Duke-NUS Medical School

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Pradeep Bist

Principal Research Scientist, Signature Research Programme in Emerging Infectious Diseases

pradeep.bist@duke-nus.edu.sg

About

Publications

Bio

Pradeep Bist is a Principal Research Scientist at Duke-NUS Medical School in the Programme in Emerging Infectious Diseases. He obtained M.Sc, M.Phil and Ph.D., in Microbiology from Bangalore, India. He has worked at different capacities from Microbiologist to Lecturer, and various postoctoral fellowships including University of California, Los Angeles.

He has gained experience in multiple biological disciplines including but not limited to molecular biology, genetics, biochemistry and cell biology, and has been trained in specialized areas of microbiology, immunology and oncology.

His research area is on Innate immunity & Inflammasomes, Virus and host determinants of viral pathogenesis, Bacterial pathogenesis & Adverse drug reactions mechanisms.

Education

Doctor of Philosophy

Bangalore University, India

Master of Philosophy in Biology

Gulbarga University, India

Master of Science in Biology

Gulbarga University, India

Bachelor of Science

Guru Nanak Dev University, India

Directory

Bio

Education

Doctor of Philosophy

Master of Philosophy in Biology

Master of Science in Biology

Bachelor of Science

Publications

A humanized mouse model to study mast cells mediated cutaneous adverse drug reactions.

MRGPR-mediated activation of local mast cells clears cutaneous bacterial infection and protects against reinfection.

Collaboration between Distinct Rab Small GTPase Trafficking Circuits Mediates Bacterial Clearance from the Bladder Epithelium.

E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP.

Annexin-1 interacts with NEMO and RIP1 to constitutively activate IKK complex and NF-κB: implication in breast cancer metastasis.

The Nod1, Nod2, and Rip2 axis contributes to host immune defense against intracellular Acinetobacter baumannii infection.

S-adenosyl-L-methionine is required for DNA cleavage by type III restriction enzymes.

Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF-kappaB activation and cell survival.

Annexin-A1 regulates TLR-mediated IFN-β production through an interaction with TANK-binding kinase 1.

Bruton's tyrosine kinase phosphorylates DDX41 and activates its binding of dsDNA and STING to initiate type 1 interferon response.

Intracellular Uropathogenic E. coli Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells.

Influenza A virus enhances its propagation through the modulation of Annexin-A1 dependent endosomal trafficking and apoptosis.

Directory

Bio

Education

Doctor of Philosophy

Master of Philosophy in Biology

Master of Science in Biology

Bachelor of Science

Publications

A humanized mouse model to study mast cells mediated cutaneous adverse drug reactions.

MRGPR-mediated activation of local mast cells clears cutaneous bacterial infection and protects against reinfection.

Collaboration between Distinct Rab Small GTPase Trafficking Circuits Mediates Bacterial Clearance from the Bladder Epithelium.

E3 Ubiquitin ligase ZNRF4 negatively regulates NOD2 signalling and induces tolerance to MDP.

Annexin-1 interacts with NEMO and RIP1 to constitutively activate IKK complex and NF-κB: implication in breast cancer metastasis.

The Nod1, Nod2, and Rip2 axis contributes to host immune defense against intracellular Acinetobacter baumannii infection.

S-adenosyl-L-methionine is required for DNA cleavage by type III restriction enzymes.

Essential role of tuberous sclerosis genes TSC1 and TSC2 in NF-kappaB activation and cell survival.

Annexin-A1 regulates TLR-mediated IFN-β production through an interaction with TANK-binding kinase 1.

Bruton's tyrosine kinase phosphorylates DDX41 and activates its binding of dsDNA and STING to initiate type 1 interferon response.

Intracellular Uropathogenic E. coli Exploits Host Rab35 for Iron Acquisition and Survival within Urinary Bladder Cells.

Influenza A virus enhances its propagation through the modulation of Annexin-A1 dependent endosomal trafficking and apoptosis.

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