molecular data, as the training set to construct Hidden Markov Models (HMMs) and train an Artificial Neural Network (ANN).
Stochastic modelling suggests that an elevated superoxide anion - hydrogen peroxide ratio can drive extravascular phagocyte transmigration by lamellipodium formation.
TL;DR: It is surmised, that superoxide anion induced directional motility, in a responding cell, results from a quasi pathway between the stimulus, surrounding interstitium, and its biochemical repertoire, a prelude to chemotactic migration.
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Mathematical modeling and stochastic simulations suggest that low-affinity peptides can bisect MHC1-mediated export of high-affinity peptides into "early"- and "late"-phases.
TL;DR: In this paper, a low-affinity peptide-driven (LAPD)-model of MHC1-mediated high affinity peptide export is formulated, implemented, analyzed and simulated.
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