prikaz prve stranice dokumenta Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse
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Scientific paper - Original scientific paper
Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse
Neuroscience Letters, 597 (2015); 176-82. https://doi.org/10.1016/j.neulet.2015.04.042
Gorup, Dunja; Bohaček, Ivan; Miličević, Tena; Pochet, Roland; Mitrečić, Dinko; Križ, Jasna; Gajović, Srećko

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Gorup, D., Bohaček, I., Miličević, T., Pochet, R., Mitrečić, D., Križ, J. & Gajović, S. (2015). Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse. Neuroscience Letters, 597., 176-82. doi: 10.1016/j.neulet.2015.04.042

Gorup, Dunja, et al. "Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse." Neuroscience Letters, vol. 597, 2015, pp. 176-82. https://doi.org/10.1016/j.neulet.2015.04.042

Gorup, Dunja, Ivan Bohaček, Tena Miličević, Roland Pochet, Dinko Mitrečić, Jasna Križ and Srećko Gajović. "Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse." Neuroscience Letters 597 (2015): 176-82. https://doi.org/10.1016/j.neulet.2015.04.042

Gorup, D., et al. (2015) 'Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse', Neuroscience Letters, 597, pp. 176-82. doi: 10.1016/j.neulet.2015.04.042

Gorup D, Bohaček I, Miličević T, Pochet R, Mitrečić D, Križ J, and sur.. Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse. Neuroscience Letters [Internet]. 2015 June 15 [cited 2024 May 15];597:176-82. doi: 10.1016/j.neulet.2015.04.042

D. Gorup, et al., "Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse", Neuroscience Letters, vol. 597, pp. 176-82, June 2015. [Online]. Available at: https://urn.nsk.hr/urn:nbn:hr:105:897203. [Accessed: 15 May 2024]

Metadata
Title (english)Increased expression and colocalization of GAP43 and CASP3 after brain ischemic lesion in mouse
AuthorDunja Gorup
AuthorIvan Bohaček
AuthorTena Miličević
AuthorRoland Pochet
AuthorDinko Mitrečić
AuthorJasna Križ
AuthorSrećko Gajović
Author's institutionUniversity of Zagreb
School of Medicine
Scientific / art field,
discipline and subdiscipline		BIOMEDICINE AND HEALTHCARE
Basic Medical Sciences
Abstract (english)
GAP43 is a protein involved in neurite outgrowth during development and axon regeneration reflecting its presynaptic localization in developing neurons. Recently, it has been demonstrated that GAP43 is a ligand of CASP3 involved in receptor endocytosis and is also localized post-synaptically. In this study, by using a transgenic mouse strain carrying a bioluminescent reporter for GAP43 combined with an in vivo bioluminescence assay for CASP3, we demonstrated that one day after brain ischemic lesion and, even more pronounced, four days after stroke, expression of both CASP3 and Gap43 in neurons increased more than 40 times. The in vivo approach of CASP3 and GAP43 colocalization imaging was further validated and quantified by immunofluorescence. Importantly, in 82% of GAP43 positive cells, colocalization with CASP3 was present. These findings suggested that one and four days after stroke CASP3 expression, not necessarily associated with neuronal death, increased and suggested that CASP3 and GAP43 might be part of a common molecular pathway involved in early response to ischemic events occurring after onset of stroke.
Keywords (english)
Languageenglish
Publication typeScientific paper - Original scientific paper
Publication statusPublished
Peer reviewPeer review
Publication versionPublished version
Journal titleNeuroscience Letters
Numberingvol. 597, pp. 176-82
p-ISSN0304-3940
DOIhttps://doi.org/10.1016/j.neulet.2015.04.042
URN:NBNurn:nbn:hr:105:897203
Publication2015-06-15
Document URLhttps://doi.org/10.1016/j.neulet.2015.04.042
Type of resourceText
Access conditionsOpen access
Terms of useLicence In copyright icon
Created on2024-03-28 08:10:50