PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
21650221-5	2011	Starting with dacinostat (LAQ824), a highly potent HDAC inhibitor, we explored the SAR to determine the pharmacophores required for HDAC and hERG inhibition.	LAQ824	14-24	ETS transcription factor ERG	Homo sapiens	141-145
34000373-6	2021	Dacinostat treatment enhances adipose thermogenesis as shown by elevated body temperature, accompanied with high mRNA expression of Ucp1 and Ppargc1alpha.	LAQ824	0-10	uncoupling protein 1 (mitochondrial, proton carrier)	Mus musculus	132-136
34000373-6	2021	Dacinostat treatment enhances adipose thermogenesis as shown by elevated body temperature, accompanied with high mRNA expression of Ucp1 and Ppargc1alpha.	LAQ824	0-10	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	141-153
34000373-7	2021	Mechanistically, we show that the thermogenic effect of Dacinostat is achieved by acetylation of histone 3 lysine 27 mediated transcriptional activation of Ucp1 and Ppargc1alpha in adipose tissue.	LAQ824	56-66	uncoupling protein 1 (mitochondrial, proton carrier)	Mus musculus	156-160
34000373-7	2021	Mechanistically, we show that the thermogenic effect of Dacinostat is achieved by acetylation of histone 3 lysine 27 mediated transcriptional activation of Ucp1 and Ppargc1alpha in adipose tissue.	LAQ824	56-66	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	165-177
30108795-2	2017	Here we describe the design and utilization of a largazole-based chemical probe to quantitatively measure the intracellular occupancy of HDAC1 and HDAC2 by dacinostat.	LAQ824	156-166	histone deacetylase 1	Homo sapiens	137-142
30108795-2	2017	Here we describe the design and utilization of a largazole-based chemical probe to quantitatively measure the intracellular occupancy of HDAC1 and HDAC2 by dacinostat.	LAQ824	156-166	histone deacetylase 2	Homo sapiens	147-152
27251006-0	2016	Transcript, methylation and molecular docking analyses of the effects of HDAC inhibitors, SAHA and Dacinostat, on SMN2 expression in fibroblasts of SMA patients.	LAQ824	99-109	survival of motor neuron 2, centromeric	Homo sapiens	114-118
27251006-2	2016	We aimed to compare the effects of suberoylanilide hydroxamic acid (SAHA) and Dacinostat, a novel HDACi, on SMN2 expression and to elucidate their acetylation effects on the methylation of the SMN2.	LAQ824	78-88	survival of motor neuron 2, centromeric	Homo sapiens	108-112
27251006-7	2016	Acetylation effects of SAHA and Dacinostat promoted demethylation of the SMN2 promoter.	LAQ824	32-42	survival of motor neuron 2, centromeric	Homo sapiens	73-77
27034410-4	2016	In the present study, we show for the first time in human induced pluripotent stem cell-derived cardiomyocytes (hiPS-CMs) that HDAC inhibitors (dacinostat, panobinostat, vorinostat, entinostat, and tubastatin-a) induce delayed dose-related cardiac dysfunction at therapeutic concentrations associated with cardiac adverse effects in humans.	LAQ824	144-154	histone deacetylase 9	Homo sapiens	127-131
22895185-6	2012	We show that the self-renewal and short-term repopulation capacity of AML1/ETO- or PLZF/RARalpha-expressing Sca1+/lin- stem and progenitor cells are profoundly inhibited by clinically applicable concentrations of the DACi dacinostat and vorinostat.	LAQ824	222-232	RUNX family transcription factor 1	Homo sapiens	70-74
22895185-6	2012	We show that the self-renewal and short-term repopulation capacity of AML1/ETO- or PLZF/RARalpha-expressing Sca1+/lin- stem and progenitor cells are profoundly inhibited by clinically applicable concentrations of the DACi dacinostat and vorinostat.	LAQ824	222-232	RUNX1 partner transcriptional co-repressor 1	Homo sapiens	75-79
22895185-6	2012	We show that the self-renewal and short-term repopulation capacity of AML1/ETO- or PLZF/RARalpha-expressing Sca1+/lin- stem and progenitor cells are profoundly inhibited by clinically applicable concentrations of the DACi dacinostat and vorinostat.	LAQ824	222-232	zinc finger and BTB domain containing 16	Homo sapiens	83-87
22895185-6	2012	We show that the self-renewal and short-term repopulation capacity of AML1/ETO- or PLZF/RARalpha-expressing Sca1+/lin- stem and progenitor cells are profoundly inhibited by clinically applicable concentrations of the DACi dacinostat and vorinostat.	LAQ824	222-232	retinoic acid receptor, alpha	Mus musculus	88-96
22194463-2	2012	The HDAC inhibitors LAQ824 and SAHA increase phosphocholine (PC) levels in human colon cancer cells and tumor xenografts as observed by magnetic resonance spectroscopy (MRS).	LAQ824	20-26	histone deacetylase 9	Homo sapiens	4-8
21650221-5	2011	Starting with dacinostat (LAQ824), a highly potent HDAC inhibitor, we explored the SAR to determine the pharmacophores required for HDAC and hERG inhibition.	LAQ824	26-32	ETS transcription factor ERG	Homo sapiens	141-145
20674020-2	2011	Treatment of normal hematopoietic progenitor cells (HPC) with LAQ824 resulted in (i) inhibition of differentiation, (ii) an G2/M cell cycle arrest exclusively in multipotent CD34(+) HPC and (iii) induction of apoptosis predominantly in committed CD34(-) HPC.	LAQ824	62-68	CD34 molecule	Homo sapiens	174-178
21368229-0	2011	Histone deacetylase inhibitor LAQ824 augments inflammatory responses in macrophages through transcriptional regulation of IL-10.	LAQ824	30-36	interleukin 10	Mus musculus	122-127
21368229-4	2011	In this study, we show for the first time, to our knowledge, that treatment of BALB/c murine macrophages with the histone deacetylase inhibitor LAQ824 induces chromatin changes at the level of the IL-10 gene promoter that lead to enhanced recruitment of the transcriptional repressors HDAC11 and PU.1.	LAQ824	144-150	interleukin 10	Mus musculus	197-202
21368229-4	2011	In this study, we show for the first time, to our knowledge, that treatment of BALB/c murine macrophages with the histone deacetylase inhibitor LAQ824 induces chromatin changes at the level of the IL-10 gene promoter that lead to enhanced recruitment of the transcriptional repressors HDAC11 and PU.1.	LAQ824	144-150	histone deacetylase 11	Mus musculus	285-291
20674020-2	2011	Treatment of normal hematopoietic progenitor cells (HPC) with LAQ824 resulted in (i) inhibition of differentiation, (ii) an G2/M cell cycle arrest exclusively in multipotent CD34(+) HPC and (iii) induction of apoptosis predominantly in committed CD34(-) HPC.	LAQ824	62-68	CD34 molecule	Homo sapiens	246-250
19014694-5	2008	We observed that the HDAC inhibitors, MS-275, trichostatin-A, phenylbutyrate, LAQ824 and depsipeptide, enhanced the antineoplastic action of 5AZA-CdR on EWS cells.	LAQ824	78-84	histone deacetylase 9	Homo sapiens	21-25
19265193-2	2009	Here we demonstrate that p53 acetylation at Lys-320/Lys-373/Lys-382 is also required for its transcription-independent functions in BAX activation, reactive oxygen species production, and apoptosis in response to the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.	LAQ824	292-298	tumor protein p53	Homo sapiens	25-28
18483381-4	2008	RESULTS: In this report, we show that the HDIs trichostatin A, sodium butyrate, and low nanomolar doses of LAQ824 combined with the glycolysis inhibitor 2-deoxy-d-glucose induce strong apoptosis in cancer cell lines of brain, breast, and cervix in a p53-independent manner.	LAQ824	107-113	tumor protein p53	Homo sapiens	250-253
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	X-ray repair cross complementing 5	Homo sapiens	181-185
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	RAD50 double strand break repair protein	Homo sapiens	190-195
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	X-ray repair cross complementing 6	Homo sapiens	207-211
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	X-ray repair cross complementing 6	Homo sapiens	236-240
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	X-ray repair cross complementing 5	Homo sapiens	245-249
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	BRCA1 DNA repair associated	Homo sapiens	308-313
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	checkpoint kinase 1	Homo sapiens	315-320
18852132-5	2008	During this interval, LAQ-824 induced early (4-8 h) increases in gamma-H2AX, which persisted (48 h) secondary to LAQ-824-mediated inhibition of DNA repair (e.g., down-regulation of Ku86 and Rad50, increased Ku70 acetylation, diminished Ku70 and Ku86 DNA-binding activity, and down-regulated DNA repair genes BRCA1, CHEK1, and RAD51).	LAQ824	22-29	RAD51 recombinase	Homo sapiens	326-331
18927309-0	2008	Phase I pharmacokinetic and pharmacodynamic study of LAQ824, a hydroxamate histone deacetylase inhibitor with a heat shock protein-90 inhibitory profile, in patients with advanced solid tumors.	LAQ824	53-59	heat shock protein 90 alpha family class A member 1	Homo sapiens	112-133
18445700-3	2008	Synergism of apoptosis induction was also observed in U251 cells when coexposing cells to other HDAC inhibitors, including LAQ824 and trichostatin A, with the proteasome inhibitor MG132, thus demonstrating a class effect.	LAQ824	123-129	histone deacetylase 9	Homo sapiens	96-100
17455259-3	2007	In biochemical assays using recombinant HDAC1, 3, 6 and 8 isoenzymes, SAHA and LAQ824/LBH589 behave as quite unselective HDAC inhibitors.	LAQ824	79-85	histone deacetylase 1	Homo sapiens	40-45
17851643-4	2008	In this paper, we report that structurally related hydroxamate LAQ824 and SK-7068 induce tumor-selective mitotic defects by depleting Aurora-A.	LAQ824	63-69	aurora kinase A	Homo sapiens	134-142
17851643-7	2008	LAQ824 or SK-7068 treatment inhibited histone deacetylase (HDAC) 6 present in Aurora-A/heat shock protein (Hsp) 90 complex.	LAQ824	0-6	aurora kinase A	Homo sapiens	78-86
17851643-11	2008	LAQ824 and SK-7068 might be more effective HDIs in cancer cells with Aurora-A overexpression.	LAQ824	0-6	aurora kinase A	Homo sapiens	69-77
17455259-3	2007	In biochemical assays using recombinant HDAC1, 3, 6 and 8 isoenzymes, SAHA and LAQ824/LBH589 behave as quite unselective HDAC inhibitors.	LAQ824	79-85	histone deacetylase 9	Homo sapiens	40-44
17699868-2	2007	By inhibiting HDAC6, the hydroxamic acid analogue pan-HDAC inhibitors (HA-HDI; e.g., LAQ824, LBH589, and vorinostat) induce hyperacetylation of the HDAC6 substrates alpha-tubulin and hsp90.	LAQ824	85-91	histone deacetylase 6	Homo sapiens	14-19
17699868-2	2007	By inhibiting HDAC6, the hydroxamic acid analogue pan-HDAC inhibitors (HA-HDI; e.g., LAQ824, LBH589, and vorinostat) induce hyperacetylation of the HDAC6 substrates alpha-tubulin and hsp90.	LAQ824	85-91	histone deacetylase 6	Homo sapiens	148-153
17699868-2	2007	By inhibiting HDAC6, the hydroxamic acid analogue pan-HDAC inhibitors (HA-HDI; e.g., LAQ824, LBH589, and vorinostat) induce hyperacetylation of the HDAC6 substrates alpha-tubulin and hsp90.	LAQ824	85-91	heat shock protein 90 alpha family class A member 1	Homo sapiens	183-188
17237267-0	2007	Antitumor effect of the histone deacetylase inhibitor LAQ824 in combination with 13-cis-retinoic acid in human malignant melanoma.	LAQ824	54-60	histone deacetylase 9	Homo sapiens	24-43
17008546-3	2007	Here, in this first systematic investigation of the role of HDACs in immunity, we show that HDAC inhibition by a small-molecule HDAC inhibitor (HDACi), LAQ824, alters Toll-like receptor 4 (TLR4)-dependent activation and function of macrophages and dendritic cells (DCs).	LAQ824	152-158	toll like receptor 4	Homo sapiens	167-187
17008546-3	2007	Here, in this first systematic investigation of the role of HDACs in immunity, we show that HDAC inhibition by a small-molecule HDAC inhibitor (HDACi), LAQ824, alters Toll-like receptor 4 (TLR4)-dependent activation and function of macrophages and dendritic cells (DCs).	LAQ824	152-158	toll like receptor 4	Homo sapiens	189-193
17237267-3	2007	In this study, we tested the antitumor effect of the HDAC inhibitor LAQ824 in combination with 13-cis-retinoic acid (CRA) on two human melanoma cell lines both in vitro and in vivo.	LAQ824	68-74	histone deacetylase 9	Homo sapiens	53-57
17237267-9	2007	The biological effect of LAQ824 was associated with p21 induction in both cell lines but G(2) cell cycle arrest in A2058 and apoptosis in HMV-I cell line.	LAQ824	25-31	H3 histone pseudogene 16	Homo sapiens	52-55
17237267-10	2007	The induction of apoptosis by LAQ824 was associated with increased reactive oxygen species and induction of SM22 gene expression in HMV-I but not in A2058 cell line.	LAQ824	30-36	transgelin	Homo sapiens	108-112
17237267-14	2007	These results suggest that the HDAC inhibitor LAQ824 has a greater antitumor activity in combination with CRA in melanoma tumors but the degree of induced apoptosis may vary.	LAQ824	46-52	histone deacetylase 9	Homo sapiens	31-35
17237267-14	2007	These results suggest that the HDAC inhibitor LAQ824 has a greater antitumor activity in combination with CRA in melanoma tumors but the degree of induced apoptosis may vary.	LAQ824	46-52	LUC7 like 3 pre-mRNA splicing factor	Homo sapiens	106-109
17172412-3	2006	In the present studies, we determined that treatment with the hydroxamate histone deacetylase inhibitor LBH589 or LAQ824 depleted the protein levels of EZH2, SUZ12, and EED in the cultured (K562, U937, and HL-60) and primary human acute leukemia cells.	LAQ824	114-120	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	152-156
17172412-3	2006	In the present studies, we determined that treatment with the hydroxamate histone deacetylase inhibitor LBH589 or LAQ824 depleted the protein levels of EZH2, SUZ12, and EED in the cultured (K562, U937, and HL-60) and primary human acute leukemia cells.	LAQ824	114-120	SUZ12 polycomb repressive complex 2 subunit	Homo sapiens	158-163
17172412-3	2006	In the present studies, we determined that treatment with the hydroxamate histone deacetylase inhibitor LBH589 or LAQ824 depleted the protein levels of EZH2, SUZ12, and EED in the cultured (K562, U937, and HL-60) and primary human acute leukemia cells.	LAQ824	114-120	embryonic ectoderm development	Homo sapiens	169-172
16783580-0	2006	Effect of histone deacetylase inhibitor LAQ824 on antineoplastic action of 5-Aza-2"-deoxycytidine (decitabine) on human breast carcinoma cells.	LAQ824	40-46	histone deacetylase 9	Homo sapiens	10-29
16783580-3	2006	LAQ824 (LAQ) is a novel inhibitor of histone deacetylase (HDAC) that shows antineoplastic activity and can activate genes that produce cell cycle arrest.	LAQ824	0-6	histone deacetylase 9	Homo sapiens	37-56
16783580-3	2006	LAQ824 (LAQ) is a novel inhibitor of histone deacetylase (HDAC) that shows antineoplastic activity and can activate genes that produce cell cycle arrest.	LAQ824	0-6	histone deacetylase 9	Homo sapiens	58-62
16783580-3	2006	LAQ824 (LAQ) is a novel inhibitor of histone deacetylase (HDAC) that shows antineoplastic activity and can activate genes that produce cell cycle arrest.	LAQ824	0-3	histone deacetylase 9	Homo sapiens	37-56
16783580-3	2006	LAQ824 (LAQ) is a novel inhibitor of histone deacetylase (HDAC) that shows antineoplastic activity and can activate genes that produce cell cycle arrest.	LAQ824	0-3	histone deacetylase 9	Homo sapiens	58-62
16861932-5	2006	In this study, LAQ824 mediated apoptosis was found to occur mainly via activation of the mitochondrial death pathway by inducing Apaf1 and caspase 9 and promoting mitochondrial release of key proapoptotic factors in lung cancer cells, but not in normal fibroblast cells.	LAQ824	15-21	apoptotic peptidase activating factor 1	Homo sapiens	129-134
16885362-2	2006	We assessed whether 3"-deoxy-3"-[(18)F]fluorothymidine-positron emission tomography ([18F]FLT-PET) could be used to noninvasively measure the biological activity of a novel HDACI LAQ824 in vivo.	LAQ824	179-185	thyroid stimulating hormone receptor	Mus musculus	94-97
16951198-5	2006	Treatment of the VHL-deficient human renal cell carcinoma cell line UMRC2 with the hydroxamic HDAC inhibitor LAQ824 resulted in a dose-dependent inhibition of HIF-1 alpha protein via a VHL-independent mechanism and reduction of HIF-1 alpha transcriptional activity.	LAQ824	109-115	hypoxia inducible factor 1 subunit alpha	Homo sapiens	159-170
16951198-5	2006	Treatment of the VHL-deficient human renal cell carcinoma cell line UMRC2 with the hydroxamic HDAC inhibitor LAQ824 resulted in a dose-dependent inhibition of HIF-1 alpha protein via a VHL-independent mechanism and reduction of HIF-1 alpha transcriptional activity.	LAQ824	109-115	hypoxia inducible factor 1 subunit alpha	Homo sapiens	228-239
16951198-6	2006	HIF-1 alpha inhibition by LAQ824 was associated with HIF-1 alpha acetylation and polyubiquitination.	LAQ824	26-32	hypoxia inducible factor 1 subunit alpha	Homo sapiens	0-11
16951198-6	2006	HIF-1 alpha inhibition by LAQ824 was associated with HIF-1 alpha acetylation and polyubiquitination.	LAQ824	26-32	hypoxia inducible factor 1 subunit alpha	Homo sapiens	53-64
16861932-5	2006	In this study, LAQ824 mediated apoptosis was found to occur mainly via activation of the mitochondrial death pathway by inducing Apaf1 and caspase 9 and promoting mitochondrial release of key proapoptotic factors in lung cancer cells, but not in normal fibroblast cells.	LAQ824	15-21	caspase 9	Homo sapiens	139-148
16861932-7	2006	Furthermore, we showed that LAQ824 only triggered the release of mitochondrial proapoptotic factors such as cytochrome C (Cyto C) and apoptosis inducing factor (AIF) in lung cancer cells but not in normal blast cells.	LAQ824	28-34	cytochrome c, somatic	Homo sapiens	108-120
16861932-7	2006	Furthermore, we showed that LAQ824 only triggered the release of mitochondrial proapoptotic factors such as cytochrome C (Cyto C) and apoptosis inducing factor (AIF) in lung cancer cells but not in normal blast cells.	LAQ824	28-34	cytochrome c, somatic	Homo sapiens	122-128
16861932-7	2006	Furthermore, we showed that LAQ824 only triggered the release of mitochondrial proapoptotic factors such as cytochrome C (Cyto C) and apoptosis inducing factor (AIF) in lung cancer cells but not in normal blast cells.	LAQ824	28-34	apoptosis inducing factor mitochondria associated 1	Homo sapiens	134-159
16861932-7	2006	Furthermore, we showed that LAQ824 only triggered the release of mitochondrial proapoptotic factors such as cytochrome C (Cyto C) and apoptosis inducing factor (AIF) in lung cancer cells but not in normal blast cells.	LAQ824	28-34	apoptosis inducing factor mitochondria associated 1	Homo sapiens	161-164
16861932-8	2006	In addition, LAQ824 was found to induce Bax translocation in lung cancer cell, which may play important role in the induction of the release of mitochondrial proapoptotic factors.	LAQ824	13-19	BCL2 associated X, apoptosis regulator	Homo sapiens	40-43
16275999-4	2005	LAQ824/roscovitine-treated cells displayed caspase-dependent down-regulation of p21(CIP1) and Mcl-1 and a pronounced caspase-independent reduction in X-linked inhibitor of apoptosis (XIAP) expression.	LAQ824	0-6	cyclin dependent kinase inhibitor 1A	Homo sapiens	80-83
16189296-4	2006	LAQ824-induced lethality in U937 cells did not involve the extrinsic apoptotic pathway, nor was it associated with death receptor up-regulation; instead, it was markedly inhibited by ectopic expression of Bcl-2, Bcl-x(L), XIAP, and Mcl-1.	LAQ824	0-6	X-linked inhibitor of apoptosis	Homo sapiens	222-226
16189296-4	2006	LAQ824-induced lethality in U937 cells did not involve the extrinsic apoptotic pathway, nor was it associated with death receptor up-regulation; instead, it was markedly inhibited by ectopic expression of Bcl-2, Bcl-x(L), XIAP, and Mcl-1.	LAQ824	0-6	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	232-237
16189296-6	2006	Together, these findings indicate that LAQ824-induced lethality represents a multifactorial process in which LAQ824-mediated ROS generation is necessary but not sufficient to induce apoptosis, and that the degree of XIAP and Mcl-1 down-regulation and ceramide generation determines whether this agent engages a maturation rather than an apoptotic program.	LAQ824	39-45	X-linked inhibitor of apoptosis	Homo sapiens	216-220
16189296-6	2006	Together, these findings indicate that LAQ824-induced lethality represents a multifactorial process in which LAQ824-mediated ROS generation is necessary but not sufficient to induce apoptosis, and that the degree of XIAP and Mcl-1 down-regulation and ceramide generation determines whether this agent engages a maturation rather than an apoptotic program.	LAQ824	39-45	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	225-230
16189296-0	2006	The histone deacetylase inhibitor LAQ824 induces human leukemia cell death through a process involving XIAP down-regulation, oxidative injury, and the acid sphingomyelinase-dependent generation of ceramide.	LAQ824	34-40	X-linked inhibitor of apoptosis	Homo sapiens	103-107
16189296-2	2006	Exposure of U937 cells to a low concentration of LAQ824 (30 nM) resulted in a delayed (2 h) increase in reactive oxygen species (ROS), induction of p21(WAF1/CIP1), pRb dephosphorylation, growth arrest of cells in G(0)/G(1) phase, and differentiation.	LAQ824	49-55	cyclin dependent kinase inhibitor 1A	Homo sapiens	148-151
16189296-2	2006	Exposure of U937 cells to a low concentration of LAQ824 (30 nM) resulted in a delayed (2 h) increase in reactive oxygen species (ROS), induction of p21(WAF1/CIP1), pRb dephosphorylation, growth arrest of cells in G(0)/G(1) phase, and differentiation.	LAQ824	49-55	cyclin dependent kinase inhibitor 1A	Homo sapiens	152-156
16189296-2	2006	Exposure of U937 cells to a low concentration of LAQ824 (30 nM) resulted in a delayed (2 h) increase in reactive oxygen species (ROS), induction of p21(WAF1/CIP1), pRb dephosphorylation, growth arrest of cells in G(0)/G(1) phase, and differentiation.	LAQ824	49-55	cyclin dependent kinase inhibitor 1A	Homo sapiens	157-161
16189296-2	2006	Exposure of U937 cells to a low concentration of LAQ824 (30 nM) resulted in a delayed (2 h) increase in reactive oxygen species (ROS), induction of p21(WAF1/CIP1), pRb dephosphorylation, growth arrest of cells in G(0)/G(1) phase, and differentiation.	LAQ824	49-55	RB transcriptional corepressor 1	Homo sapiens	164-167
16189296-3	2006	On the other hand, exposure of cells to a higher concentration of LAQ824 (75 nM) resulted in the early (30 min) generation of ROS, arrest of cells in G(2)/M phase, down-regulation of XIAP (at the transcriptional level) and Mcl-1 (through a caspase-mediated process), the acid sphingomyelinase-dependent generation of ceramide, and profound mitochondrial injury, caspase activation, and apoptosis.	LAQ824	66-72	X-linked inhibitor of apoptosis	Homo sapiens	183-187
16189296-3	2006	On the other hand, exposure of cells to a higher concentration of LAQ824 (75 nM) resulted in the early (30 min) generation of ROS, arrest of cells in G(2)/M phase, down-regulation of XIAP (at the transcriptional level) and Mcl-1 (through a caspase-mediated process), the acid sphingomyelinase-dependent generation of ceramide, and profound mitochondrial injury, caspase activation, and apoptosis.	LAQ824	66-72	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	223-228
16189296-4	2006	LAQ824-induced lethality in U937 cells did not involve the extrinsic apoptotic pathway, nor was it associated with death receptor up-regulation; instead, it was markedly inhibited by ectopic expression of Bcl-2, Bcl-x(L), XIAP, and Mcl-1.	LAQ824	0-6	BCL2 apoptosis regulator	Homo sapiens	205-210
16189296-4	2006	LAQ824-induced lethality in U937 cells did not involve the extrinsic apoptotic pathway, nor was it associated with death receptor up-regulation; instead, it was markedly inhibited by ectopic expression of Bcl-2, Bcl-x(L), XIAP, and Mcl-1.	LAQ824	0-6	BCL2 like 1	Homo sapiens	212-220
16275999-4	2005	LAQ824/roscovitine-treated cells displayed caspase-dependent down-regulation of p21(CIP1) and Mcl-1 and a pronounced caspase-independent reduction in X-linked inhibitor of apoptosis (XIAP) expression.	LAQ824	0-6	cyclin dependent kinase inhibitor 1A	Homo sapiens	84-88
16275999-4	2005	LAQ824/roscovitine-treated cells displayed caspase-dependent down-regulation of p21(CIP1) and Mcl-1 and a pronounced caspase-independent reduction in X-linked inhibitor of apoptosis (XIAP) expression.	LAQ824	0-6	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	94-99
16275999-4	2005	LAQ824/roscovitine-treated cells displayed caspase-dependent down-regulation of p21(CIP1) and Mcl-1 and a pronounced caspase-independent reduction in X-linked inhibitor of apoptosis (XIAP) expression.	LAQ824	0-6	X-linked inhibitor of apoptosis	Homo sapiens	150-181
16275999-4	2005	LAQ824/roscovitine-treated cells displayed caspase-dependent down-regulation of p21(CIP1) and Mcl-1 and a pronounced caspase-independent reduction in X-linked inhibitor of apoptosis (XIAP) expression.	LAQ824	0-6	X-linked inhibitor of apoptosis	Homo sapiens	183-187
16275999-6	2005	Combined exposure to LAQ824 and roscovitine resulted in a significant reduction in XIAP mRNA levels and diminished phosphorylation of the carboxyl-terminal domain of RNA polymerase II.	LAQ824	21-27	X-linked inhibitor of apoptosis	Homo sapiens	83-87
15937340-1	2005	The hydroxamic acid (HAA) analogue pan-histone deacetylase (HDAC) inhibitors (HDIs) LAQ824 and LBH589 have been shown to induce acetylation and inhibit the ATP binding and chaperone function of heat shock protein (HSP) 90.	LAQ824	84-90	heat shock protein 90 alpha family class A member 1	Homo sapiens	194-221
16170022-8	2005	LAQ824 induced Hsp90 acetylation in LNCaP cells, which resulted in inhibition of its ATP-binding activity, dissociation of Hsp90-androgen receptor complex, and proteasome-mediated degradation of androgen receptor.	LAQ824	0-6	heat shock protein 90 alpha family class A member 1	Homo sapiens	123-128
16170022-8	2005	LAQ824 induced Hsp90 acetylation in LNCaP cells, which resulted in inhibition of its ATP-binding activity, dissociation of Hsp90-androgen receptor complex, and proteasome-mediated degradation of androgen receptor.	LAQ824	0-6	androgen receptor	Homo sapiens	129-146
16170022-8	2005	LAQ824 induced Hsp90 acetylation in LNCaP cells, which resulted in inhibition of its ATP-binding activity, dissociation of Hsp90-androgen receptor complex, and proteasome-mediated degradation of androgen receptor.	LAQ824	0-6	androgen receptor	Homo sapiens	195-212
16170022-11	2005	These results reveal that LAQ824 is a potent agent for depletion of androgen receptor and a potential new drug for prostate cancer.	LAQ824	26-32	androgen receptor	Homo sapiens	68-85
16170022-0	2005	Chemical ablation of androgen receptor in prostate cancer cells by the histone deacetylase inhibitor LAQ824.	LAQ824	101-107	androgen receptor	Homo sapiens	21-38
16170022-3	2005	We report here that LAQ824, a cinnamyl hydroxamatic acid histone deacetylase inhibitor currently in human clinical trials, effectively depleted androgen receptor in prostate cancer cells at nanomolar concentrations.	LAQ824	20-26	androgen receptor	Homo sapiens	144-161
16170022-5	2005	Although LAQ824 may exert its effect through multiple mechanisms, several lines of evidence suggest that inactivation of the heat shock protein-90 (Hsp90) molecular chaperone is involved in LAQ824-induced androgen receptor depletion.	LAQ824	9-15	heat shock protein 90 alpha family class A member 1	Homo sapiens	125-146
16170022-5	2005	Although LAQ824 may exert its effect through multiple mechanisms, several lines of evidence suggest that inactivation of the heat shock protein-90 (Hsp90) molecular chaperone is involved in LAQ824-induced androgen receptor depletion.	LAQ824	9-15	heat shock protein 90 alpha family class A member 1	Homo sapiens	148-153
16170022-8	2005	LAQ824 induced Hsp90 acetylation in LNCaP cells, which resulted in inhibition of its ATP-binding activity, dissociation of Hsp90-androgen receptor complex, and proteasome-mediated degradation of androgen receptor.	LAQ824	0-6	heat shock protein 90 alpha family class A member 1	Homo sapiens	15-20
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	58-64	histone deacetylase 6	Homo sapiens	42-47
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	58-64	heat shock protein 90 alpha family class A member 1	Homo sapiens	88-93
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	58-64	tubulin alpha 1b	Homo sapiens	98-111
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	58-64	AKT serine/threonine kinase 1	Homo sapiens	162-165
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	58-64	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	171-176
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	124-130	histone deacetylase 6	Homo sapiens	42-47
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	124-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	153-160
15937340-7	2005	Conversely, the ectopic overexpression of HDAC6 inhibited LAQ824-induced acetylation of HSP90 and alpha-tubulin and reduced LAQ824-mediated depletion of Bcr-Abl, AKT, and c-Raf.	LAQ824	124-130	AKT serine/threonine kinase 1	Homo sapiens	162-165
15059915-0	2004	Cotreatment with histone deacetylase inhibitor LAQ824 enhances Apo-2L/tumor necrosis factor-related apoptosis inducing ligand-induced death inducing signaling complex activity and apoptosis of human acute leukemia cells.	LAQ824	47-53	TNF superfamily member 10	Homo sapiens	63-69
15183120-5	2004	However, incubation with histone deacetylase (HDAC)-inhibitors Trichostatin A (TSA) and LAQ824 or the tyrosinkinase inhibitor Imatinib (STI571) increased the rate of apoptosis in Par-4-positive K562 cells.	LAQ824	88-94	pro-apoptotic WT1 regulator	Homo sapiens	179-184
15374977-0	2004	The histone deacetylase inhibitor NVP-LAQ824 inhibits angiogenesis and has a greater antitumor effect in combination with the vascular endothelial growth factor receptor tyrosine kinase inhibitor PTK787/ZK222584.	LAQ824	34-44	vascular endothelial growth factor A	Mus musculus	126-160
15297399-0	2004	Superior activity of the combination of histone deacetylase inhibitor LAQ824 and the FLT-3 kinase inhibitor PKC412 against human acute myelogenous leukemia cells with mutant FLT-3.	LAQ824	70-76	fms related receptor tyrosine kinase 3	Homo sapiens	174-179
15297399-3	2004	Here, we determined the effects of LAQ824 and/or PKC412 (a FLT-3 kinase inhibitor) on the levels of mutant FLT-3 and its downstream signaling, as well as growth arrest and cell-death of cultured and primary human AML cells.	LAQ824	35-41	fms related receptor tyrosine kinase 3	Homo sapiens	107-112
15297399-5	2004	RESULTS: Treatment with LAQ824 promoted proteasomal degradation and attenuation of the levels of FLT-3 and p-FLT-3, associated with cell cycle G(1)-phase accumulation and apoptosis of MV4-11 cells.	LAQ824	24-30	fms related receptor tyrosine kinase 3	Homo sapiens	97-102
15297399-5	2004	RESULTS: Treatment with LAQ824 promoted proteasomal degradation and attenuation of the levels of FLT-3 and p-FLT-3, associated with cell cycle G(1)-phase accumulation and apoptosis of MV4-11 cells.	LAQ824	24-30	fms related receptor tyrosine kinase 3	Homo sapiens	109-114
15297399-8	2004	Cotreatment with LAQ824 and PKC412 synergistically induced apoptosis of MV4-11 cells and induced more apoptosis of the primary AML cells expressing mutant FLT-3.	LAQ824	17-23	fms related receptor tyrosine kinase 3	Homo sapiens	155-160
15059915-1	2004	Present studies demonstrate that treatment with the histone deacetylases inhibitor LAQ824, a cinnamic acid hydroxamate, increased the acetylation of histones H3 and H4, as well as induced p21(WAF1) in the human T-cell acute leukemia Jurkat, B lymphoblast SKW 6.4, and acute myelogenous leukemia HL-60 cells.	LAQ824	83-89	cyclin dependent kinase inhibitor 1A	Homo sapiens	188-191
15059915-1	2004	Present studies demonstrate that treatment with the histone deacetylases inhibitor LAQ824, a cinnamic acid hydroxamate, increased the acetylation of histones H3 and H4, as well as induced p21(WAF1) in the human T-cell acute leukemia Jurkat, B lymphoblast SKW 6.4, and acute myelogenous leukemia HL-60 cells.	LAQ824	83-89	cyclin dependent kinase inhibitor 1A	Homo sapiens	192-196
15059915-8	2004	Significantly, cotreatment with LAQ824 increased Apo-2L/TRAIL-induced apoptosis of primary acute myelogenous leukemia blast samples isolated from 10 patients with acute myelogenous leukemia.	LAQ824	32-38	TNF superfamily member 10	Homo sapiens	49-55
15059915-8	2004	Significantly, cotreatment with LAQ824 increased Apo-2L/TRAIL-induced apoptosis of primary acute myelogenous leukemia blast samples isolated from 10 patients with acute myelogenous leukemia.	LAQ824	32-38	TNF superfamily member 10	Homo sapiens	56-61
15059915-9	2004	Taken together, these findings indicate that LAQ824 may have promising activity in augmenting Apo-2L/TRAIL-induced death-inducing signaling complex and apoptosis of human acute leukemia cells.	LAQ824	45-51	TNF superfamily member 10	Homo sapiens	94-100
15059915-9	2004	Taken together, these findings indicate that LAQ824 may have promising activity in augmenting Apo-2L/TRAIL-induced death-inducing signaling complex and apoptosis of human acute leukemia cells.	LAQ824	45-51	TNF superfamily member 10	Homo sapiens	101-106
12941844-0	2003	Histone deacetylase inhibitor LAQ824 both lowers expression and promotes proteasomal degradation of Bcr-Abl and induces apoptosis of imatinib mesylate-sensitive or -refractory chronic myelogenous leukemia-blast crisis cells.	LAQ824	30-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	100-107
15075075-9	2004	The effect of LAQ824 was due to increased apoptosis accompanied by activation of caspase-3 and caspase-9, cleavage of poly(ADP-ribose)-polymerase (PARP) as well as by down-regulation of Bcl-2 and disruption of the mitochondrial membrane potential.	LAQ824	14-20	caspase 3	Homo sapiens	81-90
15075075-9	2004	The effect of LAQ824 was due to increased apoptosis accompanied by activation of caspase-3 and caspase-9, cleavage of poly(ADP-ribose)-polymerase (PARP) as well as by down-regulation of Bcl-2 and disruption of the mitochondrial membrane potential.	LAQ824	14-20	caspase 9	Homo sapiens	95-104
15075075-9	2004	The effect of LAQ824 was due to increased apoptosis accompanied by activation of caspase-3 and caspase-9, cleavage of poly(ADP-ribose)-polymerase (PARP) as well as by down-regulation of Bcl-2 and disruption of the mitochondrial membrane potential.	LAQ824	14-20	poly(ADP-ribose) polymerase 1	Homo sapiens	118-145
15075075-9	2004	The effect of LAQ824 was due to increased apoptosis accompanied by activation of caspase-3 and caspase-9, cleavage of poly(ADP-ribose)-polymerase (PARP) as well as by down-regulation of Bcl-2 and disruption of the mitochondrial membrane potential.	LAQ824	14-20	poly(ADP-ribose) polymerase 1	Homo sapiens	147-151
15075075-9	2004	The effect of LAQ824 was due to increased apoptosis accompanied by activation of caspase-3 and caspase-9, cleavage of poly(ADP-ribose)-polymerase (PARP) as well as by down-regulation of Bcl-2 and disruption of the mitochondrial membrane potential.	LAQ824	14-20	BCL2 apoptosis regulator	Homo sapiens	186-191
14744786-1	2004	We have synthesized a histone deacetylase inhibitor, NVP-LAQ824, a cinnamic hydroxamic acid, that inhibited in vitro enzymatic activities and transcriptionally activated the p21 promoter in reporter gene assays.	LAQ824	53-63	H3 histone pseudogene 16	Homo sapiens	174-177
15171259-0	2004	Molecular and cellular basis for the anti-proliferative effects of the HDAC inhibitor LAQ824.	LAQ824	86-92	histone deacetylase 9	Homo sapiens	71-75
14521422-0	2003	N-hydroxy-3-phenyl-2-propenamides as novel inhibitors of human histone deacetylase with in vivo antitumor activity: discovery of (2E)-N-hydroxy-3-[4-[[(2-hydroxyethyl)[2-(1H-indol-3-yl)ethyl]amino]methyl]phenyl]-2-propenamide (NVP-LAQ824).	LAQ824	129-225	histone deacetylase 9	Homo sapiens	63-82
14578462-0	2003	Histone deacetylase inhibitor LAQ824 down-regulates Her-2 and sensitizes human breast cancer cells to trastuzumab, taxotere, gemcitabine, and epothilone B.	LAQ824	30-36	erb-b2 receptor tyrosine kinase 2	Homo sapiens	52-57
14578462-2	2003	Present studies demonstrate that exposure to a novel hydroxamic acid analogue histone deacetylase inhibitor, LAQ824, induced p21WAF1 and p27KIP1 and caused growth arrest and apoptosis of human breast cancer SKBR-3 and BT-474 cells that possess amplification and overexpression of Her-2/neu.	LAQ824	109-115	cyclin dependent kinase inhibitor 1B	Homo sapiens	137-144
14578462-2	2003	Present studies demonstrate that exposure to a novel hydroxamic acid analogue histone deacetylase inhibitor, LAQ824, induced p21WAF1 and p27KIP1 and caused growth arrest and apoptosis of human breast cancer SKBR-3 and BT-474 cells that possess amplification and overexpression of Her-2/neu.	LAQ824	109-115	erb-b2 receptor tyrosine kinase 2	Homo sapiens	280-289
14578462-4	2003	LAQ824 also induced the acetylation of heat shock protein (hsp) 90, resulting in inhibition of its binding to ATP, which has been shown to impair the chaperone association of hsp 90 with its client proteins, Her-2, AKT, and c-Raf-1.	LAQ824	0-6	heat shock protein 90 alpha family class A member 1	Homo sapiens	39-66
14578462-4	2003	LAQ824 also induced the acetylation of heat shock protein (hsp) 90, resulting in inhibition of its binding to ATP, which has been shown to impair the chaperone association of hsp 90 with its client proteins, Her-2, AKT, and c-Raf-1.	LAQ824	0-6	heat shock protein 90 alpha family class A member 1	Homo sapiens	175-181
14578462-4	2003	LAQ824 also induced the acetylation of heat shock protein (hsp) 90, resulting in inhibition of its binding to ATP, which has been shown to impair the chaperone association of hsp 90 with its client proteins, Her-2, AKT, and c-Raf-1.	LAQ824	0-6	erb-b2 receptor tyrosine kinase 2	Homo sapiens	208-213
14578462-4	2003	LAQ824 also induced the acetylation of heat shock protein (hsp) 90, resulting in inhibition of its binding to ATP, which has been shown to impair the chaperone association of hsp 90 with its client proteins, Her-2, AKT, and c-Raf-1.	LAQ824	0-6	AKT serine/threonine kinase 1	Homo sapiens	215-218
14578462-4	2003	LAQ824 also induced the acetylation of heat shock protein (hsp) 90, resulting in inhibition of its binding to ATP, which has been shown to impair the chaperone association of hsp 90 with its client proteins, Her-2, AKT, and c-Raf-1.	LAQ824	0-6	TNF receptor associated factor 3	Homo sapiens	224-231
14578462-5	2003	Consistent with this, treatment with LAQ824 shifted the binding of Her-2 from hsp 90 to hsp 70, promoting proteasomal degradation of Her-2.	LAQ824	37-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	67-72
14578462-5	2003	Consistent with this, treatment with LAQ824 shifted the binding of Her-2 from hsp 90 to hsp 70, promoting proteasomal degradation of Her-2.	LAQ824	37-43	heat shock protein 90 alpha family class A member 1	Homo sapiens	78-84
14578462-5	2003	Consistent with this, treatment with LAQ824 shifted the binding of Her-2 from hsp 90 to hsp 70, promoting proteasomal degradation of Her-2.	LAQ824	37-43	heat shock protein family A (Hsp70) member 4	Homo sapiens	88-94
14578462-5	2003	Consistent with this, treatment with LAQ824 shifted the binding of Her-2 from hsp 90 to hsp 70, promoting proteasomal degradation of Her-2.	LAQ824	37-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	133-138
14578462-7	2003	Following LAQ824 treatment, the cell membrane association, autotyrosine phosphorylation, and colocalization of Her-2 with HER-3 also declined.	LAQ824	10-16	erb-b2 receptor tyrosine kinase 2	Homo sapiens	111-116
14578462-7	2003	Following LAQ824 treatment, the cell membrane association, autotyrosine phosphorylation, and colocalization of Her-2 with HER-3 also declined.	LAQ824	10-16	erb-b2 receptor tyrosine kinase 3	Homo sapiens	122-127
14578462-11	2003	These findings suggest that LAQ824 is active against human breast cancer cells and has the potential to improve the efficacy of trastuzumab, taxotere, gemcitabine, and epothilone B against breast cancer with Her-2/neuamplification.	LAQ824	28-34	erb-b2 receptor tyrosine kinase 2	Homo sapiens	208-213
12941844-1	2003	Treatment with LAQ824 (Novartis Pharmaceutical, Inc.), a cinnamyl hydroxamic acid analogue inhibitor of histone deacetylases, depleted the mRNA and protein expression of Bcr-Abl in human chronic myeloid leukemia blast crisis (CML-BC) cells.	LAQ824	15-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-177
12941844-2	2003	Exposure to LAQ824 induced the expression of the cell cycle-dependent kinase inhibitors p21 and p27 and caused cell cycle G(1)-phase accumulation and apoptosis of CML-BC cells.	LAQ824	12-18	H3 histone pseudogene 16	Homo sapiens	88-91
12941844-2	2003	Exposure to LAQ824 induced the expression of the cell cycle-dependent kinase inhibitors p21 and p27 and caused cell cycle G(1)-phase accumulation and apoptosis of CML-BC cells.	LAQ824	12-18	interferon alpha inducible protein 27	Homo sapiens	96-99
12814625-6	2003	Degradation of hY1 could also be demonstrated after treatment of A549 lung carcinoma cells treated with Staurosporin, Paclitaxel, or the histone deacetylase inhibitor LAQ824.	LAQ824	167-173	RNA, Ro60-associated Y1	Homo sapiens	15-18