PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
22261065-2	2011	Upon binding an MT, an Eg5 dimer releases one ADP molecule, undergoes a slow (~0.5 s(-1)) isomerization, and finally releases a second ADP, adopting a tightly MT-bound, nucleotide-free (APO) conformation.	Adenosine Diphosphate	46-49	kinesin family member 11	Homo sapiens	23-26
22261065-2	2011	Upon binding an MT, an Eg5 dimer releases one ADP molecule, undergoes a slow (~0.5 s(-1)) isomerization, and finally releases a second ADP, adopting a tightly MT-bound, nucleotide-free (APO) conformation.	Adenosine Diphosphate	135-138	kinesin family member 11	Homo sapiens	23-26
22261065-5	2011	We demonstrate that a critical element of Eg5, loop 5 (L5), accelerates ADP release during the initial MT-binding event.	Adenosine Diphosphate	72-75	kinesin family member 11	Homo sapiens	42-45
22261065-7	2011	Finally, we find that Eg5 having a seven-residue deletion within L5 can still hydrolyze ATP and move along MTs, suggesting that L5 is not required to accelerate subsequent steps of the motor along the MT.	Adenosine Triphosphate	88-91	kinesin family member 11	Homo sapiens	22-25
21986572-0	2011	Dimethylenastron suppresses human pancreatic cancer cell migration and invasion in vitro via allosteric inhibition of mitotic kinesin Eg5.	dimethylenastron	0-16	kinesin family member 11	Homo sapiens	134-137
21986572-2	2011	This study was undertaken to investigate the effect of dimethylenastron, a specific inhibitor of Eg5, on the migration and invasion of pancreatic cancer cells.	dimethylenastron	55-71	kinesin family member 11	Homo sapiens	97-100
21986572-7	2011	The binding of dimethylenastron to Eg5 was analyzed with a molecular modeling study, and the ADP release rate was examined with the MANT-ADP reagent.	dimethylenastron	15-31	kinesin family member 11	Homo sapiens	35-38
21986572-11	2011	However, treatment of PANC1 cells with dimethylenastron (3 and 10 mumol/L) for 24 h had no detectable effect on their proliferation, which was inhibited when the cancer cells were treated with the drug for 72 h. Molecular modeling study showed that dimethylenastron could allosterically inhibit the motor domain ATPase of Eg5 by decreasing the rate of ADP release.	dimethylenastron	39-55	kinesin family member 11	Homo sapiens	322-325
21986572-11	2011	However, treatment of PANC1 cells with dimethylenastron (3 and 10 mumol/L) for 24 h had no detectable effect on their proliferation, which was inhibited when the cancer cells were treated with the drug for 72 h. Molecular modeling study showed that dimethylenastron could allosterically inhibit the motor domain ATPase of Eg5 by decreasing the rate of ADP release.	dimethylenastron	249-265	kinesin family member 11	Homo sapiens	322-325
21872609-8	2011	We performed MD simulations in which the L5-domain of the Eg5 ADP X-ray structure was manually deformed via backbone bond rotations.	Adenosine Diphosphate	62-65	kinesin family member 11	Homo sapiens	58-61
21872609-9	2011	The L5-domain of Eg5 was sufficiently lengthy that portions of L5 could be located in proximity to bound ADP.	Adenosine Diphosphate	105-108	kinesin family member 11	Homo sapiens	17-20
21566458-5	2011	In contrast, inhibition of Eg5 and KIF4A is competitive with respect to both ATP and microtubules, indicating that Abeta interferes with their interactions with the microtubules of the mitotic spindle.	Adenosine Triphosphate	77-80	kinesin family member 11	Homo sapiens	27-30
21613548-4	2011	When satisfaction of the MC was prevented with 500 nM nocodazole or 2.5 muM dimethylenastron (an Eg5 inhibitor), 92-100% of RPE-1 cells slipped from mitosis in the presence of pan-caspase inhibitors or after simultaneously depleting caspase-3 and -9, and they did so with the same kinetics (~21-22 h) as after treatment with nocodazole or Eg5 inhibitors alone.	Nocodazole	54-64	kinesin family member 11	Homo sapiens	339-342
21613548-4	2011	When satisfaction of the MC was prevented with 500 nM nocodazole or 2.5 muM dimethylenastron (an Eg5 inhibitor), 92-100% of RPE-1 cells slipped from mitosis in the presence of pan-caspase inhibitors or after simultaneously depleting caspase-3 and -9, and they did so with the same kinetics (~21-22 h) as after treatment with nocodazole or Eg5 inhibitors alone.	dimethylenastron	76-92	kinesin family member 11	Homo sapiens	97-100
21613548-4	2011	When satisfaction of the MC was prevented with 500 nM nocodazole or 2.5 muM dimethylenastron (an Eg5 inhibitor), 92-100% of RPE-1 cells slipped from mitosis in the presence of pan-caspase inhibitors or after simultaneously depleting caspase-3 and -9, and they did so with the same kinetics (~21-22 h) as after treatment with nocodazole or Eg5 inhibitors alone.	dimethylenastron	76-92	kinesin family member 11	Homo sapiens	339-342
21765863-1	2011	INTRODUCTION: AZD4877 is a potent Eg5 inhibitor that has been shown to have an acceptable tolerability profile in a Phase I study of Western patients with solid tumors.	N-(3-aminopropyl)-N-(1-(5-benzyl-3-methyl-4-oxo-(1,2)thiazolo(5,4-d)pyrimidin-6-yl)-2-methylpropyl)-4-methylbenzamide	14-21	kinesin family member 11	Homo sapiens	34-37
21344920-0	2011	Structure-activity relationship and multidrug resistance study of new S-trityl-L-cysteine derivatives as inhibitors of Eg5.	3-tritylthio-L-alanine	70-89	kinesin family member 11	Homo sapiens	119-122
21344920-6	2011	We previously identified S-trityl-L-cysteine (STLC) as a potent allosteric inhibitor of Eg5.	3-tritylthio-L-alanine	25-44	kinesin family member 11	Homo sapiens	88-91
21344920-6	2011	We previously identified S-trityl-L-cysteine (STLC) as a potent allosteric inhibitor of Eg5.	3-tritylthio-L-alanine	46-50	kinesin family member 11	Homo sapiens	88-91
21297652-0	2011	A potent chemotherapeutic strategy in prostate cancer: S-(methoxytrityl)-L-cysteine, a novel Eg5 inhibitor.	S-(methoxytrityl)cysteine	55-83	kinesin family member 11	Homo sapiens	93-96
21297652-4	2011	The aim of this study was to investigate the anticancer efficacy of S-(methoxytrityl)-L-cysteine (S(MeO)TLC), a novel Eg5 inhibitor in prostate cancer.	S-(methoxytrityl)cysteine	68-96	kinesin family member 11	Homo sapiens	118-121
21192710-0	2011	Exploring the intermediate states of ADP-ATP exchange: a simulation study on Eg5.	adp-atp	37-44	kinesin family member 11	Homo sapiens	77-80
21192710-2	2011	Crystal structures of Eg5, one of the best-studied kinesins, have been solved in both ADP-bound and ATP-bound states.	Adenosine Diphosphate	86-89	kinesin family member 11	Homo sapiens	22-25
21192710-2	2011	Crystal structures of Eg5, one of the best-studied kinesins, have been solved in both ADP-bound and ATP-bound states.	Adenosine Triphosphate	100-103	kinesin family member 11	Homo sapiens	22-25
21192710-10	2011	These molecular simulation results provided not only a better understanding of Eg5-catalyzed ATP hydrolysis but also the structural basis for design of novel specific Eg5 inhibitors as anticancer therapeutic agents.	Adenosine Triphosphate	93-96	kinesin family member 11	Homo sapiens	79-82
20597485-0	2010	Structural basis for inhibition of Eg5 by dihydropyrimidines: stereoselectivity of antimitotic inhibitors enastron, dimethylenastron and fluorastrol.	dihydropyrimidines	42-60	kinesin family member 11	Homo sapiens	35-38
20737530-0	2010	Structure-activity relationships and molecular docking of novel dihydropyrimidine-based mitotic Eg5 inhibitors.	dihydropyrimidine	64-81	kinesin family member 11	Homo sapiens	96-99
20737530-1	2010	Dihydropyrimidine-based compounds belong to the first discovered inhibitors of the human mitotic kinesin Eg5.	dihydropyrimidine	0-17	kinesin family member 11	Homo sapiens	105-108
20597485-0	2010	Structural basis for inhibition of Eg5 by dihydropyrimidines: stereoselectivity of antimitotic inhibitors enastron, dimethylenastron and fluorastrol.	enastron	106-114	kinesin family member 11	Homo sapiens	35-38
20597485-0	2010	Structural basis for inhibition of Eg5 by dihydropyrimidines: stereoselectivity of antimitotic inhibitors enastron, dimethylenastron and fluorastrol.	dimethylenastron	116-132	kinesin family member 11	Homo sapiens	35-38
20597485-0	2010	Structural basis for inhibition of Eg5 by dihydropyrimidines: stereoselectivity of antimitotic inhibitors enastron, dimethylenastron and fluorastrol.	fluorastrol	137-148	kinesin family member 11	Homo sapiens	35-38
20597485-2	2010	Here, we report the crystal structures of the Eg5 motor domain complexed with enastron, dimethylenastron, and fluorastrol.	enastron	78-86	kinesin family member 11	Homo sapiens	46-49
20597485-2	2010	Here, we report the crystal structures of the Eg5 motor domain complexed with enastron, dimethylenastron, and fluorastrol.	dimethylenastron	88-104	kinesin family member 11	Homo sapiens	46-49
20597485-2	2010	Here, we report the crystal structures of the Eg5 motor domain complexed with enastron, dimethylenastron, and fluorastrol.	fluorastrol	110-121	kinesin family member 11	Homo sapiens	46-49
20597485-4	2010	We also noticed preferential binding of the S-enantiomer of enastron and dimethylenastron to Eg5, while the R-enantiomer of fluorastrol binds preferentially to Eg5.	dimethylenastron	73-89	kinesin family member 11	Homo sapiens	93-96
20597485-4	2010	We also noticed preferential binding of the S-enantiomer of enastron and dimethylenastron to Eg5, while the R-enantiomer of fluorastrol binds preferentially to Eg5.	fluorastrol	124-135	kinesin family member 11	Homo sapiens	160-163
20515952-0	2010	Docetaxel-resistant prostate cancer cells remain sensitive to S-trityl-L-cysteine-mediated Eg5 inhibition.	Docetaxel	0-9	kinesin family member 11	Homo sapiens	91-94
20646066-5	2010	Curcumin also perturbed the localization of the kinesin protein Eg5 and induced monopolar spindle formation.	Curcumin	0-8	kinesin family member 11	Homo sapiens	64-67
20515952-0	2010	Docetaxel-resistant prostate cancer cells remain sensitive to S-trityl-L-cysteine-mediated Eg5 inhibition.	3-tritylthio-L-alanine	62-81	kinesin family member 11	Homo sapiens	91-94
20515952-4	2010	S-Trityl-L-cysteine (STLC) is a novel Eg5-specific small-molecule inhibitor.	3-tritylthio-L-alanine	0-19	kinesin family member 11	Homo sapiens	38-41
20515952-4	2010	S-Trityl-L-cysteine (STLC) is a novel Eg5-specific small-molecule inhibitor.	3-tritylthio-L-alanine	21-25	kinesin family member 11	Homo sapiens	38-41
20515952-11	2010	Hence, although docetaxel-resistant prostate cancer cells remain responsive to Eg5 inhibition with STLC, there are key differences at the cell cycle level, which may have implication in future development.	Docetaxel	16-25	kinesin family member 11	Homo sapiens	79-82
19697325-6	2010	When Eg5, a mitotic kinesin that plays an essential role in establishing mitotic spindle bipolarity, was inhibited using S-trityl-cysteine in glyfoline-treated cells, formation of spindle multipolarity, multipolar cell division, and multinuclei was significantly reduced.	3-tritylthio-L-alanine	121-138	kinesin family member 11	Homo sapiens	5-8
20513406-7	2010	In particular, EPR probes attached to the neck linker of MT-bound Eg5 shifted to a more immobilized component in the nucleotide-free state relative to the ADP-bound state, consistent with the neck linker docking upon ADP release.	Adenosine Diphosphate	155-158	kinesin family member 11	Homo sapiens	66-69
20513406-7	2010	In particular, EPR probes attached to the neck linker of MT-bound Eg5 shifted to a more immobilized component in the nucleotide-free state relative to the ADP-bound state, consistent with the neck linker docking upon ADP release.	Adenosine Diphosphate	217-220	kinesin family member 11	Homo sapiens	66-69
20154092-0	2010	Real-time structural transitions are coupled to chemical steps in ATP hydrolysis by Eg5 kinesin.	Adenosine Triphosphate	66-69	kinesin family member 11	Homo sapiens	84-87
20154092-3	2010	Here we show time-lapse monitoring of an in vitro ATP hydrolysis reaction by the motor domain of a human Kinesin-5 protein (Eg5) using difference Fourier transform infrared spectroscopy and UV photolysis of caged ATP.	Adenosine Triphosphate	50-53	kinesin family member 11	Homo sapiens	124-127
20154092-3	2010	Here we show time-lapse monitoring of an in vitro ATP hydrolysis reaction by the motor domain of a human Kinesin-5 protein (Eg5) using difference Fourier transform infrared spectroscopy and UV photolysis of caged ATP.	Adenosine Triphosphate	213-216	kinesin family member 11	Homo sapiens	124-127
20154092-5	2010	Simultaneous examination of conformational switching in Eg5, in parallel with catalytic steps, shows structural transitions in solution consistent with published crystal structures of the prehydrolytic and ADP-bound states.	Adenosine Diphosphate	206-209	kinesin family member 11	Homo sapiens	56-59
20154092-6	2010	In addition, we detect structural modifications in the Eg5 motor domain during bond cleavage between the beta- and gamma-phosphates of ATP.	beta- and gamma-phosphates	105-131	kinesin family member 11	Homo sapiens	55-58
20154092-6	2010	In addition, we detect structural modifications in the Eg5 motor domain during bond cleavage between the beta- and gamma-phosphates of ATP.	Adenosine Triphosphate	135-138	kinesin family member 11	Homo sapiens	55-58
19896928-0	2010	Mutations in the human kinesin Eg5 that confer resistance to monastrol and S-trityl-L-cysteine in tumor derived cell lines.	3-tritylthio-L-alanine	75-94	kinesin family member 11	Homo sapiens	31-34
19937728-11	2010	In addition, kinesin Eg5 inhibitor monastrol and dynein inhibitor erythro-9-3-(2-hydroxynonyl) adenine (EHNA) significantly blocked 2ME effects.	9-(2-hydroxy-3-nonyl)adenine	104-108	kinesin family member 11	Homo sapiens	21-24
19697325-6	2010	When Eg5, a mitotic kinesin that plays an essential role in establishing mitotic spindle bipolarity, was inhibited using S-trityl-cysteine in glyfoline-treated cells, formation of spindle multipolarity, multipolar cell division, and multinuclei was significantly reduced.	glyfoline	142-151	kinesin family member 11	Homo sapiens	5-8
19751672-0	2009	Force and premature binding of ADP can regulate the processivity of individual Eg5 dimers.	Adenosine Diphosphate	31-34	kinesin family member 11	Homo sapiens	79-82
19793049-3	2009	In the present paper, we report the crystal structure of the Eg5 motor domain complexed with a potent antimitotic inhibitor STLC (S-trityl-L-cysteine) to 2.0 A (1 A=0.1 nm) resolution.	3-tritylthio-L-alanine	130-149	kinesin family member 11	Homo sapiens	61-64
19945875-0	2010	The discovery of tetrahydro-beta-carbolines as inhibitors of the kinesin Eg5.	tryptoline	17-43	kinesin family member 11	Homo sapiens	73-76
19945875-1	2010	A series of tetrahydro-beta-carbolines were identified by HTS as inhibitors of the kinesin Eg5.	tryptoline	12-38	kinesin family member 11	Homo sapiens	91-94
19713760-8	2009	By contrast, cells arrested at mitosis with the KSP/Eg5 inhibitor S-trityl-L-cysteine and induced to undergo mitotic slippage were able to successfully divide and continued to proliferate after drug removal.	3-tritylthio-L-alanine	68-85	kinesin family member 11	Homo sapiens	52-55
19751672-1	2009	Using a high-resolution optical trapping instrument, we directly observed the processive motions of individual Eg5 dimers over a range of external loads and ATP, ADP, and phosphate concentrations.	Adenosine Triphosphate	157-160	kinesin family member 11	Homo sapiens	111-114
19751672-1	2009	Using a high-resolution optical trapping instrument, we directly observed the processive motions of individual Eg5 dimers over a range of external loads and ATP, ADP, and phosphate concentrations.	Adenosine Diphosphate	162-165	kinesin family member 11	Homo sapiens	111-114
19751672-1	2009	Using a high-resolution optical trapping instrument, we directly observed the processive motions of individual Eg5 dimers over a range of external loads and ATP, ADP, and phosphate concentrations.	Phosphates	171-180	kinesin family member 11	Homo sapiens	111-114
19751672-4	2009	At a constant moderate force, maintained with a force clamp, the premature binding of ADP strongly promoted microtubule release by Eg5, whereas the addition of ATP or phosphate had little effect on dissociation.	Adenosine Diphosphate	86-89	kinesin family member 11	Homo sapiens	131-134
19481450-0	2009	Substituted benzimidazoles: A novel chemotype for small molecule hKSP inhibitors.	Benzimidazoles	12-26	kinesin family member 11	Homo sapiens	65-69
19497292-2	2009	Circular dichroism and isothermal titration calorimetry of our pyrrolotriazine-4-one series of inhibitors with Eg5 motor domain revealed enhanced binding in the presence of adenosine 5"-diphosphate (ADP).	pyrrolotriazine-4-one	63-84	kinesin family member 11	Homo sapiens	111-114
19497292-2	2009	Circular dichroism and isothermal titration calorimetry of our pyrrolotriazine-4-one series of inhibitors with Eg5 motor domain revealed enhanced binding in the presence of adenosine 5"-diphosphate (ADP).	Adenosine Diphosphate	173-197	kinesin family member 11	Homo sapiens	111-114
19497292-2	2009	Circular dichroism and isothermal titration calorimetry of our pyrrolotriazine-4-one series of inhibitors with Eg5 motor domain revealed enhanced binding in the presence of adenosine 5"-diphosphate (ADP).	Adenosine Diphosphate	199-202	kinesin family member 11	Homo sapiens	111-114
19497292-5	2009	In general, the inhibitor potency of the pyrrolotriazine-4-one series in in vitro biological assays correlated with the magnitude of the thermal stability enhancement of ADP-Eg5.	pyrrolotriazine-4-one	41-62	kinesin family member 11	Homo sapiens	174-177
19497292-5	2009	In general, the inhibitor potency of the pyrrolotriazine-4-one series in in vitro biological assays correlated with the magnitude of the thermal stability enhancement of ADP-Eg5.	Adenosine Diphosphate	170-173	kinesin family member 11	Homo sapiens	174-177
19481450-1	2009	Substituted benzimidazoles were profiled as inhibitors of kinesin spindle protein (KSP), an increasingly important target for the development of anticancer drugs.	Benzimidazoles	12-26	kinesin family member 11	Homo sapiens	83-86
19545421-6	2009	Due to the brain location of the tumor, the potential target inhibition for anticancer therapy must exhibit a manageable neurotoxicity profile in the concentration range in which the compounds show anti-proliferative activity.Kinesin KIF11 inhibition by small molecules such as Monastrol or Ispinesib is currently under investigation in the field of malignant tumors.	monastrol	278-287	kinesin family member 11	Homo sapiens	234-239
19545421-6	2009	Due to the brain location of the tumor, the potential target inhibition for anticancer therapy must exhibit a manageable neurotoxicity profile in the concentration range in which the compounds show anti-proliferative activity.Kinesin KIF11 inhibition by small molecules such as Monastrol or Ispinesib is currently under investigation in the field of malignant tumors.	ispinesib	291-300	kinesin family member 11	Homo sapiens	234-239
19545421-8	2009	RESULTS: In this study the target was validated using a set of well characterised and potentially specific small molecule inhibitors of KIF11: an ispinesib analog, Monastrol, a Merck compound and 3 simplified derivatives of the Merck compound.	ispinesib	146-155	kinesin family member 11	Homo sapiens	136-141
18266314-0	2008	Structure-activity relationship of S-trityl-L-cysteine analogues as inhibitors of the human mitotic kinesin Eg5.	3-tritylthio-L-alanine	35-54	kinesin family member 11	Homo sapiens	108-111
18591782-5	2008	A new compound CPUYL064 showed good inhibitory effect against Eg5 (IC(50) value, 100 nM).	cpuyl064	15-23	kinesin family member 11	Homo sapiens	62-65
19270519-4	2009	Here, we show that targeting the mitotic kinesin Eg5 (also known as kinesin spindle protein, KSP) by a small interfering RNA (siRNA) or by the pharmacological inhibitor dimethylenastron (DIMEN) kills tetraploid tumor cells more efficiently than their diploid precursors.	dimethylenastron	169-185	kinesin family member 11	Homo sapiens	49-52
18512732-3	2008	To investigate the functional activities of Eg5 in CaP, we used an antisense oligonucleotide (ASO) targeting Eg5 to assess the potency and anti-cancer activity of Eg5 ASO treatment for androgen-independent CaP cells in vitro and in vivo.	Oligonucleotides, Antisense	94-97	kinesin family member 11	Homo sapiens	109-112
18512732-3	2008	To investigate the functional activities of Eg5 in CaP, we used an antisense oligonucleotide (ASO) targeting Eg5 to assess the potency and anti-cancer activity of Eg5 ASO treatment for androgen-independent CaP cells in vitro and in vivo.	Oligonucleotides, Antisense	94-97	kinesin family member 11	Homo sapiens	109-112
18512732-5	2008	In both cell lines, Eg5 ASO treatment reduced mRNA and protein levels in a dose-dependent manner and a complete reduction of Eg5 protein levels was observed at 100 nM.	Oligonucleotides, Antisense	24-27	kinesin family member 11	Homo sapiens	20-23
18512732-7	2008	Surprisingly, low dose Eg5 ASO significantly antagonized cytotoxic effects of paclitaxel.	Oligonucleotides, Antisense	27-30	kinesin family member 11	Homo sapiens	23-26
18512732-7	2008	Surprisingly, low dose Eg5 ASO significantly antagonized cytotoxic effects of paclitaxel.	Paclitaxel	78-88	kinesin family member 11	Homo sapiens	23-26
18512732-8	2008	In vivo, Eg5 ASO monotherapy significantly reduced both LNCaP and PC-3 tumor growth but combination treatment with paclitaxel did not yield additive benefits.	Oligonucleotides, Antisense	13-16	kinesin family member 11	Homo sapiens	9-12
18678707-3	2008	Eg5, the vertebrate kinesin-5, has two modes of motion: an adenosine triphosphate (ATP)-dependent directional mode and a diffusive mode that does not require ATP hydrolysis.	Adenosine Triphosphate	59-81	kinesin family member 11	Homo sapiens	0-3
18678707-3	2008	Eg5, the vertebrate kinesin-5, has two modes of motion: an adenosine triphosphate (ATP)-dependent directional mode and a diffusive mode that does not require ATP hydrolysis.	Adenosine Triphosphate	83-86	kinesin family member 11	Homo sapiens	0-3
18678707-3	2008	Eg5, the vertebrate kinesin-5, has two modes of motion: an adenosine triphosphate (ATP)-dependent directional mode and a diffusive mode that does not require ATP hydrolysis.	Adenosine Triphosphate	158-161	kinesin family member 11	Homo sapiens	0-3
18266314-4	2008	S-trityl-L-cysteine (STLC) is a tight-binding inhibitor of Eg5 that prevents mitotic progression.	3-tritylthio-L-alanine	0-19	kinesin family member 11	Homo sapiens	59-62
18266314-4	2008	S-trityl-L-cysteine (STLC) is a tight-binding inhibitor of Eg5 that prevents mitotic progression.	3-tritylthio-L-alanine	21-25	kinesin family member 11	Homo sapiens	59-62
16969080-9	2006	Inhibition of Eg5 expression or its activity blocks cell cycle progression and induces cell death independent of the cellular response to Imatinib.	Imatinib Mesylate	138-146	kinesin family member 11	Homo sapiens	14-17
18037705-6	2008	By contrast to the mechanism of Kinesin-1, microtubule association triggers ADP release from both motor domains of Eg5.	Adenosine Diphosphate	76-79	kinesin family member 11	Homo sapiens	115-118
18186019-0	2008	Proteome analysis of apoptosis signaling by S-trityl-L-cysteine, a potent reversible inhibitor of human mitotic kinesin Eg5.	3-tritylthio-L-alanine	44-63	kinesin family member 11	Homo sapiens	120-123
18186019-3	2008	One potent Eg5 inhibitor is S-trityl-L-cysteine (STLC), which arrests cells in mitosis and exhibits tumor growth inhibition activity.	3-tritylthio-L-alanine	28-47	kinesin family member 11	Homo sapiens	11-14
18186019-3	2008	One potent Eg5 inhibitor is S-trityl-L-cysteine (STLC), which arrests cells in mitosis and exhibits tumor growth inhibition activity.	3-tritylthio-L-alanine	49-53	kinesin family member 11	Homo sapiens	11-14
17827400-6	2007	Interestingly, in middle-aged people, the rs1111875 C-allele of HHEX/KIF11/IDE strongly associated with lower acute insulin response during an oral glucose tolerance test (P = 6 x 10(-7)).	Glucose	148-155	kinesin family member 11	Homo sapiens	69-74
17581299-9	2007	Pharmacological inhibition of Eg5 function, with either S-trityl-L-cysteine or monastrol, prevented growth of estrogen-treated MCF-7 cells with an IC50 of 0.46 and 29.71 micromol/l, respectively.	3-tritylthio-L-alanine	56-75	kinesin family member 11	Homo sapiens	30-33
17581299-9	2007	Pharmacological inhibition of Eg5 function, with either S-trityl-L-cysteine or monastrol, prevented growth of estrogen-treated MCF-7 cells with an IC50 of 0.46 and 29.71 micromol/l, respectively.	monastrol	79-88	kinesin family member 11	Homo sapiens	30-33
17251189-3	2007	Monastrol, a specific dihydropyrimidine inhibitor of Eg5, shows stereo-specificity, since predominantly the (S)-, but not the (R)-, enantiomer has been shown to be the biologically active compound in vitro and in cell-based assays.	monastrol	0-9	kinesin family member 11	Homo sapiens	53-56
17251189-3	2007	Monastrol, a specific dihydropyrimidine inhibitor of Eg5, shows stereo-specificity, since predominantly the (S)-, but not the (R)-, enantiomer has been shown to be the biologically active compound in vitro and in cell-based assays.	dihydropyrimidine	22-39	kinesin family member 11	Homo sapiens	53-56
17251189-4	2007	Here, we solved the crystal structure (2.7A) of the complex between human Eg5 and a new keto derivative of monastrol (named mon-97), a potent antimitotic inhibitor.	monastrol	107-116	kinesin family member 11	Homo sapiens	74-77
17251189-4	2007	Here, we solved the crystal structure (2.7A) of the complex between human Eg5 and a new keto derivative of monastrol (named mon-97), a potent antimitotic inhibitor.	CHEMBL1213953	124-130	kinesin family member 11	Homo sapiens	74-77
17406591-1	2007	We present here a protocol for the synthesis of the dihydropyrimidine (DHPM) derivative monastrol, which is known to be a specific mitotic kinesin Eg5 inhibitor.	dihydropyrimidine	52-69	kinesin family member 11	Homo sapiens	147-150
17406591-1	2007	We present here a protocol for the synthesis of the dihydropyrimidine (DHPM) derivative monastrol, which is known to be a specific mitotic kinesin Eg5 inhibitor.	ethyl 6-methyl-2-oxo-4-phenyl-1,2,3,4-tetrahydropyrimidine-5-carboxylate	71-75	kinesin family member 11	Homo sapiens	147-150
17406591-1	2007	We present here a protocol for the synthesis of the dihydropyrimidine (DHPM) derivative monastrol, which is known to be a specific mitotic kinesin Eg5 inhibitor.	monastrol	88-97	kinesin family member 11	Homo sapiens	147-150
16934364-0	2006	Eg5 expression is closely correlated with the response of advanced non-small cell lung cancer to antimitotic agents combined with platinum chemotherapy.	Platinum	130-138	kinesin family member 11	Homo sapiens	0-3
16934364-3	2006	PATIENTS AND METHODS: Eg5 expression was investigated immunohistochemically in 122 formalin-fixed tumor samples from untreated stage IIIB or IV NSCLC patients.	Formaldehyde	83-91	kinesin family member 11	Homo sapiens	22-25
16934364-10	2006	CONCLUSIONS: Eg5 expression can predict a response to antimitotic agents combined with platinum chemotherapy among patients with advanced NSCLC.	Platinum	87-95	kinesin family member 11	Homo sapiens	13-16
17014086-0	2006	Pathway of ATP hydrolysis by monomeric kinesin Eg5.	Adenosine Triphosphate	11-14	kinesin family member 11	Homo sapiens	47-50
17014086-3	2006	The pre-steady-state kinetic results show that the microtubule-Eg5 complex binds MgATP tightly, followed by rapid ATP hydrolysis with a subsequent slow step that limits steady-state turnover.	Adenosine Triphosphate	81-86	kinesin family member 11	Homo sapiens	63-66
17014086-3	2006	The pre-steady-state kinetic results show that the microtubule-Eg5 complex binds MgATP tightly, followed by rapid ATP hydrolysis with a subsequent slow step that limits steady-state turnover.	Adenosine Triphosphate	83-86	kinesin family member 11	Homo sapiens	63-66
16969080-0	2006	Regulation and targeting of Eg5, a mitotic motor protein in blast crisis CML: overcoming imatinib resistance.	Imatinib Mesylate	89-97	kinesin family member 11	Homo sapiens	28-31
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	Imatinib Mesylate	25-33	kinesin family member 11	Homo sapiens	48-51
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	Imatinib Mesylate	66-74	kinesin family member 11	Homo sapiens	48-51
16969080-5	2006	Inhibition of Bcr-Abl by Imatinib downregulated Eg5 expression in Imatinib-sensitive KBM5 and HL-60p185 cells, but not in Imatinib-resistant KBM5-STI571, harboring a T315I mutation, and Bcr-Abl-negative HL-60 cells.	Imatinib Mesylate	66-74	kinesin family member 11	Homo sapiens	48-51
16969080-6	2006	Blocking Eg5 expression with antisense oligonucleotide (Eg5-ASO) or inhibiting its activity with the small-molecule Eg5 inhibitor, S-trityl-L-cysteine induced G(2)/M cell cycle block and subsequent cell death in both Imatinib-sensitive and -resistant cells.	Oligonucleotides	39-54	kinesin family member 11	Homo sapiens	9-12
16969080-6	2006	Blocking Eg5 expression with antisense oligonucleotide (Eg5-ASO) or inhibiting its activity with the small-molecule Eg5 inhibitor, S-trityl-L-cysteine induced G(2)/M cell cycle block and subsequent cell death in both Imatinib-sensitive and -resistant cells.	3-tritylthio-L-alanine	131-150	kinesin family member 11	Homo sapiens	9-12
16969080-6	2006	Blocking Eg5 expression with antisense oligonucleotide (Eg5-ASO) or inhibiting its activity with the small-molecule Eg5 inhibitor, S-trityl-L-cysteine induced G(2)/M cell cycle block and subsequent cell death in both Imatinib-sensitive and -resistant cells.	Imatinib Mesylate	217-225	kinesin family member 11	Homo sapiens	9-12
17041103-0	2006	Induction of apoptosis by monastrol, an inhibitor of the mitotic kinesin Eg5, is independent of the spindle checkpoint.	monastrol	26-35	kinesin family member 11	Homo sapiens	73-76
16814965-0	2006	Phenothiazine and carbazole-related compounds inhibit mitotic kinesin Eg5 and trigger apoptosis in transformed culture cells.	phenothiazine	0-13	kinesin family member 11	Homo sapiens	70-73
16814965-0	2006	Phenothiazine and carbazole-related compounds inhibit mitotic kinesin Eg5 and trigger apoptosis in transformed culture cells.	carbazole	18-27	kinesin family member 11	Homo sapiens	70-73
16892050-7	2006	We find that Eg5 is a processive kinesin whose motility includes, in addition to ATP-dependent directional motion, a diffusive component not requiring ATP hydrolysis.	Adenosine Triphosphate	81-84	kinesin family member 11	Homo sapiens	13-16
16892050-7	2006	We find that Eg5 is a processive kinesin whose motility includes, in addition to ATP-dependent directional motion, a diffusive component not requiring ATP hydrolysis.	Adenosine Triphosphate	151-154	kinesin family member 11	Homo sapiens	13-16
17827400-10	2007	Importantly, variations within the HHEX/KIF11/IDE and CDKN2A/B loci confer impaired glucose- and tolbutamide-induced insulin release in middle-aged and young healthy subjects, suggesting a role for these variants in the pathogenesis of pancreatic beta-cell dysfunction.	Glucose	84-91	kinesin family member 11	Homo sapiens	40-45
17827400-10	2007	Importantly, variations within the HHEX/KIF11/IDE and CDKN2A/B loci confer impaired glucose- and tolbutamide-induced insulin release in middle-aged and young healthy subjects, suggesting a role for these variants in the pathogenesis of pancreatic beta-cell dysfunction.	Tolbutamide	97-108	kinesin family member 11	Homo sapiens	40-45
17524640-0	2007	Synthesis and biological evaluation of L-cysteine derivatives as mitotic kinesin Eg5 inhibitors.	Cysteine	39-49	kinesin family member 11	Homo sapiens	81-84
17524640-2	2007	Here, we report the synthesis and structure-activity relationship of S-trityl-L-cysteine (STLC) derivatives as Eg5 inhibitors.	3-tritylthio-L-alanine	69-88	kinesin family member 11	Homo sapiens	111-114
17524640-2	2007	Here, we report the synthesis and structure-activity relationship of S-trityl-L-cysteine (STLC) derivatives as Eg5 inhibitors.	3-tritylthio-L-alanine	90-94	kinesin family member 11	Homo sapiens	111-114
17062577-0	2006	Dimeric Eg5 maintains processivity through alternating-site catalysis with rate-limiting ATP hydrolysis.	Adenosine Triphosphate	89-92	kinesin family member 11	Homo sapiens	8-11
17062577-5	2006	In addition, the kinetics of P(i) release and ATP-promoted microtubule-Eg5 dissociation were observed to be no faster than the rate of ATP hydrolysis.	Adenosine Triphosphate	46-49	kinesin family member 11	Homo sapiens	71-74
17062577-6	2006	In combination the data suggest that dimeric Eg5 is the first kinesin motor identified to have a rate-limiting ATP hydrolysis step.	Adenosine Triphosphate	111-114	kinesin family member 11	Homo sapiens	45-48
16969080-10	2006	Therefore, Eg5 could be a potential therapeutic target for the treatment of BC CML, in particular Imatinib-resistant BC CML.	Imatinib Mesylate	98-106	kinesin family member 11	Homo sapiens	11-14
15476401-0	2004	Identification of the protein binding region of S-trityl-L-cysteine, a new potent inhibitor of the mitotic kinesin Eg5.	3-tritylthio-L-alanine	48-67	kinesin family member 11	Homo sapiens	115-118
16365780-2	2006	Eg5 localises to microtubules in mitosis, but not to interphase microtubules, suggesting that Eg5 inhibitors may be useful to specifically target proliferating tumour tissue, thereby avoiding dose-limiting neuropathy observed with other antimicrotubule agents like taxanes or vinca alkaloids.	Taxoids	265-272	kinesin family member 11	Homo sapiens	0-3
16365780-2	2006	Eg5 localises to microtubules in mitosis, but not to interphase microtubules, suggesting that Eg5 inhibitors may be useful to specifically target proliferating tumour tissue, thereby avoiding dose-limiting neuropathy observed with other antimicrotubule agents like taxanes or vinca alkaloids.	Taxoids	265-272	kinesin family member 11	Homo sapiens	94-97
16365780-2	2006	Eg5 localises to microtubules in mitosis, but not to interphase microtubules, suggesting that Eg5 inhibitors may be useful to specifically target proliferating tumour tissue, thereby avoiding dose-limiting neuropathy observed with other antimicrotubule agents like taxanes or vinca alkaloids.	Vinca Alkaloids	276-291	kinesin family member 11	Homo sapiens	0-3
16365780-2	2006	Eg5 localises to microtubules in mitosis, but not to interphase microtubules, suggesting that Eg5 inhibitors may be useful to specifically target proliferating tumour tissue, thereby avoiding dose-limiting neuropathy observed with other antimicrotubule agents like taxanes or vinca alkaloids.	Vinca Alkaloids	276-291	kinesin family member 11	Homo sapiens	94-97
16365780-8	2006	The observed interaction profile of monastrol with Pgp is promising for the development of other more potent Eg5 inhibitors.	monastrol	36-45	kinesin family member 11	Homo sapiens	109-112
16402342-0	2006	Use of hydrogen/deuterium exchange mass spectrometry and mutagenesis as a tool to identify the binding region of inhibitors targeting the human mitotic kinesin Eg5.	Hydrogen	7-15	kinesin family member 11	Homo sapiens	160-163
16402342-0	2006	Use of hydrogen/deuterium exchange mass spectrometry and mutagenesis as a tool to identify the binding region of inhibitors targeting the human mitotic kinesin Eg5.	Deuterium	16-25	kinesin family member 11	Homo sapiens	160-163
16402342-1	2006	An experimental procedure associating both hydrogen/deuterium exchange mass spectrometry (H/D-MS) and mutagenesis was developed to identify the protein-binding region of small inhibitors targeting the motor domain of the human mitotic kinesin Eg5.	Deuterium	52-61	kinesin family member 11	Homo sapiens	243-246
16342954-5	2005	ATP hydrolysis and phosphate product release are rapid steps in the mechanism, and the observed rate of these steps is limited by the relatively slow isomerization of the Eg5-ATP collision complex.	Adenosine Triphosphate	0-3	kinesin family member 11	Homo sapiens	171-174
16342954-5	2005	ATP hydrolysis and phosphate product release are rapid steps in the mechanism, and the observed rate of these steps is limited by the relatively slow isomerization of the Eg5-ATP collision complex.	Phosphates	19-28	kinesin family member 11	Homo sapiens	171-174
16342954-5	2005	ATP hydrolysis and phosphate product release are rapid steps in the mechanism, and the observed rate of these steps is limited by the relatively slow isomerization of the Eg5-ATP collision complex.	Adenosine Triphosphate	175-178	kinesin family member 11	Homo sapiens	171-174
16342954-8	2005	Monastrol appears to bind weakly to the Eg5-ATP collision complex, but after tight ATP binding, the affinity for monastrol increases, thus inhibiting the conformational change required for ADP product release.	monastrol	0-9	kinesin family member 11	Homo sapiens	40-43
16342954-8	2005	Monastrol appears to bind weakly to the Eg5-ATP collision complex, but after tight ATP binding, the affinity for monastrol increases, thus inhibiting the conformational change required for ADP product release.	Adenosine Triphosphate	44-47	kinesin family member 11	Homo sapiens	40-43
16022179-5	2005	This review describes key advances made over the last year toward the design and development of inhibitors of kinesin motor proteins, with particular emphasis placed on non-ATP-competitive, small-molecule inhibitors of kinesin spindle protein (Eg5).	Adenosine Triphosphate	173-176	kinesin family member 11	Homo sapiens	244-247
16507573-0	2006	S-trityl-L-cysteine is a reversible, tight binding inhibitor of the human kinesin Eg5 that specifically blocks mitotic progression.	3-tritylthio-L-alanine	0-19	kinesin family member 11	Homo sapiens	82-85
16507573-1	2006	Human Eg5, responsible for the formation of the bipolar mitotic spindle, has been identified recently as one of the targets of S-trityl-L-cysteine, a potent tumor growth inhibitor in the NCI 60 tumor cell line screen.	3-tritylthio-L-alanine	127-146	kinesin family member 11	Homo sapiens	6-9
16507573-4	2006	In vitro, S-trityl-L-cysteine targets the catalytic domain of Eg5 and inhibits Eg5 basal and microtubule-activated ATPase activity as well as mant-ADP release.	3-tritylthio-L-alanine	10-29	kinesin family member 11	Homo sapiens	62-65
16507573-4	2006	In vitro, S-trityl-L-cysteine targets the catalytic domain of Eg5 and inhibits Eg5 basal and microtubule-activated ATPase activity as well as mant-ADP release.	3-tritylthio-L-alanine	10-29	kinesin family member 11	Homo sapiens	79-82
16507573-7	2006	S-trityl-L-cysteine inhibits Eg5-driven microtubule sliding velocity in a reversible fashion with an IC(50) of 500 nm.	3-tritylthio-L-alanine	0-19	kinesin family member 11	Homo sapiens	29-32
16507573-9	2006	Among nine different human kinesins tested, S-trityl-L-cysteine is specific for Eg5.	3-tritylthio-L-alanine	44-63	kinesin family member 11	Homo sapiens	80-83
16604065-3	2006	Individual dimers, formed by a recombinant human construct Eg5-513-5His, stepped processively along microtubules in 8-nm increments, with short run lengths averaging approximately eight steps.	5his	67-71	kinesin family member 11	Homo sapiens	59-62
16604065-4	2006	By varying the applied load (with a force clamp) and the ATP concentration, we found that the velocity of Eg5 was slower and less sensitive to external load than that of conventional kinesin, possibly reflecting the distinct demands of spindle assembly as compared with vesicle transport.	Adenosine Triphosphate	57-60	kinesin family member 11	Homo sapiens	106-109
16458511-0	2006	Inhibitors of human mitotic kinesin Eg5: characterization of the 4-phenyl-tetrahydroisoquinoline lead series.	4-phenyl-tetrahydroisoquinoline	65-96	kinesin family member 11	Homo sapiens	36-39
16458511-1	2006	In a high-throughput screening effort, a series of tetrahydroisoquinolines was identified as modest inhibitors of human Eg5.	Tetrahydroisoquinolines	51-74	kinesin family member 11	Homo sapiens	120-123
16434397-1	2006	Monastrol is a small molecule inhibitor that is specific for Eg5, a member of the kinesin 5 family of mitotic motors.	monastrol	0-9	kinesin family member 11	Homo sapiens	61-64
16084101-0	2005	Synthesis and biological evaluation of new tetrahydro-beta-carbolines as inhibitors of the mitotic kinesin Eg5.	tryptoline	43-69	kinesin family member 11	Homo sapiens	107-110
16084101-5	2005	One of these derivatives (compound trans-24) proved to be a potent and specific Eg5 inhibitor.	Eg5 Inhibitor V, trans-24	35-43	kinesin family member 11	Homo sapiens	80-83
16216042-3	2005	Here, we present the synthesis and biological investigation of 3,4-dihydrophenylquinazoline-2(1H)-thiones as selective and potent Eg5 inhibitors.	3,4-dihydrophenylquinazoline-2(1h)-thiones	63-105	kinesin family member 11	Homo sapiens	130-133
16115880-4	2005	Our results are consistent with a model in which movement in Eg5 occurs in two sequential steps, an ATP-dependent docking of the neck linker, followed by a rotation or "rolling" of the entire motor domain on the microtubule surface that occurs with ATP hydrolysis.	Adenosine Triphosphate	100-103	kinesin family member 11	Homo sapiens	61-64
16115880-4	2005	Our results are consistent with a model in which movement in Eg5 occurs in two sequential steps, an ATP-dependent docking of the neck linker, followed by a rotation or "rolling" of the entire motor domain on the microtubule surface that occurs with ATP hydrolysis.	Adenosine Triphosphate	249-252	kinesin family member 11	Homo sapiens	61-64
15665380-4	2005	In the presence of microtubules, the ATPase activity is also reduced with weakened binding of Eg5 to microtubules during steady-state ATP turnover.	Adenosine Triphosphate	37-40	kinesin family member 11	Homo sapiens	94-97
15665380-5	2005	Monastrol-treated Eg5 also shows a decreased relative affinity for microtubules under equilibrium conditions.	monastrol	0-9	kinesin family member 11	Homo sapiens	18-21
15665380-6	2005	The Mt.Eg5 presteady-state kinetics of ATP binding and the subsequent ATP-dependent isomerization are unaffected during the first ATP turnover.	Adenosine Triphosphate	39-42	kinesin family member 11	Homo sapiens	7-10
15665380-6	2005	The Mt.Eg5 presteady-state kinetics of ATP binding and the subsequent ATP-dependent isomerization are unaffected during the first ATP turnover.	Adenosine Triphosphate	70-73	kinesin family member 11	Homo sapiens	7-10
15665380-6	2005	The Mt.Eg5 presteady-state kinetics of ATP binding and the subsequent ATP-dependent isomerization are unaffected during the first ATP turnover.	Adenosine Triphosphate	70-73	kinesin family member 11	Homo sapiens	7-10
15665380-8	2005	Monastrol promotes a dramatic decrease in the observed rate of Eg5 association with microtubules, and ADP release is slowed without trapping the Mt.Eg5.ADP intermediate.	monastrol	0-9	kinesin family member 11	Homo sapiens	63-66
15665380-9	2005	We propose that S-monastrol binding to Eg5 induces a stable conformational change in the motor domain that favors ATP re-synthesis after ATP hydrolysis.	monastrol	16-27	kinesin family member 11	Homo sapiens	39-42
15665380-9	2005	We propose that S-monastrol binding to Eg5 induces a stable conformational change in the motor domain that favors ATP re-synthesis after ATP hydrolysis.	Adenosine Triphosphate	114-117	kinesin family member 11	Homo sapiens	39-42
15665380-9	2005	We propose that S-monastrol binding to Eg5 induces a stable conformational change in the motor domain that favors ATP re-synthesis after ATP hydrolysis.	Adenosine Triphosphate	137-140	kinesin family member 11	Homo sapiens	39-42
15665380-10	2005	The aberrant interactions with the microtubule and the reversals at the ATP hydrolysis step alter the ability of Eg5 to generate force, thereby yielding a nonproductive Mt.Eg5 complex that cannot establish or maintain the bipolar spindle.	Adenosine Triphosphate	72-75	kinesin family member 11	Homo sapiens	113-116
15665380-10	2005	The aberrant interactions with the microtubule and the reversals at the ATP hydrolysis step alter the ability of Eg5 to generate force, thereby yielding a nonproductive Mt.Eg5 complex that cannot establish or maintain the bipolar spindle.	Adenosine Triphosphate	72-75	kinesin family member 11	Homo sapiens	172-175
15653676-5	2005	Using affinity chromatography we first show that the compound HR22C16 is an Eg5 inhibitor and does not interact with other microtubule motor proteins tested.	HR22C16	62-69	kinesin family member 11	Homo sapiens	76-79
15653676-6	2005	Furthermore, HR22C16 along with its analogs, inhibit cell survival in both Taxol-sensitive and -resistant ovarian cancer cells with at least 15-fold greater efficacy than monastrol, the first generation Eg5 inhibitor.	monastrol	171-180	kinesin family member 11	Homo sapiens	203-206
15653676-10	2005	Taken together, our results show that Eg5 inhibitors have promising anticancer activity and can be potentially used to overcome Taxol resistance in the clinical setting.	Paclitaxel	128-133	kinesin family member 11	Homo sapiens	38-41
15476401-3	2004	We have used hydrogen-deuterium exchange mass spectrometry and directed mutagenesis to identify the secondary structure elements that form the binding sites of new Eg5 inhibitors, in particular for S-trityl-l-cysteine, a potent inhibitor of Eg5 activity in vitro and in cell-based assays.	Hydrogen	13-21	kinesin family member 11	Homo sapiens	164-167
15476401-3	2004	We have used hydrogen-deuterium exchange mass spectrometry and directed mutagenesis to identify the secondary structure elements that form the binding sites of new Eg5 inhibitors, in particular for S-trityl-l-cysteine, a potent inhibitor of Eg5 activity in vitro and in cell-based assays.	Deuterium	22-31	kinesin family member 11	Homo sapiens	164-167
15476401-3	2004	We have used hydrogen-deuterium exchange mass spectrometry and directed mutagenesis to identify the secondary structure elements that form the binding sites of new Eg5 inhibitors, in particular for S-trityl-l-cysteine, a potent inhibitor of Eg5 activity in vitro and in cell-based assays.	3-tritylthio-L-alanine	198-217	kinesin family member 11	Homo sapiens	164-167
15476401-3	2004	We have used hydrogen-deuterium exchange mass spectrometry and directed mutagenesis to identify the secondary structure elements that form the binding sites of new Eg5 inhibitors, in particular for S-trityl-l-cysteine, a potent inhibitor of Eg5 activity in vitro and in cell-based assays.	3-tritylthio-L-alanine	198-217	kinesin family member 11	Homo sapiens	241-244
15476401-5	2004	Replacement of the Tyr125-Glu145 region with the equivalent region in the Neurospora crassa conventional kinesin heavy chain prevents the inhibition of the Eg5 ATPase activity by S-trityl-l-cysteine.	3-tritylthio-L-alanine	179-198	kinesin family member 11	Homo sapiens	156-159
15476401-6	2004	We show here that S-trityl-l-cysteine and monastrol both bind to the same region on Eg5 by induced fit in a pocket formed by helix alpha3-strand beta5 and loop L5-helix alpha2, and both inhibitors trigger similar local conformational changes within the interaction site.	3-tritylthio-L-alanine	18-37	kinesin family member 11	Homo sapiens	84-87
15476401-6	2004	We show here that S-trityl-l-cysteine and monastrol both bind to the same region on Eg5 by induced fit in a pocket formed by helix alpha3-strand beta5 and loop L5-helix alpha2, and both inhibitors trigger similar local conformational changes within the interaction site.	monastrol	42-51	kinesin family member 11	Homo sapiens	84-87
15367702-3	2004	We screened preselected libraries obtained from the National Cancer Institute and identified S-trityl-L-cysteine as the most effective Eg5 inhibitor with an IC50 of 1.0 micromol/L for the inhibition of basal ATPase activity and 140 nmol/L for the microtubule-activated ATPase activity.	3-tritylthio-L-alanine	93-112	kinesin family member 11	Homo sapiens	135-138
15247293-3	2004	The steady-state parameters were: for Eg5-367: k(cat) = 5.5 s(-1), K(1/2,Mt) = 0.7 microm, and K(m,ATP) = 25 microm; and for Eg5-437: k(cat) = 2.9 s(-1), K(1/2,Mt) = 4.5 microm, and K(m,ATP) = 19 microm.	Adenosine Triphosphate	99-102	kinesin family member 11	Homo sapiens	38-41
15247293-5	2004	ATP-dependent Mt.Eg5 dissociation was relatively slow and rate-limiting at 8 s(-1) with mantADP release at 40 s(-1).	Adenosine Triphosphate	0-3	kinesin family member 11	Homo sapiens	17-20
15247293-5	2004	ATP-dependent Mt.Eg5 dissociation was relatively slow and rate-limiting at 8 s(-1) with mantADP release at 40 s(-1).	3'-O-(N-methylanthraniloyl)adenosine 5'-diphosphate	88-95	kinesin family member 11	Homo sapiens	17-20
15247293-7	2004	These results indicate that the ATPase pathway for monomeric Eg5 is more similar to conventional kinesin than the spindle motors Ncd and Kar3, where ADP product release is rate-limiting for steady-state turnover.	Adenosine Diphosphate	149-152	kinesin family member 11	Homo sapiens	61-64
15367702-6	2004	Gossypol, flexeril, and two phenothiazine analogues were also identified as Eg5 inhibitors, and we found that they all result in monoastral spindles in HeLa cells.	Gossypol	0-8	kinesin family member 11	Homo sapiens	76-79
15367702-6	2004	Gossypol, flexeril, and two phenothiazine analogues were also identified as Eg5 inhibitors, and we found that they all result in monoastral spindles in HeLa cells.	cyclobenzaprine	10-18	kinesin family member 11	Homo sapiens	76-79
15367702-6	2004	Gossypol, flexeril, and two phenothiazine analogues were also identified as Eg5 inhibitors, and we found that they all result in monoastral spindles in HeLa cells.	phenothiazine	28-41	kinesin family member 11	Homo sapiens	76-79
12678775-7	2003	Terpendole E inhibited the motor activity of mitotic kinesin, Eg5 and induced monoastral spindle in M phase.	terpendole	0-10	kinesin family member 11	Homo sapiens	62-65
15302853-6	2004	Thus, two independent pathways contribute to spindle bipolarity, with the Eg5-dependent pathway using motor force to drive spindle bipolarity and the Kif2a-dependent pathway relying on microtubule polymer dynamics to generate force for spindle bipolarity.	Polymers	197-204	kinesin family member 11	Homo sapiens	74-77
15287721-0	2004	Disparity in allosteric interactions of monastrol with Eg5 in the presence of ADP and ATP: a difference FT-IR investigation.	Adenosine Diphosphate	78-81	kinesin family member 11	Homo sapiens	55-58
15287721-0	2004	Disparity in allosteric interactions of monastrol with Eg5 in the presence of ADP and ATP: a difference FT-IR investigation.	Adenosine Triphosphate	86-89	kinesin family member 11	Homo sapiens	55-58
15287721-4	2004	Utilizing a truncated Eg5 protein, we employ difference infrared spectroscopy to probe structural changes that occur in the motor protein with monastrol in the presence of either ADP or ATP.	Adenosine Diphosphate	179-182	kinesin family member 11	Homo sapiens	22-25
15287721-4	2004	Utilizing a truncated Eg5 protein, we employ difference infrared spectroscopy to probe structural changes that occur in the motor protein with monastrol in the presence of either ADP or ATP.	Adenosine Triphosphate	186-189	kinesin family member 11	Homo sapiens	22-25
15287721-7	2004	In Eg5-monastrol complexes, exchange of ADP is associated with a decrease in random structure and an increase in alpha-helical content.	Adenosine Diphosphate	40-43	kinesin family member 11	Homo sapiens	3-6
15287721-9	2004	One or more carboxylic acid residues in Eg5 undergo unique changes when ATP, but not ADP, interacts with the motor domain in the presence of monastrol.	Carboxylic Acids	12-27	kinesin family member 11	Homo sapiens	40-43
15287721-9	2004	One or more carboxylic acid residues in Eg5 undergo unique changes when ATP, but not ADP, interacts with the motor domain in the presence of monastrol.	Adenosine Triphosphate	72-75	kinesin family member 11	Homo sapiens	40-43
15287721-9	2004	One or more carboxylic acid residues in Eg5 undergo unique changes when ATP, but not ADP, interacts with the motor domain in the presence of monastrol.	Adenosine Diphosphate	85-88	kinesin family member 11	Homo sapiens	40-43
12525161-6	2003	Enzymatic techniques indicate that monastrol partially inhibits Eg5 ATPase activity by binding directly to the motor domain.	monastrol	35-44	kinesin family member 11	Homo sapiens	64-67
12618185-0	2003	A novel action of terpendole E on the motor activity of mitotic Kinesin Eg5.	terpendole	18-28	kinesin family member 11	Homo sapiens	72-75
12618185-2	2003	We have been screening microbial products to find specific M phase inhibitors that do not directly target tubulins, and rediscovered terpendole E (TerE) as a novel Eg5 inhibitor.	terpendole E	133-145	kinesin family member 11	Homo sapiens	164-167
12618185-2	2003	We have been screening microbial products to find specific M phase inhibitors that do not directly target tubulins, and rediscovered terpendole E (TerE) as a novel Eg5 inhibitor.	terpendole E	147-151	kinesin family member 11	Homo sapiens	164-167
12618185-4	2003	TerE inhibited both motor and microtubule-stimulated ATPase activities of human Eg5, but did not affect conventional kinesin from either Drosophila or bovine brain.	terpendole E	0-4	kinesin family member 11	Homo sapiens	80-83
12618185-5	2003	Although terpendoles have been reported as inhibitors of acyl-CoA:cholesterol O-acyltransferase (ACAT), the Eg5 inhibitory activity of TerE was independent of ACAT inhibition.	terpendole E	135-139	kinesin family member 11	Homo sapiens	108-111
12618185-6	2003	Taken together, we demonstrate that TerE is a novel Eg5 inhibitor isolated from a fungal strain.	terpendole E	36-40	kinesin family member 11	Homo sapiens	52-55
12525161-10	2003	Stopped-flow fluorometry indicates that monastrol inhibits ADP release by forming an Eg5-ADP-monastrol ternary complex.	monastrol	40-49	kinesin family member 11	Homo sapiens	85-88
12525161-10	2003	Stopped-flow fluorometry indicates that monastrol inhibits ADP release by forming an Eg5-ADP-monastrol ternary complex.	Adenosine Diphosphate	59-62	kinesin family member 11	Homo sapiens	85-88
12323373-1	2002	Monastrol, a cell-permeable inhibitor of the kinesin Eg5, has been used to probe the dynamic organization of the mitotic spindle.	monastrol	0-9	kinesin family member 11	Homo sapiens	53-56
12323373-3	2002	We found that monastrol inhibits both the basal and the microtubule-stimulated ATPase activity of the Eg5 motor domain.	monastrol	14-23	kinesin family member 11	Homo sapiens	102-105
12323373-5	2002	Monastrol appears to inhibit microtubule-stimulated ADP release from Eg5 but does not compete with microtubule binding, suggesting that monastrol binds a novel allosteric site in the motor domain.	monastrol	0-9	kinesin family member 11	Homo sapiens	69-72
12323373-5	2002	Monastrol appears to inhibit microtubule-stimulated ADP release from Eg5 but does not compete with microtubule binding, suggesting that monastrol binds a novel allosteric site in the motor domain.	Adenosine Diphosphate	52-55	kinesin family member 11	Homo sapiens	69-72
12323373-6	2002	Finally, we established that (S)-monastrol, as compared to the (R)-enantiomer, is a more potent inhibitor of Eg5 activity in vitro and in vivo.	monastrol	29-42	kinesin family member 11	Homo sapiens	109-112
11328809-3	2001	We have determined the crystal structure of the Eg5 motor domain with ADP-Mg bound.	Adenosine Diphosphate	70-73	kinesin family member 11	Homo sapiens	48-51
34800719-0	2022	KIF11, a plus end-directed kinesin, as a key gene in benzo(a)pyrene-induced non-small cell lung cancer.	benzo(a)	53-61	kinesin family member 11	Homo sapiens	0-5
33808108-0	2021	Solvothermal Synthesis of Multiple Dihydropyrimidinones at a Time as Inhibitors of Eg5.	dihydropyrimidinones	35-55	kinesin family member 11	Homo sapiens	83-86
34800719-0	2022	KIF11, a plus end-directed kinesin, as a key gene in benzo(a)pyrene-induced non-small cell lung cancer.	pyrene	61-67	kinesin family member 11	Homo sapiens	0-5
34800719-7	2022	In summary, the present study revealed that KIF11 might be a key gene in the tumorigenesis of BPDE-related lung cancer, raising the possibility of KIF11 as a target for BPDE-induced lung cancer prevention and therapy.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	94-98	kinesin family member 11	Homo sapiens	44-49
34800719-7	2022	In summary, the present study revealed that KIF11 might be a key gene in the tumorigenesis of BPDE-related lung cancer, raising the possibility of KIF11 as a target for BPDE-induced lung cancer prevention and therapy.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	94-98	kinesin family member 11	Homo sapiens	147-152
34800719-7	2022	In summary, the present study revealed that KIF11 might be a key gene in the tumorigenesis of BPDE-related lung cancer, raising the possibility of KIF11 as a target for BPDE-induced lung cancer prevention and therapy.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	169-173	kinesin family member 11	Homo sapiens	44-49
34800719-7	2022	In summary, the present study revealed that KIF11 might be a key gene in the tumorigenesis of BPDE-related lung cancer, raising the possibility of KIF11 as a target for BPDE-induced lung cancer prevention and therapy.	7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide	169-173	kinesin family member 11	Homo sapiens	147-152
34800881-15	2021	According to further verification of related genes, the mRNA and protein levels of KIF11, CCNA2 and CDC25A decrease significantly after treatment with dehydroabietic acid.	dehydroabietic acid	151-170	kinesin family member 11	Homo sapiens	83-88
34264310-0	2021	Kolaflavanone, a biflavonoid derived from medicinal plant Garcinia, is an inhibitor of mitotic kinesin Eg5.	kolaviron	0-13	kinesin family member 11	Homo sapiens	103-106
34264310-0	2021	Kolaflavanone, a biflavonoid derived from medicinal plant Garcinia, is an inhibitor of mitotic kinesin Eg5.	Biflavonoids	17-28	kinesin family member 11	Homo sapiens	103-106
34264310-4	2021	Herein, we report the inhibitory effect of kolaflavanone (KLF), a Garcinia biflavonoid, on the ATPase and microtubule-gliding activities of mitotic kinesin Eg5.	kolaviron	43-56	kinesin family member 11	Homo sapiens	156-159
34264310-4	2021	Herein, we report the inhibitory effect of kolaflavanone (KLF), a Garcinia biflavonoid, on the ATPase and microtubule-gliding activities of mitotic kinesin Eg5.	klf	58-61	kinesin family member 11	Homo sapiens	156-159
35382311-3	2022	Furthermore, in silico based structure activity analysis of the synthesized BIM derivatives divulges their potential ability to bind antineoplastic drug target and spindle motor protein kinesin Eg5.	1,1-bis(3'-indolyl)methane	76-79	kinesin family member 11	Homo sapiens	194-197
34264310-9	2021	The Eg5-KLF model obtained from molecular docking showed that the biflavonoid exists within the alpha2/alpha3/L5 (alpha2: Lys111-Glu116 and Ile135-Asp149, alpha3: Asn206-Thr226; L5: Gly117-Gly134) pocket, with a binding pose comparable to known Eg5 inhibitors.	Biflavonoids	66-77	kinesin family member 11	Homo sapiens	4-7
34264310-9	2021	The Eg5-KLF model obtained from molecular docking showed that the biflavonoid exists within the alpha2/alpha3/L5 (alpha2: Lys111-Glu116 and Ile135-Asp149, alpha3: Asn206-Thr226; L5: Gly117-Gly134) pocket, with a binding pose comparable to known Eg5 inhibitors.	Biflavonoids	66-77	kinesin family member 11	Homo sapiens	245-248
34958711-5	2022	Our lead compound is a cell permeable azobenzene that inhibits Eg5 more potently in its light-induced cis form.	azobenzene	38-48	kinesin family member 11	Homo sapiens	63-66
34711161-5	2021	N1-substituted DHPMs are explored mainly due to their effects on cancer cell proliferation via numerous targets, such as kinesin Eg5, heat shock protein 70, heat shock protein 90 and the epidermal growth factor receptor.	dhpms	15-20	kinesin family member 11	Homo sapiens	129-132
35619540-0	2022	KIF11 manipulates SREBP2-dependent mevalonate cross talk to promote tumor progression in pancreatic ductal adenocarcinoma.	Mevalonic Acid	35-45	kinesin family member 11	Homo sapiens	0-5
35619540-5	2022	This study aims to elucidate the oncogenic functions of KIF11 in stimulating cholesterol metabolism, thereby driving PDAC progression.	Cholesterol	77-88	kinesin family member 11	Homo sapiens	56-61
35619540-8	2022	Gene set enrichment analysis (GSEA) revealed that KIF11 correlated intensively with the mevalonate (MVA) metabolic pathway.	Mevalonic Acid	88-98	kinesin family member 11	Homo sapiens	50-55
35619540-8	2022	Gene set enrichment analysis (GSEA) revealed that KIF11 correlated intensively with the mevalonate (MVA) metabolic pathway.	Mevalonic Acid	100-103	kinesin family member 11	Homo sapiens	50-55
35619540-10	2022	KIF11 could elevate the free cholesterol content of PDAC cells and targeting MVA inhibited the in vitro growth of KIF11-overexpressing cells.	Cholesterol	29-40	kinesin family member 11	Homo sapiens	0-5
35619540-14	2022	Accordingly, KIF11 stimulated the expressions of MVA-signature and free cholesterol contents depending on SREBP2.	Cholesterol	72-83	kinesin family member 11	Homo sapiens	13-18
35619540-16	2022	The subcutaneous xenograft models indicated that targeting MVA biogenesis (atorvastatin) is effective to restrict the in vivo growth of KIF11high PDAC.	Atorvastatin	75-87	kinesin family member 11	Homo sapiens	136-141
35312942-0	2022	The kinesin Eg5 inhibitor K858 exerts antiproliferative and proapoptotic effects and attenuates the invasive potential of head and neck squamous carcinoma cells.	K 858	26-30	kinesin family member 11	Homo sapiens	12-15
35312942-1	2022	Our group recently demonstrated that K858, an inhibitor of motor kinesin Eg5, has important antiproliferative and apoptotic effects on breast cancer, prostatic cancer, melanoma and glioblastoma cells.	K 858	37-41	kinesin family member 11	Homo sapiens	73-76
35382311-4	2022	The precise binding mode of BIM derivatives with the ATPase motor domain of Eg5 is structurally reminiscent with previously reported allosteric inhibitor Arry520, which is under phase III clinical trials.	1,1-bis(3'-indolyl)methane	28-31	kinesin family member 11	Homo sapiens	76-79
35382311-4	2022	The precise binding mode of BIM derivatives with the ATPase motor domain of Eg5 is structurally reminiscent with previously reported allosteric inhibitor Arry520, which is under phase III clinical trials.	filanesib	154-161	kinesin family member 11	Homo sapiens	76-79
35382311-5	2022	Nevertheless, detailed analysis of the binding poses indicates that BIM derivatives bind the allosteric pocket of the Eg5 motor domain more robustly than Arry520; moreover, unlike Arry520, BIM binding is found to be resistant to drug-resistant mutations of Eg5.	1,1-bis(3'-indolyl)methane	68-71	kinesin family member 11	Homo sapiens	118-121
35382311-5	2022	Nevertheless, detailed analysis of the binding poses indicates that BIM derivatives bind the allosteric pocket of the Eg5 motor domain more robustly than Arry520; moreover, unlike Arry520, BIM binding is found to be resistant to drug-resistant mutations of Eg5.	1,1-bis(3'-indolyl)methane	68-71	kinesin family member 11	Homo sapiens	257-260
35382311-5	2022	Nevertheless, detailed analysis of the binding poses indicates that BIM derivatives bind the allosteric pocket of the Eg5 motor domain more robustly than Arry520; moreover, unlike Arry520, BIM binding is found to be resistant to drug-resistant mutations of Eg5.	1,1-bis(3'-indolyl)methane	189-192	kinesin family member 11	Homo sapiens	118-121
35382311-5	2022	Nevertheless, detailed analysis of the binding poses indicates that BIM derivatives bind the allosteric pocket of the Eg5 motor domain more robustly than Arry520; moreover, unlike Arry520, BIM binding is found to be resistant to drug-resistant mutations of Eg5.	1,1-bis(3'-indolyl)methane	189-192	kinesin family member 11	Homo sapiens	257-260
35382311-6	2022	Accordingly, a structure-guided mechanism of Eg5 inhibition by synthesized BIM derivatives is proposed.	1,1-bis(3'-indolyl)methane	75-78	kinesin family member 11	Homo sapiens	45-48
34972948-1	2022	This paper describes an easy method to enrich the harvest of adherent mammalian cells at each stage of mitosis (from prometaphase to cytokinesis) by combining Eg5 inhibition using dimethylenastron (DMA) with mitotic shake-off, followed by timed release from the drug.	dimethylenastron	180-196	kinesin family member 11	Homo sapiens	159-162
35164221-3	2022	Docking studies confirmed a similar interaction with Eg5 to that of the parent compound K858.	K 858	88-92	kinesin family member 11	Homo sapiens	53-56
34972948-1	2022	This paper describes an easy method to enrich the harvest of adherent mammalian cells at each stage of mitosis (from prometaphase to cytokinesis) by combining Eg5 inhibition using dimethylenastron (DMA) with mitotic shake-off, followed by timed release from the drug.	dimethylenastron	198-201	kinesin family member 11	Homo sapiens	159-162
34057639-0	2021	Vanadocene dichloride induces apoptosis in HeLa cells through depolymerization of microtubules and inhibition of Eg5.	vanadocene dichloride	0-21	kinesin family member 11	Homo sapiens	113-116
33995648-7	2021	We found that KIF11 was upregulated in CRC tissues and was associated with advanced clinical stage and vessel invasion and that knockdown of KIF11 led to tumor growth arrest and increased sensitivity to oxaliplatin via enhanced DNA damage and apoptosis.	Oxaliplatin	203-214	kinesin family member 11	Homo sapiens	141-146
34050874-5	2022	Molecular docking and molecular dynamics (MD) simulations were applied to explore binding potential and realistic binding model of the assessed derivatives through identification of key amino acid residues within L5/alpha2/alpha3 allosteric site of kinesin 5 (Eg5) as a validated microtubule-dependent target for monastrol as a privileged DHPM derivative.	ethyl 6-methyl-2-oxo-4-phenyl-1,2,3,4-tetrahydropyrimidine-5-carboxylate	339-343	kinesin family member 11	Homo sapiens	260-263
33995648-9	2021	Thus, our data firmly demonstrated that KIF11 could serve as a potential oncogene and proper biomarker for assessing oxaliplatin sensitivity in CRC.	Oxaliplatin	117-128	kinesin family member 11	Homo sapiens	40-45
33310050-4	2021	The identification of monastrol as specific inhibitor of the ATPase activity of the motor domain of Eg5 inhibiting the Eg5 microtubule motility in vitro and in cellulo sparked an intense interest in academia and industry to pursue the identification of novel small molecules that target Eg5 in order to be used in cancer chemotherapy based on the anti-mitotic strategy.	monastrol	22-31	kinesin family member 11	Homo sapiens	100-103
33995648-0	2021	KIF11 is upregulated in colorectal cancer and silencing of it impairs tumor growth and sensitizes colorectal cancer cells to oxaliplatin via p53/GSK3beta signaling.	Oxaliplatin	125-136	kinesin family member 11	Homo sapiens	0-5
33864298-7	2021	The current study discusses two separate proteomics experiments using BLM and TGF-beta1-treated cells with the proteomics approach, various unique target proteins were identified, and proteomic analysis revealed that curcumin reversed the expressions of unique proteins like DNA topoisomerase 2-alpha (TOP2A), kinesin-like protein (KIF11), centromere protein F (CENPF), and so on BLM or TGF-beta1 injury.	Curcumin	217-225	kinesin family member 11	Homo sapiens	332-337
33513284-3	2021	An ATP hydrolysis mechanism involving two water molecules has been proposed based on the structure of the kinesin-5 Eg5 bound to an ATP analog.	Adenosine Triphosphate	3-6	kinesin family member 11	Homo sapiens	116-119
33513284-3	2021	An ATP hydrolysis mechanism involving two water molecules has been proposed based on the structure of the kinesin-5 Eg5 bound to an ATP analog.	Water	42-47	kinesin family member 11	Homo sapiens	116-119
33513284-3	2021	An ATP hydrolysis mechanism involving two water molecules has been proposed based on the structure of the kinesin-5 Eg5 bound to an ATP analog.	Adenosine Triphosphate	132-135	kinesin family member 11	Homo sapiens	116-119
33513284-9	2021	Moreover, the OSM-3 nucleotide binding site is virtually identical to that of ATP-like Eg5, demonstrating a shared ATPase mechanism.	Adenosine Triphosphate	78-81	kinesin family member 11	Homo sapiens	87-90
33752234-3	2021	In this study, we synthesized a novel functional photoresponsive inhibitor composed of spiropyran and azobenzene derivatives to control Eg5 function with multi-stage inhibitory activity accompanied by the formation of different isomerization states.	spiropyran	87-97	kinesin family member 11	Homo sapiens	136-139
33752234-3	2021	In this study, we synthesized a novel functional photoresponsive inhibitor composed of spiropyran and azobenzene derivatives to control Eg5 function with multi-stage inhibitory activity accompanied by the formation of different isomerization states.	azobenzene	102-112	kinesin family member 11	Homo sapiens	136-139
33310050-4	2021	The identification of monastrol as specific inhibitor of the ATPase activity of the motor domain of Eg5 inhibiting the Eg5 microtubule motility in vitro and in cellulo sparked an intense interest in academia and industry to pursue the identification of novel small molecules that target Eg5 in order to be used in cancer chemotherapy based on the anti-mitotic strategy.	monastrol	22-31	kinesin family member 11	Homo sapiens	119-122
33310050-4	2021	The identification of monastrol as specific inhibitor of the ATPase activity of the motor domain of Eg5 inhibiting the Eg5 microtubule motility in vitro and in cellulo sparked an intense interest in academia and industry to pursue the identification of novel small molecules that target Eg5 in order to be used in cancer chemotherapy based on the anti-mitotic strategy.	monastrol	22-31	kinesin family member 11	Homo sapiens	119-122
33310050-7	2021	However, one Eg5 inhibitor, Arry-520 (clinical name filanesib), has demonstrated clinical efficacy in patients with multiple myeloma and is scheduled to enter phase III clinical trials.	filanesib	28-36	kinesin family member 11	Homo sapiens	13-16
33310050-7	2021	However, one Eg5 inhibitor, Arry-520 (clinical name filanesib), has demonstrated clinical efficacy in patients with multiple myeloma and is scheduled to enter phase III clinical trials.	filanesib	52-61	kinesin family member 11	Homo sapiens	13-16
32031402-6	2020	In this study, we applied recently developed diazirine reagents to obtain deep coverage of the large motor domain of Eg5 (a mitotic kinesin), and together with computational methods we correlated labeling yields with accessibility data in a number of ways.	Diazomethane	45-54	kinesin family member 11	Homo sapiens	117-120
32171585-0	2020	Corrigendum to "Biochemical and biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	64-72	kinesin family member 11	Homo sapiens	106-109
33465289-3	2021	v-Src directly phosphorylates Tyr-15 of cyclin-dependent kinase 1 (CDK1), thereby causing mitotic slippage and reduction in Eg5 inhibitor cytotoxicity.	Tyrosine	30-33	kinesin family member 11	Homo sapiens	124-127
32835667-6	2020	As a class of hopeful beta-carboline derivatives, growing evidence has indicated their auspicious roles in combating cancer by inhibiting topoisomerase (TOPO), kinesin Eg5, telomerase, cyclin-dependent kinase (CDK), IkappaB kinase (IKK), and polo-like kinase-1 (PLK1) in the transition phases of cell cycle.	norharman	22-36	kinesin family member 11	Homo sapiens	168-171
32911668-8	2020	Therapeutic targeting of Kif11 to block the Id1-Kif11 axis was carried out using small molecular inhibitor ispinesib.	ispinesib	107-116	kinesin family member 11	Homo sapiens	25-30
32911668-9	2020	We finally leveraged our findings to target the Id/Kif11 pathway using the small molecule inhibitor ispinesib in the Id+ CSC results combined with chemotherapy for better response in TNBC subtypes.	ispinesib	100-109	kinesin family member 11	Homo sapiens	51-56
32873777-7	2020	In addition, bis(maleimido)hexane-mediated protein-protein crosslinking and proximity ligation assays revealed that HSP70 inhibition deregulates the interaction between Eg5 tetramers and TPX2 at the spindle pole, leading to their accumulation in high-molecular-weight complexes.	1,1'-hexane-1,6-diyldipyrrolidine-2,5-dione	13-33	kinesin family member 11	Homo sapiens	169-172
32346924-11	2020	Meanwhile, downregulation of KIF11 could enhance the cytotoxicity of adriamycin in breast cancer cell lines MCF-7 and MDA-MB-231.	Doxorubicin	69-79	kinesin family member 11	Homo sapiens	29-34
32171585-0	2020	Corrigendum to "Biochemical and biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	64-72	kinesin family member 11	Homo sapiens	165-168
32171585-0	2020	Corrigendum to "Biochemical and biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	153-161	kinesin family member 11	Homo sapiens	106-109
32171585-0	2020	Corrigendum to "Biochemical and biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	153-161	kinesin family member 11	Homo sapiens	165-168
30995725-0	2019	Insights into the Molecular Mechanisms of Eg5 Inhibition by (+)-Morelloflavone.	morelloflavone	60-78	kinesin family member 11	Homo sapiens	42-45
31864780-0	2020	Corrigendum to "Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	153-161	kinesin family member 11	Homo sapiens	106-109
31864780-0	2020	Corrigendum to "Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	153-161	kinesin family member 11	Homo sapiens	165-168
31882607-4	2019	While both monastrol and S-trityl-L-cysteine inhibit Eg5 motility, our data reveal an unexpected ability of these loop5 targeting inhibitors to differentially control a novel Eg5 microtubule depolymerizing activity.	monastrol	11-20	kinesin family member 11	Homo sapiens	53-56
31882607-4	2019	While both monastrol and S-trityl-L-cysteine inhibit Eg5 motility, our data reveal an unexpected ability of these loop5 targeting inhibitors to differentially control a novel Eg5 microtubule depolymerizing activity.	monastrol	11-20	kinesin family member 11	Homo sapiens	175-178
31882607-4	2019	While both monastrol and S-trityl-L-cysteine inhibit Eg5 motility, our data reveal an unexpected ability of these loop5 targeting inhibitors to differentially control a novel Eg5 microtubule depolymerizing activity.	3-tritylthio-L-alanine	25-44	kinesin family member 11	Homo sapiens	53-56
31882607-4	2019	While both monastrol and S-trityl-L-cysteine inhibit Eg5 motility, our data reveal an unexpected ability of these loop5 targeting inhibitors to differentially control a novel Eg5 microtubule depolymerizing activity.	3-tritylthio-L-alanine	25-44	kinesin family member 11	Homo sapiens	175-178
31488701-6	2019	Surprisingly, when the cells were challenged with ispinesib, another Eg5 inhibitor, the Eg5(D130A) cells were resistant, but those expressing Eg5(L214A) were strikingly sensitive.	ispinesib	50-59	kinesin family member 11	Homo sapiens	69-72
31488701-6	2019	Surprisingly, when the cells were challenged with ispinesib, another Eg5 inhibitor, the Eg5(D130A) cells were resistant, but those expressing Eg5(L214A) were strikingly sensitive.	ispinesib	50-59	kinesin family member 11	Homo sapiens	88-91
31488701-6	2019	Surprisingly, when the cells were challenged with ispinesib, another Eg5 inhibitor, the Eg5(D130A) cells were resistant, but those expressing Eg5(L214A) were strikingly sensitive.	ispinesib	50-59	kinesin family member 11	Homo sapiens	88-91
31280993-5	2019	Colchicine-like inhibitors that stabilize the bent conformation of tubulin allosterically inhibit Eg5 binding, consistent with a model in which Eg5 induces a curved-to-straight transition in tubulin.	Colchicine	0-10	kinesin family member 11	Homo sapiens	98-101
31280993-5	2019	Colchicine-like inhibitors that stabilize the bent conformation of tubulin allosterically inhibit Eg5 binding, consistent with a model in which Eg5 induces a curved-to-straight transition in tubulin.	Colchicine	0-10	kinesin family member 11	Homo sapiens	144-147
31864780-0	2020	Corrigendum to "Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	64-72	kinesin family member 11	Homo sapiens	106-109
31864780-0	2020	Corrigendum to "Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5" [Int.	Curcumin	64-72	kinesin family member 11	Homo sapiens	165-168
31679979-5	2019	Monastrol and STLC induce monopolar spindle formation and M phase arrest via inhibition of the ATPase activity of Eg5.	monastrol	0-9	kinesin family member 11	Homo sapiens	114-117
31679979-5	2019	Monastrol and STLC induce monopolar spindle formation and M phase arrest via inhibition of the ATPase activity of Eg5.	3-tritylthio-L-alanine	14-18	kinesin family member 11	Homo sapiens	114-117
31129050-0	2019	Systemic delivery of Eg5 shRNA-expressing plasmids using PEGylated DC-Chol/DOPE cationic liposome: Long-term silencing and anticancer effects in vivo.	3-(N-(N',N'-dimethylaminoethane)carbamoyl)cholesterol	67-74	kinesin family member 11	Homo sapiens	21-24
31129050-0	2019	Systemic delivery of Eg5 shRNA-expressing plasmids using PEGylated DC-Chol/DOPE cationic liposome: Long-term silencing and anticancer effects in vivo.	1,2-dielaidoylphosphatidylethanolamine	75-79	kinesin family member 11	Homo sapiens	21-24
31673316-0	2019	Dihydropyrimidine-2-thiones as Eg5 inhibitors and L-type calcium channel blockers: potential antitumour dual agents.	dihydropyrimidine-2-thiones	0-27	kinesin family member 11	Homo sapiens	31-34
30047307-3	2019	Interestingly, the crystal structure of Eg-5 bound to benzimidazole unveils two chemically different allosteric pockets (PDB ID: 3ZCW).	benzimidazole	54-67	kinesin family member 11	Homo sapiens	40-44
30995725-9	2019	Altered structural conformations were also visible within various regions of Eg5, including switch I, switch II, alpha2/alpha3 helices, and the tubulin-binding region, indicating that MF might induce modifications in the Eg5 structure to compromise its ATP/ADP binding and conversion process as well as its interaction with microtubules.	Adenosine Diphosphate	257-260	kinesin family member 11	Homo sapiens	221-224
31105832-9	2019	In a word, our study found that miR-186-5p could inhibit tumor proliferation by targeting Eg5 in neuroblastoma.	CHEMBL3740941	40-42	kinesin family member 11	Homo sapiens	90-93
30410329-7	2018	Results: Results are obtained to depict the dynamics induced by ispinesib, when used as an inhibitor of kinesin Eg5, on cancer cell lines.	ispinesib	64-73	kinesin family member 11	Homo sapiens	112-115
30594885-0	2019	Structure-activity relationship of pyrazolo pyrimidine derivatives as inhibitors of mitotic kinesin Eg5 and anticancer agents.	pyrazolo pyrimidine	35-54	kinesin family member 11	Homo sapiens	100-103
30594885-3	2019	Here, we report the pyrazolopyrimidine derivates as potent inhibitors of Eg5 that prevents mitotic kinesin progression.	1H-pyrazolo[4,3-d]pyrimidine	20-38	kinesin family member 11	Homo sapiens	73-76
30594885-7	2019	Out of fifteen pyrazolopyrimidine derivates, three compounds (12, 25, and 27) have shown significant inhibition of Eg5.	1H-pyrazolo[4,3-d]pyrimidine	15-33	kinesin family member 11	Homo sapiens	115-118
30279037-0	2018	Corrigendum to "Design and synthesis of novel thiadiazole-thiazolone hybrids as potential inhibitors of the human mitotic kinesin Eg5 [Bioorg Med Chem Lett 28 (17) (2018) 2930-2938]".	thiadiazole-thiazolone	46-68	kinesin family member 11	Homo sapiens	130-133
30325216-2	2018	In the present study the antiproliferative activity of 4-benzyl-5-phenyl-3,4-dihydropyrimidine-2(1H)-thione (1) and its pyridine bioisoster (2) were evaluated and compared with monastrol (MON), the first known cell-permeable small molecule which disrupts bipolar spindle formation by inhibiting Eg5-kinesin activity.	pyridine	120-128	kinesin family member 11	Homo sapiens	295-298
30031975-0	2018	Crystal structure of the Eg5 - K858 complex and implications for structure-based design of thiadiazole-containing inhibitors.	Thiadiazoles	91-102	kinesin family member 11	Homo sapiens	25-28
31459302-1	2018	For a better understanding of protein-inhibitor interactions, we report structural, thermodynamic, and biological analyses of the interactions between S-trityl-l-cysteine (STLC) derivatives and the motor domain of kinesin spindle protein Eg5.	3-tritylthio-L-alanine	151-170	kinesin family member 11	Homo sapiens	238-241
31459302-6	2018	Further introduction of an ethylene linkage between two phenyl rings enhances Eg5 inhibitory activity by reducing the loss of entropy in forming the complex.	ethylene	27-35	kinesin family member 11	Homo sapiens	78-81
29860530-0	2018	Highly efficient photocontrol of mitotic kinesin Eg5 ATPase activity using a novel photochromic compound composed of two azobenzene derivatives.	azobenzene	121-131	kinesin family member 11	Homo sapiens	49-52
29860530-4	2018	Photochromic compounds of azobenzene derivatives, mimicking Eg5-specific inhibitors of STLC, indicated photoreversible inhibitory effects on Eg5 ATPase activity; however, the photoreversible switching efficiency was not significant.	azobenzene	26-36	kinesin family member 11	Homo sapiens	60-63
29860530-4	2018	Photochromic compounds of azobenzene derivatives, mimicking Eg5-specific inhibitors of STLC, indicated photoreversible inhibitory effects on Eg5 ATPase activity; however, the photoreversible switching efficiency was not significant.	azobenzene	26-36	kinesin family member 11	Homo sapiens	141-144
29860530-5	2018	This study presents a novel synthesized photochromic Eg5 inhibitor 2, 3-bis[(2,5-dioxo-1-{4-[(E)-2-phenyldiazen-1-yl]phenyl}pyrrolidin-3-yl)sulfanyl] butanedioic acid (BDPSB), which is composed of two azobenzenes.	2, 3-bis[(2,5-dioxo-1-{4-[(e)-2-phenyldiazen-1-yl]phenyl}pyrrolidin-3-yl)sulfanyl] butanedioic acid	67-166	kinesin family member 11	Homo sapiens	53-56
29860530-5	2018	This study presents a novel synthesized photochromic Eg5 inhibitor 2, 3-bis[(2,5-dioxo-1-{4-[(E)-2-phenyldiazen-1-yl]phenyl}pyrrolidin-3-yl)sulfanyl] butanedioic acid (BDPSB), which is composed of two azobenzenes.	bdpsb	168-173	kinesin family member 11	Homo sapiens	53-56
29860530-5	2018	This study presents a novel synthesized photochromic Eg5 inhibitor 2, 3-bis[(2,5-dioxo-1-{4-[(E)-2-phenyldiazen-1-yl]phenyl}pyrrolidin-3-yl)sulfanyl] butanedioic acid (BDPSB), which is composed of two azobenzenes.	azobenzene	201-212	kinesin family member 11	Homo sapiens	53-56
30055887-0	2018	Design and synthesis of novel thiadiazole-thiazolone hybrids as potential inhibitors of the human mitotic kinesin Eg5.	Thiadiazoles	30-41	kinesin family member 11	Homo sapiens	114-117
30055887-0	2018	Design and synthesis of novel thiadiazole-thiazolone hybrids as potential inhibitors of the human mitotic kinesin Eg5.	thiazolone	42-52	kinesin family member 11	Homo sapiens	114-117
30055887-1	2018	A novel series of 1,3,4-thiadiazole-thiazolone hybrids 5a-v were designed, synthesized, characterized, and evaluated against the basal and the microtubule (MT)-stimulated ATPase activity of Eg5.	1,3,4-thiadiazole-thiazolone	18-46	kinesin family member 11	Homo sapiens	190-193
30055887-2	2018	From the evaluated derivatives, 5h displayed the highest inhibition with an IC50 value of 13.2 microM against the MT-stimulated Eg5 ATPase activity.	5h	32-34	kinesin family member 11	Homo sapiens	128-131
29718428-3	2018	DSPPA induced reversible changes in the inhibitory effect on Eg5 ATPase and motor activities, which correlates with the spiropyran-merocyanine photo-isomerization.	dsppa	0-5	kinesin family member 11	Homo sapiens	61-64
29718428-3	2018	DSPPA induced reversible changes in the inhibitory effect on Eg5 ATPase and motor activities, which correlates with the spiropyran-merocyanine photo-isomerization.	spiropyran-merocyanine	120-142	kinesin family member 11	Homo sapiens	61-64
29738338-0	2018	Growth arrest and apoptosis induced by kinesin Eg5 inhibitor K858 and by its 1,3,4-thiadiazoline analogue in tumor cells.	K 858	61-65	kinesin family member 11	Homo sapiens	47-50
30031975-2	2018	For example, the 2,4,5-substituted 1,3,4-thiadiazole scaffold is present in a lead compound and at least two clinical candidates targeting the human motor protein Eg5, against neoplastic diseases.	2,4,5-substituted 1,3,4-thiadiazole	17-52	kinesin family member 11	Homo sapiens	163-166
30031975-4	2018	Astonishingly, structural data are lacking for all thiadiazole-containing Eg5 inhibitors.	Thiadiazoles	51-62	kinesin family member 11	Homo sapiens	74-77
30031975-5	2018	Here we report the structure determination of two crystal forms of the ternary Eg5-ADP-K858 complex, locking the motor in the so-called final inhibitor bound state, thus blocking ADP release, a crucial stage for Eg5 activity.	Adenosine Diphosphate	83-86	kinesin family member 11	Homo sapiens	79-82
30031975-5	2018	Here we report the structure determination of two crystal forms of the ternary Eg5-ADP-K858 complex, locking the motor in the so-called final inhibitor bound state, thus blocking ADP release, a crucial stage for Eg5 activity.	Adenosine Diphosphate	83-86	kinesin family member 11	Homo sapiens	212-215
30031975-7	2018	The structure of the complex has far reaching consequences for thiadiazole containing Eg5 inhibitors.	Thiadiazoles	63-74	kinesin family member 11	Homo sapiens	86-89
29749513-8	2018	From the protein-protein interaction network, DNA topoisomerase IIalpha, kinesin family member 11, cyclin B1 and BUB1 mitotic checkpoint serine/threonine were identified as foremost hub genes.	Serine	137-143	kinesin family member 11	Homo sapiens	46-97
29749513-8	2018	From the protein-protein interaction network, DNA topoisomerase IIalpha, kinesin family member 11, cyclin B1 and BUB1 mitotic checkpoint serine/threonine were identified as foremost hub genes.	Threonine	144-153	kinesin family member 11	Homo sapiens	46-97
29162464-0	2018	Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5.	Curcumin	48-56	kinesin family member 11	Homo sapiens	90-93
29162464-2	2018	Curcumin bound to the purified Eg5 (Eg5-437H) with a Kd value of 7.8muM.	Curcumin	0-8	kinesin family member 11	Homo sapiens	36-44
29162464-4	2018	Evidences from competition experiment with monastrol indicated that curcumin bound to Eg5 at a novel druggable site.	Curcumin	68-76	kinesin family member 11	Homo sapiens	86-89
29162464-5	2018	Using Forster resonance energy transfer the distance between curcumin and monastrol binding site from TRP127 on Eg5-437H was found to be 33A and 17A respectively.	Curcumin	61-69	kinesin family member 11	Homo sapiens	112-120
29162464-5	2018	Using Forster resonance energy transfer the distance between curcumin and monastrol binding site from TRP127 on Eg5-437H was found to be 33A and 17A respectively.	monastrol	74-83	kinesin family member 11	Homo sapiens	112-120
29162464-6	2018	Curcumin inhibited the ATPase activity of Eg5 motor and perturbed the dynamic interactions between Eg5 and microtubules.	Curcumin	0-8	kinesin family member 11	Homo sapiens	42-45
29162464-6	2018	Curcumin inhibited the ATPase activity of Eg5 motor and perturbed the dynamic interactions between Eg5 and microtubules.	Curcumin	0-8	kinesin family member 11	Homo sapiens	99-102
29162464-7	2018	Results from circular dichroism studies and molecular dynamics simulations suggest that curcumin binding might perturb the Eg5-437H secondary structure which could be the reason behind its inhibitory effects on Eg5.	Curcumin	88-96	kinesin family member 11	Homo sapiens	123-131
29162464-7	2018	Results from circular dichroism studies and molecular dynamics simulations suggest that curcumin binding might perturb the Eg5-437H secondary structure which could be the reason behind its inhibitory effects on Eg5.	Curcumin	88-96	kinesin family member 11	Homo sapiens	123-126
29963178-0	2018	S-trityl-L-cysteine, a novel Eg5 inhibitor, is a potent chemotherapeutic strategy in neuroblastoma.	3-tritylthio-L-alanine	0-19	kinesin family member 11	Homo sapiens	29-32
29963178-4	2018	In the present study, the expression of Eg5 was examined in clinical tissue samples and neuroblastoma cell lines, SK-N-SH, SH-SY5Y and SK-N-BE2.	sk-n-be2	135-143	kinesin family member 11	Homo sapiens	40-43
29963178-5	2018	Additionally, the antitumor activity of the Eg5 inhibitor, S-trityl-L-cysteine (STLC), was confirmed in vitro.	3-tritylthio-L-alanine	59-78	kinesin family member 11	Homo sapiens	44-47
29963178-5	2018	Additionally, the antitumor activity of the Eg5 inhibitor, S-trityl-L-cysteine (STLC), was confirmed in vitro.	3-tritylthio-L-alanine	80-84	kinesin family member 11	Homo sapiens	44-47
29454915-7	2018	All these compounds form hydrophobic interaction, aromatic pi-pi stacking and hydrogen bond efficiently with the Eg5.	Hydrogen	78-86	kinesin family member 11	Homo sapiens	113-116
29162464-0	2018	Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5.	Curcumin	48-56	kinesin family member 11	Homo sapiens	149-152
29162464-0	2018	Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5.	Curcumin	137-145	kinesin family member 11	Homo sapiens	90-93
29162464-0	2018	Biochemical and Biophysical characterization of curcumin binding to human mitotic kinesin Eg5: Insights into the inhibitory mechanism of curcumin on Eg5.	Curcumin	137-145	kinesin family member 11	Homo sapiens	149-152
29162464-1	2018	In this study we have characterized the biochemical and biophysical interactions of curcumin with the mitotic kinesin Eg5 which plays a pivotal role in the separation of centrosomes during cell division.	Curcumin	84-92	kinesin family member 11	Homo sapiens	118-121
29162464-2	2018	Curcumin bound to the purified Eg5 (Eg5-437H) with a Kd value of 7.8muM.	Curcumin	0-8	kinesin family member 11	Homo sapiens	31-34
29041840-3	2018	All drug candidates considered for Eg5 so far binds to the binding site (Site 1) formed by the loop L5, helices alpha2 and alpha3 and are uncompetitive to ATP/ADP.	Adenosine Triphosphate	155-158	kinesin family member 11	Homo sapiens	35-38
29432173-2	2018	We investigated one of these-acetylation of lysine 146 in Eg5-by creating an acetylation mimetic lysine to glutamine substitution (K146Q).	Glutamine	107-116	kinesin family member 11	Homo sapiens	58-61
29041840-9	2018	Our studies suggest that pyridazine analogs have good MDCK, permeability properties and high binding affinity to the human Eg5.	pyridazine	25-35	kinesin family member 11	Homo sapiens	123-126
29181100-4	2017	Immunohistochemical analysis revealed that KIF11 expression was upregulated in 256/268 (95.8%) paraffin-embedded archival breast cancer biopsies.	Paraffin	95-103	kinesin family member 11	Homo sapiens	43-48
29432173-2	2018	We investigated one of these-acetylation of lysine 146 in Eg5-by creating an acetylation mimetic lysine to glutamine substitution (K146Q).	Lysine	44-50	kinesin family member 11	Homo sapiens	58-61
29432173-2	2018	We investigated one of these-acetylation of lysine 146 in Eg5-by creating an acetylation mimetic lysine to glutamine substitution (K146Q).	Lysine	97-103	kinesin family member 11	Homo sapiens	58-61
29736710-4	2018	This screen is based on the analysis of monopolar mitotic spindle structures, which form upon inhibition of the mitotic kinesin Eg5/KSP by the small-molecule inhibitor dimethylenastron (DME) or similar compounds.	dimethylenastron	168-184	kinesin family member 11	Homo sapiens	128-131
29736710-4	2018	This screen is based on the analysis of monopolar mitotic spindle structures, which form upon inhibition of the mitotic kinesin Eg5/KSP by the small-molecule inhibitor dimethylenastron (DME) or similar compounds.	dimethylenastron	186-189	kinesin family member 11	Homo sapiens	128-131
29078367-10	2017	Strikingly, BTB-1 binding is close to that of well-characterized Kif11 inhibitors that block tight microtubule binding, whereas BTB-1 traps Kif18A on the microtubule.	4-Chloro-2-nitro-1-(phenylsulfonyl)benzene	12-17	kinesin family member 11	Homo sapiens	65-70
29190901-0	2017	KIF11 is required for proliferation and self-renewal of docetaxel resistant triple negative breast cancer cells.	Docetaxel	56-65	kinesin family member 11	Homo sapiens	0-5
29190901-6	2017	We found that the expression of KIF11 was significantly increased in CD44+/CD24- subpopulation of docetaxel resistant TNBC cells.	Docetaxel	98-107	kinesin family member 11	Homo sapiens	32-37
29190901-9	2017	Further docetaxel resistant TNBC xenograft models demonstrated that KIF11 inhibitor exerts growth inhibitory effect in vivo.	Docetaxel	8-17	kinesin family member 11	Homo sapiens	68-73
28625631-14	2017	Based on their expression, activity of agents targeting CD52, CD 22, CD26 and EG5 could be further explored in TET patients.	tetramethylenedisulfotetramine	111-114	kinesin family member 11	Homo sapiens	78-81
28314282-2	2017	Monastrol inhibits the mitotic kinesin family member 11 (EG5), which has been studied for its potential use in cancer therapy.	monastrol	0-9	kinesin family member 11	Homo sapiens	57-60
28062800-0	2017	Novel Allosteric Pathway of Eg5 Regulation Identified through Multivariate Statistical Analysis of Hydrogen-Exchange Mass Spectrometry (HX-MS) Ligand Screening Data.	Hydrogen	99-107	kinesin family member 11	Homo sapiens	28-31
28097385-0	2017	Two Phase 1 dose-escalation studies exploring multiple regimens of litronesib (LY2523355), an Eg5 inhibitor, in patients with advanced cancer.	litronesib	67-77	kinesin family member 11	Homo sapiens	94-97
28097385-0	2017	Two Phase 1 dose-escalation studies exploring multiple regimens of litronesib (LY2523355), an Eg5 inhibitor, in patients with advanced cancer.	litronesib	79-88	kinesin family member 11	Homo sapiens	94-97
28097385-1	2017	PURPOSE: This first-in-human report examined the recommended Phase 2 dose and schedule of litronesib, a selective allosteric kinesin Eg5 inhibitor.	litronesib	90-100	kinesin family member 11	Homo sapiens	133-136
28062800-4	2017	Terpendole E, a natural-product Eg5 inhibitor, is active against mutants resistant to canonical loop L5 inhibitors and appears to offer a unique mode of inhibition.	terpendole	0-10	kinesin family member 11	Homo sapiens	32-35
25622007-3	2015	The biphenyl-type inhibitor PVZB1194 binds to the alpha4/alpha6 allosteric pocket 15 A from the ATP-binding pocket, which differs from conventional allosteric inhibitors that bind to the allosteric L5/alpha2/alpha3 pocket of Eg5.	PVZB1194	28-36	kinesin family member 11	Homo sapiens	225-228
27402829-3	2016	First, upon microtubule binding, dimeric Eg5 releases both bound ADPs.	adenosine 5'-O-(2-thiodiphosphate)	65-69	kinesin family member 11	Homo sapiens	41-44
27402829-8	2016	This 2HB state may enable Eg5 to stabilize incoming tubulin at the growing microtubule plus-end.	2hb	5-8	kinesin family member 11	Homo sapiens	26-29
26994617-0	2016	The kinesin Eg5 inhibitor K858 induces apoptosis but also survivin-related chemoresistance in breast cancer cells.	K 858	26-30	kinesin family member 11	Homo sapiens	12-15
26994617-2	2016	Our group has recently synthesized and screened a library of 1,3,4-thiadiazoline analogues with the pharmacophoric structure of K858, an Eg5 inhibitor.	1,3,4-thiadiazoline	61-80	kinesin family member 11	Homo sapiens	137-140
26994617-2	2016	Our group has recently synthesized and screened a library of 1,3,4-thiadiazoline analogues with the pharmacophoric structure of K858, an Eg5 inhibitor.	K 858	128-132	kinesin family member 11	Homo sapiens	137-140
27121275-5	2016	We performed a chemical genetic suppression screen to identify compounds that restore spindle bipolarity in cells treated with Monastrol, an inhibitor of the mitotic kinesin Eg5.	monastrol	127-136	kinesin family member 11	Homo sapiens	174-177
26864917-6	2016	Experiments with the saturation-transfer difference NMR demonstrated that the identified Eg5 inhibitor SRI35566 binds directly to Eg5 without involving microtubules.	CHEMBL1355162	103-111	kinesin family member 11	Homo sapiens	89-92
26864917-6	2016	Experiments with the saturation-transfer difference NMR demonstrated that the identified Eg5 inhibitor SRI35566 binds directly to Eg5 without involving microtubules.	CHEMBL1355162	103-111	kinesin family member 11	Homo sapiens	130-133
27840795-4	2016	THS-PAMAM protects siRNA from degradation by RNase A and traffics KIF11 and GAPDH siRNA into U87 cancer cells.	ths-pamam	0-9	kinesin family member 11	Homo sapiens	66-71
26658059-0	2015	A Potent Chemotherapeutic Strategy with Eg5 Inhibitor against Gemcitabine Resistant Bladder Cancer.	gemcitabine	62-73	kinesin family member 11	Homo sapiens	40-43
26658059-2	2015	Eg5 has been recently identified as an attractive target in cancer chemotherapy, so novel targeted chemotherapy with Eg5 inhibitor is expected to improve the anticancer effect in gemcitabine-resistant bladder cancer.	gemcitabine	179-190	kinesin family member 11	Homo sapiens	0-3
26658059-2	2015	Eg5 has been recently identified as an attractive target in cancer chemotherapy, so novel targeted chemotherapy with Eg5 inhibitor is expected to improve the anticancer effect in gemcitabine-resistant bladder cancer.	gemcitabine	179-190	kinesin family member 11	Homo sapiens	117-120
26304237-0	2015	A Novel Eg5 Inhibitor (LY2523355) Causes Mitotic Arrest and Apoptosis in Cancer Cells and Shows Potent Antitumor Activity in Xenograft Tumor Models.	litronesib	23-32	kinesin family member 11	Homo sapiens	8-11
26304237-5	2015	Here, we show that a novel selective Eg5 inhibitor, LY2523355, has broad target-mediated anticancer activity in vitro and in vivo.	litronesib	52-61	kinesin family member 11	Homo sapiens	37-40
25885813-3	2015	METHODS: An in vitro screening was performed for identification of DHPMs with potent antitumor effects on MCF-7 and MDA-MB-231 cells and the selected DHPMs were evaluated for their inhibitory activity on Eg5 both in silico, using Molecular dynamics, and in vitro Eg5 inhibition assays.	dhpms	150-155	kinesin family member 11	Homo sapiens	204-207
24023007-10	2015	When genes with more than a threefold change were analyzed, KIF11, ITGAV, SEMA3C, IBTK, and DEK were selected as candidate genes induced by TiO2 -stimulated BEAS-2B cells.	titanium dioxide	140-144	kinesin family member 11	Homo sapiens	60-65
25885813-0	2015	Impact of kinesin Eg5 inhibition by 3,4-dihydropyrimidin-2(1H)-one derivatives on various breast cancer cell features.	thiazolo(2,3-b)dihydropyrimidinone	36-66	kinesin family member 11	Homo sapiens	18-21
25885813-2	2015	In addressing the need for treatments of this life-threatening illness, we studied 3,4-dihydropyrimidin-2(1H)-one (or thione) derivatives (DHPMs), a class of inhibitor molecules of the Eg5 motor spindle protein that shows pronounced antitumor activity against several cancer cell lines.	thiazolo(2,3-b)dihydropyrimidinone	83-113	kinesin family member 11	Homo sapiens	185-188
25885813-2	2015	In addressing the need for treatments of this life-threatening illness, we studied 3,4-dihydropyrimidin-2(1H)-one (or thione) derivatives (DHPMs), a class of inhibitor molecules of the Eg5 motor spindle protein that shows pronounced antitumor activity against several cancer cell lines.	Thiones	118-124	kinesin family member 11	Homo sapiens	185-188
25885813-2	2015	In addressing the need for treatments of this life-threatening illness, we studied 3,4-dihydropyrimidin-2(1H)-one (or thione) derivatives (DHPMs), a class of inhibitor molecules of the Eg5 motor spindle protein that shows pronounced antitumor activity against several cancer cell lines.	dhpms	139-144	kinesin family member 11	Homo sapiens	185-188
24023007-12	2015	We conclude that KIF11, ITGAV, SEMA3C, IBTK, and DEK are candidate genes expressed by epithelial cells when stimulated with TiO2 particles.	titanium dioxide	124-128	kinesin family member 11	Homo sapiens	17-22
24801905-3	2014	In this paper, we evaluated, for the first time, the therapeutic benefit of blocking Eg5 by S-(methoxytrityl)-L-cysteine (S(MeO)TLC) in RCC both in vitro and vivo.	S-(methoxytrityl)cysteine	92-120	kinesin family member 11	Homo sapiens	85-88
25001485-0	2014	Synthetic studies on mitotic kinesin Eg5 inhibitors: synthesis and structure-activity relationships of novel 2,4,5-substituted-1,3,4-thiadiazoline derivatives.	2,4,5-substituted-1,3,4-thiadiazoline	109-146	kinesin family member 11	Homo sapiens	37-40
25001485-1	2014	The 2,4,5-substituted-1,3,4-thiadiazoline derivative 1a has been identified as a new class of mitotic kinesin Eg5 inhibitor.	2,4,5-substituted-1,3,4-thiadiazoline	4-41	kinesin family member 11	Homo sapiens	110-113
25660025-3	2015	One such compound, BRD9876, displayed selectivity over normal hematopoietic progenitors and was discovered to be an unusual ATP non-competitive kinesin-5 (Eg5) inhibitor.	Adenosine Triphosphate	124-127	kinesin family member 11	Homo sapiens	155-158
25660025-3	2015	One such compound, BRD9876, displayed selectivity over normal hematopoietic progenitors and was discovered to be an unusual ATP non-competitive kinesin-5 (Eg5) inhibitor.	kinesin-5	144-153	kinesin family member 11	Homo sapiens	155-158
25184606-1	2015	The first synthesis of the racemate of terpendole E, a specific inhibitor of the mitotic kinesin Eg5, has been achieved from a known tricyclic dihydroxy ketone by a 13-step sequence that involves diastereoselective installation of its C3 quaternary stereocenter via a cyclopropyl ketone intermediate and Pd-mediated two-step construction of the indole ring moiety as the key transformations.	terpendole E	39-51	kinesin family member 11	Homo sapiens	97-100
25277178-0	2014	Nuclear Eg5 (kinesin spindle protein) expression predicts docetaxel response and prostate cancer aggressiveness.	Docetaxel	58-67	kinesin family member 11	Homo sapiens	8-11
25277178-6	2014	Nuclear Eg5-expression was significantly related to docetaxel response (p=0.036) in tissues acquired within three years before docetaxel initiation.	Docetaxel	52-61	kinesin family member 11	Homo sapiens	8-11
25277178-6	2014	Nuclear Eg5-expression was significantly related to docetaxel response (p=0.036) in tissues acquired within three years before docetaxel initiation.	Docetaxel	127-136	kinesin family member 11	Homo sapiens	8-11
25277178-9	2014	Analyzing samples taken before hormonal therapy, overall survival and time to docetaxel use were significantly decreased in patients with nuclear Eg5-expressing tumors (p<0.01).	Docetaxel	78-87	kinesin family member 11	Homo sapiens	146-149
25277178-13	2014	In conclusion, nuclear Eg5-expression may be a predictive biomarker for docetaxel response in metastatic castrate-resistant PCa patients and a prognostic biomarker for hormone-naive PCa patients.	Docetaxel	72-81	kinesin family member 11	Homo sapiens	23-26
24801905-5	2014	The anti-proliferative activity of Eg5 inhibitors, (S)-trityl-L-cysteine (STLC) and S(MeO)TLC, was evaluated by a cell viability assay.	3-tritylthio-L-alanine	51-72	kinesin family member 11	Homo sapiens	35-38
24752449-0	2014	A phase 1 and dose-finding study of LY2523355 (litronesib), an Eg5 inhibitor, in Japanese patients with advanced solid tumors.	litronesib	36-45	kinesin family member 11	Homo sapiens	63-66
24752449-2	2014	LY2523355 (litronesib) is an allosteric inhibitor of Eg5.	litronesib	0-9	kinesin family member 11	Homo sapiens	53-56
24752449-2	2014	LY2523355 (litronesib) is an allosteric inhibitor of Eg5.	litronesib	11-21	kinesin family member 11	Homo sapiens	53-56
24752449-0	2014	A phase 1 and dose-finding study of LY2523355 (litronesib), an Eg5 inhibitor, in Japanese patients with advanced solid tumors.	litronesib	47-57	kinesin family member 11	Homo sapiens	63-66
24732354-0	2014	Significant decrease of ADP release rate underlies the potent activity of dimethylenastron to inhibit mitotic kinesin Eg5 and cancer cell proliferation.	Adenosine Diphosphate	24-27	kinesin family member 11	Homo sapiens	118-121
24488929-3	2014	In this study, we provide evidence that Tat interacts with Eg5, a microtubule-associated motor protein, and allosterically modulates the ATPase activity of Eg5 by affecting ADP release from the enzyme"s active centre.	Adenosine Diphosphate	173-176	kinesin family member 11	Homo sapiens	59-62
24488929-3	2014	In this study, we provide evidence that Tat interacts with Eg5, a microtubule-associated motor protein, and allosterically modulates the ATPase activity of Eg5 by affecting ADP release from the enzyme"s active centre.	Adenosine Diphosphate	173-176	kinesin family member 11	Homo sapiens	156-159
24488929-5	2014	Further studies reveal that lysine 85 in the carboxyl terminus of Tat is critical for its interaction with Eg5 and hence its effects on Eg5 activity, mitotic progression, and apoptosis.	Lysine	28-34	kinesin family member 11	Homo sapiens	107-110
24488929-5	2014	Further studies reveal that lysine 85 in the carboxyl terminus of Tat is critical for its interaction with Eg5 and hence its effects on Eg5 activity, mitotic progression, and apoptosis.	Lysine	28-34	kinesin family member 11	Homo sapiens	136-139
24732354-0	2014	Significant decrease of ADP release rate underlies the potent activity of dimethylenastron to inhibit mitotic kinesin Eg5 and cancer cell proliferation.	dimethylenastron	74-90	kinesin family member 11	Homo sapiens	118-121
24732354-1	2014	Eg5 is a mitotic kinesin that plays a crucial role in the formation of bipolar mitotic spindles, by hydrolyzing ATP to push apart anti-parallel microtubules.	Adenosine Triphosphate	112-115	kinesin family member 11	Homo sapiens	0-3
24732354-2	2014	Dimethylenastron is potent specific small molecule inhibitor of Eg5.	dimethylenastron	0-16	kinesin family member 11	Homo sapiens	64-67
24732354-3	2014	The mechanism by which dimethylenastron inhibits Eg5 function remains unclear.	dimethylenastron	23-39	kinesin family member 11	Homo sapiens	49-52
24732354-5	2014	We analyze their interactions with ADP-bound Eg5 crystal structure, and find that dimethylenastron binds Eg5 motor domain with higher affinity.	Adenosine Diphosphate	35-38	kinesin family member 11	Homo sapiens	45-48
24732354-5	2014	We analyze their interactions with ADP-bound Eg5 crystal structure, and find that dimethylenastron binds Eg5 motor domain with higher affinity.	dimethylenastron	82-98	kinesin family member 11	Homo sapiens	45-48
24732354-5	2014	We analyze their interactions with ADP-bound Eg5 crystal structure, and find that dimethylenastron binds Eg5 motor domain with higher affinity.	dimethylenastron	82-98	kinesin family member 11	Homo sapiens	105-108
24334276-0	2014	Photocontrol of mitotic kinesin Eg5 facilitated by thiol-reactive photochromic molecules incorporated into the loop L5 functional loop.	Sulfhydryl Compounds	51-56	kinesin family member 11	Homo sapiens	32-35
24648249-0	2014	Terpendole E and its derivative inhibit STLC- and GSK-1-resistant Eg5.	terpendole	0-10	kinesin family member 11	Homo sapiens	66-69
24648249-1	2014	Terpendole E is first natural product found to inhibit mitotic kinesin Eg5, but its inhibitory mechanism remains to be revealed.	terpendole E	0-12	kinesin family member 11	Homo sapiens	71-74
24648249-2	2014	Here, we report the effects of terpendole E and 11ketopaspaline (a new natural terpendole E analogue) on the Eg5-microtubule interaction and in several Eg5 mutants.	terpendole E	31-43	kinesin family member 11	Homo sapiens	109-112
24648249-2	2014	Here, we report the effects of terpendole E and 11ketopaspaline (a new natural terpendole E analogue) on the Eg5-microtubule interaction and in several Eg5 mutants.	terpendole E	31-43	kinesin family member 11	Homo sapiens	152-155
24648249-2	2014	Here, we report the effects of terpendole E and 11ketopaspaline (a new natural terpendole E analogue) on the Eg5-microtubule interaction and in several Eg5 mutants.	11-ketopaspaline	48-63	kinesin family member 11	Homo sapiens	109-112
24648249-2	2014	Here, we report the effects of terpendole E and 11ketopaspaline (a new natural terpendole E analogue) on the Eg5-microtubule interaction and in several Eg5 mutants.	11-ketopaspaline	48-63	kinesin family member 11	Homo sapiens	152-155
24648249-2	2014	Here, we report the effects of terpendole E and 11ketopaspaline (a new natural terpendole E analogue) on the Eg5-microtubule interaction and in several Eg5 mutants.	terpendole E	79-91	kinesin family member 11	Homo sapiens	109-112
24648249-3	2014	11-Ketopaspaline is a shunt product from terpendole E, and it shows potent inhibitory activity against the microtubule-stimulated ATPase activity of Eg5.	11-ketopaspaline	0-16	kinesin family member 11	Homo sapiens	149-152
24648249-3	2014	11-Ketopaspaline is a shunt product from terpendole E, and it shows potent inhibitory activity against the microtubule-stimulated ATPase activity of Eg5.	terpendole E	41-53	kinesin family member 11	Homo sapiens	149-152
24648249-4	2014	Unlike other Eg5 inhibitors, such as S-trityl-L-cysteine (STLC) and GSK-1, both terpendole E and 11-ketopaspaline only partially inhibited Eg5-microtubule interaction.	terpendole E	80-92	kinesin family member 11	Homo sapiens	13-16
24648249-4	2014	Unlike other Eg5 inhibitors, such as S-trityl-L-cysteine (STLC) and GSK-1, both terpendole E and 11-ketopaspaline only partially inhibited Eg5-microtubule interaction.	terpendole E	80-92	kinesin family member 11	Homo sapiens	139-142
24648249-4	2014	Unlike other Eg5 inhibitors, such as S-trityl-L-cysteine (STLC) and GSK-1, both terpendole E and 11-ketopaspaline only partially inhibited Eg5-microtubule interaction.	11-ketopaspaline	97-113	kinesin family member 11	Homo sapiens	139-142
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	terpendole E	13-25	kinesin family member 11	Homo sapiens	65-68
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	terpendole E	13-25	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	terpendole E	13-25	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	terpendole E	13-25	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	terpendole E	13-25	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	terpendole E	13-25	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	11-ketopaspaline	30-46	kinesin family member 11	Homo sapiens	65-68
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	11-ketopaspaline	30-46	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	11-ketopaspaline	30-46	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	11-ketopaspaline	30-46	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	11-ketopaspaline	30-46	kinesin family member 11	Homo sapiens	105-108
24648249-5	2014	Furthermore, terpendole E and 11-ketopaspaline inhibited several Eg5 mutants that are resistant to STLC (Eg5(D130A), Eg5(L214A)) or GSK-1 (Eg5(I299F), Eg5(A356T)), but with the same extent of inhibition against wild-type Eg5.	11-ketopaspaline	30-46	kinesin family member 11	Homo sapiens	105-108
24648249-6	2014	Because Eg5(D130A) and Eg5(L214A) show cross-resistance to most known Eg5 inhibitors, which bind the L5 loop, these results suggest that terpendole E and its analogues have a different binding site and/or inhibitory mechanism to those for L5 loop-binding type Eg5 inhibitors.	terpendole E	137-149	kinesin family member 11	Homo sapiens	8-11
24648249-6	2014	Because Eg5(D130A) and Eg5(L214A) show cross-resistance to most known Eg5 inhibitors, which bind the L5 loop, these results suggest that terpendole E and its analogues have a different binding site and/or inhibitory mechanism to those for L5 loop-binding type Eg5 inhibitors.	terpendole E	137-149	kinesin family member 11	Homo sapiens	23-26
24648249-6	2014	Because Eg5(D130A) and Eg5(L214A) show cross-resistance to most known Eg5 inhibitors, which bind the L5 loop, these results suggest that terpendole E and its analogues have a different binding site and/or inhibitory mechanism to those for L5 loop-binding type Eg5 inhibitors.	terpendole E	137-149	kinesin family member 11	Homo sapiens	23-26
24648249-6	2014	Because Eg5(D130A) and Eg5(L214A) show cross-resistance to most known Eg5 inhibitors, which bind the L5 loop, these results suggest that terpendole E and its analogues have a different binding site and/or inhibitory mechanism to those for L5 loop-binding type Eg5 inhibitors.	terpendole E	137-149	kinesin family member 11	Homo sapiens	23-26
24451491-0	2014	Photocontrol of the mitotic kinesin Eg5 using a novel S-trityl-L-cysteine analogue as a photochromic inhibitor.	3-tritylthio-L-alanine	54-73	kinesin family member 11	Homo sapiens	36-39
24451491-3	2014	S-trityl-L-cysteine is one of the inhibitors of Eg5 whose molecular mechanism of inhibition was well studied.	3-tritylthio-L-alanine	0-19	kinesin family member 11	Homo sapiens	48-51
24334276-5	2014	We prepared five kinesin Eg5 motor domain mutants, E116C, E118C, Y125C, W127C and D130C, which contained a single reactive cysteine residue in loop L5.	Cysteine	123-131	kinesin family member 11	Homo sapiens	25-28
24334276-6	2014	The ability of S-trityl-l-cysteine (STLC), a specific Eg5 inhibitor, to inhibit E116C, W127C and D130C was significantly reduced.	3-tritylthio-L-alanine	15-34	kinesin family member 11	Homo sapiens	54-57
24334276-6	2014	The ability of S-trityl-l-cysteine (STLC), a specific Eg5 inhibitor, to inhibit E116C, W127C and D130C was significantly reduced.	3-tritylthio-L-alanine	36-40	kinesin family member 11	Homo sapiens	54-57
24334276-6	2014	The ability of S-trityl-l-cysteine (STLC), a specific Eg5 inhibitor, to inhibit E116C, W127C and D130C was significantly reduced.	e116c	80-85	kinesin family member 11	Homo sapiens	54-57
24334276-6	2014	The ability of S-trityl-l-cysteine (STLC), a specific Eg5 inhibitor, to inhibit E116C, W127C and D130C was significantly reduced.	w127c	87-92	kinesin family member 11	Homo sapiens	54-57
24334276-6	2014	The ability of S-trityl-l-cysteine (STLC), a specific Eg5 inhibitor, to inhibit E116C, W127C and D130C was significantly reduced.	d130c	97-102	kinesin family member 11	Homo sapiens	54-57
24285623-6	2014	Conversely, treatment with FCPT, which induces a rigor-like interaction of Eg5 with microtubules, reduced the rate of spindle elongation.	fcpt	27-31	kinesin family member 11	Homo sapiens	75-78
24285623-8	2014	Spindle fluorescence of GFP-Eg5 was decreased following treatment with STLC and increased in cells treated with FCPT.	fcpt	112-116	kinesin family member 11	Homo sapiens	28-31
23899248-2	2013	elucidated the molecular basis of resistance by characterizing the binding interactions between Eg5 and the allosteric inhibitor SB743921.	SB 743921	129-137	kinesin family member 11	Homo sapiens	96-99
24689846-0	2014	Synthesis of potential pyrimidine derivatives via Suzuki cross-coupling reaction as HIV and kinesin Eg5 inhibitors.	pyrimidine	23-33	kinesin family member 11	Homo sapiens	100-103
24689846-5	2014	Two of the newly synthesized pyrimidines 12 and 29 exhibited moderate kinesin Eg5 inhibition.	Pyrimidines	29-40	kinesin family member 11	Homo sapiens	78-81
23895133-6	2013	AZ82 effectively engaged with the minus end-directed KIFC1 motor inside cells to reverse the monopolar spindle phenotype induced by the inhibition of the plus end-directed kinesin Eg5.	AZ82	0-4	kinesin family member 11	Homo sapiens	180-183
23751065-3	2013	Here, we study ATP hydrolysis mechanisms in the kinesin-5 protein Eg5 by using combined quantum mechanics/molecular mechanics metadynamics simulations.	Adenosine Triphosphate	15-18	kinesin family member 11	Homo sapiens	66-69
23329066-1	2013	BACKGROUND: AZD4877 is a potent inhibitor of the mitotic spindle kinesin, Eg5.	N-(3-aminopropyl)-N-(1-(5-benzyl-3-methyl-4-oxo-(1,2)thiazolo(5,4-d)pyrimidin-6-yl)-2-methylpropyl)-4-methylbenzamide	12-19	kinesin family member 11	Homo sapiens	74-77
23658017-0	2013	"Snapshots" of ispinesib-induced conformational changes in the mitotic kinesin Eg5.	ispinesib	15-24	kinesin family member 11	Homo sapiens	79-82
23658017-4	2013	This loop is longest in the mitotic kinesin Eg5 and is the target for a number of small molecule inhibitors, including ispinesib, which is being used in clinical trials in patients with cancer.	ispinesib	119-128	kinesin family member 11	Homo sapiens	44-47
23658017-5	2013	In this study, we have used x-ray crystallography to identify a new structure of an Eg5-ispinesib complex and have combined this with transient state kinetics to identify a plausible sequence of conformational changes that occur in response to ispinesib binding.	ispinesib	88-97	kinesin family member 11	Homo sapiens	84-87
23658017-6	2013	Our results demonstrate that ispinesib-induced structural changes in L5 from Eg5 lead to subsequent changes in the conformation of the switch II loop and helix and in the neck linker.	ispinesib	29-38	kinesin family member 11	Homo sapiens	77-80
23658017-7	2013	We conclude that L5 in Eg5 simultaneously regulates the structure of both the ATP binding site and the motor"s mechanical elements that generate force.	Adenosine Triphosphate	78-81	kinesin family member 11	Homo sapiens	23-26
23840313-7	2013	Of the genes that affect both of these processes, CAMK1D, TSPAN8 and KIF11 affect the localization of a mediator of both gluconeogenesis and glycolysis regulation, CRTC2, to the nucleus in response to glucagon.	Glucagon	201-209	kinesin family member 11	Homo sapiens	69-74
23751065-10	2013	When ATP is placed in the ADP-bound conformation of Eg5, the ATP-Mg moiety is surrounded by many water molecules and Thr107 blocks the water chain, which together make the hydrolysis reaction less favorable.	Adenosine Triphosphate	5-8	kinesin family member 11	Homo sapiens	52-55
23751065-10	2013	When ATP is placed in the ADP-bound conformation of Eg5, the ATP-Mg moiety is surrounded by many water molecules and Thr107 blocks the water chain, which together make the hydrolysis reaction less favorable.	Adenosine Diphosphate	26-29	kinesin family member 11	Homo sapiens	52-55
23751065-10	2013	When ATP is placed in the ADP-bound conformation of Eg5, the ATP-Mg moiety is surrounded by many water molecules and Thr107 blocks the water chain, which together make the hydrolysis reaction less favorable.	Adenosine Triphosphate	61-64	kinesin family member 11	Homo sapiens	52-55
23751065-10	2013	When ATP is placed in the ADP-bound conformation of Eg5, the ATP-Mg moiety is surrounded by many water molecules and Thr107 blocks the water chain, which together make the hydrolysis reaction less favorable.	Water	97-102	kinesin family member 11	Homo sapiens	52-55
23751065-10	2013	When ATP is placed in the ADP-bound conformation of Eg5, the ATP-Mg moiety is surrounded by many water molecules and Thr107 blocks the water chain, which together make the hydrolysis reaction less favorable.	Water	135-140	kinesin family member 11	Homo sapiens	52-55
23399639-5	2013	Taccalonolide AJ causes centrosome separation and disjunction failure to a much greater extent than paclitaxel or laulimalide, which is consistent with the distinct defects in expression and activation of Plk1 and Eg5 caused by each stabilizer.	taccalonolide	0-13	kinesin family member 11	Homo sapiens	214-217
23875972-2	2013	The aim of this study was to investigate the underlying molecular mechanism of resistance developed by the mitotic kinesin Eg5 against the potent second-generation ispinesib analogue SB743921 (1), a phase I/II clinical candidate.	ispinesib	164-173	kinesin family member 11	Homo sapiens	123-126
23875972-2	2013	The aim of this study was to investigate the underlying molecular mechanism of resistance developed by the mitotic kinesin Eg5 against the potent second-generation ispinesib analogue SB743921 (1), a phase I/II clinical candidate.	SB 743921	183-191	kinesin family member 11	Homo sapiens	123-126
23394180-2	2013	Previously, we identified S-trityl-L-cysteine as a selective inhibitor of Eg5 and developed triphenylbutanamine analogues with improved potency, favorable drug-like properties, but moderate in vivo activity.	3-tritylthio-L-alanine	26-45	kinesin family member 11	Homo sapiens	74-77
22615058-0	2013	A Phase I trial of the kinesin spindle protein (Eg5) inhibitor AZD4877 in patients with solid and lymphoid malignancies.	N-(3-aminopropyl)-N-(1-(5-benzyl-3-methyl-4-oxo-(1,2)thiazolo(5,4-d)pyrimidin-6-yl)-2-methylpropyl)-4-methylbenzamide	63-70	kinesin family member 11	Homo sapiens	48-51
23247925-1	2013	Bovine serum albumin (BSA) promoted simple and efficient one-pot procedure was developed for the direct synthesis of 3,4-dihydropyrimidin-2(1H)-ones including potent mitotic kinesin Eg5 inhibitor monastrol under mild reaction conditions.	3,4-dihydropyrimidin-2(1h)-ones	117-148	kinesin family member 11	Homo sapiens	182-185
23316706-8	2013	The power of the triplex-IPTL approach in combination with IsobariQ was demonstrated through temporal profiling of HeLa cells incubated with the kinesin Eg5 inhibitor S-Trityl-l-cysteine (STLC).	triplex-iptl	17-29	kinesin family member 11	Homo sapiens	153-156
23316706-8	2013	The power of the triplex-IPTL approach in combination with IsobariQ was demonstrated through temporal profiling of HeLa cells incubated with the kinesin Eg5 inhibitor S-Trityl-l-cysteine (STLC).	3-tritylthio-L-alanine	167-186	kinesin family member 11	Homo sapiens	153-156
23316706-8	2013	The power of the triplex-IPTL approach in combination with IsobariQ was demonstrated through temporal profiling of HeLa cells incubated with the kinesin Eg5 inhibitor S-Trityl-l-cysteine (STLC).	3-tritylthio-L-alanine	188-192	kinesin family member 11	Homo sapiens	153-156
22337772-10	2012	However, motion of Eg5 on midzone microtubules was not altered.	midzone	26-33	kinesin family member 11	Homo sapiens	19-22
22993085-5	2012	In this study, the crystal structure of the Eg5 motor domain in complex with ispinesib, supported by kinetic and thermodynamic binding data, is reported.	ispinesib	77-86	kinesin family member 11	Homo sapiens	44-47
22993085-6	2012	Ispinesib occupies the same induced-fit pocket in Eg5 as other allosteric inhibitors, making extensive hydrophobic interactions with the protein.	ispinesib	0-9	kinesin family member 11	Homo sapiens	50-53
22749640-0	2012	Doing the methylene shuffle--further insights into the inhibition of mitotic kinesin Eg5 with S-trityl L-cysteine.	3-tritylthio-L-alanine	94-113	kinesin family member 11	Homo sapiens	85-88
22749640-1	2012	S-Trityl L-cysteine (STLC) is an inhibitor of the mitotic kinesin Eg5 with potential as an antimitotic chemotherapeutic agent.	3-tritylthio-L-alanine	0-19	kinesin family member 11	Homo sapiens	66-69
22749640-1	2012	S-Trityl L-cysteine (STLC) is an inhibitor of the mitotic kinesin Eg5 with potential as an antimitotic chemotherapeutic agent.	3-tritylthio-L-alanine	21-25	kinesin family member 11	Homo sapiens	66-69
22887948-6	2012	Interestingly, five kinesin family proteins including KIF11, KIF20A, KIF22, KIF23, and CENPF were found to be simultaneously downregulated by genistein.	Genistein	142-151	kinesin family member 11	Homo sapiens	54-59
22691177-1	2012	Biginelli dihydropyrimidinone derivatives as structural analogs of monastrol, a known human kinesin Eg5 inhibitor, were synthesized.	biginelli dihydropyrimidinone	0-29	kinesin family member 11	Homo sapiens	100-103
21494838-2	2012	This Phase I/II, open-label, multicenter, two-part study investigated AZD4877, a potent Eg5 inhibitor, in patients with acute myeloid leukemia.	N-(3-aminopropyl)-N-(1-(5-benzyl-3-methyl-4-oxo-(1,2)thiazolo(5,4-d)pyrimidin-6-yl)-2-methylpropyl)-4-methylbenzamide	70-77	kinesin family member 11	Homo sapiens	88-91
22343406-0	2012	3D-QSAR studies of dihydropyrazole and dihydropyrrole derivatives as inhibitors of human mitotic kinesin Eg5 based on molecular docking.	dihydropyrazole	19-34	kinesin family member 11	Homo sapiens	105-108
22361733-0	2012	p63 expression correlates with sensitivity to the Eg5 inhibitor ZD4877 in bladder cancer cells.	zd4877	64-70	kinesin family member 11	Homo sapiens	50-53
22361733-2	2012	Here we examined the cytotoxic effects of a novel antimitotic, the Eg5 inhibitor AZD4877, in a molecularly diverse panel of human bladder cancer cell lines.	N-(3-aminopropyl)-N-(1-(5-benzyl-3-methyl-4-oxo-(1,2)thiazolo(5,4-d)pyrimidin-6-yl)-2-methylpropyl)-4-methylbenzamide	81-88	kinesin family member 11	Homo sapiens	67-70
22309208-3	2012	We employed structure-based virtual screening of a database of 700, 000 compounds to identify three novel Eg5 inhibitors bearing quinazoline (24) or thioxoimidazolidine (30 and 37) scaffolds.	Quinazolines	129-140	kinesin family member 11	Homo sapiens	106-109
22309208-3	2012	We employed structure-based virtual screening of a database of 700, 000 compounds to identify three novel Eg5 inhibitors bearing quinazoline (24) or thioxoimidazolidine (30 and 37) scaffolds.	thioxoimidazolidine	149-168	kinesin family member 11	Homo sapiens	106-109
22343406-0	2012	3D-QSAR studies of dihydropyrazole and dihydropyrrole derivatives as inhibitors of human mitotic kinesin Eg5 based on molecular docking.	pyrroline	39-53	kinesin family member 11	Homo sapiens	105-108
22343406-2	2012	To find the correlation between Eg5 and its inhibitors, structure-based 3D-quantitative structure-activity relationship (QSAR) studies were performed on a series of dihydropyrazole and dihydropyrrole derivatives using comparative molecular field analysis (CoMFA) and comparative molecular similarity indices analysis (CoMSIA) methods.	dihydropyrazole	165-180	kinesin family member 11	Homo sapiens	32-35
22343406-2	2012	To find the correlation between Eg5 and its inhibitors, structure-based 3D-quantitative structure-activity relationship (QSAR) studies were performed on a series of dihydropyrazole and dihydropyrrole derivatives using comparative molecular field analysis (CoMFA) and comparative molecular similarity indices analysis (CoMSIA) methods.	pyrroline	185-199	kinesin family member 11	Homo sapiens	32-35
23071517-6	2012	Similarly to KIF11 siRNA, the KIF11 inhibitor monastrol induced lysosomal membrane permeabilization and sensitized several cancer cell lines to siramesine.	monastrol	46-55	kinesin family member 11	Homo sapiens	30-35
22248262-2	2012	We previously identified S-trityl-l-cysteine (STLC) and related analogues as selective potent inhibitors of Eg5.	3-tritylthio-L-alanine	25-44	kinesin family member 11	Homo sapiens	108-111
22248262-2	2012	We previously identified S-trityl-l-cysteine (STLC) and related analogues as selective potent inhibitors of Eg5.	3-tritylthio-L-alanine	46-50	kinesin family member 11	Homo sapiens	108-111
22248262-5	2012	Crystallographic studies reveal that they adopt the same overall binding configuration as S-trityl analogues at an allosteric site formed by loop L5 of Eg5.	trityl	92-98	kinesin family member 11	Homo sapiens	152-155
21638123-0	2012	A Phase I study to assess the safety, tolerability, and pharmacokinetics of AZD4877, an intravenous Eg5 inhibitor in patients with advanced solid tumors.	N-(3-aminopropyl)-N-(1-(5-benzyl-3-methyl-4-oxo-(1,2)thiazolo(5,4-d)pyrimidin-6-yl)-2-methylpropyl)-4-methylbenzamide	76-83	kinesin family member 11	Homo sapiens	100-103
21638123-2	2012	AZD4877 is a specific, potent inhibitor of Eg5.	N-(3-aminopropyl)-N-(1-(5-benzyl-3-methyl-4-oxo-(1,2)thiazolo(5,4-d)pyrimidin-6-yl)-2-methylpropyl)-4-methylbenzamide	0-7	kinesin family member 11	Homo sapiens	43-46
23071517-6	2012	Similarly to KIF11 siRNA, the KIF11 inhibitor monastrol induced lysosomal membrane permeabilization and sensitized several cancer cell lines to siramesine.	Lu 28-179	144-154	kinesin family member 11	Homo sapiens	30-35