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Articles by Panpan Hou
Mechanosensitive ion channels in immunity from biophysics to mechanomedicine
Affiliations & Notes 1Dr. Neher’s Biophysics Laboratory for Innovative Drug Discovery, State Key Laboratory of Mechanism and Quality of Chinese Medicine, School of Pharmacy, Faculty of Chinese Medicine, Macau University of Science and Technology, Macau SAR, China 2Macau University of Science and Technology Innovation Technology Research Institute.
Structural basis of the neuronal M-current generated by an asymmetric KCNQ2/3 assembly
Dear Editor, The voltage-gated KCNQ2/3 heteromer channel underlies the neuronal M-current, a slow-activating potassium current that stabilizes membrane potential and prevents neuronal hyperexcitability.1 Mutations in KCNQ2 or KCNQ3 disrupt this current, causing epileptic encephalopathies and implicating channel dysfunction in neuropathic pain and auditory disorders.2 Despite differences in gating, trafficking, and phosphatidylinositol 4,5-bisphosphate (PIP₂) sensitivity in homomers, KCNQ2/3...
Coronaviral nsp6 hijacks ERAD machinery to facilitate lipolysis and supply membrane components for DMV growth - Nature Communications
Abstract The positive-strand RNA ( + RNA) viruses extensively remodel cellular endomembranes to facilitate viral replication, with coronaviruses forming a specialized viral replication organelle (RO) known as double-membrane vesicles (DMVs). These DMVs serve as platforms for viral replication and shield viral RNA from host immune recognition. However, the biogenesis, structural organization, and physiological properties of DMVs remain poorly understood.
The fully activated open state of KCNQ1 controls the cardiac 'fight-or-flight' response
Abstract The cardiac KCNQ1+KCNE1 (IKs) channel regulates heart rhythm in both normal and stress conditions. Under stress, the β-adrenergic stimulation elevates the intracellular cAMP level, leading to KCNQ1 phosphorylation by protein kinase A and increased IKs, which shortens action potentials to adapt to accelerated heart rate.
Predicting Patient Response to the Antiarrhythmic Mexiletine Based on Genetic Variation
Personalized Medicine for Long QT Syndrome Originally published18 Dec 2018https://doi.org/10.1161/CIRCRESAHA.118.314050Circulation Research. 2018;124:539–552 Abstract Rationale: Mutations in the SCN5A gene, encoding the α subunit of the Nav1.5 channel, cause a life-threatening form of cardiac arrhythmia, long QT syndrome type 3 (LQT3). Mexiletine, which is structurally related to the Na+ channel-blocking anesthetic lidocaine, is used to treat LQT3 patients.
Predicting Patient Response to the Antiarrhythmic Mexiletine Based on Genetic Variation: Personalized Medicine for Long QT Syndrome
Abstract Rationale: Mutations in the SCN5A gene, encoding the α subunit of the Nav1.5 channel, cause a life-threatening form of cardiac arrhythmia, Long QT Syndrome Type 3 (LQT3). Mexiletine, which is structurally related to the Na+ channel-blocking anesthetic lidocaine, is used to treat LQT3 patients. However, the patient response is variable, depending on the genetic mutation in SCN5A.
A Genome-Wide CRISPR Screen Identifies Genes Critical for Resistance to FLT3 Inhibitor AC220
Therapeutics, Targets, and Chemical Biology A Genome-Wide CRISPR Screen Identifies Genes Critical for Resistance to FLT3 Inhibitor AC220 Panpan Hou, Chao Wu, Yuchen Wang, Rui Qi, Dheeraj Bhavanasi, Zhixiang Zuo, Cedric Dos Santos, Shuliang Chen, Yu Chen, Hong Zheng, Hong Wang, Alexander Perl, Deyin Guo and Jian Huang
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