ArticleProceedings of the National Academy of Sciences of the United States of America1996
Expression of calbindin-D28K in motoneuron hybrid cells after retroviral infection with calbindin-D28K cDNA prevents amyotrophic lateral sclerosis IgG-mediated cytotoxicity.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 91 citations in OpenAlex.
- Molecular and cellular mechanisms of selective vulnerability in neurodegenerative diseases.Nature reviews. Neuroscience · 2024Review
- Increased Calbindin D28k Expression via Long-Term Alternate-Day Fasting Does Not Protect against Ischemia-Reperfusion Injury: A Focus on Delayed Neuronal Death, Gliosis and Immunoglobulin G Leakage.International journal of molecular sciences · 2021Article
- P2X7 Receptor Antagonism as a Potential Therapy in Amyotrophic Lateral Sclerosis.Frontiers in molecular neuroscience · 2020Review
- Role of VEGF and VEGFR2 Receptor in Reversal of ALS-CSF Induced Degeneration of NSC-34 Motor Neuron Cell Line.Molecular neurobiology · 2015Article
- Calpain inhibition prevents ethanol-induced alterations in spinal motoneurons.Neurochemical research · 2013Article
- Roles of vitamin D in amyotrophic lateral sclerosis: possible genetic and cellular signaling mechanisms.Molecular brain · 2013Review
- Calpain inhibition protected spinal cord motoneurons against 1-methyl-4-phenylpyridinium ion and rotenone.Neuroscience · 2011Article
- Distribution of calcium-binding proteins in the cerebellum.Cerebellum (London, England) · 2003Review
- 'New' functions for 'old' proteins: the role of the calcium-binding proteins calbindin D-28k, calretinin and parvalbumin, in cerebellar physiology. Studies with knockout mice.Cerebellum (London, England) · 2002Review
- Control of IP(3)-mediated Ca2+ puffs in Xenopus laevis oocytes by the Ca2+-binding protein parvalbumin.The Journal of physiology · 2001Article
- Calcium dynamics and buffering in oculomotor neurones from mouse that are particularly resistant during amyotrophic lateral sclerosis (ALS)-related motoneurone disease.The Journal of physiology · 2000Article
- Calcium dynamics and buffering in motoneurones of the mouse spinal cord.The Journal of physiology · 1999Article
- Transgenic mice in the study of ALS: the role of neurofilaments.Brain pathology (Zurich, Switzerland) · 1998Review
- Protective effect of neurofilament heavy gene overexpression in motor neuron disease induced by mutant superoxide dismutase.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Absence of neurofilaments reduces the selective vulnerability of motor neurons and slows disease caused by a familial amyotrophic lateral sclerosis-linked superoxide dismutase 1 mutant.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Mutant superoxide dismutase-1-linked familial amyotrophic lateral sclerosis: molecular mechanisms of neuronal death and protection.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
- Androgen mitigates axotomy-induced decreases in calbindin expression in motor neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Calbindin-D28K and/or parvalbumin appear to influence the selective vulnerability of motoneurons in amyotrophic lateral sclerosis (ALS). Their immunoreactivity is undetectable in motoneurons readily damaged in human ALS, and in differentiated motoneuron hybrid cells [ventral spinal cord (VSC 4.1 cells)] that undergo calcium-dependent apoptotic cell death in the presence of ALS immunoglobulins. To provide additional evidence for the role of calcium-binding proteins in motoneuron vulnerability, VSC 4.1 cells were infected with a retrovirus carrying calbindin-D28K cDNA under the control of the promoter of the phosphoglycerate kinase gene. Differentiated calbindin-D28K cDNA-infected cells expressed high calbindin-D28K and demonstrated increased resistance to ALS IgG-mediated toxicity. Treatment with calbindin-D28K antisense oligodeoxynucleotides, which significantly decreased calbindin-D28K expression, rendered these cells vulnerable again to ALS IgG toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.