Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P17931 (galectin-3)
 2,860 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using an electron histochemical technique, we have observed the binding of a D-galactose-specific lectin to the muscle cell plasma membrane in muscle biopsies taken from patients with various neuromuscular disorders. In spinal muscular atrophy, the only neurogenic disease studied, the plasma membrane stained as in normal muscle. However, in the myopathies Becker and limb-girdle muscular dystrophy and in the polymyositis there was a reduction in both the occurrence and the intensity of staining of the plasma membrane. Reduced lectin binding by the plasma membrane probably reflects secondary changes in the composition of glycoproteins and/or glycolipids in the membrane and seems to be common to all these myopathies to varying degrees.
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PMID:Binding of Ricinus communis I lectin to the muscle cell plasma membrane in diseased muscle. 647 Jul 42

Muscle atrophy is a major hallmark of amyotrophic lateral sclerosis (ALS), the most frequent adult-onset motor neuron disease. To define the full set of alterations in gene expression in skeletal muscle during the course of the disease, we used the G86R superoxide dismutase-1 transgenic mouse model of ALS and performed high-density oligonucleotide microarrays. We compared these data to those obtained by axotomy-induced denervation. A major set of gene regulations in G86R muscles resembled those of surgically denervated muscles, but many others appeared specific to the ALS condition. The first significant transcriptional changes appeared in a subpopulation of mice before the onset of overt clinical symptoms and motor neuron death. These early changes affected genes involved in detoxification (e.g., ALDH3, metallothionein-2, and thioredoxin-1) and regeneration (e.g., BTG1, RB1, and RUNX1) but also tissue degradation (e.g., C/EBPdelta and DDIT4) and cell death (e.g., ankyrin repeat domain-1, CDKN1A, GADD45alpha, and PEG3). Of particular interest, metallothionein-1 and -2, ATF3, cathepsin-Z, and galectin-3 genes appeared, among others, commonly regulated in both skeletal muscle (our present data) and spinal motor neurons (as previously reported) of paralyzed ALS mice. The importance of these findings is twofold. First, they designate the distal part of the motor unit as a primary site of disease. Second, they identify specific gene regulations to be explored in the search for therapeutic strategies that could alleviate disease before motor neuron death manifests clinically.
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PMID:Gene profiling of skeletal muscle in an amyotrophic lateral sclerosis mouse model. 1800 Jan 59