CEP-1347/KT7515 prevents motor neuronal programmed cell death and injury-induced dedifferentiationin vivo
✍ Scribed by Glicksman, M. A. ;Chiu, A. Y. ;Dionne, C. A. ;Harty, M. ;Kaneko, M. ;Murakata, C. ;Oppenheim, R. W. ;Prevette, D. ;Sengelaub, D. R. ;Vaught, J. L. ;Neff, N. T.
- Book ID
- 101259223
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 140 KB
- Volume
- 35
- Category
- Article
- ISSN
- 0022-3034
No coin nor oath required. For personal study only.
✦ Synopsis
CEP-1347, also known as KT7515, 1347/KT7515 during the 4-day postnatal window of a derivative of a natural product indolocarbazole, inmotor neuronal death resulted in persistent long-term hibited motor neuronal death in vitro, inhibited activamotor neuronal survival in adult animals that received tion of the stress-activated kinase JNK1 (c-jun NH no additional CEP-1347/KT7515. In a model of adult terminal kinase) in cultured spinal motor neurons, motor neuronal dedifferentiation following axotomy, but had no effect on the mitogen-activated protein local application of CEP-1347/KT7515 to the trankinase ERK1 in these cells. Results reported here prosected hypoglossal nerve substantially reduced the loss file the functional activity of CEP-1347/KT7515 in of choline acetyl transferase immunoreactivity obvivo in models of motor neuronal death or dedifferenserved 7 days postaxotomy compared to untreated antiation. Application of CEP-1347/KT7515 to the choimals. Results from these experiments demonstrate rioallantoic membrane of embryonic chicks rescued that a small organic molecule that inhibits a signaling 40% of the lumbar motor neurons that normally die pathway associated with stress and injury also reduces during the developmental period assessed. Peripheral neuronal death and degeneration in vivo. ᭧ 1998 John administration of low doses (0.5 and 1 mg/kg daily)