Lunbin Deng
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Explore the profile of Lunbin Deng including associated specialties, affiliations and a list of published articles.
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20
Citations
1206
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Recent Articles
1.
Deng L, Dourado M, Reese R, Huang K, Shields S, Stark K, et al.
Neuron
. 2023 Jun;
111(17):2642-2659.e13.
PMID: 37352856
Loss-of-function mutations in Nav1.7, a voltage-gated sodium channel, cause congenital insensitivity to pain (CIP) in humans, demonstrating that Nav1.7 is essential for the perception of pain. However, the mechanism by...
2.
Kschonsak M, Jao C, Arthur C, Rohou A, Bergeron P, Ortwine D, et al.
Elife
. 2023 Mar;
12.
PMID: 36975198
The voltage-gated sodium (Na) channel Na1.7 has been identified as a potential novel analgesic target due to its involvement in human pain syndromes. However, clinically available Na channel-blocking drugs are...
3.
McKerrall S, Nguyen T, Lai K, Bergeron P, Deng L, DiPasquale A, et al.
J Med Chem
. 2019 Apr;
62(8):4091-4109.
PMID: 30943032
Using structure- and ligand-based design principles, a novel series of piperidyl chromane arylsulfonamide Na1.7 inhibitors was discovered. Early optimization focused on improvement of potency through refinement of the low energy...
4.
Sun S, Jia Q, Zenova A, Wilson M, Chowdhury S, Focken T, et al.
J Med Chem
. 2018 Dec;
62(2):908-927.
PMID: 30499663
Herein, we report the discovery and optimization of a series of orally bioavailable acyl sulfonamide Na1.7 inhibitors that are selective for Na1.7 over Na1.5 and highly efficacious in in vivo...
5.
Shields S, Deng L, Reese R, Dourado M, Tao J, Foreman O, et al.
J Neurosci
. 2018 Oct;
38(47):10180-10201.
PMID: 30301756
Strong human genetic evidence points to an essential contribution of the voltage-gated sodium channel Nav1.7 to pain sensation: loss of Nav1.7 function leads to congenital insensitivity to pain, whereas gain-of-function...
6.
Wang T, Brown B, Deng L, Sellers B, Lupardus P, Wallweber H, et al.
Neuropharmacology
. 2017 May;
121:204-218.
PMID: 28457974
Ionotropic glutamate receptors (iGluRs) mediate fast excitatory neurotransmission and are key nervous system drug targets. While diverse pharmacological tools have yielded insight into iGluR extracellular domain function, less is known...
7.
Ahuja S, Mukund S, Deng L, Khakh K, Chang E, Ho H, et al.
Science
. 2015 Dec;
350(6267):aac5464.
PMID: 26680203
Voltage-gated sodium (Nav) channels propagate action potentials in excitable cells. Accordingly, Nav channels are therapeutic targets for many cardiovascular and neurological disorders. Selective inhibitors have been challenging to design because...
8.
Hanson J, Pare J, Deng L, Smith Y, Zhou Q
Neurobiol Dis
. 2014 Dec;
74:254-62.
PMID: 25484285
GluN2B subunit containing NMDARs (GluN2B-NMDARs) mediate pathophysiological effects of acutely applied amyloid beta (Aβ), including impaired long-term potentiation (LTP). However, in transgenic Alzheimer's disease (AD) mouse models which feature gradual...
9.
Hanson J, Deng L, Hackos D, Lo S, Lauffer B, Steiner P, et al.
J Neurosci
. 2013 Apr;
33(14):5924-9.
PMID: 23554474
Histone deacetylase 2 (HDAC2) negatively regulates excitatory synapse number and memory performance. However, whether HDAC2 regulation of excitatory synapses occurs in a cell-autonomous manner and whether HDAC2 regulates inhibitory synaptic...
10.
Hanson J, Weber M, Meilandt W, Wu T, Luu T, Deng L, et al.
Neuropsychopharmacology
. 2013 Jan;
38(7):1221-33.
PMID: 23340518
Although antagonists to GluN2B-containing N-methyl-D-aspartate receptors (NMDARs) have been widely considered to be neuroprotective under certain pathological conditions, their immediate and lasting impacts on synaptic, circuit, and cognitive functions are...