Dr. Sandip Chorghade

Postdoctoral Fellow

Ph.D Indian Institue of Science
M.S. Microbiology - University of Pune

Worked in the Lab: February 2013 - September 2016

Current position: Post-doc Fellow at Duke-NUS Medical School

Email: sandipgc@illinois.edu


Chorghade S*, Seimetz J*, Emmons, RS, Yang J, Bresson SM, De Lisio M, Parise, G, Conrad NK and Kalsotra A (2017) Poly(A) tail length regulates PABPC1 expression to tune translation in the heart. eLIFE doi:10.7554/eLife.24139.
| * denotes equal authors

Aguero T, Jin Z, Chorghade S, Kalsotra A, King ML, Yang J (2017) Maternal dead-end 1 promotes translation of nanos1 through binding the eIF3 complex. Development DOI: 10.1242/dev.152611.

Bhate A*, Parker DJ*, Bebee TW, Ahn J, Arif W, Rashan EH, Chorghade S, Chau A, Lee JH, Anakk S, Carstens RP, Xiao X and Kalsotra A (2015) ESRP2 controls an adult splicing program in hepatocytes to support postnatal liver maturation.
Nature Commun. 6:8768 | DOI: 10.1038/ncomms9768.
| * denotes equal authors


Hi I am Sandip. I have done my Masters in Microbiology from University of Pune, India. After receiving Junior Research Fellowship from the Council for Scientific and Industrial Research (CSIR), I joined Prof C. Durga Rao’s laboratory in Microbiology and Cell Biology Department at the Indian Institute of Science, Bangalore, India for graduate studies. During my Ph.D., I have studied a novel role of AU-rich element binding proteins in pre-mRNA splicing. I am fun loving person. During free time, I like to read books, go for hiking and camping. I also like to paint and watch movies. I love nature photography.


(Click image to enlarge)

Alternative splicing in Liver

Alternative splicing is a key to the vast proteomic diversity found in the metazoan species. It performs an important role in post-transcriptional regulation of gene expression during development as well as in pathogenic conditions. Alternative splicing is highly regulated and its mis-regulation contributes to many diseases. The liver is a vital organ and a highly specialized tissue to perform several metabolic functions. Its ability to regenerate adds an extra layer of complexity. My current project is focused on identifying the RNA-binding proteins and their role in splicing regulation during liver regeneration.

Poly (A) binding proteins and their role in cardiac development and cardiac hypertrophy

Cardiac hypertrophy is the adaptive cellular response to an increase in biomechanical stress, which can be result of physiological (as occurs during postnatal development and in response to exercise) or pathological stress. Physiological cardiac hypertrophy eventually normalizes the increase in wall tension, thereby abolishing the initial stimulus while pathological cardiac hypertrophy eventually leads to heart failure. Cardiac hypertrophy is characterized by increase in cardiomyocyte size, enhanced protein synthesis, and a higher organization of the sarcomere. Several factors including re-induction of fetal gene program are involved in these changes. It is important to stimulate the physiological and inhibit pathological hypertrophy in order to avoid heart failure. In my current project, I am exploring the role of Poly-A Binding proteins in cardiac hypertrophy using mouse as model system.