Research Interests

Our body cells deal with a large number of external and internal threats. The external threats involve invasion of pathogenic bacteria, viruses, and fungi. The internal threats involve damaged cell organelles for example mitochondria. Damaged organelles or other internal threats including inflammation if not cleared could cause cell death or could lead to genomic mutations. Significant genomic alteration could make cells cancerous.

Our body has different mechanisms to take care of these threats and mostly the processes/pathways are similar whether the threats are internal or external. Our lab tries to understand how these mechanisms work and whether we can artificially boost (therapy) these mechanisms to remove or reduce threats.

Specifically, our lab works on autophagy and inflammatory pathways. Autophagy is a cell autonomous cleaning process, which removes both internal and external threats and allows the cells to perform their work efficiently. We know that excess inflammation is highly detrimental and could lead to autoimmune diseases. We are interested how autophagy reduces inflammation of the cells and prevent inflammatory cell death and autoimmunity.

In addition, our lab is interested in knowing how host anti-viral innate immune system works. One of the most efficient host anti-viral systems is interferon response. We are interested understanding how different interferon induced proteins could kill or restrict viral growth. Interestingly, the interferon response is not only anti-viral (external threat) but also anti-cancer (internal threat). Our lab is also interested in understanding the anti-cancer role of interferon stimulated proteins.

Moreover, we are taking both unbiased and structure-based approaches to screen and identify small molecules that could boost anti-viral and anti-cancer immunity. We use multiple biochemical, cell biological and molecular biological techniques to elucidate the mechanisms by which small molecules could enhance cell immunity.

Broad areas of research in lab:

1. Cell autonomous defense systems: Autophagy and inflammatory processes
2. Innate Immunity: anti-viral immunity and anti-cancer immunity
3. Immunogenic Cell Death: Pyroptosis and Necroptosis
4. Drug discovery: Antiviral and anti-cancer by inducing host immune responses

For more details please visit https://www.autophagylab.com/

Selected Publications

Jena KK, Mehto S, Yadav R, Priyadarsini S, Samal P, Krishna S, Dhar K, Jain A, Chauhan NR, Murmu KC, Bal R, Sahu R, Jaiswal P, Sahoo BS, Patnaik S, Kufer TS, Rusten TE, Chauhan S, Prasad P, Chauhan S. Selective Autophagy of RIPosomes Maintains Innate Immune Homeostasis during Bacterial Infection. EMBO J. 2022 Dec 1;41(23):e111289.

Nath P, Chauhan NR, Jena KK, Datey A, Kumar ND, Mehto S, De S, Nayak TK, Priyadarsini S, Rout K, Bal R, Murmu KC, Kalia M, Patnaik S, Prasad P, Reggiori F, Chattopadhyay S*, Chauhan S*. Inhibition of IRGM establishes a robust antiviral immune state to restrict pathogenic viruses. EMBO Rep. 2021 Sep 1:e52948. (Cover page article)

Kolapalli SP, Sahu R, Chauhan NR, Jena KK, Mehto S, Das SK, Jain A, Rout M, Dash R, Swain R, Lee DY, Rusten TE, Chauhan S*, Chauhan S*. RNA binding RING E3-ligase DZIP3/hRUL138 is a novel driver of cell cycle and cancer progression by employing a unique mechanism to stabilize Cyclin D1. Cancer Research, 2021 Jan 15;81(2):315-331. (Cover page article)

Jena KK, Mehto S, Nath P, Chauhan NR, Sahu R, Dhar K, Das SK, Kolapalli SP, Murmu KC, Jain A, Krishna S, Sahoo BS, Chattopadhyay S, Rusten TE, Prasad P, Chauhan S, Chauhan S*. Autoimmunity gene IRGM suppresses cGAS-STING and RIG-I-MAVS signaling to control interferon response. EMBO Rep. 2020 Jul 27:e50051.

Mehto S, Jena KK, Nath P, Chauhan S, Kolapalli SP, Das SK, Sahoo PK, Jain A, Taylor GA, Chauhan S*. The Crohn's disease risk factor IRGM limits NLRP3 inflammasome activation by impeding its assembly and by mediating its selective autophagy. Molecular Cell. 2019 Feb 7;73(3):429-445.e7. (Publication highlighted in the issue)

Jena KK, Kolapalli SP, Mehto S, Nath P, Das B, Sahoo PK, Ahad A, Syed GH, Raghav SK, Senapati S, Chauhan S, Chauhan S*. TRIM16 controls assembly and degradation of protein aggregates by modulating the p62-NRF2 axis and autophagy. EMBO J. 2018 Sep 14;37(18).