Pluripotent stem cells establish and maintain a state of equilibrium between self-renewal and differentiation. The pluripotent embryonic stem cells exit this equilibrium to differentiate to any cell type of the body. The molecular mechanisms underlying fate choice of pluripotent cells to enter and exit different states of pluripotency and early lineages commitments are being studied. We are attempting to understand molecular mechanisms by which novel factors; particularly transcription factors regulate the cell fate decisions in pluripotent stem cells and in early developmental stages of mouse embryogenesis. The lab uses genetic approaches(gene knock out/ transgenics)in mice, somatic cell reprogramming (iPSC) and biochemical approaches in Embryonic stem cells to understand these mechanisms.

Selected Publications

Fidalgo M*, Shekar PC*, Ang YS, Fujiwara Y, Orkin SH, Wang J. Zfp281 functions as a transcriptional repressor for pluripotency of mouse embryonic stem cells.Stem Cells. 2011 Nov; 29 (11): 1705-16. doi: 10.1002/stem.736.

P. Chandra Shekar, Adnan Naim, D ParthaSarathi, Satishkumar.Argonaute 2 deficient embryonic stem cells are retarded in self-renewal and differentiation. 2011 J. Biosci.36 649-657 DOI10.1007/s12038-011-9094-1

P. Chandra Shekar*, SandeepGoel*, S. DeepaSelvi Rani, D. ParthaSarathi, Jomini Liza Alex, Shashi Singh, and Satish Kumar; K-Casein-deficient mice fail to lactate. Proc. Natl. Acad. Sci. USA.2006,103,8000-8005 

*Equal contribution