2000
DOI: 10.1016/s0304-3940(00)01024-7
|View full text |Cite
|
Sign up to set email alerts
|

c-Jun N-terminal kinase (JNK) and JNK interacting protein response in rat brain after transient middle cerebral artery occlusion

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1

Citation Types

1
52
0
1

Year Published

2002
2002
2014
2014

Publication Types

Select...
5
3

Relationship

0
8

Authors

Journals

citations
Cited by 71 publications
(54 citation statements)
references
References 17 publications
1
52
0
1
Order By: Relevance
“…[25][26][27] In this study, we extended these observations by demonstrating the presence of IB1/JIP-1 in human AD brain colocalized with JNK and phosphorylated tau proteins in neurofibrillary tangles. IB1/JIP-1 interacts with many cellular components including the reelin receptor ApoER2, LRP, a-synuclein, 190 RhoGEF, kinesin and APP [13][14][15][16][17][18]40 .…”
Section: Discussionsupporting
confidence: 63%
See 1 more Smart Citation
“…[25][26][27] In this study, we extended these observations by demonstrating the presence of IB1/JIP-1 in human AD brain colocalized with JNK and phosphorylated tau proteins in neurofibrillary tangles. IB1/JIP-1 interacts with many cellular components including the reelin receptor ApoER2, LRP, a-synuclein, 190 RhoGEF, kinesin and APP [13][14][15][16][17][18]40 .…”
Section: Discussionsupporting
confidence: 63%
“…25 In vivo, following a transient middle cerebral occlusion, the expression of IB1/JIP-1 and JNK is enhanced 8 h during reperfusion. 26 It has been also reported that JNK activation is increased following transient global focal ischaemia, in particular in the CA1 neurons of the hippocampus. 27 In other cell systems, IB1/JIP-1 was shown to be downregulated once cells were exposed to various stresses such as UV, cytokines, parietal stress or starving 10,28 .…”
Section: Introductionmentioning
confidence: 95%
“…Evidence has accumulated showing that the JNK signaling pathway is activated during focal ischemia (Herdegen et al, 1998;Hayashi et al, 2000). MCA occlusion provokes a strong expression of p-c-Jun that became detectable 3 h after the onset of ischemia and was maximal at 72 h. Although the mechanism of action of AS601245 has not been studied in the model of focal ischemia, these previous studies support the hypothesis that the pharmacological efficacy of AS601245 could be due to JNK inhibition.…”
Section: Discussionmentioning
confidence: 79%
“…It is interesting to note that increased JNK phosphorylation has been reported 15 min after global ischemia in the gerbil (Ferrer et al, 1997;Sugino et al, 2000;Tsuji et al, 2000), and increased phospho-c-Jun levels were detected in the hippocampus after 15 min of global ischemia in rats (Gillardon et al, 1999;Hu et al, 2000). Increased activity of the JNK signaling pathways was also observed after focal ischemia (Herdegen et al, 1998;Hayashi et al, 2000). Supporting the idea that neuronal death-induced by ischemia is in part due to JNK activation, Tsuji et al (2000) have demonstrate that the neuroprotective effect of ␣-phenyl-N-tert-butylnitrone, a spin trap agent, on the CA1 region of hippocampus after global ischemia, is due to its ability to block JNK activation.…”
mentioning
confidence: 85%
“…JNK2 is a negative regulator of cell proliferation, whereas JNK1 seems to be a positive regulator (17). Finally, JNK3 deficiency protects against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced dopaminergic cell loss (18), kainic acid-induced seizures (19), stroke (20), oxidative stress (21,22), nerve growth factor deprivation (21), and ␤-amyloid-induced neuronal death (23).…”
mentioning
confidence: 99%