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CHAT — IGF1

Text-mined interactions from Literome

Corse et al., Neurobiol Dis 1999 (Motor Neuron Disease...) : Using organotypic spinal cord cultures from postnatal rats, we have demonstrated that insulin-like growth factor-I (IGF-I) and glial derived neurotrophic factor (GDNF) significantly increase choline acetyltransferase (ChAT) activity, but brain derived neurotrophic factor (BDNF), neurotrophin-4 ( NT-4/5 ), and neurotrophin-3 (NT-3) do not
Guan et al., Neuroscience 2000 (Brain Ischemia) : Insulin-like growth factor-1 markedly prevented the loss of calbindin-28kd ( n = 7, P < 0.05 ), choline acetyltransferase ( n = 7, P < 0.05 ), neuropeptide Y ( n = 7, P < 0.05 ), neuronal nitric oxide synthase ( n = 8, P < 0.05 ) and glutamate acid decarboxylase ( n = 9, P < 0.05 ) immunopositive neurons, but failed to protect parvalbumin ( n = 6 ) immunopositive neurons
Brass et al., J Neurochem 1992 : Insulin-like growth factor-1 (IGF-1) reduced ChAT activity at concentrations 10-fold lower than insulin, suggesting that insulin 's effect on ChAT may involve the IGF-1 receptor
Rivera et al., J Alzheimers Dis 2005 (Alzheimer Disease...) : Further studies demonstrated that : 1 ) ChAT expression increases with insulin or IGF-I stimulation ; 2 ) ChAT is expressed in insulin and IGF-I receptor positive cortical neurons ; and 3 ) ChAT co-localization in insulin or IGF-I receptor positive neurons is reduced in AD
McManaman et al., J Neurochem 1991 (Neuroblastoma) : In contrast, neither insulin-like growth factor-1 , epidermal growth factor, nor nerve growth factor affected the ChAT activity of LA-N-2 cells
Konishi et al., Brain Res 1994 : IGFI also stimulated ChAT activity, but with less potency than IGFII