PMID- 10479680
OWN - NLM
STAT- MEDLINE
DCOM- 19991004
LR  - 20191023
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 19
IP  - 18
DP  - 1999 Sep 15
TI  - Neuronal interleukin-16 (NIL-16): a dual function PDZ domain protein.
PG  - 7770-80
AB  - Interleukin (IL)-16 is a proinflammatory cytokine that has attracted widespread
      attention because of its ability to block HIV replication. We describe the
      identification and characterization of a large neuronal IL-16 precursor, NIL-16. 
      The N-terminal half of NIL-16 constitutes a novel PDZ domain protein sequence,
      whereas the C terminus is identical with splenocyte-derived mouse pro-IL-16.
      IL-16 has been characterized only in the immune system, and the identification of
      NIL-16 marks a previously unsuspected connection between the immune and the
      nervous systems. NIL-16 is a cytosolic protein that is detected only in neurons
      of the cerebellum and the hippocampus. The N-terminal portion of NIL-16 interacts
      selectively with a variety of neuronal ion channels, which is similar to the
      function of many other PDZ domain proteins that serve as intracellular
      scaffolding proteins. Among the NIL-16-interacting proteins is the class C alpha1
      subunit of a mouse brain calcium channel (mbC alpha1). The C terminus of NIL-16
      can be processed by caspase-3, resulting in the release of secreted IL-16.
      Furthermore, in cultured cerebellar granule neurons undergoing apoptosis, NIL-16 
      proteolysis parallels caspase-3 activation. Cerebellar granule neurons express
      the IL-16 receptor CD4. Exposure of these cells to IL-16 induces expression of
      the immediate-early gene, c-fos, via a signaling pathway that involves tyrosine
      phosphorylation. This suggests that IL-16 provides an autocrine function in the
      brain. Therefore, we hypothesize that NIL-16 is a dual function protein in the
      nervous system that serves as a secreted signaling molecule as well as a
      scaffolding protein.
FAU - Kurschner, C
AU  - Kurschner C
AD  - Department of Developmental Neurobiology, Saint Jude Children's Research
      Hospital, Memphis, Tennessee 38105, USA.
FAU - Yuzaki, M
AU  - Yuzaki M
LA  - eng
GR  - P30 CA21765/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for
      Neuroscience
JID - 8102140
RN  - 0 (Interleukin-16)
RN  - 0 (Ion Channels)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Recombinant Proteins)
RN  - 0 (neuronal interleukin-16)
SB  - IM
MH  - Aging/metabolism
MH  - Amino Acid Sequence
MH  - Animals
MH  - Cells, Cultured
MH  - Cerebellum/growth & development/*metabolism
MH  - Cloning, Molecular
MH  - Gene Expression Regulation, Developmental
MH  - Gene Library
MH  - Hippocampus/growth & development/metabolism
MH  - Interleukin-16/*chemistry/genetics/*metabolism/pharmacology
MH  - Ion Channels/metabolism
MH  - Mice
MH  - Molecular Sequence Data
MH  - Nerve Tissue Proteins/*chemistry/genetics/*metabolism/pharmacology
MH  - Neurons/cytology/drug effects/*metabolism
MH  - Recombinant Proteins/chemistry/metabolism
MH  - Saccharomyces cerevisiae
PMC - PMC6782450
EDAT- 1999/09/10 00:00
MHDA- 1999/09/10 00:01
CRDT- 1999/09/10 00:00
PHST- 1999/09/10 00:00 [pubmed]
PHST- 1999/09/10 00:01 [medline]
PHST- 1999/09/10 00:00 [entrez]
PST - ppublish
SO  - J Neurosci. 1999 Sep 15;19(18):7770-80.