Jenny Gao

ORCID: 0000-0003-4682-7428
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About
Contact & Profiles
Research Areas
  • RNA modifications and cancer
  • RNA and protein synthesis mechanisms
  • Uterine Myomas and Treatments
  • Endometrial and Cervical Cancer Treatments
  • CAR-T cell therapy research
  • RNA Research and Splicing
  • Sphingolipid Metabolism and Signaling
  • Lipid metabolism and biosynthesis
  • Integrated Circuits and Semiconductor Failure Analysis
  • Cancer Research and Treatments
  • Bacteriophages and microbial interactions
  • Advancements in Semiconductor Devices and Circuit Design
  • Chronic Lymphocytic Leukemia Research
  • Management of metastatic bone disease
  • Endoplasmic Reticulum Stress and Disease
  • Colorectal Cancer Surgical Treatments
  • Lymphoma Diagnosis and Treatment

University of Massachusetts Chan Medical School
2022-2023

Rockefeller University
2018-2023

Utilization of specific codons varies between organisms. Cancer represents a model for understanding DNA sequence evolution and could reveal causal factors underlying codon evolution. We found that across human cancer, arginine are frequently mutated to other codons. Moreover, limitation—a feature tumor microenvironments—is sufficient induce codon–switching mutations in colon cancer cells. Such switching events encode mutant proteins with residue substitutions. Mechanistically, limitation...

10.1126/sciadv.ade9120 article EN cc-by-nc Science Advances 2023-01-06

Sphingolipids play important signaling and structural roles in cells. Here, we find that during de novo sphingolipid biosynthesis, a toxic metabolite is formed with critical implications for cancer cell survival. The enzyme catalyzing the first step this pathway, serine palmitoyltransferase complex (SPT), upregulated breast other cancers. SPT dispensable proliferation, as sphingolipids can be salvaged from environment. However, activity introduces liability its product,...

10.1016/j.celrep.2022.111415 article EN cc-by-nc-nd Cell Reports 2022-09-01

SUMMARY Eukaryotic transfer RNAs can become selectively fragmented upon various stresses, generating tRNA-derived small RNA fragments. Such fragmentation has been reported to impact a fraction of the tRNA pool and thus presumed not directly translation. We report that oxidative stress rapidly generate tyrosine GUA fragments in human cells—causing significant depletion precursor tRNA. Tyrosine impaired translation growth metabolic genes enriched cognate codons. Depletion or its...

10.1101/416727 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2018-09-13

Abstract Utilization of specific codons varies significantly across organisms. Cancer represents a model for understanding DNA sequence evolution and could reveal causal factors underlying codon evolution. We found that human cancer, arginine are frequently mutated to other codons. Moreover, restriction—a feature tumor microenvironments—is sufficient induce codon-switching mutations in colon cancer cells. Such switching events encode mutant proteins with residue substitutions....

10.1101/2023.01.02.521806 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-01-02
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