Disease relevance of mercaptomethanethione

• A plasmid-encoded regulatory gene, rns, required for expression of the CS1 and CS2 adhesins of enterotoxigenic Escherichia coli [1].
• A comparison of the physical and kinetic properties of clavaminate synthase from S. antibioticus (CS3) and the two isozymes from Streptomyces clavuligerus (CS1 and CS2) has been conducted [2].
• Disulfiram and CS2 toxicity [3].
• Expression of CS2 and CS3 reduced the invasiveness of Shigella for HeLa cells and slowed the intracellular growth rate [4].
• Purification, properties and cellular localization of the stereospecific CS2 secondary alkylsulphohydrolase of Comamonas terrigena [5].

Psychiatry related information on mercaptomethanethione

• Exposure to CS2 increased the intensity of apomorphine-induced stereotypy in male rats without increasing the reaction time [6].
• Ethanol did not change the exploratory motor activity and behaviour of CS2-exposed rats in the open-field and passive avoidance tests but it affected their performance in the conditioned avoidance test [7].
• Development of gait, motor coordination, and activity, avoidance learning and swimming were tested in the offspring of CFY rat mothers, exposed to CS2 inhalation (0, less than 10, 700 and 2000 mg/m3) and to Aromatol (0, 600, 1000 and 2000 mg/m3) on days 7-15 gestation [8].
• Only the group exposed to values exceeding three times the recommended TLV for CS2; had significant impairments in both the speed and the quality of psychomotor performance [9].
• Data were from 222 workers in the viscose industry exposed to CS2 and 191 employees from the same factory with similar physical and psychological stress factors but without occupational contact with neurotoxic substances [10].

High impact information on mercaptomethanethione

• In the shocked jovian atmosphere, HCS could further decompose to H and CS, and CS could react with SH and OH to yield the observed CS2 and COS [11].
• Mutating the CS1 sequence within the context of the 302-bp promoter abolished all activity of the promoter, while mutating the CS2 sequence alone had little effect [12].
• Multimer constructs linking CS1- or CS2-spanning oligonucleotides to a heterologous promotor revealed that the CS1 construct had the greater enhancer activity in EL4 cells [12].
• Expression of two of these specific adherence structures, CS1 and CS2, requires the presence of a plasmid in an ETEC strain of a particular serotype and biotype [1].
• In addition, CS2 is responsible for ABF1-mediated chromatin remodeling [13].

Chemical compound and disease context of mercaptomethanethione

• None of the monkeys developed retinal microaneurysms or hemorrhages, major accepted signs of visual toxicity in CS2 exposed humans; thus, permanent visual loss may result from carbon disulfide exposure even in the absence of retinal vascular effects [14].
• The reactivities of CO2 and the related compounds COS and CS2 with the nickel- and iron- sulfur-containing carbon monoxide dehydrogenase (CODH) from Rhodospirillum rubrum have been investigated [15].
• Purification and characterization of CS2, a sialic acid-specific haemagglutinin of enterotoxigenic Escherichia coli [16].
• Guinea pigs immunized intranasally with CVD 1204(pGA1-CS2) or CVD 1204(pGA1-CS3), or with a mixture of these strains, developed secretory immunoglobulin A (IgA) in tears and serum IgG antibodies against Shigella lipopolysaccharide, CS2, and CS3 antigens [4].
• It is concluded that the elevation of adrenal dopamine content and catecholamine synthesis in CS2 exposed rats satisfy part of the demand placed on the adrenal medulla by hypothermia and hypoglycaemia.(ABSTRACT TRUNCATED AT 250 WORDS)[17]

Biological context of mercaptomethanethione

• We examined CS1 in further detail, as well as a second consensus sequence, CS2, located at nucleotides -75 through -65; both are within a minimal 83-bp construct that expresses full promoter activity [12].
• When tethered to specific regions of the genome, a 30-aa fragment that contains CS2 alone is sufficient for activation of transcription and chromosomal replication [13].
• Dephosphorylation by the catalytic subunits of protein phosphatases 1 (CS1) and 2A (CS2) reveals that mature protein kinase C is phosphorylated at two distinct sites [18].
• Replicons containing individual deletions of CS2, repeated CS2 (RCS2), CS3, or RCS3 were viable, but their RNA replication was dramatically compromised [19].
• These results demonstrate that genome cyclization through the 5'CS-CS1 interaction is essential for WNV RNA replication, whereas CS2, RCS2, CS3, and RCS3 facilitate, but are dispensable for, WNV replication [19].

Anatomical context of mercaptomethanethione

• In addition, the binding of enterotoxigenic E. coli strains expressing CFA/I, CS2, CS4, and PCFO166 to enterocyte-like cell-line Caco-2 was inhibited by both MAbs [20].
• A single TMS pulse (110% resting motor threshold, RMT) to the left dorsal premotor cortex (PMd) (CS2) suppresses the amplitude of motor evoked potentials (MEPs) from a test pulse (TS) over the right motor cortex (M1), and facilitates MEPs from the left motor cortex [21].
• In the present study, the structure of one type of stable protein cross-link produced on erythrocyte spectrin by CS2 in vivo is determined [22].
• In microsomes, CS2 metabolism was increased by phenobarbital pretreatment of the rats and decreased with pretreatment of the rats with cobaltous chloride [23].
• Kupffer cells are also stained with CS2 antiserum but hepatocyte expression is undetectable [24].

Associations of mercaptomethanethione with other chemical compounds

• Five monkeys were exposed by inhalation for 6 hr a day, 5 days a week to 256 ppm carbon disulfide (CS2) [14].
• In this work, the quenching ability (i.e., reactivity) was examined for H2S, CS2, and NO2- acting on tryptophan phosphorescence in parvalbumin, azurin, horse liver alcohol dehydrogenase, and alkaline phosphatase [25].
• The adrenal dopamine content increased during cold exposure with immobilization or after insulin treatment both in CS2 exposed and control rats [17].
• Acetazolamide, a carbonic anhydrase inhibitor, significantly decreased COS metabolism but not CS2 metabolism in isolated hepatocytes or microsomes fortified with dialyzed cytosol [23].
• Unlike the case for thiourea and acetylene, saturating concentrations of CS2 did not fully inhibit AMO, and the inhibition resulted in a low but significant rate of ammonia-dependent O2 uptake [26].

Gene context of mercaptomethanethione

• CONCLUSION: These studies support a central role for MT4-MMP in IL-1-induced cartilage aggrecanolysis and are consistent with the identification of p68 as the aggrecanase that cleaves within the CS2 domain, and of p53 as the aggrecanase that generates G1-NITEGE [27].
• Both aggrecanases showed a similar ability to cleave within the CS2 domain of bovine aggrecan irrespective of age, but showed a much lower ability to cleave within the CS2 domain of human aggrecan [28].
• Multiple alignment and phylogenetic analysis of the proteins encoded by each operon define three subclasses, 5a (CFA/I, CS4, and CS14), 5b (CS1, CS17, CS19, and PCFO71), and 5c (CS2) [29].
• The results of PCR and nucleotide sequencing of the fliD region of eight different P. aeruginosa strains (laboratory strains PAK, PAO1, and PA103; clinical strains 1244, CS2, and CS32; cystic fibrosis strains CS29 and MDR) suggested that there were two distinct types of FliD in P. aeruginosa, which we named A type and B type [30].
• The CS2 cotA to -D genes, isolated from ETEC strain C91F, and the CS3 cstA to -H genes, subcloned from plasmid pCS100, were cloned into ~15-copy-number-stabilized pGA1 behind the osmotically regulated ompC promoter, resulting in high expression of both fimbriae [4].

Analytical, diagnostic and therapeutic context of mercaptomethanethione

• CS1- and CS2-spanning oligonucleotides bound apparently distinct PMA-inducible, sequence-specific factors in mobility-shift assays [12].
• Off-resonant fifth-order response function for two-dimensional Raman spectroscopy of liquids CS2 and H2O [31].
• In all patients standard 12-lead ECG investigations were performed, as well as 24-h ECG monitoring, using an Oxford Medical System device with two precordial leads CM5 and CS2, according to the Holter method [32].
• Oral administration of diethyldithiocarbamate (DTC) and carbon disulfide (CS2) protected mice against CHCl3-induced kidney injury, as evidenced by normalization of delayed plasma phenolsulfonphthalein clearance, suppression of increased kidney calcium content and prevention of renal tubular necrosis [33].
• All of the neurofilament associated CS2 carbon was bound to protein in control group 3 h after the injection [34].

References