PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
8624380-9	1996	In stromal cells expressing the membrane-bound form of SCF, the presence of MAb RG7.6, even at low concentrations, interfered with thymidine uptake and proliferation.	Thymidine	131-140	KIT ligand	Canis lupus familiaris	55-58
26020315-4	2015	The SCF also contained 26% starch and 8% resistant starch and had a TMEn value of 2.6 kcal/g.	Starch	27-33	KIT ligand	Canis lupus familiaris	4-7
26020315-4	2015	The SCF also contained 26% starch and 8% resistant starch and had a TMEn value of 2.6 kcal/g.	Starch	51-57	KIT ligand	Canis lupus familiaris	4-7
24867932-3	2014	The second generation (G2) SCF included those prepared using phosphoric acid catalyzation in both a liquid [G2-SCF-phos (Lq)] and powder [G2-SCF-phos (Pw)] form, and SCF that were prepared using hydrochloric acid catalyzation in both a liquid [G2-SCF-HCl (Lq)] and powder [G2-SCF-HCl (Pw)] form.	phosphoric acid	61-76	KIT ligand	Canis lupus familiaris	27-30
24867932-7	2014	Glucose was the major free sugar and bound monosaccharide in all SCF except for G1-SCF-hydrog that had greater concentrations of sorbitol.	Glucose	0-7	KIT ligand	Canis lupus familiaris	65-68
24867932-7	2014	Glucose was the major free sugar and bound monosaccharide in all SCF except for G1-SCF-hydrog that had greater concentrations of sorbitol.	Monosaccharides	43-57	KIT ligand	Canis lupus familiaris	65-68
24867932-7	2014	Glucose was the major free sugar and bound monosaccharide in all SCF except for G1-SCF-hydrog that had greater concentrations of sorbitol.	Sorbitol	129-137	KIT ligand	Canis lupus familiaris	80-93
24867932-8	2014	All SCF had intermediate to low amounts of monosaccharides released as a result of in vitro hydrolytic digestion, with glucose being the primary sugar component released.	Monosaccharides	43-58	KIT ligand	Canis lupus familiaris	4-7
24867932-8	2014	All SCF had intermediate to low amounts of monosaccharides released as a result of in vitro hydrolytic digestion, with glucose being the primary sugar component released.	Glucose	119-126	KIT ligand	Canis lupus familiaris	4-7
24867932-8	2014	All SCF had intermediate to low amounts of monosaccharides released as a result of in vitro hydrolytic digestion, with glucose being the primary sugar component released.	Sugars	145-150	KIT ligand	Canis lupus familiaris	4-7
24867932-12	2014	All SCF had low free sugar concentrations with varying degrees of resistance to digestion, reduced caloric content, and attenuated glycemic and insulinemic responses in adult dogs.	Sugars	21-26	KIT ligand	Canis lupus familiaris	4-7
23736045-1	2013	The objective of these experiments was to measure in vitro hydrolytic digestion and glycemic and insulinemic responses of select carbohydrate blends, all containing the novel carbohydrate soluble corn fiber (SCF).	Carbohydrates	175-187	KIT ligand	Canis lupus familiaris	208-211
23736045-2	2013	Two SCF that varied in their method of production were used to formulate the carbohydrate blends.	Carbohydrates	77-89	KIT ligand	Canis lupus familiaris	4-7
23736045-5	2013	Free sugar concentrations found in the individual SCFsd and SCF substrates were low but varied.	Sugars	5-10	KIT ligand	Canis lupus familiaris	50-53
23736045-7	2013	Glucose was the main free sugar found in both SCFsd and SCF but at different concentrations (2.7 vs. 12.7%, respectively).	Glucose	0-7	KIT ligand	Canis lupus familiaris	46-49
23736045-7	2013	Glucose was the main free sugar found in both SCFsd and SCF but at different concentrations (2.7 vs. 12.7%, respectively).	Sugars	26-31	KIT ligand	Canis lupus familiaris	46-49
23736045-10	2013	Hydrolyzed monosaccharide concentrations for the SCF:pullulan:sorbitol:fructose blends followed similar trends to the SCFsd blends where greater percentages of fructose and sorbitol resulted in decreased (P < 0.05) hydrolyzed monosaccharide concentrations.	Monosaccharides	11-25	KIT ligand	Canis lupus familiaris	49-52
23736045-10	2013	Hydrolyzed monosaccharide concentrations for the SCF:pullulan:sorbitol:fructose blends followed similar trends to the SCFsd blends where greater percentages of fructose and sorbitol resulted in decreased (P < 0.05) hydrolyzed monosaccharide concentrations.	Sorbitol	62-70	KIT ligand	Canis lupus familiaris	49-52
23736045-14	2013	The SCF:pullulan:sorbitol:fructose blends also had intermediate to high released monosaccharides as a result of in vitro hydrolytic digestion.	Sorbitol	17-25	KIT ligand	Canis lupus familiaris	4-7
23736045-14	2013	The SCF:pullulan:sorbitol:fructose blends also had intermediate to high released monosaccharides as a result of in vitro hydrolytic digestion.	Fructose	26-34	KIT ligand	Canis lupus familiaris	4-7
23736045-14	2013	The SCF:pullulan:sorbitol:fructose blends also had intermediate to high released monosaccharides as a result of in vitro hydrolytic digestion.	Monosaccharides	81-96	KIT ligand	Canis lupus familiaris	4-7
23736045-15	2013	All SCF blends resulted in decreased glycemic and insulinemic responses compared with the maltodextrin control (P < 0.05) using a canine model.	maltodextrin	90-102	KIT ligand	Canis lupus familiaris	4-7
23535662-5	2013	Here, we find that yeast SCF (Skp1-Cdc53-F-box) Cullin-RING complexes are remodelled in a CAND1-dependent manner, when cells are switched from growth in fermentable to non-fermentable carbon sources.	Carbon	184-190	KIT ligand	Canis lupus familiaris	25-28
20033487-3	2010	A strong relationship exists between the SCF/c-KIT pathway and pathogenesis of CAD, suggesting that masitinib may potentially fulfil the above role.	masitinib	100-109	KIT ligand	Canis lupus familiaris	41-44
11844224-4	2001	Histamine release by skin cell suspensions after stimulation with SCF, concanavalin A (ConA) or rabbit anticanine IgE antibodies was compared between normal and atopic dogs.	Histamine	0-9	KIT ligand	Canis lupus familiaris	66-69
11844224-8	2001	Median histamine release stimulated by SCF in the absence of IgE from lesional skin cells was higher in atopic than normal dogs (P = 0.04).	Histamine	7-16	KIT ligand	Canis lupus familiaris	39-42
11844224-9	2001	These experiments suggest that dermal SCF secretion could potentiate histamine release following IgE receptor cross-linking and thus, could be one of the explanations for the inherent mast cell hyperexcitability observed in canine atopic dermatitis.	Histamine	69-78	KIT ligand	Canis lupus familiaris	38-41
10889302-0	2000	Stem cell factor enhances IgE-mediated histamine and TNF-alpha release from dispersed canine cutaneous mast cells.	Histamine	39-48	KIT ligand	Canis lupus familiaris	0-16
10889302-3	2000	To investigate the effect of SCF on canine cutaneous MC function, we have characterized the ability of SCF to modulate the release by mature canine MC of preformed (histamine) and newly generated (TNF-alpha) mediators.	Histamine	165-174	KIT ligand	Canis lupus familiaris	103-106
10889302-6	2000	However, we observed that SCF used as a co-stimulus significantly potentiated histamine and TNF-alpha release in canine MC activated through Fc epsilon RI regardless of whether or not SCF was added to the medium during culturing.	Histamine	78-87	KIT ligand	Canis lupus familiaris	26-29
10889302-7	2000	Thus, the mean histamine release (%) and TNF-alpha production (pg/ml) were found to be significantly higher if cells were maintained in culture in SCF-supplemented medium compared with cells cultured in the absence of exogenous SCF.	Histamine	15-24	KIT ligand	Canis lupus familiaris	147-150
10228034-7	1999	Induction of progelatinase B is blocked by U-73122, Ro31-8220, and thapsigargin, implicating phospholipase C, protein kinase C, and Ca2+, respectively, in the kit ligand effect.	Thapsigargin	67-79	KIT ligand	Canis lupus familiaris	159-169