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Profil bibliographique

Jaehoon Shim

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

24Publications signalées
363Citations signalées
4Affiliations récentes

Les institutions déclarées

Les domaines associés

Neuroscience and Neuropharmacology ResearchIon channel regulation and functionPain Mechanisms and TreatmentsAdvanced Memory and Neural ComputingIon Channels and Receptors

Les publications récentes

Accès ouvert 2025 article OpenAlex

Discovery of Na v 1.7 Inhibitors through the Screening of Marine Natural Product Extracts

Adetola H. Adewole, Bhuwan K. Chhetri, Ghada M. Abdelwahab, Riya Bhanushali et autres

High Resolution Image Download MS PowerPoint Slide Automated high-throughput screening of a prefractionated extract library of marine macroorganisms identified 239 hits (hit rate 2.5%), including a marine algal extract that blocked the Na v 1.7 channel in a fluorescent-based flux assay. Bioactivity-guided …

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1 citation Journal of Natural Products
Accès ouvert 2025 article OpenAlex

Validation of human sensory neurons derived from inducible pluripotent stem cells as a model for latent infection and reactivation by herpes simplex virus 1

Hyung Suk Oh, Shu-Fan Chou, Priya Raja, Jaehoon Shim et autres

Herpes simplex virus 1 (HSV-1) undergoes primary acute lytic replication in mucosal epithelial cells and then spreads to establish latent infection in peripheral neurons including sensory and autonomic neurons. Latent HSV-1 reactivates to cause recurrent cold sores but can also cause more …

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8 citations mBio
Accès ouvert 2025 erratum OpenAlex

Correction of sodium channel mutations in sensory neurons reverses aberrant properties

Jaehoon Shim, Brian S. Tanaka, Daniel G. Taub, Malgorzata A. Mis et autres

Inherited erythromelalgia, small fibre neuropathy and paroxysmal extreme pain disorder are caused by gain-of-function mutations in the voltage-gated sodium channel Nav1.7. It remains unknown how different mutations in the same channel enhancing electrogenesis in sensory neurons results in such distinct disease presentations. …

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1 citation Brain
2025 article OpenAlex

Increased Na V 1.2 expression and its interaction with CaM contribute to the hyperexcitability induced by prolonged inhibition of CaMKII

Hongyue Liang, Ling Qin, Rui Feng, Jaehoon Shim et autres

Abstract Objective Dysfunction of calcium/calmodulin (CaM)–dependent kinase II (CaMKII) has been involved in hyperexcitability‐related disorders including epilepsy. However, the relationship between CaMKII and neuronal excitability remains unclear. Methods Neuronal excitability was detected in vivo and in vitro by electroencephalography (EEG), patch clamp …

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2 citations Epilepsia
Accès ouvert 2024 article OpenAlex

A Novel Quaternary Ammonium N-Propylamiodarone Bromide Provides Long-Lasting Analgesia Against Corneal Pain

Yumi Kotoda, Sohei Hishiyama, Jaehoon Shim, Hiroki Kobayashi et autres

Purpose: Corneal pain is one of the most common eye symptoms caused by various types of epithelial injuries, including traumatic abrasion, chemical injury, ulcers, ultraviolet exposure, and infection. However, current therapeutic options for corneal pain are limited. In this study, we synthesized …

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0 citations Drug Design Development and Therapy
Accès ouvert 2023 article OpenAlex

Scalable generation of sensory neurons from human pluripotent stem cells

Tao Deng, Vukasin M. Jovanovic, Carlos A. Tristan, Claire Weber et autres

Development of new non-addictive analgesics requires advanced strategies to differentiate human pluripotent stem cells (hPSCs) into relevant cell types. Following principles of developmental biology and translational applicability, here we developed an efficient stepwise differentiation method for peptidergic and non-peptidergic nociceptors. By modulating …

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58 citations Stem Cell Reports
Accès ouvert 2023 article OpenAlex

Nav1.7 gain-of-function mutation I228M triggers age-dependent nociceptive insensitivity and C-LTMR dysregulation

Nivanthika K. Wimalasena, Daniel G. Taub, Jaehoon Shim, Sara Hakim et autres

Gain-of-function mutations in Scn9a, which encodes the peripheral sensory neuron-enriched voltage-gated sodium channel Nav1.7, cause paroxysmal extreme pain disorder (PEPD), inherited erythromelalgia (IEM), and small fiber neuropathy (SFN). Conversely, loss-of-function mutations in the gene are linked to congenital insensitivity to pain (CIP). …

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18 citations Experimental Neurology
Accès ouvert 2022 article OpenAlex

The sigma‐1 receptor curtails endogenous opioid analgesia during sensitization of TRPV1 nociceptors

M. Carmen Ruiz‐Cantero, Elsa Cortés‐Montero, Aakanksha Jain, Ángeles Montilla‐García et autres

BACKGROUND AND PURPOSE: -sensing chaperone known to modulate opoid analgesia. This receptor binds both to TRPV1 and the μ opioid receptor, although the functional repercussions of these physical interactions in peripheral sensitization are unknown. EXPERIMENTAL APPROACH: We tested the effects of sigma-1 …

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30 citations British Journal of Pharmacology
Accès ouvert 2022 dataset OpenAlex

Prolonged inhibition of CaMKII results in hyperexcitability by increasing NaV1.2 expression and its interaction with CaM

Hongyue Liang, Ling Qin, Rui Feng, Jaehoon Shim et autres

Dysfunction of calcium/calmodulin (CaM)-dependent kinase II (CaMKII) has been involved in hyperexcitability-related disorders including epilepsy. However, the exact mechanism by which CaMKII inhibits neuronal excitability remains to be elucidated. In the present study, we found that seizure-like events recorded by EEG in …

us, cn, pl (code pays fourni par la source)

0 citations Zenodo (CERN European Organization for Nuclear Research)
Accès ouvert 2022 dataset OpenAlex

Prolonged inhibition of CaMKII results in hyperexcitability by increasing NaV1.2 expression and its interaction with CaM

Hongyue Liang, Ling Qin, Rui Feng, Jaehoon Shim et autres

Dysfunction of calcium/calmodulin (CaM)-dependent kinase II (CaMKII) has been involved in hyperexcitability-related disorders including epilepsy. However, the exact mechanism by which CaMKII inhibits neuronal excitability remains to be elucidated. In the present study, we found that seizure-like events recorded by EEG in …

us, cn, pl (code pays fourni par la source)

0 citations Zenodo (CERN European Organization for Nuclear Research)
Accès ouvert 2022 dataset OpenAlex

Prolonged inhibition of CaMKII results in hyperexcitability by increasing NaV1.2 expression and its interaction with CaM

Hongyue Liang, Ling Qin, Rui Feng, Jaehoon Shim et autres

Dysfunction of calcium/calmodulin (CaM)-dependent kinase II (CaMKII) has been involved in hyperexcitability-related disorders including epilepsy. However, the exact mechanism by which CaMKII inhibits neuronal excitability remains to be elucidated. In the present study, we found that seizure-like events recorded by EEG in …

us, cn, pl (code pays fourni par la source)

0 citations Zenodo (CERN European Organization for Nuclear Research)
Accès ouvert 2022 dataset OpenAlex

Prolonged inhibition of CaMKII results in hyperexcitability by increasing NaV1.2 expression and its interaction with CaM

Hongyue Liang, Ling Qin, Rui Feng, Jaehoon Shim et autres

Dysfunction of calcium/calmodulin (CaM)-dependent kinase II (CaMKII) has been involved in hyperexcitability-related disorders including epilepsy. However, the exact mechanism by which CaMKII inhibits neuronal excitability remains to be elucidated. In the present study, we found that seizure-like events recorded by EEG in …

us, cn, pl (code pays fourni par la source)

0 citations Zenodo (CERN European Organization for Nuclear Research)

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