Type 3 inositol 1,4,5-trisphosphate receptor modulates cell death

Research output: Contribution to journalArticle

Abstract

Mechanisms accounting for the cellular entry of calcium that mediates cellular proliferation and apoptosis have been obscure. Previously we reported selective augmentation of type 3 inositol (1,4,5) trisphosphate receptors (IP3R3) in lymphocytes undergoing programmed cell death, which was prevented by antisense constructs to IP3R3. We now report increases in mRNA and protein levels for IP3R3 associated with cell death in several apoptotic paradigms in diverse tissues. Elevations of IP3R3 occur during developmental apoptosis in early postnatal cerebellar granule cells, dorsal root ganglia, embryonic hair follicles, and intestinal villi. Neurotoxic damage elicited by the glutamate agonist kainate is also associated with IP3R3 augmentation. In chick dorsal root ganglia neurons undergoing apoptosis due to deprivation of nerve growth factor, levels of IP3R3 are selectively increased and cell death is selectively prevented by antisense oligonucleotides to IP3R3. Thus, IP3R3 appears to participate actively in cell death in a diversity of tissues.

Original languageEnglish (US)
Pages (from-to)1375-1379
Number of pages5
JournalFASEB Journal
Volume14
Issue number10
StatePublished - 2000

Fingerprint

Inositol 1,4,5-Trisphosphate Receptors
Cell death
cell death
Cell Death
apoptosis
receptors
Spinal Ganglia
Apoptosis
Tissue
Excitatory Amino Acid Agonists
nerve growth factor
hair follicles
Lymphocytes
Hair Follicle
Antisense Oligonucleotides
Kainic Acid
Nerve Growth Factor
villi
oligonucleotides
glutamates

Keywords

  • Dorsal root ganglia
  • IPR3 expression
  • Nerve growth factor
  • PCD

ASJC Scopus subject areas

  • Agricultural and Biological Sciences (miscellaneous)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry
  • Cell Biology

Cite this

Type 3 inositol 1,4,5-trisphosphate receptor modulates cell death. / Blackshaw, Seth; Sawa, Akira; Sharp, Alan H.; Ross, Christopher A; Snyder, Solomon H; Khan, Adil A.

In: FASEB Journal, Vol. 14, No. 10, 2000, p. 1375-1379.

Research output: Contribution to journalArticle

@article{65ce600f70794d85b39f8ce204768038,
title = "Type 3 inositol 1,4,5-trisphosphate receptor modulates cell death",
abstract = "Mechanisms accounting for the cellular entry of calcium that mediates cellular proliferation and apoptosis have been obscure. Previously we reported selective augmentation of type 3 inositol (1,4,5) trisphosphate receptors (IP3R3) in lymphocytes undergoing programmed cell death, which was prevented by antisense constructs to IP3R3. We now report increases in mRNA and protein levels for IP3R3 associated with cell death in several apoptotic paradigms in diverse tissues. Elevations of IP3R3 occur during developmental apoptosis in early postnatal cerebellar granule cells, dorsal root ganglia, embryonic hair follicles, and intestinal villi. Neurotoxic damage elicited by the glutamate agonist kainate is also associated with IP3R3 augmentation. In chick dorsal root ganglia neurons undergoing apoptosis due to deprivation of nerve growth factor, levels of IP3R3 are selectively increased and cell death is selectively prevented by antisense oligonucleotides to IP3R3. Thus, IP3R3 appears to participate actively in cell death in a diversity of tissues.",
keywords = "Dorsal root ganglia, IPR3 expression, Nerve growth factor, PCD",
author = "Seth Blackshaw and Akira Sawa and Sharp, {Alan H.} and Ross, {Christopher A} and Snyder, {Solomon H} and Khan, {Adil A.}",
year = "2000",
language = "English (US)",
volume = "14",
pages = "1375--1379",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "10",

}

TY - JOUR

T1 - Type 3 inositol 1,4,5-trisphosphate receptor modulates cell death

AU - Blackshaw, Seth

AU - Sawa, Akira

AU - Sharp, Alan H.

AU - Ross, Christopher A

AU - Snyder, Solomon H

AU - Khan, Adil A.

PY - 2000

Y1 - 2000

N2 - Mechanisms accounting for the cellular entry of calcium that mediates cellular proliferation and apoptosis have been obscure. Previously we reported selective augmentation of type 3 inositol (1,4,5) trisphosphate receptors (IP3R3) in lymphocytes undergoing programmed cell death, which was prevented by antisense constructs to IP3R3. We now report increases in mRNA and protein levels for IP3R3 associated with cell death in several apoptotic paradigms in diverse tissues. Elevations of IP3R3 occur during developmental apoptosis in early postnatal cerebellar granule cells, dorsal root ganglia, embryonic hair follicles, and intestinal villi. Neurotoxic damage elicited by the glutamate agonist kainate is also associated with IP3R3 augmentation. In chick dorsal root ganglia neurons undergoing apoptosis due to deprivation of nerve growth factor, levels of IP3R3 are selectively increased and cell death is selectively prevented by antisense oligonucleotides to IP3R3. Thus, IP3R3 appears to participate actively in cell death in a diversity of tissues.

AB - Mechanisms accounting for the cellular entry of calcium that mediates cellular proliferation and apoptosis have been obscure. Previously we reported selective augmentation of type 3 inositol (1,4,5) trisphosphate receptors (IP3R3) in lymphocytes undergoing programmed cell death, which was prevented by antisense constructs to IP3R3. We now report increases in mRNA and protein levels for IP3R3 associated with cell death in several apoptotic paradigms in diverse tissues. Elevations of IP3R3 occur during developmental apoptosis in early postnatal cerebellar granule cells, dorsal root ganglia, embryonic hair follicles, and intestinal villi. Neurotoxic damage elicited by the glutamate agonist kainate is also associated with IP3R3 augmentation. In chick dorsal root ganglia neurons undergoing apoptosis due to deprivation of nerve growth factor, levels of IP3R3 are selectively increased and cell death is selectively prevented by antisense oligonucleotides to IP3R3. Thus, IP3R3 appears to participate actively in cell death in a diversity of tissues.

KW - Dorsal root ganglia

KW - IPR3 expression

KW - Nerve growth factor

KW - PCD

UR - http://www.scopus.com/inward/record.url?scp=0033945128&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0033945128&partnerID=8YFLogxK

M3 - Article

C2 - 10877830

AN - SCOPUS:0033945128

VL - 14

SP - 1375

EP - 1379

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 10

ER -