Nhi Lang

ORCID: 0000-0001-7187-1194
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroscience and Neuropharmacology Research
  • Phosphodiesterase function and regulation
  • RNA modifications and cancer
  • Cancer-related gene regulation
  • RNA Research and Splicing
  • Connective tissue disorders research
  • Wnt/β-catenin signaling in development and cancer
  • Kruppel-like factors research
  • Epigenetics and DNA Methylation
  • Nuclear Structure and Function

Scripps Research Institute
2023-2025

Children’s Institute
2020-2021

University of California, San Diego
2020-2021

cAMP response element-binding protein (CREB)-regulated transcription coactivator 1 (CRTC1) plays an important role in synaptic plasticity, learning, and long-term memory formation through the regulation of neuronal activity-dependent gene expression, CRTC1 dysregulation is implicated Alzheimer’s disease (AD). Here, we show that increased S-nitrosylation (forming SNO-CRTC1), as seen cell-based, animal-based, human-induced pluripotent stem cell (hiPSC)-derived cerebrocortical neuron-based AD...

10.1073/pnas.2418179122 article EN cc-by-nc-nd Proceedings of the National Academy of Sciences 2025-02-27

Abstract DNA methyltransferases (DNMTs) catalyze methylation at the C5 position of cytosine with S -adenosyl- l -methionine. Methylation regulates gene expression, serving a variety physiological and pathophysiological roles. The chemical mechanisms regulating DNMT enzymatic activity, however, are not fully elucidated. Here, we show that protein S-nitrosylation cysteine residue in DNMT3B attenuates activity consequent aberrant upregulation expression. These genes include Cyclin D2 ( Ccnd2 ),...

10.1038/s41467-023-36232-6 article EN cc-by Nature Communications 2023-02-04

SUMMARY CREB-regulated transcription coactivator 1 (CRTC1) plays an important role in synaptic plasticity, learning and long-term memory formation through regulation of neuronal activity-dependent gene expression, CRTC1 dysregulation is implicated Alzheimer’s disease (AD). Here, we show that increased S-nitrosylation (forming SNO-CRTC1), as seen cell-based, animal-based, human induced pluripotent stem cell (hiPSC)-derived cerebrocortical neuron-based AD models, disrupts its binding with CREB...

10.1101/2023.08.25.554320 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-08-27
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