PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
31001109-2	2019	In humans, SOX deficiency causes the formation of the glutamate analog S-Sulfocysteine (SSC) resulting in a constant overstimulation of ionotropic glutamatergic receptors.	S-sulphocysteine	71-86	sulfite oxidase	Homo sapiens	11-14
32535071-6	2020	Analysis of the interaction between protein and drug discovered ASAP1 interacts with cysteine sulfonic acid and double oxidized cysteine drug compounds.	S-sulphocysteine	85-107	ArfGAP with SH3 domain, ankyrin repeat and PH domain 1	Homo sapiens	64-69
31001109-2	2019	In humans, SOX deficiency causes the formation of the glutamate analog S-Sulfocysteine (SSC) resulting in a constant overstimulation of ionotropic glutamatergic receptors.	S-sulphocysteine	88-91	sulfite oxidase	Homo sapiens	11-14
21305354-4	2011	Low PLP levels were also seen in a group of children with transiently elevated urinary excretion of sulfite and/or sulfocysteine, suggesting that there may be other situations in which sulfite accumulates and inactivates PLP.	S-sulphocysteine	115-128	pyridoxal phosphatase	Homo sapiens	4-7
27523630-1	2016	Patients affected by sulfite oxidase (SO) deficiency present severe seizures early in infancy and progressive neurological damage, as well as tissue accumulation of sulfite, thiosulfate and S-sulfocysteine.	S-sulphocysteine	190-205	sulfite oxidase	Rattus norvegicus	21-36
27523630-1	2016	Patients affected by sulfite oxidase (SO) deficiency present severe seizures early in infancy and progressive neurological damage, as well as tissue accumulation of sulfite, thiosulfate and S-sulfocysteine.	S-sulphocysteine	190-205	sulfite oxidase	Rattus norvegicus	38-40
24793416-1	2014	Sulfite oxidase (SO) deficiency is biochemically characterized by the accumulation of sulfite, thiosulfate and S-sulfocysteine in tissues and biological fluids of the affected patients.	S-sulphocysteine	111-126	sulfite oxidase	Homo sapiens	0-15
24793416-1	2014	Sulfite oxidase (SO) deficiency is biochemically characterized by the accumulation of sulfite, thiosulfate and S-sulfocysteine in tissues and biological fluids of the affected patients.	S-sulphocysteine	111-126	sulfite oxidase	Homo sapiens	17-19
20388560-4	2010	The absorption of the aggregated TTR molecules increased more with incubation time and the concentration of cysteine-S-sulfonate at pH 4 than at pH 8.	S-sulphocysteine	108-128	transthyretin	Homo sapiens	33-36
17913710-7	2007	Using mass spectrometry and limited proteolysis, this upper band was identified as an oxidized subunit of SOD1; the sulfhydryl group (Cys-SH) of Cys(111) was selectively oxidized to cysteine sulfinic acid (Cys-SO(2)H) and to cysteine sulfonic acid (Cys-SO(3)H).	S-sulphocysteine	225-247	superoxide dismutase 1	Homo sapiens	106-110
17063874-4	2006	During the process of TTR analysis, we found unique isoforms of TTR, which showed changes of the cysteine (10th from amino terminal) residue to glycine, dehydroalanine, and S-sulfocysteine residues.	S-sulphocysteine	173-188	transthyretin	Homo sapiens	22-25
17063874-4	2006	During the process of TTR analysis, we found unique isoforms of TTR, which showed changes of the cysteine (10th from amino terminal) residue to glycine, dehydroalanine, and S-sulfocysteine residues.	S-sulphocysteine	173-188	transthyretin	Homo sapiens	64-67
34426590-5	2021	Fasting glucose was associated with metabolites of intracellular insulin action and beta-cell dysfunction, namely cysteine-s-sulphate and n-acetylgarginine, whereas fasting insulin was predicted by myristoleoylcarnitine, propionylcarnitine and other metabolites of beta-oxidation of fatty acids.	S-sulphocysteine	114-133	insulin	Homo sapiens	65-72
15063314-2	2004	By electrospray ionization mass spectrometry (ESI-MS), we previously found derivatives of serum transthyretin (TTR) in which cysteine residue at position 10 was changed to glycine residue and sulfocysteine residue.	S-sulphocysteine	192-205	transthyretin	Homo sapiens	96-109
15063314-2	2004	By electrospray ionization mass spectrometry (ESI-MS), we previously found derivatives of serum transthyretin (TTR) in which cysteine residue at position 10 was changed to glycine residue and sulfocysteine residue.	S-sulphocysteine	192-205	transthyretin	Homo sapiens	111-114
11397793-10	2001	To functionally characterize the new protein, human and mouse Grx2 proteins were expressed in Escherichia coli, and the purified proteins were shown to reduce mixed disulfides formed between GSH and S-sulfocysteine, hydroxyethyldisulfide, or cystine.	S-sulphocysteine	199-214	glutaredoxin 2 (thioltransferase)	Mus musculus	62-66
7659277-1	1995	An elevated, sustained expression of c-fos mRNA was found in primary cultures of mouse cerebellar granule cells following exposure to toxic concentrations of the excitatory amino acids, L-glutamate, L-homocysteate, S-sulpho-L-cysteine and N-methyl-D-aspartate (NMDA), using leakage of lactate dehydrogenase (LDH) as an indicator of cytotoxicity.	S-sulphocysteine	215-234	FBJ osteosarcoma oncogene	Mus musculus	37-42
7659277-3	1995	Both LDH release and elevated, sustained c-fos mRNA induction were blocked (in the case of L-homocysteate) or reduced (in the case of L-glutamate and S-sulpho-L-cysteine) by the selective NMDA receptor antagonist (DL(+/-)-2-amino- 5-phosphonopentanoic acid) whereas 6-cyano-7-nitroquinoxaline-2,3-dione (a selective antagonist at non-NMDA ionotropic receptors) had no effect.	S-sulphocysteine	150-169	FBJ osteosarcoma oncogene	Mus musculus	41-46
2221913-7	1990	Plots of thioltransferase activity as a function of S-sulfocysteine or hydroxyethyl disulfide concentration did not show normal Michaelis-Menten kinetics.	S-sulphocysteine	52-67	glutaredoxin	Homo sapiens	9-25
33877450-1	2021	In this study, we examined neuronal excitability and skeletal muscle physiology and histology in homozygous knockout mice lacking cysteine sulfonic acid decarboxylase (CSAD-KO).	S-sulphocysteine	130-152	cysteine sulfinic acid decarboxylase	Mus musculus	168-172
3605592-7	1987	The plots of thioltransferase activity as a function of S-sulfocysteine, 2-hydroxyethyl disulfide, and reduced glutathione concentrations did not display Michaelis-Menten kinetics.	S-sulphocysteine	56-71	glutaredoxin-1	Sus scrofa	13-29
3944096-12	1986	The plots of the activity of thioltransferase as a function of S-sulfocysteine and 2-hydroxyethyl disulfide concentrations showed sigmoidal relationships.	S-sulphocysteine	63-78	glutaredoxin-1	Bos taurus	29-45