Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The enzymatic transfer of the sugar portion from UDP-N-acetylgalactosamine to pyridylamino (PA) lacto-N-fucopentaose I (Fuc alpha 1-2Gal beta 1-3GlcNAc beta 1-4Glc-PA) was detected by high-performance liquid chromatography. Separation of the fluorescent product from the fluorescence-labeled acceptor was achieved within 10 min by reversed-phase high-performance liquid chromatography. Rat stomach enzyme activity was detected in the microsomal fraction from antrum but not corpus. Ohara et al. (1986, Comp. Biochem. Physiol. 83B, 273-275) reported that the N-acetylgalactosamine content in antrum mucin was greater than that in corpus mucin and antrum mucin had strong blood group A activity. The prominent asymmetrical distribution of the enzyme detected here well supports these findings. The elution position of the fluorescent product was the same as that of the product formed by the action of type A human serum toward the acceptor. Its hydrolysis by alpha-N-acetylgalactosaminidase yielded the acceptor. It is thus evident that the detected enzyme is the same as that producing the blood group A structure.
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PMID:Detection of UDP-N-acetylgalactosamine-oligosaccharide N-acetylgalactosaminyltransferase activity in rat stomach and human serum by high-performance liquid chromatography. 314 99

In January 1993, a 43-year-old man was admitted to our hospital for left wrist-drop. Neurological examinations revealed asymmetrical distal weakness in the upper limbs. Deep tendon reflexes were normal in all 4 limbs. Sensory and autonomic nervous functions were intact. CSF examinations were within normal limits. Thin-layer chromatography with immunostaining revealed serum antibodies that reacted with GM1 and GalNAc-GD1a. Motor nerve conduction studies revealed abnormal temporal dispersion, and a low amplitude of compound muscle action potential in the left radial nerve. Neurological symptoms gradually improved with prednisolone over one and a half years. He was hospitalized again in January 1995, because of right wrist-drop and slight sensory loss of the limbs. Those findings were improved by methylprednisolone (1,000 mg/day) for 3 days. The interval until maximal disability in this patient was more than one month for each admission. This case must belong to inflammatory demyelinating neuropathy.
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PMID:[A case of chronic inflammatory demyelinating neuropathy associated with antibodies to gangliosides GM1 and GalNAc-GD1a]. 921 22

The patient was a 25-year-old male with acute multifocal motor neuropathy with conduction block (MMNCB) after Campylobacter jejuni enteritis. After having suffered from diarrhea for 3 days, he rapidly developed asymmetrical distal-dominant muscle weakness in all extremities. Sensory disturbance was unremarkable except for slight disturbance in deep sensation. Deep tendon reflexes were normal throughout the course of present illness. CSF analysis revealed increased protein up to 66 mg/dl without pleocytosis. In electrophysiological examinations, persistant multifocal conduction blocks in the motor nerves were predominantly noted in the distal part of the extremities. Serum titers of anti-Campylobacter jejuni antibody, anti-GM1 antibody and anti-GalNAc-GD1a antibody were elevated. Muscle weakness resolved completely within 7 weeks. The sural nerve biopsy did not reveal either axonal degeneration, nor demyelination. These clinical and laboratory findings suggested that this case was most likely an acute type of MMNCB after Campylobacter jejuni enteritis.
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PMID:[A case of acute multifocal motor neuropathy with conduction block after Campylobacter jejuni enteritis]. 959 9

A 14-year-old boy developed a distinct asymmetrical muscle atrophy and weakness with no sensory disturbance in the lower extremities after enteritis. He had an elevated titre of the IgG antibody against GalNAc-GD1a, but none of the others. A nerve conduction study revealed motor axonopathy. Intravenous immunoglobulin therapy improved the status gradually, with low titres of IgG anti-GalNAc-GD1a.
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PMID:Subacute motor axonal neuropathy associated with the IgG anti-GalNAc-GD1a antibody. 2270 Apr 88