Institute Affiliations

  • Member, Maternal & Child Health Research Institute (MCHRI)

Professional Education

  • Doctor of Philosophy, Unlisted School (2018)
  • Master of Science, Unlisted School (2014)
  • Bachelor of Science, Unlisted School (2013)

Stanford Advisors


All Publications

  • HOTAIRM1 regulates neuronal differentiation by modulating NEUROGENIN 2 and the downstream neurogenic cascade. Cell death & disease Rea, J., Menci, V., Tollis, P., Santini, T., Armaos, A., Garone, M. G., Iberite, F., Cipriano, A., Tartaglia, G. G., Rosa, A., Ballarino, M., Laneve, P., Caffarelli, E. 2020; 11 (7): 527


    Neuronal differentiation is a timely and spatially regulated process, relying on precisely orchestrated gene expression control. The sequential activation/repression of genes driving cell fate specification is achieved by complex regulatory networks, where transcription factors and noncoding RNAs work in a coordinated manner. Herein, we identify the long noncoding RNA HOTAIRM1 (HOXA Transcript Antisense RNA, Myeloid-Specific 1) as a new player in neuronal differentiation. We demonstrate that the neuronal-enriched HOTAIRM1 isoform epigenetically controls the expression of the proneural transcription factor NEUROGENIN 2 that is key to neuronal fate commitment and critical for brain development. We also show that HOTAIRM1 activity impacts on NEUROGENIN 2 downstream regulatory cascade, thus contributing to the achievement of proper neuronal differentiation timing. Finally, we identify the RNA-binding proteins HNRNPK and FUS as regulators of HOTAIRM1 biogenesis and metabolism. Our findings uncover a new regulatory layer underlying NEUROGENIN 2 transitory expression in neuronal differentiation and reveal a previously unidentified function for the neuronal-induced long noncoding RNA HOTAIRM1.

    View details for DOI 10.1038/s41419-020-02738-w

    View details for PubMedID 32661334

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