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Journal Abstract Search

247 related items for PubMed ID: 37030595

  • 1. N-Terminomic Changes in Neurons During Excitotoxicity Reveal Proteolytic Events Associated With Synaptic Dysfunctions and Potential Targets for Neuroprotection.
    Ameen SS, Griem-Krey N, Dufour A, Hossain MI, Hoque A, Sturgeon S, Nandurkar H, Draxler DF, Medcalf RL, Kamaruddin MA, Lucet IS, Leeming MG, Liu D, Dhillon A, Lim JP, Basheer F, Zhu HJ, Bokhari L, Roulston CL, Paradkar PN, Kleifeld O, Clarkson AN, Wellendorph P, Ciccotosto GD, Williamson NA, Ang CS, Cheng HC.
    Mol Cell Proteomics; 2023 May; 22(5):100543. PubMed ID: 37030595
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  • 2. A truncated fragment of Src protein kinase generated by calpain-mediated cleavage is a mediator of neuronal death in excitotoxicity.
    Hossain MI, Roulston CL, Kamaruddin MA, Chu PWY, Ng DCH, Dusting GJ, Bjorge JD, Williamson NA, Fujita DJ, Cheung SN, Chan TO, Hill AF, Cheng HC.
    J Biol Chem; 2013 Apr 05; 288(14):9696-9709. PubMed ID: 23400779
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  • 4. Conventional protein kinase Cβ-mediated phosphorylation inhibits collapsin response-mediated protein 2 proteolysis and alleviates ischemic injury in cultured cortical neurons and ischemic stroke-induced mice.
    Yang X, Zhang X, Li Y, Han S, Howells DW, Li S, Li J.
    J Neurochem; 2016 May 05; 137(3):446-59. PubMed ID: 26788931
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  • 5. Development of a neuroprotective peptide that preserves survival pathways by preventing Kidins220/ARMS calpain processing induced by excitotoxicity.
    Gamir-Morralla A, López-Menéndez C, Ayuso-Dolado S, Tejeda GS, Montaner J, Rosell A, Iglesias T, Díaz-Guerra M.
    Cell Death Dis; 2015 Oct 22; 6(10):e1939. PubMed ID: 26492372
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  • 6. CaMKII phosphorylates collapsin response mediator protein 2 and modulates axonal damage during glutamate excitotoxicity.
    Hou ST, Jiang SX, Aylsworth A, Ferguson G, Slinn J, Hu H, Leung T, Kappler J, Kaibuchi K.
    J Neurochem; 2009 Nov 22; 111(3):870-81. PubMed ID: 19735446
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  • 7. Prevention of excitotoxicity-induced processing of BDNF receptor TrkB-FL leads to stroke neuroprotection.
    Tejeda GS, Esteban-Ortega GM, San Antonio E, Vidaurre ÓG, Díaz-Guerra M.
    EMBO Mol Med; 2019 Jul 22; 11(7):e9950. PubMed ID: 31273936
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  • 8. Excitotoxic targeting of Kidins220 to the Golgi apparatus precedes calpain cleavage of Rap1-activation complexes.
    López-Menéndez C, Simón-García A, Gamir-Morralla A, Pose-Utrilla J, Luján R, Mochizuki N, Díaz-Guerra M, Iglesias T.
    Cell Death Dis; 2019 Jul 11; 10(7):535. PubMed ID: 31296845
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  • 9. Quantitative proteomic analyses of dynamic signalling events in cortical neurons undergoing excitotoxic cell death.
    Hoque A, Williamson NA, Ameen SS, Ciccotosto GD, Hossain MI, Oakhill JS, Ng DCH, Ang CS, Cheng HC.
    Cell Death Dis; 2019 Mar 01; 10(3):213. PubMed ID: 30824683
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  • 13. A beacon of hope in stroke therapy-Blockade of pathologically activated cellular events in excitotoxic neuronal death as potential neuroprotective strategies.
    Hoque A, Hossain MI, Ameen SS, Ang CS, Williamson N, Ng DC, Chueh AC, Roulston C, Cheng HC.
    Pharmacol Ther; 2016 Apr 01; 160():159-79. PubMed ID: 26899498
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  • 19. Gephyrin Cleavage in In Vitro Brain Ischemia Decreases GABAA Receptor Clustering and Contributes to Neuronal Death.
    Costa JT, Mele M, Baptista MS, Gomes JR, Ruscher K, Nobre RJ, de Almeida LP, Wieloch T, Duarte CB.
    Mol Neurobiol; 2016 Aug 01; 53(6):3513-3527. PubMed ID: 26093381
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