c-Jun N-Terminal Kinases and Their Pharmacological Modulation in Ischemic and Reperfusion Brain Injury

Shvedova, Maria; Anfinogenova, Yana; Щепеткин, И. А.; Atochin, Dmitriy N.

doi:10.1007/s11055-018-0622-4

Cited by 3 publications

(2 citation statements)

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“…In contrast, in ischemia and reperfusion injury, the inhibition of JNK signaling has been an attractive target to prevent apoptosis for the protection of tissues [ 87 , 88 ]. Inhibiting JNK3 has been proposed for treating ALS as JNK inhibition prevents the apoptosis of motor neurons derived from human iPS cells [ 89 ].…”

Section: Pharmacological Inhibition Of Apoptotic Machinery—implicatiomentioning

confidence: 99%

Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins

2020

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Axonal degeneration and neuronal cell death are fundamental processes in development and contribute to the pathology of neurological disease in adults. Both processes are regulated by BCL-2 family proteins which orchestrate the permeabilization of the mitochondrial outer membrane (MOM). MOM permeabilization (MOMP) results in the activation of pro-apoptotic molecules that commit neurons to either die or degenerate. With the success of small-molecule inhibitors targeting anti-apoptotic BCL-2 proteins for the treatment of lymphoma, we can now envision the use of inhibitors of apoptosis with exquisite selectivity for BCL-2 family protein regulation of neuronal apoptosis in the treatment of nervous system disease. Critical to this development is deciphering which subset of proteins is required for neuronal apoptosis and axon degeneration, and how these two different outcomes are separately regulated. Moreover, noncanonical BCL-2 family protein functions unrelated to the regulation of MOMP, including impacting necroptosis and other modes of cell death may reveal additional potential targets and/or confounders. This review highlights our current understanding of BCL-2 family mediated neuronal cell death and axon degeneration, while identifying future research questions to be resolved to enable regulating neuronal survival pharmacologically.

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Section: Pharmacological Inhibition Of Apoptotic Machinery—implicatiomentioning

confidence: 99%

Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins

2020

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“…Enzymes of the c-Jun N-terminal kinase (JNK) family are known to play an important role in human body functioning [ 2 ]. JNKs are involved in the regulation of inflammation [ 3 ], participate in signaling pathways leading to apoptosis and necrosis [ 4 , 5 ], and regulate some transcriptional and non-transcriptional processes that damage the brain neurons and cardiomyocytes during ischemia/reperfusion [ 6 , 7 ]. JNKs are also involved in the embryonic development of the heart, the regulation of metabolism [ 8 ], and the normal functioning of the myocardium.…”

Section: Introductionmentioning

confidence: 99%

Experimental and Computational Investigation of the Oxime Bond Stereochemistry in c-Jun N-terminal Kinase 3 Inhibitors 11H-Indeno[1,2-b]quinoxalin-11-one Oxime and Tryptanthrin-6-oxime

et al. 2023

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11H-Indeno[1,2-b]quinoxalin-11-one oxime (IQ-1) and tryptanthrin-6-oxime are potent c-Jun N-terminal kinase 3 (JNK-3) inhibitors demonstrating neuroprotective, anti-inflammatory and anti-arthritic activity. However, the stereochemical configuration of the oxime carbon–nitrogen double bond (E- or Z-) in these compounds was so far unknown. In this contribution, we report the results of the determination of the double bond configuration in the solid state by single crystal X-ray diffraction and in solution by 1D and 2D NMR techniques and DFT calculations. It was found that both in the solid state and in solution, IQ-1 adopts the E-configuration stabilized by intermolecular hydrogen bonds, in contrast to previously assumed Z-configuration that could be stabilized only by an intramolecular hydrogen bond.

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Emerging paradigms in nanotechnology for imaging and treatment of cerebral ischemia

Kaviarasi

Yuba

Harada

et al. 2019

Journal of Controlled Release

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c-Jun N-Terminal Kinases and Their Pharmacological Modulation in Ischemic and Reperfusion Brain Injury

Cited by 3 publications

References 64 publications

Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins

Neuronal cell life, death, and axonal degeneration as regulated by the BCL-2 family proteins

Experimental and Computational Investigation of the Oxime Bond Stereochemistry in c-Jun N-terminal Kinase 3 Inhibitors 11H-Indeno[1,2-b]quinoxalin-11-one Oxime and Tryptanthrin-6-oxime

Emerging paradigms in nanotechnology for imaging and treatment of cerebral ischemia

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