Key Specifications Table
|Application||The NS225 Neurite Outgrowth Assay Kit (1 μm) is based on the use of Millicell cell culture inserts (chambers) containing a permeable membrane with 1 μm pores at the base.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||When stored at 2-8° C, the kit components are stable up to the expiration date. Do not freeze or expose to elevated temperatures. Discard any remaining reagents after the expiration date.|
|Material Size||12 assays|
Neurite Outgrowth Assay Kit (1 µm) SDS
|Reference overview||Pub Med ID|
|Neural progenitor cells derived from adult bone marrow mesenchymal stem cells promote neuronal regeneration.|
Yue Tang,Yong-Chun Cui,Xiao-Juan Wang,Ai-Li Wu,Guang-Fu Hu,Fu-Liang Luo,Jia-Kang Sun,Jing Sun,Li-Ke Wu
Life sciences 91 2012
It is well known that neural stem/progenitor cells (NS/PC) are an ideal cell type for the treatment of central nervous system (CNS) disease. However, ethical problems have severely hampered fetal NS/PC from being widely used as a source for stem cell therapy. Recently, it has been demonstrated that autologous bone marrow mesenchymal stem cells (BMSC) can transdifferentiate into neural progenitor cells (NPC). The biological function of BMSC derived NPC (MDNPC) in neuronal systems remains unknown. In the present study, we aimed to investigate whether MDNPC can promote in vitro neural regeneration, a process comprising mainly the generation of neurons and neurotransmitters.
|Small GTPase Tc10 and its homologue RhoT induce N-WASP-mediated long process formation and neurite outgrowth.|
Abe, Tomoyuki, et al.
J. Cell. Sci., 116: 155-68 (2003) 2003
Rho family small GTPases regulate multiple cellular functions through reorganization of the actin cytoskeleton. Among them, Cdc42 and Tc10 induce filopodia or peripheral processes in cultured cells. We have identified a member of the family, designated as RhoT, which is closely related to Tc10. Tc10 was highly expressed in muscular tissues and brain and remarkably induced during differentiation of C2 skeletal muscle cells and neuronal differentiation of PC12 and N1E-115 cells. On the other hand, RhoT was predominantly expressed in heart and uterus and induced during neuronal differentiation of N1E-115 cells. Tc10 exogenously expressed in fibroblasts generated actin-filament-containing peripheral processes longer than the Cdc42-formed filopodia, whereas RhoT produced much longer and thicker processes containing actin filaments. Furthermore, both Tc10 and RhoT induced neurite outgrowth in PC12 and N1E-115 cells, but Cdc42 did not do this by itself. Tc10 and RhoT as well as Cdc42 bound to the N-terminal CRIB-motif-containing portion of N-WASP and activated N-WASP to induce Arp2/3-complex-mediated actin polymerization. The formation of peripheral processes and neurites by Tc10 and RhoT was prevented by the coexpression of dominant-negative mutants of N-WASP. Thus, N-WASP is essential for the process formation and neurite outgrowth induced by Tc10 and RhoT. Neuronal differentiation of PC12 and N1E-115 cells induced by dibutyryl cyclic AMP and by serum starvation, respectively, was prevented by dominant-negative Cdc42, Tc10 and RhoT. Taken together, all these Rho family proteins are required for neuronal differentiation, but they exert their functions differentially in process formation and neurite extension. Consequently, N-WASP activated by these small GTPases mediates neuronal differentiation in addition to its recently identified role in glucose uptake.
|Spinal cord repair: strategies to promote axon regeneration.|
Neurobiol. Dis., 8: 11-8 (2001) 2001
Neurons in the central nervous system have a remarkable capacity to regenerate their transected axons when provided with an appropriate growth environment. Advances in our understanding of axon regeneration have allowed the development of different experimental strategies to stimulate axon regeneration in animal models of spinal cord injury. Growth inhibitory proteins block axon regeneration in the CNS, and many of these proteins have been identified. Various methods that are now used to stimulate regeneration in the injured spinal cord are directed at overcoming the growth inhibitory environment of the CNS. Three general approaches tested in vivo stimulate regeneration in the spinal cord. First, antibodies that bind inhibitory proteins in myelin allow axon regeneration in the CNS. Second, methods that modulate neuronal intracellular signaling allow axons to grow directly on the inhibitory substrate of the CNS. Third, transplantation of cells to the lesioned spinal cord promotes repair. In this paper we review current advances in each of these research domains.
|Repulsive factors and axon regeneration in the CNS|
Fournier, A E and Strittmatter, S M
Curr Opin Neurobiol, 11:89-94 (2001) 2001
|Axon regeneration: Vaccinating against spinal cord injury|
Filbin, M T
Curr Biol, 10:R100-R103 (2000) 2000
|Glial inhibition of nerve regeneration in the mature mammalian CNS.|
Qiu, J, et al.
Glia, 29: 166-74 (2000) 2000
The lack of axonal regeneration in the adult mammalian CNS is due to both unfavorable environmental glial factors and the intrinsic neuronal state. Inhibitors associated with myelin and the glial scar have been extensively studies and it has been shown that neutralizing at least some of the inhibitors can lead to improved growth. Meanwhile, important advances have also been made towards our understanding of the neuronal intrinsic state, particularly the intracellular levels of cyclic nucleotide, that influence the capacity of mature CNS neurons to initiate and maintain a regrowth response. It is well recognized that successful regeneration may only be achieved by application of a combination of strategies that both block glial inhibitors and enhance the intrinsic neuronal growth capacity.
|Extracellular matrix allows PC12 neurite elongation in the absence of microtubules|
Lamoureux, P, et al.
J Cell Biol, 110:71-79 (1990) 1990
|Nerve growth factor-induced neurite outgrowth in PC12 cells involves the coordinate induction of microtubule assembly and assembly-promoting factors|
Drubin, D G, et al
J Cell Biol, 101:1799-1807 (1985) 1985
|Poster: High Throughput Screening To Identify Novel Molecular Pathways Involved In Neurite Outgrowth|