|1.||Tetzlaff, Wolfram: 4 articles (05/2007 - 04/2002)|
|2.||Ohtori, Seiji: 3 articles (04/2010 - 12/2004)|
|3.||Takahashi, Kazuhisa: 3 articles (04/2010 - 12/2004)|
|4.||Perrone-Bizzozero, Nora I: 3 articles (12/2007 - 02/2005)|
|5.||Kwon, Brian K: 3 articles (05/2007 - 04/2002)|
|6.||Liu, Jie: 3 articles (05/2007 - 09/2004)|
|7.||Kleinman, J E: 3 articles (09/2003 - 02/2001)|
|8.||Hyde, T M: 3 articles (09/2003 - 02/2001)|
|9.||Nagashima, Mikiko: 2 articles (01/2014 - 07/2008)|
|10.||Mawatari, Kazuhiro: 2 articles (01/2014 - 07/2008)|
02/01/2014 - "Notably, GAP-43 levels in the cervical spinal cord were significantly increased after FL-SMC lesion, but the temporal window of elevated structural plasticity was more finite in spinal cord relative to ipsilesional cortical expression (returning to baseline levels by 28 post-stroke). "
02/01/2014 - "Growth-associated protein 43 (GAP-43), measured at 3, 7, 14, or 28 days after photothrombotic stroke of the forelimb sensorimotor cortex (FL-SMC) to provide an index of periods of heightened structural plasticity, varied as a function of lesion size and time after stroke in the cortical hemispheres and the spinal cord. "
03/01/2014 - "Relative to controls, melatonin-treated stroke animals caused a significant improvement in GAP-43 and PSD-95 expressions as well as the MMP-9 activity in the ischemic brain (P<0.05). "
12/01/2013 - "Despite the unaltered infarct size in nude rats, IPostC increased levels of phosphorylated Akt (p-Akt) and Akt isoforms (Akt1, Akt2, Akt3), and p-mTOR, p-S6K and p-4EBP1 in the mTOR pathway, as well as growth associated Protein 43 (GAP43), both in the peri-infarct area and core, 24 h after stroke. "
03/01/2014 - "Together, melatonin upregulates GAP-43, PSD-95, and MMP-9 proteins, which likely accounts for its actions to improve neuroplasticity in cultured neurons exposed to glutamate excitotoxicity and to enhance long-term neuroprotection, neuroplasticity, and brain remodeling in stroke rats."
|2.||Schizophrenia (Dementia Praecox)
02/01/2012 - "Our study lends support to the hypothesis of multiple rare mutations in schizophrenia, and it provides genetic clues that indicate the involvement of GAP-43 in this disorder."
02/01/2012 - "We searched for genetic variants in the promoter region and 3 exons (including both UTR ends) of the GAP-43 gene using direct sequencing in a sample of patients with schizophrenia (n=586) and non-psychotic controls (n=576), both being Han Chinese from Taiwan, and conducted an association and functional study. "
02/01/2012 - "In this study, we investigated the involvement of the gene encoding GAP-43 in the susceptibility to schizophrenia. "
02/01/2012 - "In earlier reports, growth-associated protein 43 (GAP-43) has been shown to be critical for initial establishment or reorganization of synaptic connections, a process thought to be disrupted in schizophrenia. "
02/01/2012 - "Genetic and functional analysis of the gene encoding GAP-43 in schizophrenia."
09/01/2011 - "The expressions of bFGF and GAP-43 increased significantly in the boundary zone of the infarction area when compared to model group. "
11/01/1998 - "The GAP-43 was elevated to statistically significant levels in forelimb, hindlimb, and parietal neocortical regions ipsilateral to the infarction only at days 3, 7, and 14. "
11/01/1995 - "The GAP-43 was elevated to statistically significant levels in forelimb, hindlimb, and parietal neocortical regions medial and lateral to the infarction only at days 3, 7, and 14. "
11/12/1993 - "We hypothesize that this increase in GAP-43 reaction product is due to axonal sprouting in the cortex surrounding an area of infarction. "
09/01/2011 - "The possible mechanism of protecting neuronal injury of IA may be related to inhibition on neuronal apoptosis, upregulation of bFGF and GAP-43, and neurogenesis in boundary zone of infarction after cerebral ischemia-reperfusion."
10/27/2011 - "GAP-43 up-regulation in VCN was significantly greater in Noise-No-Tinnitus rats than in Noise-Tinnitus rats. "
10/27/2011 - "Our results suggest that noise-induced tinnitus is suppressed by strong up-regulation of GAP-43 in the medial VCN. "
10/27/2011 - "One Noise-No-Tinnitus rat showed no up-regulation of GAP-43 in auditory nerve fibers and only little VCN shrinkage, suggesting that auditory nerve degeneration plays a role in tinnitus generation. "
|5.||Alzheimer Disease (Alzheimer's Disease)
01/01/2000 - "Growth-associated protein GAP-43 in the frontal cortex and in the hippocampus in Alzheimer's disease: an immunohistochemical and quantitative study."
03/06/1992 - "In the present study, involvement of APP in aberrant sprouting in Alzheimer's disease (AD) was studied by comparing immunolabeling patterns of anti-APP and anti-growth-associated protein 43 (anti-GAP43). "
02/01/1996 - "The preservation of normal GAP-43 message levels in the cerebellum in AD is consistent with the hypothesis that events related to NFT formation have a major impact on the expression of GAP-43 in Alzheimer's disease."
02/01/1996 - "Gap-43 message levels in anterior cerebellum in Alzheimer's disease."
10/01/1995 - "The widespread aberrant neuritic growth accompanied by impaired synaptic plasticity in Alzheimer's disease (AD) suggests that abnormal GAP-43 gene expression may contribute to the cascade of neurodegeneration. "
|1.||Messenger RNA (mRNA)
|2.||Nerve Growth Factor (NGF)
|3.||Brain-Derived Neurotrophic Factor (BDNF)
|4.||Nerve Growth Factors (Neurotrophins)
|10.||GAP-43 Protein (GAP 43 Protein)
|3.||Transplantation (Transplant Recipients)