The novel neurotrophin-regulated neuronal development-associated protein, NDAP, mediates apoptosis.

Item request has been placed! ×
Item request cannot be made. ×
loading   Processing Request
Read More Add to Saved list
  • Author(s): Li HL;Li HL; Li Z; Qin LY; Liu S; Lau LT; Han JS; Yu AC
  • Source:
    FEBS letters [FEBS Lett] 2006 Mar 20; Vol. 580 (7), pp. 1723-8. Date of Electronic Publication: 2006 Feb 20.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: John Wiley & Sons Ltd Country of Publication: England NLM ID: 0155157 Publication Model: Print-Electronic Cited Medium: Print ISSN: 0014-5793 (Print) Linking ISSN: 00145793 NLM ISO Abbreviation: FEBS Lett Subsets: MEDLINE
    • Publication Information:
      Publication: Jan. 2016- : West Sussex : John Wiley & Sons Ltd.
      Original Publication: Amsterdam, North-Holland on behalf of the Federation of European Biochemical Societies.
    • Subject Terms:
      Apoptosis*; Acyltransferases/*physiology ; Nerve Tissue Proteins/*physiology ; Neurons/*cytology ; Neurons/*metabolism; Acyltransferases/analysis ; Acyltransferases/genetics ; Animals ; Astrocytes/chemistry ; Astrocytes/metabolism ; Base Sequence ; Brain Chemistry ; Cells, Cultured ; Cerebral Cortex ; Gene Expression Regulation/drug effects ; Growth Substances/pharmacology ; Hippocampus ; Mice ; Mice, Inbred ICR ; Molecular Sequence Data ; Nerve Tissue Proteins/analysis ; Nerve Tissue Proteins/genetics ; Neurons/chemistry ; Neurotrophin 3/pharmacology ; RNA, Messenger/analysis ; Time Factors ; Tissue Distribution
    • Abstract:
      We identified a novel gene and named it, "neuronal development-associated protein (NDAP)". We detected NDAP mRNA presence in most tissues including the brain where it was present in the area from the external granular layer to the multiform layer in the cerebral cortex, and in CA1, CA2, CA3 and the dentate gyrus in the hippocampus. Its expression increased transiently in primary cultures of 2-4 day neurons and 1-2 week astrocytes and was significantly reduced in older cultures. Treatment by the neurotrophin, NT-3, significantly attenuated the decline of NDAP in neurons from days 2 to 10, whereas growth factors such as GDNF and insulin, and high potassium levels did not. To elucidate the effects of neurotrophins, we treated day 5 neurons with NT-3, BDNF or NGF for 48 h. NT-3 and BDNF both inhibited downregulation of NDAP mRNA levels but NGF slightly enhanced the already present downregulation; this effect of NGF was significant when examined in day 3 neurons. To investigate the potential function of NDAP, we over-expressed an NDAP-EGFP fusion protein in 4-week-old astrocytes. The newly expressed NDAP gradually aggregated into membrane-bound structures and eventually led to cell death through apoptosis by 24 h. Significant levels of cell death were also observed in NDAP-EGFP transfected HEK293 cells. Thus maintenance of high NDAP levels may cause apoptosis. The different regulations of NDAP expression by neurotrophins indicate that the expression of NDAP might be a checkpoint for apoptosis during neuronal development.
    • Molecular Sequence:
      GENBANK AJ308886
    • Accession Number:
      0 (Growth Substances)
      0 (Nerve Tissue Proteins)
      0 (Neurotrophin 3)
      0 (RNA, Messenger)
      EC 2.3.- (Acyltransferases)
      EC 2.3.2.- (COOH-terminal signal transamidase)
    • Publication Date:
      Date Created: 20060307 Date Completed: 20060607 Latest Revision: 20061115
    • Publication Date:
      20221213
    • Accession Number:
      10.1016/j.febslet.2006.02.022
    • Accession Number:
      16516892