نتایج جستجو برای: artemin

تعداد نتایج: 155  

Journal: :Neuron 1999
Jinsuke Nishino Kyoko Mochida Yasuhisa Ohfuji Takuya Shimazaki Chikara Meno Sachiko Ohishi Yoichi Matsuda Hideta Fujii Yukio Saijoh Hiroshi Hamada

GFR alpha3 is a component of the receptor for the neurotrophic factor artemin. The role of GFR alpha3 in nervous system development was examined by generating mice in which the Gfr alpha3 gene was disrupted. The Gfr alpha3-/- mice exhibited severe defects in the superior cervical ganglion (SCG), whereas other ganglia appeared normal. SCG precursor cells in the mutant embryos failed to migrate t...

Journal: :Development 2001
H Enomoto P A Crawford A Gorodinsky R O Heuckeroth E M Johnson J Milbrandt

Sympathetic axons use blood vessels as an intermediate path to reach their final target tissues. The initial contact between differentiating sympathetic neurons and blood vessels occurs following the primary sympathetic chain formation, where precursors of sympathetic neurons migrate and project axons along or toward blood vessels. We demonstrate that, in Ret-deficient mice, neuronal precursors...

Journal: :European Journal of Biochemistry 1990

Journal: :Molecular and cellular biology 2006
Stefanie M Hauck Norbert Kinkl Cornelia A Deeg Magdalena Swiatek-de Lange Stephanie Schöffmann Marius Ueffing

Apoptotic cell death of photoreceptors is the final event leading to blindness in the heterogeneous group of inherited retinal degenerations. GDNF (glial cell-line-derived neurotrophic factor) was found to rescue photoreceptor function and survival very effectively in an animal model of retinal degeneration (M. Frasson, S. Picaud, T. Leveillard, M. Simonutti, S. Mohand-Said, H. Dreyfus, D. Hick...

2012
Xavier Fontana Mariya Hristova Clive Da Costa Smriti Patodia Laura Thei Milan Makwana Bradley Spencer-Dene Morwena Latouche Rhona Mirsky Kristjan R. Jessen Rüdiger Klein Gennadij Raivich Axel Behrens

The AP-1 transcription factor c-Jun is a master regulator of the axonal response in neurons. c-Jun also functions as a negative regulator of myelination in Schwann cells (SCs) and is strongly reactivated in SCs upon axonal injury. We demonstrate here that, after injury, the absence of c-Jun specifically in SCs caused impaired axonal regeneration and severely increased neuronal cell death. c-Jun...

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