NDLI: Activation of LA-N-2 Cell Phospholipase D by Amyloid Beta Protein (25

Content Provider	Springer Nature Link
Author	Singh, Indrapal N. Sorrenti, Giuseppe Kanfer, Julian N.
Copyright Year	1998
Abstract	Amyloid β protein is the major protein component of neuritic plaques found in the brain of Alzheimer's disease. The activation of phospholipase D by amyloid beta protein (25–35), quisqualate and phorbol 12, 13-dibutyrate was investigated in LA-N-2 cells by measuring phosphatidylethanol formation. The activation of phospholipase D by quisqualate and AβP (25–35) was calcium-independent. The AβP (25–35) and quisqualate activation of phospholipase D appeared to be mediated through a pertussis toxin-sensitive GTP-binding protein. Phospholipase D activation by AβP (25–35), quisqualate and phorbol dibutyrate was not blunted by the protein kinase C inhibitors, staurosporine, H-7 and RO-31-8220. However, it was abolished by overnight exposure to phorbol dibutyrate. This activation of phospholipase D was prevented by the tyrosine kinase inhibitor, genistein but not by tyrophostin A. Several excitatory amino acid antagonists were tested for their ability to prevent the phospholipase D activation by quisqualate and AβP (25–35). Only NBQX was effective with an IC$_{50}$ of 75 μM for AβP (25–35) and quisqualate. Activation of phospholipase D by AβP or quisqualate was absent in LA-N-2 cells previously desensitized by quisqualate or AβP (25–35), but the activation by phorbol dibutyrate was unaltered. The responsiveness to AβP and quisqualate in previously desensitized cells reappeared subsequent to a period of resensitization. The observations with the antagonist NBQX, and the desensitization and resensitization experiments, are consistent with a receptor occupancy mediated activation of phospholipase D by quisqualate and by AβP (25–35).
Starting Page	1225
Ending Page	1232
Page Count	8
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	23
Issue Number	10
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	1998-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

1,8-Cineole (Eucalyptol) Mitigates Inflammation in Amyloid Beta Toxicated PC12 Cells: Relevance to Alzheimer’s Disease

Amyloid β peptide 25–35 modulates hydrolysis of phosphoinositides by membrane phospholipase(s) C of adult brain cortex

The Neuroprotective Effects of Justicidin A on Amyloid Beta$_{25–35}$-Induced Neuronal Cell Death Through Inhibition of Tau Hyperphosphorylation and Induction of Autophagy in SH-SY5Y Cells

Eriodictyol Attenuates β-Amyloid 25–35 Peptide-Induced Oxidative Cell Death in Primary Cultured Neurons by Activation of Nrf2

Activation of Phospholipases A$_{2}$ and D of a Human Neuroblastoma Cell Line (LA-N-2) by N-Dodecyl-l-Lysine Amide (Compound 24), a Putative G Protein Activator: Characteristics of Inhibition by (−)-Nicotine

β-Amyloid 25-35 Peptide Reduces the Expression of Glutamine Transporter SAT1 in Cultured Cortical Neurons

Beta Amyloid Peptide (25-35) Leading to Inflammation Through Toll-Like Receptors and the Anti-inflammatory Effect of Genistein in BV-2 Cells

Genistein alleviates the mitochondria-targeted DNA damage induced by β-amyloid peptides 25–35 in C6 glioma cells

Neuroprotective Effects of New Protein Kinase C Activator TPPB Against Aβ$_{25–35}$ Induced Neurotoxicity in PC12 Cells

Activation of LA-N-2 Cell Phospholipase D by Amyloid Beta Protein (25–35)

Similar Documents

1,8-Cineole (Eucalyptol) Mitigates Inflammation in Amyloid Beta Toxicated PC12 Cells: Relevance to Alzheimer’s Disease

Amyloid β peptide 25–35 modulates hydrolysis of phosphoinositides by membrane phospholipase(s) C of adult brain cortex

The Neuroprotective Effects of Justicidin A on Amyloid Beta$_{25–35}$-Induced Neuronal Cell Death Through Inhibition of Tau Hyperphosphorylation and Induction of Autophagy in SH-SY5Y Cells

Eriodictyol Attenuates β-Amyloid 25–35 Peptide-Induced Oxidative Cell Death in Primary Cultured Neurons by Activation of Nrf2

Activation of Phospholipases A$_{2}$ and D of a Human Neuroblastoma Cell Line (LA-N-2) by N-Dodecyl-l-Lysine Amide (Compound 24), a Putative G Protein Activator: Characteristics of Inhibition by (−)-Nicotine

β-Amyloid 25-35 Peptide Reduces the Expression of Glutamine Transporter SAT1 in Cultured Cortical Neurons

Beta Amyloid Peptide (25-35) Leading to Inflammation Through Toll-Like Receptors and the Anti-inflammatory Effect of Genistein in BV-2 Cells

Genistein alleviates the mitochondria-targeted DNA damage induced by β-amyloid peptides 25–35 in C6 glioma cells

Neuroprotective Effects of New Protein Kinase C Activator TPPB Against Aβ$_{25–35}$ Induced Neurotoxicity in PC12 Cells

Activation of LA-N-2 Cell Phospholipase D by Amyloid Beta Protein (25–35)