An NF-κB-like transcription factor in axoplasm is rapidly inactivated after nerve injury in Aplysia

Journal of Neuroscience

Volumn 17, Issue 13, 1997, Pages 4915-4920

  Povelones, Michael ^a   Tran, Kathy ^a   Thanos, Dimitris ^a   Ambron, Richard T ^a,b  

^a Columbia University ^*  (United States)

^b NewYork Presbyterian Hospital   (United States)

Author keywords

Axon injury; Axoplasm; DNA binding; Injury signal; NF B; Nuclear localization signal; Transcription factor

Indexed keywords

BETA INTERFERON; MAJOR HISTOCOMPATIBILITY ANTIGEN CLASS 1; TRANSCRIPTION FACTOR; CARRIER PROTEIN; IMMUNOGLOBULIN ENHANCER BINDING PROTEIN; SEROTONIN;

ANIMAL CELL; APLYSIA; ARTICLE; AXOPLASM; DNA BINDING; ENHANCER REGION; GENETIC TRANSCRIPTION; ISOTOPE LABELING; MAMMAL; NERVE INJURY; NONHUMAN; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; SYNAPTIC TRANSMISSION; ANIMAL; CYTOPLASM; DRUG EFFECT; HUMAN; METABOLISM; NERVE FIBER; NERVOUS SYSTEM INJURY; PHYSIOLOGY; TIME;

ANIMALS; APLYSIA; AXONS; CARRIER PROTEINS; CYTOPLASM; HUMANS; NF-KAPPA B; SEROTONIN; TIME FACTORS; TRAUMA, NERVOUS SYSTEM;

EID: 0030610403     PISSN: 02706474     EISSN: None     Source Type: Journal    
DOI: 10.1523/jneurosci.17-13-04915.1997     Document Type: Article

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