Literature summary for 7.1.1.2 extracted from

Alvira, D.; Yeste-Velasco, M.; Folch, J.; Casadesus, G.; Smith, M.A.; Pallas, M.; Camins, A.
Neuroprotective effects of caffeine against complex I inhibition-induced apoptosis are mediated by inhibition of the Atm/p53/E2F-1 path in cerebellar granule neurons (2007), J. Neurosci. Res., 85, 3079-3088.

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Application

Application	Comment	Organism
medicine	enzymes activated by DNA damage, e.g. mediated by complex I inhibition, are an important feature in the process of neuronal apoptosis	Rattus norvegicus

Inhibitors

Inhibitors	Comment	Organism	Structure
1-methyl-4-phenylpyridinium ion	inhibition of mitochondrial complex I. Neuroprotective effects of caffeine in the MPP+ model of apoptosis are mediated through activation of the ataxia telangiectasia mutated enzyme/p53 pathway. Caffeine decreases the expression of cyclin D and the transcription factor E2F-1, a regulator of apoptosis in neurons. Caffeine-mediated neuroprotection is not mediated through blockade of adenosine receptors because DPCPX and CGS-15943, two antagonists of these receptors, fail to attenuate apoptosis produced by 1-methyl-4-phenylpyridinium ion treatment	Rattus norvegicus
additional information	inhibition of mitochondrial complex I by serum and potassium deprivation. Caffeine does not exert neuroprotective effects after serum and potassium withdrawal, a p53-independent model of apoptosis	Rattus norvegicus

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
mitochondrion	-	Rattus norvegicus	5739	-

Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	-	7-day-old Sprague-Dawley rat	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
additional information	cerebellar granule neuron	Rattus norvegicus	-

Synonyms

Synonyms	Comment	Organism
complex I	-	Rattus norvegicus

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Release 2023.1 (January 2023)