| RONGGUI HU LAB
| RONGGUI HU LAB
Autism Spectrum Disorder (ASD) research focuses on uncovering the biological underpinnings of ASD. The studies explore how genetic mutations, neurodevelopmental abnormalities, immune responses, and environmental factors interact to affect neural circuits, leading to core ASD symptoms. Through multidisciplinary approaches, including molecular genetics, neuroimaging, and systems biology, researchers aim to understand ASD's complex pathophysiology, paving the way for early intervention and personalized therapies.The Hu's research investigates the impact of triclosan (TCS), a commonly used antimicrobial agent, on autism-like behaviors in mice. The study reveals that TCS inhibits retinoic acid (RA) signaling, which is crucial for synaptic plasticity. Mice exposed to TCS during pregnancy displayed significant autism-like behaviors, suggesting that TCS could be an environmental factor contributing to neurodevelopmental disorders such as autism. The findings highlight the need to reassess the safety of TCS, particularly its potential impact on mental health.
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Virology research delves into how viruses enter host cells and manipulate cellular mechanisms for replication and propagation. The focus is on virus-host protein interactions, immune evasion strategies, and viral genome replication and assembly. Utilizing advanced “omics” technologies and imaging techniques, scientists are uncovering the molecular mechanisms of viral infections, providing a scientific basis for developing antiviral drugs and vaccines. The Hu's research reveals that the E3 ubiquitin ligase TRIM21 inhibits hepatitis B virus (HBV) replication through non-proteolytic ubiquitination of the viral X protein (HBx). This modification disrupts the interaction between HBx and DDB1, a host protein, thereby suppressing HBV replication. Unlike traditional ubiquitination, which typically leads to protein degradation, TRIM21-mediated ubiquitination alters HBx's function without degrading it. This discovery offers a novel therapeutic target for treating HBV infections.
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Cancer research aims to understand the molecular foundations of tumor initiation, progression, and metastasis. This field covers gene mutations, signal transduction pathways, tumor microenvironment, and immune evasion mechanisms. Through a variety of molecular biology and immunology techniques, the research drives the development of targeted therapies, immunotherapies, and personalized medicine, with the goal of improving cancer diagnosis and treatment outcomes.The Hu's team discovered that the E3 ubiquitin ligase HERC3 suppresses epithelial-mesenchymal transition (EMT) and metastasis in colorectal cancer (CRC) by promoting the ubiquitination degradation of EIF5A2. HERC3 was found to be downregulated in CRC tissues, correlating with poor prognosis. It regulates EMT via the EIF5A2/TGF-β/Smad2/3 signaling pathway, ultimately inhibiting cancer cell migration, invasion, and metastasis. This research offers new insights into CRC treatment, particularly in targeting cancer metastasis.
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Immunology studies the body's mechanisms for recognizing and defending against pathogens, cancer cells, and other abnormal cells, while inflammation biology focuses on the physiological and pathological processes of inflammation. The findings may provide a theoretical basis for developing new therapeutic strategies for inflammatory diseases.The Hu's research reveals a novel role of ER-localized Hrd1 in regulating TLR4-induced inflammation during bacterial infection. Hrd1 ubiquitinates and inactivates the deubiquitinase Usp15, promoting IκBα degradation, thus enhancing NF-κB activation and the inflammatory response. Mice lacking Hrd1 show increased resistance to LPS-induced sepsis, highlighting the importance of Hrd1 and Usp15 in inflammation regulation. This study offers new insights into the role of Hrd1 and the endoplasmic reticulum in inflammation and immune responses.
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