Disease relevance of CSAD

• Analysis of antibody reactivity against cysteine sulfinic acid decarboxylase, a pyridoxal phosphate-dependent enzyme, in endocrine autoimmune disease [1].
• Three prostate cancer susceptibility genes have been reported to be linked to different regions on chromosome 1: HPC1 at 1q24-25, PCAP at 1q42-43, and CAPB at 1p36 [2].
• The clinical significance of plasma cell acid phosphatase (PCAP) was evaluated in 143 patients with monoclonal gammapathies, using a semiquantitative cytological scoring method [3].
• CSD is a well recognised cause of cervical lymphadenopathy, and parotid involvement occurs in 3 per cent of cases [4].
• Hence, they support novel therapeutic strategies that consider CSD and cortical hyperexcitability as key targets for preventive migraine treatment [5].

High impact information on CSAD

• Coexistence of neurotransmitter-synthesizing enzymes choline acetyltransferase, cysteine sulfinic acid decarboxylase, tyrosine hydroxylase, and L-glutamic acid decarboxylase was demonstrated at human and primate neuromuscular junctions with specific antibodies directed against these enzymes [6].
• Concomitantly, a whole-genome shotgun (WGS) sequencing of paired-end reads from plasmids and fosmids were assembled with PCAP, providing a predicted genome size of up to 43.5 Mbp and 17% repetitive DNA [7].
• Differences between our sequence data on CSAD and those reported previously were observed at two positions, which arose from a single amino acid substitution and frame shift mutation [8].
• Thus, we propose that the high-titer CSAD autoantibody resulted from increased CSAD gene expression in the liver due to stimulation by the HCC [8].
• CSAD activity was readily measured in extracts of spinal cord from the same species, except those from rhesus monkey and man [9].

Chemical compound and disease context of CSAD

• Bolus injection of Lx (200 microM) caused insidious and significant lung weight gain, which was not associated with remarkable elevation of Ppa or Pcap but was associated with an increase of perfusate LDH activity and nitrite levels [10].

Biological context of CSAD

• Each virus of this series contains the cat reporter gene under the control of Pcap or portions thereof [11].
• According to the sensitivity of the HPLC analysis this indicates that the decarboxylation of HCA, if any, was 130-fold and 50-fold less than that of CSA by CSD from liver and brain, respectively, in our experimental conditions [12].
• Blockade of synaptic transmission with aminophosphonobutyric + kynurenic acids simplified the CSD profiles through the retina [13].

Anatomical context of CSAD

• The most noteworthy observation was the complete absence of CSAD activity in extracts of optic nerves and of sciatic nerves from all seven mammals [9].
• The greatest difference between Huntington's and normal tissues occurred in putamen, in which the apparent CSAD activity was reduced by 85%, while no difference was observed in frontal cortex [14].
• The results indicate that the CSD was often depolarized earlier than a more proximal site by impulses that conducted to the atria retrogradely via the AV node while the quadripolar recording catheter was placed at the CSD [15].
• Among various clinical and laboratory parameters, PCAP was significantly related to the percentage of bone marrow plasma cells, the neoplastic growth fraction, as determined by Ki67 monoclonal antibody, and to serum levels of C-reactive protein [3].
• Cysteine sulfinate decarboxylase in brain: identification, characterization and immunocytochemical location in astrocytes [16].

Associations of CSAD with chemical compounds

• We determined whether Cu deficiency would decrease taurine status and the hepatic activities of cysteine dioxygenase (CDO) and/or cysteine sulfinic acid decarboxylase (CSAD) in rats [17].
• The ratio of formation of taurine to that of hypotaurine was similar for CSD from liver and brain [12].
• We therefore investigated the specificity of CSD vs CSA and HCA as well as the related analogs homocysteine sulfinic acid (HCSA) and cysteic acid (CA) [12].
• Similar inhibition of glutamate decarboxylase and cysteine sulfinic acid decarboxylase by two different radical-containing compounds (O2 and NO) is consistent with the notion that these reactions proceed via radical mechanisms [18].
• However, in the multivariate analysis, beta 2-microglobulin, growth fraction, performance status, and serum levels of thymidine kinase and C-reactive protein, but not PCAP, maintained a significant prognostic relevance [3].

Other interactions of CSAD

• Oxygen-induced seizures and inhibition of human glutamate decarboxylase and porcine cysteine sulfinic acid decarboxylase by oxygen and nitric oxide [18].

Analytical, diagnostic and therapeutic context of CSAD

• Three of 83 patients (3.6%) with autoimmune polyendocrine syndrome type 1 (APS1) were anti-CSAD positive in a radioimmunoprecipitation assay [1].
• Sequence analysis of this clone showed it to exhibit 90 and 60% similarity with the rat cysteine sulfinic acid decarboxylase (CSAD) and mammalian glutamic acid decarboxylases (GAD), respectively [8].
• If such an approach is followed, lasting limb salvage with minimal morbidity should be achieved in most patients with CSAD [19].
• In the program, PCAP, we provide a methodology for choosing synthetic oligonucleotide probes to be used in contig mapping experiments [20].
• We would also advise that in those cases of parotid CSD in which either the diagnosis is equivocal, CS antigen is unavailable or intense parotid pain is a predominant feature, excision of the primary lesion together with surgical decompression of the parotid capsule should be performed [4].

References