Publications by authors named "Kang-Sik Park"

Tumor necrosis factor α (TNF-α) is a major pro-inflammatory cytokine, important in many diseases, that sensitizes nociceptors through its action on a variety of ion channels, including voltage-gated sodium (Na) channels. We show here that TNF-α acutely upregulates sensory neuron excitability and current density of threshold channel Na1.7.

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Liquid chromatography-tandem mass spectrometry (LC-MS)-based profiling of proteomes with isobaric tag labeling from low-quantity biological and clinical samples, including needle-core biopsies and laser capture microdissection, has been challenging due to the limited amount and sample loss during preparation. To address this problem, we developed OnM (On-Column from Myers et al. and mPOP)-modified on-column method combining freeze-thaw lysis of mPOP with isobaric tag labeling of On-Column method to minimize sample loss.

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  • T-type Ca channels are important for functions like low-threshold spikes in neurons, visceral pain, and pacemaker activity, and their activity is significantly impacted by phosphorylation.
  • In this study, researchers identified 30 phosphorylation sites on the Ca 3.1 channel using mass spectrometry and created a phosphorylation map, revealing how these sites affect channel function.
  • Mutations of specific phosphorylation sites led to decreased current amplitude and changes in channel properties, indicating that these phosphorylated regions are key regulators of the channel's activity and voltage sensitivity.
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In mammals, environmental cold sensing conducted by peripheral cold thermoreceptor neurons mostly depends on TRPM8, an ion channel that has evolved to become the main molecular cold transducer. This TRP channel is activated by cold, cooling compounds, such as menthol, voltage, and rises in osmolality. TRPM8 function is regulated by kinase activity that phosphorylates the channel under resting conditions.

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Ca1.2 channel phosphorylation plays an important role in regulating neuronal plasticity by action potential-dependent Ca entry. Most studies of Ca1.

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Aging is a gradual biological process characterized by a decrease in cellular and organism functions. Aging-related processes involve changes in the expression and activity of several proteins. Here, we identified the transmembrane protease serine 11a (TMPRSS11a) as a new age-specific protein that plays an important role in skin wound healing.

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Mesenchymal stem cells (MSCs) have the potential to be a viable therapy against various diseases due to their paracrine effects, such as secretion of immunomodulatory, trophic and protective factors. These cells are known to be distributed within various organs and tissues. Although they possess the same characteristics, MSCs from different sources are believed to have different secretion potentials and patterns, which may influence their therapeutic effects in disease environments.

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  • Brain ischemia causes oxidative stress that leads to neuronal cell death, primarily by increasing the activity of the K2.1 potassium channel, resulting in potassium loss from cells.
  • This study found that the process of apoptosis during ischemia is linked to the rapid tyrosine phosphorylation of the K2.1 channel, specifically at the Y810 site, which plays a key role in this cell death mechanism.
  • In experiments, cells lacking the ability to phosphorylate the Y810 site showed improved survival, suggesting that targeting this modification on K2.1 could be a promising strategy for treating brain ischemia.
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  • Quetiapine is an atypical antipsychotic used to treat schizophrenia and mania, and it has been deemed mostly safe regarding heart-related side effects despite previous concerns about its impact on potassium channels.
  • This study utilized the whole-cell patch-clamp technique to assess how both quetiapine and its metabolite norquetiapine affect human cardiac sodium channels (hNa1.5), finding that norquetiapine is more potent in blocking these channels.
  • The research indicates that norquetiapine causes a concentration-dependent blockade of hNa1.5, slows the recovery of the channel from inactivation, and potentially reduces heart risks by affecting the cardiac action potential duration without significantly increasing the risk of
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  • The text discusses the introduction of cRFP (common Repository of FBS Proteins) for improving mass spectrometry raw data analysis in cell secretomes by supplementing the reference database with abundant fetal bovine serum proteins.
  • The primary goal of cRFP is to reduce misidentification of these serum proteins as other proteins during data analysis, similar to the use of cRAP for adventitious proteins.
  • The authors anticipate that cRFP will be beneficial in experiments using serum-free media, complex media like SILAC, or extracellular vesicles.
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Introduction: Most cases of Parkinson's disease (PD) are sporadic, but genetic variations have been discovered in PD patients. PARK7/DJ-1 is a known cause of early-onset autosomal-recessive PD and is implicated in neuroprotection against oxidative stress. Although several post-translational modifications of DJ-1 have been proposed, phospho-modification of DJ-1 and its functional consequences have been less studied.

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An excess of reactive oxygen species (ROS) relative to the antioxidant capacity causes oxidative stress, which plays a role in the development of Parkinson's disease (PD). Because mitochondria are both sites of ROS generation and targets of ROS damage, the delivery of antioxidants to mitochondria might prevent or alleviate PD. To transduce the antioxidant protein human metallothionein 1A (hMT1A) into mitochondria, we computationally designed a cell-penetrating artificial mitochondria-targeting peptide (CAMP).

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  • Ginsenoside Rg1 shows protective effects against Alzheimer's disease, but its mechanisms are not fully understood.
  • A proteomic analysis revealed that Rg1 significantly alters 49 proteins in SH-SY5Y cells treated with β-amyloid peptides, including those related to ribosomal function and mitochondria.
  • The study highlights that mitochondrial proteins could play a key role in Rg1's protective mechanisms in Alzheimer's disease.
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  • Nephrotic syndrome (NS) is a kidney disorder often caused by conditions like minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), and membranous nephropathy (MN), prompting researchers to analyze urinary protein profiles for specific biomarkers.
  • In the study, urine samples from 16 NS patients and healthy controls were analyzed using advanced techniques (LC-MS/MS) and further validated with ELISA across 61 samples, identifying 228 proteins, with 22 showing different expressions among the three diseases.
  • The findings included the validation of proteins C9, CD14, and SERPINA1, which were elevated in MCD, MN, and FSGS, and supported developing
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The potassium ion channel Kv3.1b is a member of a family of voltage-gated ion channels that are glycosylated in their mature form. In the present study, we demonstrate the impact of N-glycosylation at specific asparagine residues on the trafficking of the Kv3.

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  • * Researchers investigated how Rb1 protects neuronal cells exposed to β-amyloid using advanced mass spectrometry techniques, identifying 1,231 proteins, with 40 significantly affected by Rb1.
  • * The study suggests that changes in actin cytoskeleton proteins, particularly CAP1, CAPZB, TOMM40, and DSTN, may be linked to Rb1’s protective effects against Alzheimer’s disease.
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Cellular migration and contractility are fundamental processes that are regulated by a variety of concerted mechanisms such as cytoskeleton rearrangements, focal adhesion turnover, and Ca2+ oscillations. TRPM4 is a Ca2+-activated non-selective cationic channel (Ca2+-NSCC) that conducts monovalent but not divalent cations. Here, we used a mass spectrometry-based proteomics approach to identify putative TRPM4-associated proteins.

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  • The study identifies glypican 4 (GPC-4) as a specific binding partner for the protein PTPσ, which is involved in organizing synapse development.
  • GPC-4 interacts with PTPσ in a strong and specific manner, primarily when GPC-4 is cleaved, and forms a complex with another protein, LRRTM4, in rat brains.
  • Reducing PTPσ levels in neurons hampers the ability of LRRTM4 to promote synapse formation and decreases excitatory synaptic activity, effects that can be reversed by the normal PTPσ but not a mutant version that can't bind heparan sulfate.
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Transient receptor potential melastatin-like 4 (TRPM4) is a Ca(2+)-activated non-selective cation channel expressed in a wide range of human tissues. TRPM4 participates in a variety of physiological processes such as T cell activation, myogenic vasoconstriction, and allergic reactions. TRPM4 Ca(2+) sensitivity is enhanced by calmodulin (CaM) and phosphathydilinositol 4, 5-bisphosphate (PI(4,5)P2) binding, as well as, under certain conditions, PKC activation.

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  • Parkinson's disease (PD) is characterized by the loss of dopamine-producing neurons in a specific brain region, the substantia nigra.
  • A proteomic analysis using advanced techniques identified 1740 proteins in cells treated to mimic PD, revealing 39 proteins that were differentially expressed.
  • Among these, 14 were linked to mitochondria, highlighting their significant role in PD and introducing new proteins that may contribute to the disease's mechanisms.
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Cyclin-dependent kinase 5 (CDK5), a member of atypical serine/threonine cyclin-dependent kinase family, plays a crucial role in pathophysiology of neurodegenerative disorders. Its kinase activity and substrate specificity are regulated by several independent pathways including binding with its activator, phosphorylation and S-nitrosylation. In the present study, we report that acetylation of CDK5 comprises an additional posttranslational modification within the cells.

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Multiple synaptic adhesion molecules govern synapse formation. Here, we propose calsyntenin-3/alcadein-β as a synapse organizer that specifically induces presynaptic differentiation in heterologous synapse-formation assays. Calsyntenin-3 (CST-3) is highly expressed during various postnatal periods of mouse brain development.

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The Kv3.1 channel plays a crucial role in regulating the high-frequency firing properties of neurons. Here, we determined whether Src regulates the subcellular distributions of the Kv3.

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  • Cadmium and nickel are classified as human carcinogens by the World Health Organization, raising concerns about their low-dose exposure in the environment leading to diseases like cancer.
  • The study utilized advanced techniques like genomic hybridization and gene expression analysis to investigate the toxic effects of chronic low-dose exposure to these heavy metals.
  • Key findings revealed distinct signaling networks for cadmium and nickel exposure, identifying important mediators such as HSP90AA1 involved in apoptosis and potential cancer development pathways.
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