PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19229879-5	2009	Pim-3 was dispersed from lamellipodia when ECs were treated with cytochalasin D, an inhibitor of actin polymerization.	Cytochalasin D	65-79	Pim-3 proto-oncogene, serine/threonine kinase	Homo sapiens	0-5
19385049-5	2009	In the present study,the well-characterized human neuroblastoma cell line SH-SY5Y served as a model system to separate physiological and pro-apoptotic JNK actions in the response to the cytoskeleton-interfering substances colchicine, cytochalasin D and taxol.	Cytochalasin D	234-248	mitogen-activated protein kinase 8	Homo sapiens	151-154
19213846-9	2009	Cytochalasin D eliminated this difference and normalized insulin and glucagon secretion in NCAM(-/-) islets.	Cytochalasin D	0-14	neural cell adhesion molecule 1	Mus musculus	91-95
19385049-7	2009	Using the chemical JNK inhibitor SP600125 as well as compartment-specific JNK-inhibiting constructs and dominant negative isoform mutants, we show that the nuclear subgroup of JNK2 is the dominant effector in colchicine and taxol-induced apoptosis, while cell cycle promotion is mediated by both cytoplasmic and nuclear JNK2.In contrast, cytochalasin D-triggered apoptosis is independent of JNK signaling.	Cytochalasin D	338-352	mitogen-activated protein kinase 9	Homo sapiens	176-180
19282659-8	2009	By using this screening system, daunorubicin, doxorubicin and cytochalasin D, which enhanced the green fluorescent, were selected and then were confirmed to actually increase the expression of Melan-A/MART-1 mRNA and protein in human melanoma cells of MU89, MM96L(+) and SK-MEL-28, but also in low-antigen presenting cells such as MM96L(-), MUX, and A375.	Cytochalasin D	62-76	melan-A	Homo sapiens	193-200
19245805-6	2009	The destruction of microfilaments with cytochalasin D, which is known to delocalize beta-actin mRNAs, led to an increase in D(MACRO) to 0.2 microm(2)/s in the perinuclear region.	Cytochalasin D	39-53	actin, beta	Gallus gallus	84-94
19114730-7	2009	Cytochalasin D, an actin polymerization inhibitor, suppressed the PCOOH-induced cell adhesion to ICAM-1 and the membrane protrusions.	Cytochalasin D	0-14	intercellular adhesion molecule 1	Homo sapiens	97-103
19107907-7	2009	Cytochalasin D (an actin filament disruptor) partially inhibited CSE-induced ICAM-1 and E-selectin surface expression.	Cytochalasin D	0-14	intercellular adhesion molecule 1	Homo sapiens	77-83
19107907-7	2009	Cytochalasin D (an actin filament disruptor) partially inhibited CSE-induced ICAM-1 and E-selectin surface expression.	Cytochalasin D	0-14	selectin E	Homo sapiens	88-98
18760941-4	2009	RESULTS: Here we demonstrate that several CTGF/Cyr61/Nov (CCN) family members are differentially affected by either inhibition of actin polymerization (cytochalasin D treatment), promotion of actin polymerization (jasplakinolide treatment), inhibition of RhoA/rho kinase (ROCK) signaling (Y27632 treatment) and Rac1 signaling.	Cytochalasin D	152-166	cellular communication network factor 2	Homo sapiens	42-46
18760941-4	2009	RESULTS: Here we demonstrate that several CTGF/Cyr61/Nov (CCN) family members are differentially affected by either inhibition of actin polymerization (cytochalasin D treatment), promotion of actin polymerization (jasplakinolide treatment), inhibition of RhoA/rho kinase (ROCK) signaling (Y27632 treatment) and Rac1 signaling.	Cytochalasin D	152-166	cellular communication network factor 1	Homo sapiens	47-52
18760941-4	2009	RESULTS: Here we demonstrate that several CTGF/Cyr61/Nov (CCN) family members are differentially affected by either inhibition of actin polymerization (cytochalasin D treatment), promotion of actin polymerization (jasplakinolide treatment), inhibition of RhoA/rho kinase (ROCK) signaling (Y27632 treatment) and Rac1 signaling.	Cytochalasin D	152-166	cellular communication network factor 3	Homo sapiens	53-56
18760941-5	2009	We also show that the Smad site in the CTGF/CCN2 promoter is responsive to both Rac1 inhibition and cytochalasin D treatment, suggesting a role of TGFbeta/Smad signaling in mediating the effects of actin dynamics and Rac1.	Cytochalasin D	100-114	cellular communication network factor 2	Homo sapiens	39-43
18760941-5	2009	We also show that the Smad site in the CTGF/CCN2 promoter is responsive to both Rac1 inhibition and cytochalasin D treatment, suggesting a role of TGFbeta/Smad signaling in mediating the effects of actin dynamics and Rac1.	Cytochalasin D	100-114	cellular communication network factor 2	Homo sapiens	44-48
18760941-5	2009	We also show that the Smad site in the CTGF/CCN2 promoter is responsive to both Rac1 inhibition and cytochalasin D treatment, suggesting a role of TGFbeta/Smad signaling in mediating the effects of actin dynamics and Rac1.	Cytochalasin D	100-114	transforming growth factor beta 1	Homo sapiens	147-154
18760941-5	2009	We also show that the Smad site in the CTGF/CCN2 promoter is responsive to both Rac1 inhibition and cytochalasin D treatment, suggesting a role of TGFbeta/Smad signaling in mediating the effects of actin dynamics and Rac1.	Cytochalasin D	100-114	Rac family small GTPase 1	Homo sapiens	217-221
19282659-8	2009	By using this screening system, daunorubicin, doxorubicin and cytochalasin D, which enhanced the green fluorescent, were selected and then were confirmed to actually increase the expression of Melan-A/MART-1 mRNA and protein in human melanoma cells of MU89, MM96L(+) and SK-MEL-28, but also in low-antigen presenting cells such as MM96L(-), MUX, and A375.	Cytochalasin D	62-76	melan-A	Homo sapiens	201-207
18566755-8	2008	Cytochalasin D treatment immediately following release of gels inhibited contraction in a dose-dependent manner as well as prevented upregulation of MMP-1, MMP-3, and alpha2 integrin mRNA levels in contracting gels.	Cytochalasin D	0-14	matrix metallopeptidase 1	Homo sapiens	149-154
19073604-3	2009	The uptake of zymosan by CHO/CL-P1 was dependent upon the level of CL-P1 expressed on the membrane and was inhibited by cytochalasin D and wortmannin.	Cytochalasin D	120-134	cleavage factor polyribonucleotide kinase subunit 1	Homo sapiens	29-34
19073604-3	2009	The uptake of zymosan by CHO/CL-P1 was dependent upon the level of CL-P1 expressed on the membrane and was inhibited by cytochalasin D and wortmannin.	Cytochalasin D	120-134	cleavage factor polyribonucleotide kinase subunit 1	Homo sapiens	67-72
19183835-7	2009	The protein kinase C (PKC)/PKD inhibitor Go6976 suppressed cytochalasin D-induced acceleration of osteoblastic differentiation, whereas Go6983, a specific inhibitor of conventional PKCs, did not.	Cytochalasin D	59-73	protein kinase D1	Mus musculus	27-30
18789311-2	2008	In the present study, we demonstrated that reorganization of actin cytoskeleton induced by Cytochalasin D (CytD), an actin-polymerization inhibitor, enhanced il-8 gene expression induced by TNFalpha and LPS in HL-60 monocyte-like cells.	Cytochalasin D	91-105	C-X-C motif chemokine ligand 8	Homo sapiens	158-162
18789311-2	2008	In the present study, we demonstrated that reorganization of actin cytoskeleton induced by Cytochalasin D (CytD), an actin-polymerization inhibitor, enhanced il-8 gene expression induced by TNFalpha and LPS in HL-60 monocyte-like cells.	Cytochalasin D	91-105	tumor necrosis factor	Homo sapiens	190-198
18675249-5	2008	When the nuclear deformation was recovered by cytochalasin D treatment, aggrecan expression was up-regulated and type I collagen (Col1a2) expression was down-regulated.	Cytochalasin D	46-60	collagen type I alpha 2 chain	Homo sapiens	130-136
18703153-7	2008	Moreover, cytochalasin D inhibited the phosphorylation of Akt and p38 mitogen activated protein kinase (MAPK), induced during redifferentiation on chitosan membrane.	Cytochalasin D	10-24	adapter molecule crk	Gallus gallus	66-69
18665919-5	2008	Translocation of Bid and Bax to the mitochondria was reduced by cytochalasin D, latrunculin A or jasplakinolide.	Cytochalasin D	64-78	BH3 interacting domain death agonist	Homo sapiens	17-20
18665919-5	2008	Translocation of Bid and Bax to the mitochondria was reduced by cytochalasin D, latrunculin A or jasplakinolide.	Cytochalasin D	64-78	BCL2 associated X, apoptosis regulator	Homo sapiens	25-28
18566755-8	2008	Cytochalasin D treatment immediately following release of gels inhibited contraction in a dose-dependent manner as well as prevented upregulation of MMP-1, MMP-3, and alpha2 integrin mRNA levels in contracting gels.	Cytochalasin D	0-14	matrix metallopeptidase 3	Homo sapiens	156-161
18650426-4	2008	Depolymerization of the actin cytoskeleton by cytochalasin D or disruption of transit between the endoplasmic reticulum and the Golgi apparatus by brefeldin A prevented the second phase of ERK1/2 phosphorylation.	Cytochalasin D	46-60	mitogen-activated protein kinase 3	Homo sapiens	189-195
18571158-5	2008	Additionally, ginsenoside Rg1 or Rb1-mediated facilitation of ionomycin-evoked glutamate release was occluded by cytochalasin D, a membrane-permeant inhibitor of actin polymerization.	Cytochalasin D	113-127	RB transcriptional corepressor 1	Rattus norvegicus	33-36
18697831-5	2008	P-Rex1 inhibition of neurite outgrowth was rescued by low-dose cytochalasin D treatment, which prevents actin polymerisation.	Cytochalasin D	63-77	phosphatidylinositol-3,4,5-trisphosphate-dependent Rac exchange factor 1	Rattus norvegicus	0-6
18758068-10	2008	TRPC5 was inhibited by cytochalasin D treatment.	Cytochalasin D	23-37	transient receptor potential cation channel subfamily C member 5	Homo sapiens	0-5
18460599-8	2008	Silencing of p38 MAPK, inhibition of PI 3-kinase, or preincubation with cytochalasin D prevented the increases in LPL activity.	Cytochalasin D	72-86	lipoprotein lipase	Rattus norvegicus	114-117
18753385-7	2008	Gain of function of PKD can rescue the disruption of polarized membrane trafficking and neuronal polarity caused by cytochalasin D, which results in F-actin depolymerization.	Cytochalasin D	116-130	protein kinase D1	Homo sapiens	20-23
18690644-6	2008	Moreover, treatment with cytochalasin D, an inhibitor of F-actin polymerization, completely blocked the upregulation of GnT-III expression in the dense culture.	Cytochalasin D	25-39	beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase	Homo sapiens	120-127
18506372-8	2008	Cytochalasin D, a destructive agent of the cytoskeleton, inhibits ECM-induced FAK activation and cell proliferation in HaCaT cells.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	78-81
18306405-7	2008	Similar to SNP, cytochalasin D, an inhibitor of F-actin formation, disturbed F-actin polymerization and increased MEKK1 and JNK activations.	Cytochalasin D	16-30	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	114-119
18306405-7	2008	Similar to SNP, cytochalasin D, an inhibitor of F-actin formation, disturbed F-actin polymerization and increased MEKK1 and JNK activations.	Cytochalasin D	16-30	mitogen-activated protein kinase 8	Homo sapiens	124-127
18587263-8	2008	In addition, phalloidin or cytochalasin D inhibited CD98-mediated induction of cell-ECM adhesion, but not surface expression and clustering of beta1 integrins.	Cytochalasin D	27-41	solute carrier family 3 member 2	Homo sapiens	52-56
18587263-9	2008	The inhibitory effects of PP2, cytochalasin D or phalloidin on CD98-stimulated cell adhesion were diminished by pretreatment of cells with Mn2+, which is shown to induce conformational change of integrins.	Cytochalasin D	31-45	solute carrier family 3 member 2	Homo sapiens	63-67
18355291-8	2008	The intracytoplasmatic transport seems to depend on the contractile apparatus, because cell pretreatment with cytochalasin D prevented lipopolysaccharide internalization and reduced both TNF-alpha and NO release.	Cytochalasin D	110-124	lipopolysaccharide induced TNF factor	Gallus gallus	187-196
18331289-3	2008	In cells transfected with either 0.5 microg/mL or 3 microg/mL of alpha-Syn and 1 microg/mL of NET DNA, treatment with cytochalasin D, an actin depolymerizing agent, caused a dose-dependent decrease and increase, respectively, in [3H]-NE uptake.	Cytochalasin D	118-132	synuclein alpha	Homo sapiens	65-74
18326801-6	2008	The inclusion of the actin polymerization inhibitor cytochalasin D (CD) during culture prevented gross morphological changes including a loss of T tubules and a rounding of intercalated discs, but CD alone did not rescue the responsiveness to ET-1 or prevent ET(A) downregulation.	Cytochalasin D	68-70	endothelin receptor type A	Rattus norvegicus	259-264
18432521-5	2008	Binding of platelets to collagen also leads to activation of alpha2beta1 integrin, which is dependent upon actin polymerization and cdc42 activity, since activation is blocked by cytochalasin D and secramine A respectively.	Cytochalasin D	179-193	cell division cycle 42	Homo sapiens	132-137
18207700-13	2008	Depolymerization of actin by cytochalasin D prevented US-induced Src, ERK, and p38 activation.	Cytochalasin D	29-43	Rous sarcoma oncogene	Mus musculus	65-68
18230622-7	2008	Its inhibitory action was dependent on the association of TRPC4alpha with actin cytoskeleton as it was prevented by cytochalasin D treatment or by the deletion of the C-terminal PDZ-binding motif (Thr-Thr-Arg-Leu) that links TRPC4 to F-actin through the sodium-hydrogen exchanger regulatory factor and ezrin.	Cytochalasin D	116-130	transient receptor potential cation channel subfamily C member 4	Homo sapiens	58-63
18204471-8	2008	Thrombin-promoted nucleotide release was inhibited by BAPTA-AM, brefeldin A and cytochalasin D, and was insensitive to Pertussis toxin and PI3-kinase inhibitors.	Cytochalasin D	80-94	coagulation factor II, thrombin	Homo sapiens	0-8
18207700-13	2008	Depolymerization of actin by cytochalasin D prevented US-induced Src, ERK, and p38 activation.	Cytochalasin D	29-43	mitogen-activated protein kinase 14	Mus musculus	79-82
17884942-5	2007	Cytochalasin D, jasplakinolide, latrunculin B, and swinholide A altered the actin cytoskeleton of GH4 cells, as assessed by Alexa Fluor phalloidin staining, and inhibited insulin-increased prolactin gene transcription.	Cytochalasin D	0-14	insulin	Homo sapiens	171-178
18215660-6	2008	Disruption of cytoskeleton by cytochalasin D prior to treatment with TNF-alpha led to increase of p65 nuclear translocation.	Cytochalasin D	30-44	lipopolysaccharide induced TNF factor	Gallus gallus	69-78
18215660-6	2008	Disruption of cytoskeleton by cytochalasin D prior to treatment with TNF-alpha led to increase of p65 nuclear translocation.	Cytochalasin D	30-44	synaptotagmin 1	Gallus gallus	98-101
17977944-8	2008	Similarly, cytochalasin D-induced actin depolymerization and intercellular gap formation and cell detachment in response to the Ca(2+)/calmodulin antagonist trifluperazine (TFP) as well as thrombin-induced cell dissociation were also reduced by hydrostatic pressure.	Cytochalasin D	11-25	coagulation factor II	Mus musculus	189-197
20084179-7	2008	Addition of cytochalasin D to disrupt actin polymerization served to suppress the magnitude of flow-mediated actin remodeling in both subconfluent confluent EC monolayers.	Cytochalasin D	12-26	actin epsilon 1	Bos taurus	38-43
20084179-7	2008	Addition of cytochalasin D to disrupt actin polymerization served to suppress the magnitude of flow-mediated actin remodeling in both subconfluent confluent EC monolayers.	Cytochalasin D	12-26	actin epsilon 1	Bos taurus	109-114
17916773-6	2007	The effect of statins on eNOS polyadenylation was related to cytoskeleton organization; there was increased eNOS mRNA polyadenylation after Rho inhibition and cytochalasin D treatment.	Cytochalasin D	159-173	nitric oxide synthase 3	Homo sapiens	25-29
17916773-6	2007	The effect of statins on eNOS polyadenylation was related to cytoskeleton organization; there was increased eNOS mRNA polyadenylation after Rho inhibition and cytochalasin D treatment.	Cytochalasin D	159-173	nitric oxide synthase 3	Homo sapiens	108-112
17884942-5	2007	Cytochalasin D, jasplakinolide, latrunculin B, and swinholide A altered the actin cytoskeleton of GH4 cells, as assessed by Alexa Fluor phalloidin staining, and inhibited insulin-increased prolactin gene transcription.	Cytochalasin D	0-14	prolactin	Rattus norvegicus	189-198
17717051-5	2007	The cellular uptake of Pax4 PTD can be completely blocked by heparin, whereas cytochalasin D and amiloride were partially effective in blocking the Pax4 protein entry.	Cytochalasin D	78-92	paired box 4	Homo sapiens	148-152
17936423-8	2007	Cytochalasin D and paclitaxel, but not phalloidin and colchicine, blocked ERK1/2 phosphorylation.	Cytochalasin D	0-14	mitogen-activated protein kinase 3	Homo sapiens	74-80
17690101-8	2007	AMF uptake in these cells was reduced by phosphatidylinositol 3-kinase inhibition but not by regulators of macropinocytosis such as amiloride, phorbol ester, or actin cytoskeleton disruption by cytochalasin D.	Cytochalasin D	194-208	glucose-6-phosphate isomerase	Homo sapiens	0-3
17825818-7	2007	Finally, C3G- and C3GDeltaCat-mediated inhibition of ERK phosphorylation is reverted by incubation with cytochalasin D.	Cytochalasin D	104-118	Rap guanine nucleotide exchange factor 1	Homo sapiens	9-19
17825818-7	2007	Finally, C3G- and C3GDeltaCat-mediated inhibition of ERK phosphorylation is reverted by incubation with cytochalasin D.	Cytochalasin D	104-118	mitogen-activated protein kinase 1	Homo sapiens	53-56
17699564-6	2007	Preincubation with ryanodine, cytochalasin-D, or colchicine substantially reduced the occurrence of Ca(2+) sparks triggered by fibronectin-coated beads.	Cytochalasin D	30-44	fibronectin 1	Rattus norvegicus	127-138
17804730-4	2007	Elevated expression of RNF5 was seen in breast cancer cell lines that became more sensitive to cytochalasin D- and paclitaxel-induced apoptosis following its knockdown with specific short interfering RNA.	Cytochalasin D	95-109	ring finger protein 5	Homo sapiens	23-27
17487456-6	2007	And the upregulation in c-fos expression was blocked by cytochalasin D (Depolymerizing agent of microfilament).	Cytochalasin D	56-70	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	24-29
17711354-6	2007	Both the cytoskeleton-disrupting agent cytochalasin D and the cholesterol-depleting agent methyl-beta-cyclodextrin (mbetaCD) increased the lateral mobility of the YFP-DAT but not that of the EGFP-EGFR.	Cytochalasin D	39-53	solute carrier family 6 (neurotransmitter transporter, dopamine), member 3	Mus musculus	167-170
17711354-6	2007	Both the cytoskeleton-disrupting agent cytochalasin D and the cholesterol-depleting agent methyl-beta-cyclodextrin (mbetaCD) increased the lateral mobility of the YFP-DAT but not that of the EGFP-EGFR.	Cytochalasin D	39-53	epidermal growth factor receptor	Mus musculus	196-200
17617603-4	2007	Cytochalasin D treatment impaired T cell activation by causing a reduction in TCR/CD28-mediated calcium flux, and blocked activation of two regulatory elements within the IL-2 promoter, NFAT/AP-1 and CD28RE/AP.	Cytochalasin D	0-14	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	78-81
17617603-4	2007	Cytochalasin D treatment impaired T cell activation by causing a reduction in TCR/CD28-mediated calcium flux, and blocked activation of two regulatory elements within the IL-2 promoter, NFAT/AP-1 and CD28RE/AP.	Cytochalasin D	0-14	CD28 molecule	Homo sapiens	82-86
17617603-4	2007	Cytochalasin D treatment impaired T cell activation by causing a reduction in TCR/CD28-mediated calcium flux, and blocked activation of two regulatory elements within the IL-2 promoter, NFAT/AP-1 and CD28RE/AP.	Cytochalasin D	0-14	interleukin 2	Homo sapiens	171-175
17403879-7	2007	In contrast, cytochalasin D treatment of RAW 264.7 cells decreased TNF-alpha secretion after infection with either the wild type or the mutant.	Cytochalasin D	13-27	tumor necrosis factor	Mus musculus	67-76
17395152-6	2007	The inhibition by PMA was partially prevented by cytochalasin D, suggesting that PKC reduces the hNaDC-3 activity, at least in part, by increased endocytosis.	Cytochalasin D	49-63	solute carrier family 13 member 3	Homo sapiens	97-104
17942824-7	2008	AICAR also appreciably enhanced LPL, an effect reduced by preincubation with the p38 MAPK inhibitor SB202190 or by cytochalasin D, which inhibits actin polymerization.	Cytochalasin D	115-129	lipoprotein lipase	Rattus norvegicus	32-35
17202227-5	2007	Disruption of the actin cytoskeleton by latrunculin A and cytochalasin D induced a decrease in FMLP-stimulated CD35 expression after an initial increase.	Cytochalasin D	58-72	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	111-115
17451552-11	2007	Similar alterations were observed upon cytochalasin D treatment, suggesting that the Rab27a-Myrip-MyoVIIa complex regulates tethering of melanosomes onto actin filaments, a process that ensures melanosome movement towards the cell periphery.	Cytochalasin D	39-53	RAB27A, member RAS oncogene family	Mus musculus	85-91
17460268-3	2007	RESULTS: Treatment of HTM cells with cytochalasin D and latrunculin A led to significant activation of MMP-2, p38 MAPK, and ERK1/2, which appeared to correlate with changes in cell morphology and actin depolymerization.	Cytochalasin D	37-51	matrix metallopeptidase 2	Homo sapiens	103-108
17460268-3	2007	RESULTS: Treatment of HTM cells with cytochalasin D and latrunculin A led to significant activation of MMP-2, p38 MAPK, and ERK1/2, which appeared to correlate with changes in cell morphology and actin depolymerization.	Cytochalasin D	37-51	mitogen-activated protein kinase 14	Homo sapiens	110-118
17460268-3	2007	RESULTS: Treatment of HTM cells with cytochalasin D and latrunculin A led to significant activation of MMP-2, p38 MAPK, and ERK1/2, which appeared to correlate with changes in cell morphology and actin depolymerization.	Cytochalasin D	37-51	mitogen-activated protein kinase 3	Homo sapiens	124-130
17451552-11	2007	Similar alterations were observed upon cytochalasin D treatment, suggesting that the Rab27a-Myrip-MyoVIIa complex regulates tethering of melanosomes onto actin filaments, a process that ensures melanosome movement towards the cell periphery.	Cytochalasin D	39-53	myosin VIIA and Rab interacting protein	Mus musculus	92-97
17229686-6	2007	Cells expressing NSP4-EGFP for 24 h were also resistant to cell rounding induced by cytochalasin D.	Cytochalasin D	84-98	serine protease 57	Homo sapiens	17-21
17197512-9	2007	Of note, internalization of this G-actin-sequestering peptide into HCE-T cells was found to be essential in cell death prevention, in that disruption of the cellular entry of Tbeta(4) by cytochalasin D abrogated its cytoprotective effects.	Cytochalasin D	187-201	thymosin beta 4 X-linked	Homo sapiens	175-183
17123483-5	2007	Overexpression of hNP22 resulted in process formation in these cells that increased upon treatment with cytochalasin D, an actin depolymerising agent.	Cytochalasin D	104-118	transgelin 3	Homo sapiens	18-23
17009330-5	2007	In contrast, observations of streaming and actin organisation during treatments with cytochalasin D (CD) suggested GFP-mTn-labelled actin to remain more stable.	Cytochalasin D	85-99	actin-12	Arabidopsis thaliana	43-48
17009330-5	2007	In contrast, observations of streaming and actin organisation during treatments with cytochalasin D (CD) suggested GFP-mTn-labelled actin to remain more stable.	Cytochalasin D	85-99	actin-12	Arabidopsis thaliana	132-137
17108132-4	2006	Treatment of 2008 cells with DDP in combination with inhibitors of various endosomal pathways (amiloride, cytochalasin D, nystatin, and methyl-beta-cyclodextrin) showed that hCTR1 degradation was blocked by amiloride and cytochalasin D, indicating that hCTR1 was internalized primarily by macropinocytosis.	Cytochalasin D	106-120	solute carrier family 31 member 1	Homo sapiens	174-179
17050539-3	2006	Here we show that endogenous SOX9 mRNA can be rapidly up-regulated in subcultured human articular chondrocytes if grown in alginate, in monolayer with cytochalasin D, or with specific inhibition of the RhoA effector kinases ROCK1 and -2, which all prevent actin stress fiber formation.	Cytochalasin D	151-165	SRY-box transcription factor 9	Homo sapiens	29-33
16563724-3	2006	Biochemical modification of the actin and microtubule network by (1) okadaic acid (OA), which disrupts MT-based vesicular trafficking; (2) cytochalasin D and latrunculin B, which promote actin depolymerization; and (3) 2,3-butanedione monoxime (BDM), which inhibits myosin-actin interaction, was confirmed by immunofluorescence microscopy using actin- and tubulin-specific antibodies.	Cytochalasin D	139-153	myosin heavy chain 14	Homo sapiens	266-272
17108132-4	2006	Treatment of 2008 cells with DDP in combination with inhibitors of various endosomal pathways (amiloride, cytochalasin D, nystatin, and methyl-beta-cyclodextrin) showed that hCTR1 degradation was blocked by amiloride and cytochalasin D, indicating that hCTR1 was internalized primarily by macropinocytosis.	Cytochalasin D	221-235	solute carrier family 31 member 1	Homo sapiens	174-179
16979163-3	2006	We demonstrate that vinblastin and cytochalasin D, which respectively disorganize microtubules and actin microfilaments, trigger the activation of the p38/MAPKAP2 kinase pathway and lead to the specific alphaB-crystallin phosphorylation at serine 59.	Cytochalasin D	35-49	mitogen-activated protein kinase 14	Homo sapiens	151-154
16672691-6	2006	Inhibition of phosphoinositide 3-kinase (PI3K), but not JNK, significantly decreased the amount of active MMP-2 following cytochalasin D stimulation with a concurrent decrease in MT1-MMP protein.	Cytochalasin D	122-136	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	14-39
17002579-1	2006	UNLABELLED: Disruption of the actin cytoskeleton with cytochalasin D enhanced the mechanically induced increase in intracellular Ca(2+) ([Ca(2+)](i)) in osteoblasts in a manner similar to that of PTH.	Cytochalasin D	54-68	parathyroid hormone	Homo sapiens	196-199
17002579-11	2006	RESULTS AND CONCLUSIONS: Depolymerization of actin with 1-5 microM cytochalasin D (cyto D) augmented the peak [Ca(2+)](i) response and increased the number of cells responding to shear, similar to the increased responses induced by pretreatment with 50 nM PTH.	Cytochalasin D	67-81	parathyroid hormone	Homo sapiens	256-259
16920067-2	2006	Paxillin tyrosine phosphorylation is inhibited by cytochalasin D (CD), but slightly increased by colchicine and paclitaxol (taxol).	Cytochalasin D	50-64	paxillin	Bos taurus	0-8
16672691-6	2006	Inhibition of phosphoinositide 3-kinase (PI3K), but not JNK, significantly decreased the amount of active MMP-2 following cytochalasin D stimulation with a concurrent decrease in MT1-MMP protein.	Cytochalasin D	122-136	matrix metallopeptidase 2	Homo sapiens	106-111
16823880-8	2006	This process appears mediated through actin cytoskeleton since incubation of the cells with cytochalasin D totally reversed the T3 stimulatory effect on Cx43-GFP gap junction plaques.	Cytochalasin D	92-106	gap junction protein alpha 1	Homo sapiens	153-157
17029595-3	2006	Cells treated with vinblastine, colchicine or cytochalasin D, and zinc deficient cells, all showed a low nuclear NF-kappaB binding activity, and low nuclear concentrations of RelA and p50.	Cytochalasin D	46-60	nuclear factor kappa B subunit 1	Homo sapiens	113-122
16887096-7	2006	In the CD-treated cells, Oct4 and Sox2, representing undifferentiation, were down-regulated as well as Sox1, AFP, and CTN-1, representing ectoderm, endoderm, and cardiogenesis, respectively.	Cytochalasin D	7-9	POU domain, class 5, transcription factor 1, related sequence 1	Mus musculus	25-29
16887096-7	2006	In the CD-treated cells, Oct4 and Sox2, representing undifferentiation, were down-regulated as well as Sox1, AFP, and CTN-1, representing ectoderm, endoderm, and cardiogenesis, respectively.	Cytochalasin D	7-9	SRY (sex determining region Y)-box 2	Mus musculus	34-38
16887096-7	2006	In the CD-treated cells, Oct4 and Sox2, representing undifferentiation, were down-regulated as well as Sox1, AFP, and CTN-1, representing ectoderm, endoderm, and cardiogenesis, respectively.	Cytochalasin D	7-9	SRY (sex determining region Y)-box 1	Mus musculus	103-107
16887096-7	2006	In the CD-treated cells, Oct4 and Sox2, representing undifferentiation, were down-regulated as well as Sox1, AFP, and CTN-1, representing ectoderm, endoderm, and cardiogenesis, respectively.	Cytochalasin D	7-9	alpha fetoprotein	Mus musculus	109-112
16984628-5	2006	In addition, Atf3 mRNA levels are increased in response to cytochalasin D treatment, an inducer of chondrocyte maturation.	Cytochalasin D	59-73	activating transcription factor 3	Mus musculus	13-17
17029595-3	2006	Cells treated with vinblastine, colchicine or cytochalasin D, and zinc deficient cells, all showed a low nuclear NF-kappaB binding activity, and low nuclear concentrations of RelA and p50.	Cytochalasin D	46-60	RELA proto-oncogene, NF-kB subunit	Homo sapiens	175-179
17029595-3	2006	Cells treated with vinblastine, colchicine or cytochalasin D, and zinc deficient cells, all showed a low nuclear NF-kappaB binding activity, and low nuclear concentrations of RelA and p50.	Cytochalasin D	46-60	nuclear factor kappa B subunit 1	Homo sapiens	184-187
16818493-3	2006	Depolymerization of microtubules with colchicine (Colch) or actin microfilaments with cytochalasin D (CD) dramatically reduced the amount of caveolin-3 in buoyant (sucrose density) fractions of adult rat cardiac myocytes.	Cytochalasin D	86-100	caveolin 3	Rattus norvegicus	141-151
16818493-3	2006	Depolymerization of microtubules with colchicine (Colch) or actin microfilaments with cytochalasin D (CD) dramatically reduced the amount of caveolin-3 in buoyant (sucrose density) fractions of adult rat cardiac myocytes.	Cytochalasin D	102-104	caveolin 3	Rattus norvegicus	141-151
16818493-6	2006	Treatment of S49 T-lymphoma cells (which possess lipid rafts but lack caveolae) with CD or Colch redistributed a lipid raft marker (linker for activation of T cells (LAT)) and Galpha(s) from lipid raft domains.	Cytochalasin D	85-87	GNAS (guanine nucleotide binding protein, alpha stimulating) complex locus	Mus musculus	176-185
16818493-4	2006	Colch or CD treatment led to the exclusion of caveolin-1, caveolin-2, beta1-adrenergic receptors (beta1-AR), beta2-AR, Galpha(s), and adenylyl cyclase (AC)5/6 from buoyant fractions, decreasing AC5/6 and tyrosine-phosphorylated caveolin-1 in caveolin-1 immunoprecipitates but in parallel increased isoproterenol (beta-AR agonist)-stimulated cAMP production.	Cytochalasin D	9-11	adenylate cyclase 6	Rattus norvegicus	194-238
16818493-4	2006	Colch or CD treatment led to the exclusion of caveolin-1, caveolin-2, beta1-adrenergic receptors (beta1-AR), beta2-AR, Galpha(s), and adenylyl cyclase (AC)5/6 from buoyant fractions, decreasing AC5/6 and tyrosine-phosphorylated caveolin-1 in caveolin-1 immunoprecipitates but in parallel increased isoproterenol (beta-AR agonist)-stimulated cAMP production.	Cytochalasin D	9-11	caveolin 1	Rattus norvegicus	228-238
16872432-7	2006	The filamentous structure was identified as an actin cortical cytoskeleton, investigating its disaggregation induced by cytochalasin D treatment.	Cytochalasin D	120-134	actin like 6A S homeolog	Xenopus laevis	47-52
16740972-5	2006	However, treatment of cells with hCG or dbcAMP in the presence of hormones significantly (P < 0.05) decreased the percentage of annexin-V-stained cells compared with cells treated with cytochalasin D alone.	Cytochalasin D	188-202	annexin A5	Homo sapiens	131-140
16740972-7	2006	The inhibition of apoptosis by hCG and dbcAMP was via the intrinsic pathway because the cytochalasin-D-treated cells stained intensely for Bax, whereas the cells treated with hormones, hCG, or dbcAMP stained predominantly for Bcl-2.	Cytochalasin D	88-102	BCL2 associated X, apoptosis regulator	Homo sapiens	139-142
16740972-8	2006	Treatment of cytochalasin-D-treated cells with hormones and dbcAMP resulted in an increase in the secretion of IGF-binding protein-1 (IGFBP-1) and prolactin.	Cytochalasin D	13-27	insulin like growth factor binding protein 1	Homo sapiens	111-132
16740972-8	2006	Treatment of cytochalasin-D-treated cells with hormones and dbcAMP resulted in an increase in the secretion of IGF-binding protein-1 (IGFBP-1) and prolactin.	Cytochalasin D	13-27	insulin like growth factor binding protein 1	Homo sapiens	134-141
16740972-8	2006	Treatment of cytochalasin-D-treated cells with hormones and dbcAMP resulted in an increase in the secretion of IGF-binding protein-1 (IGFBP-1) and prolactin.	Cytochalasin D	13-27	prolactin	Homo sapiens	147-156
16740972-9	2006	Treatment of cytochalasin-D-treated cells with recombinant IGFBP-1 and prolactin also inhibited apoptosis.	Cytochalasin D	13-27	insulin like growth factor binding protein 1	Homo sapiens	59-66
16740972-9	2006	Treatment of cytochalasin-D-treated cells with recombinant IGFBP-1 and prolactin also inhibited apoptosis.	Cytochalasin D	13-27	prolactin	Homo sapiens	71-80
16762926-9	2006	TEM8 anchorage to actin was relevant as spreading was inhibited by the cytoskeleton-disrupting drug cytochalasin D, but persisted in the presence of the microtubule-depolymerizing drug nocodazole, and in cells lacking intermediate filaments.	Cytochalasin D	100-114	ANTXR cell adhesion molecule 1	Homo sapiens	0-4
16300929-7	2006	Inhibition of actin polymerization by cytochalasin D inhibits translocation and activation of both caspases, suggesting that thrombin stimulates caspase 3 and 9 activation and association with the reorganizing actin cytoskeleton.	Cytochalasin D	38-52	caspase 9	Homo sapiens	99-107
16300929-7	2006	Inhibition of actin polymerization by cytochalasin D inhibits translocation and activation of both caspases, suggesting that thrombin stimulates caspase 3 and 9 activation and association with the reorganizing actin cytoskeleton.	Cytochalasin D	38-52	coagulation factor II, thrombin	Homo sapiens	125-133
16849490-7	2006	In human monocytic cells, in the presence of cytochalasin D meso-DAP induced slightly but significantly increased production of cytokines, although the cells did not respond to meso-DAP in the absent of cytochalasin D.	Cytochalasin D	45-59	death associated protein	Homo sapiens	65-68
16849490-7	2006	In human monocytic cells, in the presence of cytochalasin D meso-DAP induced slightly but significantly increased production of cytokines, although the cells did not respond to meso-DAP in the absent of cytochalasin D.	Cytochalasin D	203-217	death associated protein	Homo sapiens	65-68
16719903-3	2006	RESULTS: Using a fluorescent conjugate of the actin binding drug cytochalasin D (CD-BODIPY) we provide evidence that polymerising actin accumulates in vicinity to the NE.	Cytochalasin D	65-79	actin-7	Triticum aestivum	46-51
16569755-7	2006	The FK-induced NKCC1 augmentation after exposure to basolateral H2O2 was counteracted by cytochalasin D, an inhibitor of microfilament function, but not by charybdotoxin, a blocker of the intermediate conductance Ca2+-activated K+ channel, whose activation could be related to NKCC1-mediated Cl- secretion.	Cytochalasin D	89-103	solute carrier family 12 member 2	Homo sapiens	15-20
16569755-7	2006	The FK-induced NKCC1 augmentation after exposure to basolateral H2O2 was counteracted by cytochalasin D, an inhibitor of microfilament function, but not by charybdotoxin, a blocker of the intermediate conductance Ca2+-activated K+ channel, whose activation could be related to NKCC1-mediated Cl- secretion.	Cytochalasin D	89-103	solute carrier family 12 member 2	Homo sapiens	277-282
16702038-2	2006	We have previously reported that cytochalasin D (Cyt D) inhibits thapsigargin-evoked store-operated Ca(2+) entry (SOCE), which is believed to contribute a major component of thrombin-evoked Ca(2+) entry in platelets.	Cytochalasin D	33-47	coagulation factor II, thrombin	Homo sapiens	174-182
16159311-8	2006	The cortical distribution in mitotic cells was dependent on F-actin, because the actin-depolymerization-inducing drugs cytochalasin D or latrunculin A prevented pEg3 cortical localization.	Cytochalasin D	119-133	paternally expressed 3	Homo sapiens	161-165
16461767-10	2006	Further, cytochalasin D inhibited FAK phosphorylation and cleavage, cell adhesion, locomotion, and ERK phosphorylation, thus showing FAK activation downstream of actin assembly.	Cytochalasin D	9-23	protein tyrosine kinase 2	Homo sapiens	34-37
16461767-10	2006	Further, cytochalasin D inhibited FAK phosphorylation and cleavage, cell adhesion, locomotion, and ERK phosphorylation, thus showing FAK activation downstream of actin assembly.	Cytochalasin D	9-23	mitogen-activated protein kinase 1	Homo sapiens	99-102
16461767-10	2006	Further, cytochalasin D inhibited FAK phosphorylation and cleavage, cell adhesion, locomotion, and ERK phosphorylation, thus showing FAK activation downstream of actin assembly.	Cytochalasin D	9-23	protein tyrosine kinase 2	Homo sapiens	133-136
16707113-11	2006	The phenotypic changes resembled changes observed after treatment of the cells with cytochalasin D, which has been shown to interfere with CTGF induction.	Cytochalasin D	84-98	cellular communication network factor 2	Homo sapiens	139-143
16565087-5	2006	In contrast, inhibition of the RhoA/ROCK pathway and cytochalasin D treatment in monolayer culture results in the enhancement of a number of markers of chondrogenesis such as Sox9 activity and collagen II and aggrecan transcripts levels.	Cytochalasin D	53-67	SRY-box transcription factor 9	Homo sapiens	175-179
16469749-5	2006	Timp-3 deficiency accelerated pro-MMP-2 activation in response to both cytochalasin D and concanavalin A. Exogenous TIMP-2 and N-TIMP-3 inhibited this activation, whereas TIMP-3 containing matrix from wild-type MEFs did not rescue the enhanced MMP-2 activation in Timp-3(-/-) cells.	Cytochalasin D	71-85	tissue inhibitor of metalloproteinase 3	Mus musculus	0-6
16469749-5	2006	Timp-3 deficiency accelerated pro-MMP-2 activation in response to both cytochalasin D and concanavalin A. Exogenous TIMP-2 and N-TIMP-3 inhibited this activation, whereas TIMP-3 containing matrix from wild-type MEFs did not rescue the enhanced MMP-2 activation in Timp-3(-/-) cells.	Cytochalasin D	71-85	matrix metallopeptidase 2	Mus musculus	34-39
16469749-5	2006	Timp-3 deficiency accelerated pro-MMP-2 activation in response to both cytochalasin D and concanavalin A. Exogenous TIMP-2 and N-TIMP-3 inhibited this activation, whereas TIMP-3 containing matrix from wild-type MEFs did not rescue the enhanced MMP-2 activation in Timp-3(-/-) cells.	Cytochalasin D	71-85	tissue inhibitor of metalloproteinase 1	Mus musculus	0-4
16392133-8	2006	We also demonstrate that while cytochalasin D, a potent inhibitor of phagocytosis, suppressed the titanium particle effect on IL-8 protein release in human bone marrow-derived osteoblasts, the inhibitor had no effect on IL-8 expression in MG-63 osteoblast-like cells.	Cytochalasin D	31-45	C-X-C motif chemokine ligand 8	Homo sapiens	126-130
16527992-9	2006	Pretreatment with 3 micromol/L cytochalasin D, an actin depolymerizing agent, abrogated CyPA secretion.	Cytochalasin D	31-45	peptidylprolyl isomerase A	Homo sapiens	88-92
16221736-3	2006	After we treated cells with cytochalasin D, NCX1.1 protein colocalized with patches of fragmented filamentous actin (F-actin).	Cytochalasin D	28-42	solute carrier family 8 member A1	Bos taurus	44-48
16221736-3	2006	After we treated cells with cytochalasin D, NCX1.1 protein colocalized with patches of fragmented filamentous actin (F-actin).	Cytochalasin D	28-42	actin epsilon 1	Bos taurus	110-115
16221736-3	2006	After we treated cells with cytochalasin D, NCX1.1 protein colocalized with patches of fragmented filamentous actin (F-actin).	Cytochalasin D	28-42	actin epsilon 1	Bos taurus	119-124
19521476-6	2006	Both latrunculin B and cytochalasin D treatments inhibited root growth but restored gravibending of the decapped root apices, indicating that there is a strong potential for effective actin-mediated gravity sensing outside the cap.	Cytochalasin D	23-37	actin-7	Zea mays	184-189
16239402-6	2006	The actin depolymerizer cytochalasin D resulted in a decreased transepithelial resistance (TER) more quickly than NH(2)Cl but caused a more modest and slower reduction in ZO-1 levels and in occludin redistribution.	Cytochalasin D	24-38	tight junction protein 1	Homo sapiens	171-175
16239402-6	2006	The actin depolymerizer cytochalasin D resulted in a decreased transepithelial resistance (TER) more quickly than NH(2)Cl but caused a more modest and slower reduction in ZO-1 levels and in occludin redistribution.	Cytochalasin D	24-38	occludin	Homo sapiens	190-198
16719903-3	2006	RESULTS: Using a fluorescent conjugate of the actin binding drug cytochalasin D (CD-BODIPY) we provide evidence that polymerising actin accumulates in vicinity to the NE.	Cytochalasin D	65-79	actin-7	Triticum aestivum	130-135
16014575-6	2005	However, disruption of the actin cytoskeleton with cytochalasin D or latrunculin B in parental GEC (on collagen) and in GEC that express R4F-MEK or CD2-FAK (on plastic) decreased ERK activation and increased apoptosis.	Cytochalasin D	51-65	Eph receptor B1	Rattus norvegicus	179-182
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	Cytochalasin D	31-45	nitric oxide synthase 3	Homo sapiens	90-94
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	Cytochalasin D	31-45	nitric oxide synthase 3	Homo sapiens	120-124
16113046-9	2006	Moreover, PAEC incubation with cytochalasin D and jasplakinolide resulted in increases in eNOS/actin association and in eNOS activity without changes in eNOS protein content.	Cytochalasin D	31-45	nitric oxide synthase 3	Homo sapiens	120-124
16186248-7	2006	Cytochalasin D decreased the interaction between ACE and MYH9 and stimulated ACE shedding.	Cytochalasin D	0-14	myosin heavy chain 9	Homo sapiens	57-61
16006481-3	2005	In type II cells, uptake of SP-A, compared with controls, was decreased by 60% on incubation with clathrin inhibitors (amantadine and phenylarsine oxide) or with the actin inhibitor cytochalasin D.	Cytochalasin D	182-196	surfactant protein A1	Rattus norvegicus	28-32
16006481-6	2005	Inhibitors of clathrin and actin significantly reduced SP-A uptake by approximately 54%, whereas cytochalasin D inhibited SP-A degradation.	Cytochalasin D	97-111	surfactant protein A1	Rattus norvegicus	122-126
16373510-6	2006	Cytochalasin D blocked the Francisella internalization and the Francisella-induced monocyte IL-1beta processing and release but not that induced by the exogenous stimulus E. coli LPS.	Cytochalasin D	0-14	interleukin 1 beta	Homo sapiens	92-100
15887250-10	2005	Additionally, the effect of Ang II on Na+/K+ATPase activity was also blocked by the phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002, and by the actin depolymerizing agents, cytochalasin D.	Cytochalasin D	198-212	angiogenin	Homo sapiens	28-31
16236262-4	2005	This appears to be linked to a particular change in cell shape and cytoskeletal (actin) reorganisation, as treatment of these cells with cytochalasin D (Cyt D), but not with latrunculin B, recapitulates and potentiates TF upregulation.	Cytochalasin D	137-151	coagulation factor III	Mus musculus	219-221
16236262-4	2005	This appears to be linked to a particular change in cell shape and cytoskeletal (actin) reorganisation, as treatment of these cells with cytochalasin D (Cyt D), but not with latrunculin B, recapitulates and potentiates TF upregulation.	Cytochalasin D	153-158	coagulation factor III	Mus musculus	219-221
16153249-4	2005	Rickettsia inactivation by heat or formaldehyde abolished the activation of p38 kinase and inhibition of cellular invasion by infection at low temperature, pre-treatment of host EC with cytochalasin D, or pre-incubation of rickettsiae with an irreversible phospholipase inhibitor led to a diminished p38 phosphorylation, suggesting requirement of invasion by viable rickettsiae for this host cell response.	Cytochalasin D	186-200	mitogen-activated protein kinase 14	Homo sapiens	76-79
15917311-9	2005	Phalloidin, cytochalasin D, latrunculin B and colchicine prevented pressure-induced SW620 FAK phosphorylation but not Src phosphorylation.	Cytochalasin D	12-26	protein tyrosine kinase 2	Homo sapiens	90-93
16321206-4	2005	Cytochalasin D (CD) was added to the culture fluid to inhibit the phagocytizing, secreting, and moving functions of the hRPE.	Cytochalasin D	0-14	ribulose-5-phosphate-3-epimerase	Homo sapiens	120-124
15855657-6	2005	Activation of ERK was attenuated by drugs that disassemble the actin cytoskeleton (cytochalasin D, latrunculin B), and these compounds interfered with the activation of ERK by mitogen-activated protein kinase kinase (MEK).	Cytochalasin D	83-97	mitogen-activated protein kinase 1	Homo sapiens	14-17
15855657-6	2005	Activation of ERK was attenuated by drugs that disassemble the actin cytoskeleton (cytochalasin D, latrunculin B), and these compounds interfered with the activation of ERK by mitogen-activated protein kinase kinase (MEK).	Cytochalasin D	83-97	mitogen-activated protein kinase 1	Homo sapiens	169-172
15855657-6	2005	Activation of ERK was attenuated by drugs that disassemble the actin cytoskeleton (cytochalasin D, latrunculin B), and these compounds interfered with the activation of ERK by mitogen-activated protein kinase kinase (MEK).	Cytochalasin D	83-97	mitogen-activated protein kinase kinase 7	Homo sapiens	176-215
15855657-6	2005	Activation of ERK was attenuated by drugs that disassemble the actin cytoskeleton (cytochalasin D, latrunculin B), and these compounds interfered with the activation of ERK by mitogen-activated protein kinase kinase (MEK).	Cytochalasin D	83-97	mitogen-activated protein kinase kinase 7	Homo sapiens	217-220
16321206-4	2005	Cytochalasin D (CD) was added to the culture fluid to inhibit the phagocytizing, secreting, and moving functions of the hRPE.	Cytochalasin D	16-18	ribulose-5-phosphate-3-epimerase	Homo sapiens	120-124
16321206-10	2005	After cytochalasin D pretreated, the expression and secretion of both MCP-1 and IL-8 of the hRPE cells were significantly decreased to the levels of 2.36 ng/L +/- 0.27 ng/L and 1.64 ng/L +/- 0.08 ng/L, and 353.80 ng/L +/- 16.68 ng/L and 101.86 ng/L +/- 15.92 ng/L respectively.	Cytochalasin D	6-20	chemokine (C-C motif) ligand 2	Mus musculus	70-75
15856282-3	2005	We demonstrated by using rhodamine-phalloidin staining, the localization of actin filaments on the mitotic spindles of tobacco BY-2 cells when the cells were treated with cytochalasin D.	Cytochalasin D	171-185	actin	Nicotiana tabacum	76-81
16321206-10	2005	After cytochalasin D pretreated, the expression and secretion of both MCP-1 and IL-8 of the hRPE cells were significantly decreased to the levels of 2.36 ng/L +/- 0.27 ng/L and 1.64 ng/L +/- 0.08 ng/L, and 353.80 ng/L +/- 16.68 ng/L and 101.86 ng/L +/- 15.92 ng/L respectively.	Cytochalasin D	6-20	chemokine (C-X-C motif) ligand 15	Mus musculus	80-84
16321206-10	2005	After cytochalasin D pretreated, the expression and secretion of both MCP-1 and IL-8 of the hRPE cells were significantly decreased to the levels of 2.36 ng/L +/- 0.27 ng/L and 1.64 ng/L +/- 0.08 ng/L, and 353.80 ng/L +/- 16.68 ng/L and 101.86 ng/L +/- 15.92 ng/L respectively.	Cytochalasin D	6-20	ribulose-5-phosphate-3-epimerase	Homo sapiens	92-96
16321206-11	2005	CONCLUSION: Mechanical stress induces the RPE cells to express MCP-1 and IL-8, and this effect was inhibited in part by pretreatment of CD, indicating that the cytoskeleton may be involved in the effect and that these two inflammatory cytokines take a part in the early stage of development of primary retinal detachment.	Cytochalasin D	136-138	ribulose-5-phosphate-3-epimerase	Homo sapiens	42-45
16321206-11	2005	CONCLUSION: Mechanical stress induces the RPE cells to express MCP-1 and IL-8, and this effect was inhibited in part by pretreatment of CD, indicating that the cytoskeleton may be involved in the effect and that these two inflammatory cytokines take a part in the early stage of development of primary retinal detachment.	Cytochalasin D	136-138	C-C motif chemokine ligand 2	Homo sapiens	63-68
16321206-11	2005	CONCLUSION: Mechanical stress induces the RPE cells to express MCP-1 and IL-8, and this effect was inhibited in part by pretreatment of CD, indicating that the cytoskeleton may be involved in the effect and that these two inflammatory cytokines take a part in the early stage of development of primary retinal detachment.	Cytochalasin D	136-138	C-X-C motif chemokine ligand 8	Homo sapiens	73-77
15535802-5	2005	Actin cytoskeleton disruption by cytochalasin D induced O2- release from human monocytes, through the activation of the NADPH oxidase, as confirmed by the phosphorylation and by the membrane translocation of p47phox.	Cytochalasin D	33-47	neutrophil cytosolic factor 1	Homo sapiens	208-215
15845576-6	2005	Acute addition of cytochalasin D (CD, 5 microg ml-1) to reconstituted hST apical membranes transiently increased K+ -permeable channel activity.	Cytochalasin D	18-32	sulfotransferase family 2A member 1	Homo sapiens	70-73
15845576-6	2005	Acute addition of cytochalasin D (CD, 5 microg ml-1) to reconstituted hST apical membranes transiently increased K+ -permeable channel activity.	Cytochalasin D	34-36	sulfotransferase family 2A member 1	Homo sapiens	70-73
15845576-8	2005	CD treatment of hST vesicles resulted in a re-distribution of actin filaments, in agreement with the effect of CD on K+ channel activity.	Cytochalasin D	0-2	sulfotransferase family 2A member 1	Homo sapiens	16-19
15845576-8	2005	CD treatment of hST vesicles resulted in a re-distribution of actin filaments, in agreement with the effect of CD on K+ channel activity.	Cytochalasin D	111-113	sulfotransferase family 2A member 1	Homo sapiens	16-19
15845576-11	2005	The acute (<15 min) CD stimulation of K+ channel activity was mimicked by addition of the actin-severing protein gelsolin in the presence, but not in the absence, of micromolar Ca2+.	Cytochalasin D	23-25	gelsolin	Homo sapiens	116-124
15987604-6	2005	Calcein transfer assay showed that calcein transfer was inhibited when cells were treated with Brefeldin A or cytochalasin D, but not when treated with nocodazole or a-glycyrrhetinic acid, suggesting that Golgi apparatus and actin filaments, but not microtubules, are crucial to the trafficking and assembly of connexin 31, as well as the formation of gap junction intercellular communication by connexin 31.	Cytochalasin D	110-124	gap junction protein beta 3	Homo sapiens	311-322
15987604-6	2005	Calcein transfer assay showed that calcein transfer was inhibited when cells were treated with Brefeldin A or cytochalasin D, but not when treated with nocodazole or a-glycyrrhetinic acid, suggesting that Golgi apparatus and actin filaments, but not microtubules, are crucial to the trafficking and assembly of connexin 31, as well as the formation of gap junction intercellular communication by connexin 31.	Cytochalasin D	110-124	gap junction protein beta 3	Homo sapiens	396-407
16083715-7	2005	EGF potentiation of transport responses in DSS-treated colon was completely blocked by the cytoskeletal disruptor cytochalasin D and the phosphatidylinositol 3-kinase inhibitor wortmannin, whereas the novel and conventional protein kinase C isoform inhibitor Go6850 and the extracellular signal-regulated kinase inhibitor PD98059 partially reduced EGF effects.	Cytochalasin D	114-128	epidermal growth factor	Mus musculus	0-3
16049696-8	2005	The disruption of actin filaments with cytochalasin D or latrunculin B induced the accumulation of AQP2 in EEA1-positive early endosomes.	Cytochalasin D	39-53	aquaporin 2	Canis lupus familiaris	99-103
16049696-8	2005	The disruption of actin filaments with cytochalasin D or latrunculin B induced the accumulation of AQP2 in EEA1-positive early endosomes.	Cytochalasin D	39-53	early endosome antigen 1	Canis lupus familiaris	107-111
15904659-5	2005	Furthermore, cytochalasin D inhibited the distribution of EGFP-SGLT1 at the apical surface.	Cytochalasin D	13-27	solute carrier family 5 member 1	Canis lupus familiaris	58-68
15705737-6	2005	Cytochalasin D (CD; 0.5 microM) and latrunculin A (LA; 0.5 microM) that disrupted actin filaments, blocked cPLA(2) translocation elicited by NE.	Cytochalasin D	0-14	cytosolic phospholipase A2	Oryctolagus cuniculus	107-114
15389641-9	2005	The actin cytoskeleton disruptor, cytochalasin D (20 microM), abolished FAK phosphorylation in response to CCh but did not alter CCh-induced EGFr or ERK MAPK activation.	Cytochalasin D	34-48	protein tyrosine kinase 2	Homo sapiens	72-75
15803134-4	2005	Movement is directed, temperature- and energy-dependent, sensitive to the putative myosin inhibitor 2,3-butanedione monoxime (BDM) and to actin depolymerization with latrunculin-A, but insensitive to actin depolymerization with cytochalasin-D.	Cytochalasin D	228-242	myosin heavy chain 14	Homo sapiens	83-89
15557012-7	2005	Posttreatment with cytochalasin D abolished thrombin-induced cell stiffening.	Cytochalasin D	19-33	coagulation factor II, thrombin	Homo sapiens	44-52
15671060-5	2005	Interestingly, the interaction between cortactin and dynamin 2 in cells was dependent on actin polymerization and was attenuated upon cell exposure to cytochalasin D as analyzed by immunofluorescence and immunoprecipitation.	Cytochalasin D	151-165	cortactin	Homo sapiens	39-48
15706082-6	2005	Cytochalasin D or a phorbol ester also induced nuclear accumulation of Hic-5, which was inhibited by scavengers of reactive oxygen species (ROS), suggesting that besides oxidants, endogenously produced ROS induced the nuclear accumulation of Hic-5.	Cytochalasin D	0-14	transforming growth factor beta 1 induced transcript 1	Homo sapiens	71-76
15706082-6	2005	Cytochalasin D or a phorbol ester also induced nuclear accumulation of Hic-5, which was inhibited by scavengers of reactive oxygen species (ROS), suggesting that besides oxidants, endogenously produced ROS induced the nuclear accumulation of Hic-5.	Cytochalasin D	0-14	transforming growth factor beta 1 induced transcript 1	Homo sapiens	242-247
15963258-8	2005	Disruption of Calu-1 cell cytoskeleton integrity by 1-5 muM Cytochalasin D resulted in the inhibition of cell adhesion (50% to 75%, p<0.19 - 6.6 x 10(7)) and ERKs phosphorylation (2 fold) without any effect on FAK phosphorylation.	Cytochalasin D	60-74	protein tyrosine kinase 2	Homo sapiens	213-216
15737330-8	2005	Hence, the disruption of the cytoskeleton with cytochalasin D prevented ET-1-stimulated aspartate uptake.	Cytochalasin D	47-61	endothelin 1	Homo sapiens	72-76
15567062-9	2005	Cytoskeletal disruption with cytochalasin D and the Rho-kinase inhibitor, Y-27632, however, blocked both Raf-1 phosphorylation and activation.	Cytochalasin D	29-43	Raf-1 proto-oncogene, serine/threonine kinase	Rattus norvegicus	105-110
15671060-5	2005	Interestingly, the interaction between cortactin and dynamin 2 in cells was dependent on actin polymerization and was attenuated upon cell exposure to cytochalasin D as analyzed by immunofluorescence and immunoprecipitation.	Cytochalasin D	151-165	dynamin 2	Homo sapiens	53-62
15494512-6	2004	Strikingly, blocking actin polymerization with a high dose of cytochalasin D also substantially decreased clustering of KIR as well as KIR-induced clustering of HLA-C-GFP in target cells.	Cytochalasin D	62-76	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	120-123
15371259-7	2005	However, disrupting the actin cytoskeleton with cytochalasin D did block the multiaxial signaling to p70(S6k), with no effect on signaling to PKB/Akt.	Cytochalasin D	48-62	annexin A6	Homo sapiens	101-104
15371259-7	2005	However, disrupting the actin cytoskeleton with cytochalasin D did block the multiaxial signaling to p70(S6k), with no effect on signaling to PKB/Akt.	Cytochalasin D	48-62	ribosomal protein S6 kinase B1	Homo sapiens	105-108
16473595-6	2005	This association is increased by cytochalasin D and phorbol esters that also induced the translocation of both Rabin8 and Rab8 to lamellipodia-like structures.	Cytochalasin D	33-47	RAB3A interacting protein	Homo sapiens	111-117
16473595-6	2005	This association is increased by cytochalasin D and phorbol esters that also induced the translocation of both Rabin8 and Rab8 to lamellipodia-like structures.	Cytochalasin D	33-47	RAB8A, member RAS oncogene family	Homo sapiens	122-126
15619425-7	2004	The treatment of cytochalasin D, which effectively inhibited invasion of L. pneumophila into A549, significantly reduced the production of IL-6 and TNF-alpha, but not IL-8.	Cytochalasin D	17-31	interleukin 6	Homo sapiens	139-143
15619425-7	2004	The treatment of cytochalasin D, which effectively inhibited invasion of L. pneumophila into A549, significantly reduced the production of IL-6 and TNF-alpha, but not IL-8.	Cytochalasin D	17-31	tumor necrosis factor	Homo sapiens	148-157
15485691-7	2004	When mouse embryonic fibroblasts were cultured in the presence of cytochalasin D or doxorubicin, the number of apoptotic cells in the Nd1-/- cell culture was larger that that in the wild-type cell culture.	Cytochalasin D	66-80	NADH dehydrogenase 1, mitochondrial	Mus musculus	134-137
15494512-6	2004	Strikingly, blocking actin polymerization with a high dose of cytochalasin D also substantially decreased clustering of KIR as well as KIR-induced clustering of HLA-C-GFP in target cells.	Cytochalasin D	62-76	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	135-138
15466888-8	2004	Latrunculin B, cytochalasin D and jasplakinolide, which disrupt actin dynamics, prevented insulin- and PDGF-induced actin remodeling but significantly inhibited GLUT4myc translocation only in response to insulin (75-85%, P<0.05), not to PDGF (20-30% inhibition).	Cytochalasin D	15-29	insulin	Homo sapiens	90-97
15466888-8	2004	Latrunculin B, cytochalasin D and jasplakinolide, which disrupt actin dynamics, prevented insulin- and PDGF-induced actin remodeling but significantly inhibited GLUT4myc translocation only in response to insulin (75-85%, P<0.05), not to PDGF (20-30% inhibition).	Cytochalasin D	15-29	solute carrier family 2 member 4	Homo sapiens	161-166
15466888-8	2004	Latrunculin B, cytochalasin D and jasplakinolide, which disrupt actin dynamics, prevented insulin- and PDGF-induced actin remodeling but significantly inhibited GLUT4myc translocation only in response to insulin (75-85%, P<0.05), not to PDGF (20-30% inhibition).	Cytochalasin D	15-29	insulin	Homo sapiens	204-211
15189814-8	2004	Expression of l-CaD protected transcellular resistance through primary effects on membrane capacitance and independently of actin solubility and effects on pre-stress, as measured by the decline in isometric tension in response to cytochalasin D.	Cytochalasin D	231-245	caldesmon 1	Homo sapiens	14-19
15292185-9	2004	CD47-activated SS RBC adhesion absolutely requires the Src family tyrosine kinases and is also enhanced by treatment of SS RBCs with low concentrations of cytochalasin D, which may release alpha4beta1 from cytoskeletal restraints.	Cytochalasin D	155-169	CD47 molecule	Homo sapiens	0-4
15287896-5	2004	In contrast, cytochalasin D, lovastatin (a 3-hydroxy-3-methylglutaryl-CoA reductase inhibitor) and Y-27632 (a rho-kinase inhibitor) prevented both cyclin D3 expression and BrdU incorporation.	Cytochalasin D	13-27	cyclin D3	Rattus norvegicus	147-156
15383621-3	2004	In wash-off assays, cytochalasin D (1 microM) reduced intercellular adhesion by threefold, confirming the importance of cortical actin filaments in strengthening of N-cadherin-mediated adhesions.	Cytochalasin D	20-34	cadherin 2	Homo sapiens	165-175
15068974-9	2004	Disrupting the actin cytoskeleton with cytochalasin D (10 microM) reduced flow-induced NO production by 62% (from 37.1 +/- 3.4 to 14.0 +/- 2.4 pA/mm tubule, n = 7, P < 0.04) and blocked flow-induced eNOS translocation.	Cytochalasin D	39-53	nitric oxide synthase 3	Rattus norvegicus	202-206
15518663-4	2004	To investigate oligomeric lectins as a possible extracellular driving force affecting cell shape changes, we examined lectin-mediated reactions in lepidopteran haemocytes after cytochalasin D-treatment and observed that while cell-spreading was dependent on F-actin, lectin-uptake was less dependent on F-actin.	Cytochalasin D	177-191	lectin-37Db	Drosophila melanogaster	26-32
15518663-4	2004	To investigate oligomeric lectins as a possible extracellular driving force affecting cell shape changes, we examined lectin-mediated reactions in lepidopteran haemocytes after cytochalasin D-treatment and observed that while cell-spreading was dependent on F-actin, lectin-uptake was less dependent on F-actin.	Cytochalasin D	177-191	Actin 79B	Drosophila melanogaster	258-265
15518663-4	2004	To investigate oligomeric lectins as a possible extracellular driving force affecting cell shape changes, we examined lectin-mediated reactions in lepidopteran haemocytes after cytochalasin D-treatment and observed that while cell-spreading was dependent on F-actin, lectin-uptake was less dependent on F-actin.	Cytochalasin D	177-191	lectin-37Db	Drosophila melanogaster	118-124
15247260-8	2004	CFTR endocytosis was decreased by cytochalasin D, an actin-filament depolymerizing agent.	Cytochalasin D	34-48	CF transmembrane conductance regulator	Homo sapiens	0-4
15254973-5	2004	Actinomycin D or cytochalasin D, which interacts with the cytoskeleton, but not the protein synthesis inhibitor cycloheximide, prevented EGF from downregulating AngII receptor binding.	Cytochalasin D	17-31	epidermal growth factor like 1	Rattus norvegicus	137-140
15254973-5	2004	Actinomycin D or cytochalasin D, which interacts with the cytoskeleton, but not the protein synthesis inhibitor cycloheximide, prevented EGF from downregulating AngII receptor binding.	Cytochalasin D	17-31	angiotensinogen	Rattus norvegicus	161-166
15320955-11	2004	Disruption of actin cytoskeleton by cytochalasin D abolished phospho-C3G staining at the periphery of the cell without affecting its Golgi localization.	Cytochalasin D	36-50	Rap guanine nucleotide exchange factor 1	Homo sapiens	69-72
15287896-6	2004	FAK phosphorylation by ET-1 was inhibited by cytochalasin D, lovastatin and Y-27632, but not by PD98059 or PP-2.	Cytochalasin D	45-59	protein tyrosine kinase 2	Rattus norvegicus	0-3
15287896-6	2004	FAK phosphorylation by ET-1 was inhibited by cytochalasin D, lovastatin and Y-27632, but not by PD98059 or PP-2.	Cytochalasin D	45-59	endothelin 1	Rattus norvegicus	23-27
15060825-3	2004	After cytochalasin D-induced disruption of the actin cytoskeleton, the regeneration of actin microfilaments (MFs) starts with the reappearance of a flat, brightly fluorescing actin array in the outermost tip.	Cytochalasin D	6-20	TOR signaling pathway regulator	Homo sapiens	204-207
15254085-4	2004	At the distal end of C6 glioma cell processes, GLT-1 clusters undergo rapid morphological changes in both shape and size, and these changes are inhibited by cytochalasin D treatment, suggesting that the morphogenesis of GLT-1 clusters is highly dependent on the actin network.	Cytochalasin D	157-171	solute carrier family 1 member 2	Homo sapiens	47-52
15254085-4	2004	At the distal end of C6 glioma cell processes, GLT-1 clusters undergo rapid morphological changes in both shape and size, and these changes are inhibited by cytochalasin D treatment, suggesting that the morphogenesis of GLT-1 clusters is highly dependent on the actin network.	Cytochalasin D	157-171	solute carrier family 1 member 2	Homo sapiens	220-225
15137059-8	2004	Cytochalasin D also activated p38 MAP kinase, which pathway contributed to the cytochalasin D-induced increase in IL-8 production.	Cytochalasin D	0-14	mitogen-activated protein kinase 14	Homo sapiens	30-33
15137059-8	2004	Cytochalasin D also activated p38 MAP kinase, which pathway contributed to the cytochalasin D-induced increase in IL-8 production.	Cytochalasin D	0-14	C-X-C motif chemokine ligand 8	Homo sapiens	114-118
15137059-8	2004	Cytochalasin D also activated p38 MAP kinase, which pathway contributed to the cytochalasin D-induced increase in IL-8 production.	Cytochalasin D	79-93	mitogen-activated protein kinase 14	Homo sapiens	30-33
15137059-8	2004	Cytochalasin D also activated p38 MAP kinase, which pathway contributed to the cytochalasin D-induced increase in IL-8 production.	Cytochalasin D	79-93	C-X-C motif chemokine ligand 8	Homo sapiens	114-118
15149849-8	2004	Conversely, cytochalasin D and the Rho kinase inhibitor Y-27632, both of which cause stress fiber disruption, increased p70(S6K) activity.	Cytochalasin D	12-26	ubiquitin associated and SH3 domain containing B	Homo sapiens	120-123
15207617-5	2004	DC uptake of and signalling by VLP was inhibited by amiloride or cytochalasin D (CCD), but not by filipin treatment, and was blocked by several sulfated and non-sulfated polysaccharides and anti-CD16.	Cytochalasin D	65-79	VHL like	Homo sapiens	31-34
15207617-5	2004	DC uptake of and signalling by VLP was inhibited by amiloride or cytochalasin D (CCD), but not by filipin treatment, and was blocked by several sulfated and non-sulfated polysaccharides and anti-CD16.	Cytochalasin D	81-84	VHL like	Homo sapiens	31-34
15207617-5	2004	DC uptake of and signalling by VLP was inhibited by amiloride or cytochalasin D (CCD), but not by filipin treatment, and was blocked by several sulfated and non-sulfated polysaccharides and anti-CD16.	Cytochalasin D	81-84	Fc gamma receptor IIIa	Homo sapiens	195-199
15149849-8	2004	Conversely, cytochalasin D and the Rho kinase inhibitor Y-27632, both of which cause stress fiber disruption, increased p70(S6K) activity.	Cytochalasin D	12-26	ribosomal protein S6 kinase B1	Homo sapiens	124-127
15102784-4	2004	CEACAM1 and CEACAM3 each contain proteinaceous transmembrane and cytoplasmic domains; however, the processes of neisserial uptake mediated by these receptors differ with respect to their susceptibilities to both tyrosine kinase inhibitors and the actin microfilament-disrupting agent cytochalasin D.	Cytochalasin D	284-298	CEA cell adhesion molecule 1	Homo sapiens	0-7
15102784-4	2004	CEACAM1 and CEACAM3 each contain proteinaceous transmembrane and cytoplasmic domains; however, the processes of neisserial uptake mediated by these receptors differ with respect to their susceptibilities to both tyrosine kinase inhibitors and the actin microfilament-disrupting agent cytochalasin D.	Cytochalasin D	284-298	CEA cell adhesion molecule 3	Homo sapiens	12-19
15087385-7	2004	This shift is mimicked in subconfluent cells treated with cytochalasin D, suggesting that the shift results from merlin dissociation from the actin cytoskeleton, but not from lipid rafts.	Cytochalasin D	58-72	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	113-119
14751227-7	2004	Cytochalasin D markedly increased the basal shedding of wild-type ACE but had little effect on the shedding of ACE-DeltaCYT.	Cytochalasin D	0-14	angiotensin I converting enzyme	Homo sapiens	66-69
15034928-6	2004	A functioning actin cytoskeleton was important for VCAM-1 and ICAM-1 expression as both cytochalasin D, an actin filament disruptor, and jasplakinolide, an actin filament stabilizer, attenuated the expression of these CAMs.	Cytochalasin D	88-102	intercellular adhesion molecule 1	Homo sapiens	62-68
15013092-7	2004	Disruption of the actin cytoskeleton with cytochalasin D abolished the inhibitory effect of ex vivo static tensile loading on MMP-1 expression.	Cytochalasin D	42-56	matrix metallopeptidase 1	Rattus norvegicus	126-131
14660592-9	2004	Agents that modulate the actin cytoskeleton (cytochalasin D and jasplakinolide) altered the plasma membrane mobility of CFTR but not CFTR- DeltaTRL.	Cytochalasin D	45-59	CF transmembrane conductance regulator	Canis lupus familiaris	120-124
14581479-6	2004	Cytochalasin D, an inhibitor of actin polymerization, significantly reduced H2O2-induced pp60(src) activation.	Cytochalasin D	0-14	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	94-97
14551056-3	2004	Pretreatment (>or=1 h) of HEK cells with 5 microM cytochalasin D to disrupt the actin microfilaments greatly augmented whole cell Kv4.2 currents at potentials positive to -20 mV.	Cytochalasin D	53-67	potassium voltage-gated channel subfamily D member 2	Homo sapiens	133-138
14745949-6	2004	Surprisingly, agents that interfere with actin dynamics, such as cytochalasin D, produced only minor organizational disruptions in actin, capZ, and titin staining.	Cytochalasin D	65-79	capping actin protein of muscle Z-line subunit alpha 2	Homo sapiens	138-142
14745949-6	2004	Surprisingly, agents that interfere with actin dynamics, such as cytochalasin D, produced only minor organizational disruptions in actin, capZ, and titin staining.	Cytochalasin D	65-79	titin	Homo sapiens	148-153
14559894-7	2004	The activation of the distal downstream effector ERK1/2 was demonstrated to be sensitive to the disrupters of cytoskeletal rearrangement, cytochalasin D and latrunculin B.	Cytochalasin D	138-152	mitogen-activated protein kinase 3	Homo sapiens	49-55
14749378-6	2004	Increased surface expression of the plasma membrane Ca(2+) ATPase was observed upon stimulation, which was inhibited by cytochalasin D, suggesting that actin polymerization contributes to calcium export.	Cytochalasin D	120-134	ATPase plasma membrane Ca2+ transporting 2	Homo sapiens	36-65
14717982-8	2004	Ligand binding to the activated alpha IIb beta 3 in the GPIbhigh CMK cells is totally abolished by an alpha IIb beta 3-specific antagonist, and inhibited by wortmannin, cytochalasin-D and prostaglandin E1, and the effects of these inhibitors on alpha IIb beta 3 activation in the GPIbhigh CMK cells were compatible with those in platelets.	Cytochalasin D	169-183	cytidine/uridine monophosphate kinase 1	Homo sapiens	65-68
14717692-4	2004	Cytochalasin D, an actin depolymerizing agent, inhibited chemokine-induced internalization of CCR5 and recycling of the receptor in stably transfected CHO cells and in the monocytic cell line, THP-1.	Cytochalasin D	0-14	C-C chemokine receptor type 5	Cricetulus griseus	94-98
14717692-4	2004	Cytochalasin D, an actin depolymerizing agent, inhibited chemokine-induced internalization of CCR5 and recycling of the receptor in stably transfected CHO cells and in the monocytic cell line, THP-1.	Cytochalasin D	0-14	GLI family zinc finger 2	Homo sapiens	193-198
14688373-8	2004	Inhibition of LPS internalization by cytochalasin D or treatment with dibutyryl cAMP attenuated ICAM-1 expression and TNF production by PBMC.	Cytochalasin D	37-51	intercellular adhesion molecule 1	Homo sapiens	96-102
14688373-8	2004	Inhibition of LPS internalization by cytochalasin D or treatment with dibutyryl cAMP attenuated ICAM-1 expression and TNF production by PBMC.	Cytochalasin D	37-51	tumor necrosis factor	Homo sapiens	118-121
14559906-4	2003	The betaPIX.WASP.SPIN90.Nck interaction was abolished in suspended and cytochalasin D-treated cells, but was recovered when cells were replated on fibronectin-coated dishes.	Cytochalasin D	71-85	Rho guanine nucleotide exchange factor 7	Homo sapiens	4-11
15747836-8	2004	Pretreatment of A431 cells with cytochalasin D or wortmannin prior to EGF treatment increases p65/RelA and alpha-actinin-4 accumulation in nuclear extracts.	Cytochalasin D	32-46	RELA proto-oncogene, NF-kB subunit	Homo sapiens	94-97
15747836-8	2004	Pretreatment of A431 cells with cytochalasin D or wortmannin prior to EGF treatment increases p65/RelA and alpha-actinin-4 accumulation in nuclear extracts.	Cytochalasin D	32-46	RELA proto-oncogene, NF-kB subunit	Homo sapiens	98-102
15747836-8	2004	Pretreatment of A431 cells with cytochalasin D or wortmannin prior to EGF treatment increases p65/RelA and alpha-actinin-4 accumulation in nuclear extracts.	Cytochalasin D	32-46	actinin alpha 4	Homo sapiens	107-122
15283963-8	2004	In the investigation of synaptic targets for the enhancement, we found that IP(3)R agonist-enhanced GABA(A)R-gated IPSCs were attenuated by co-infusing colchicine (30 microM), vincristine (3 microM) or cytochalasin D (1 microM) that inhibits tubulin or actin polymerization, implying that actin filament and microtubules are involved.	Cytochalasin D	202-216	inositol 1,4,5-trisphosphate receptor type 3	Homo sapiens	76-82
14559906-4	2003	The betaPIX.WASP.SPIN90.Nck interaction was abolished in suspended and cytochalasin D-treated cells, but was recovered when cells were replated on fibronectin-coated dishes.	Cytochalasin D	71-85	WASP actin nucleation promoting factor	Homo sapiens	12-16
14559906-4	2003	The betaPIX.WASP.SPIN90.Nck interaction was abolished in suspended and cytochalasin D-treated cells, but was recovered when cells were replated on fibronectin-coated dishes.	Cytochalasin D	71-85	NCK interacting protein with SH3 domain	Homo sapiens	17-23
14559906-4	2003	The betaPIX.WASP.SPIN90.Nck interaction was abolished in suspended and cytochalasin D-treated cells, but was recovered when cells were replated on fibronectin-coated dishes.	Cytochalasin D	71-85	NCK adaptor protein 1	Homo sapiens	24-27
14559906-4	2003	The betaPIX.WASP.SPIN90.Nck interaction was abolished in suspended and cytochalasin D-treated cells, but was recovered when cells were replated on fibronectin-coated dishes.	Cytochalasin D	71-85	fibronectin 1	Homo sapiens	147-158
14507877-5	2003	Cytochalasin D (an inhibitor of microfilament formation) and the peptide GRGDSP (Gly-Arg-Gly-Asp-Ser-Pro), a fibronectin receptor antagonist, each inhibited this effect of fibronectin, whereas nocodazole (an inhibitor of microtubule polymerization) and the control peptide GRGESP (Gly-Arg-Gly-Glu-Ser-Pro) did not.	Cytochalasin D	0-14	fibronectin 1	Bos taurus	172-183
12951326-9	2003	Given the fact that cytochalasin D sequesters G-actin, a decrease in G-actin increased CTGF, while increased levels of G-actin corresponded to reduced CTGF expression.	Cytochalasin D	20-34	cellular communication network factor 2	Homo sapiens	87-91
12951326-9	2003	Given the fact that cytochalasin D sequesters G-actin, a decrease in G-actin increased CTGF, while increased levels of G-actin corresponded to reduced CTGF expression.	Cytochalasin D	20-34	cellular communication network factor 2	Homo sapiens	151-155
12839837-9	2003	Haptoglobin, cytochalasin D, and actinomycin inhibited the MHb-induced responses, whereas zinc protoporphyrin IX (a heme oxygenase inhibitor) or desferroxamine (an iron chelator) did not inhibit MHb-induced responses.	Cytochalasin D	13-27	hemoglobin subunit gamma 2	Homo sapiens	59-62
12907684-3	2003	Disruption of the actin cytoskeleton by cytochalasin D (CD) inhibited NO-induced apoptosis, dedifferentiation, COX-2 expression, and prostaglandin E2 production in chondrocytes cultured on plastic or during cartilage explants culture.	Cytochalasin D	40-54	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	111-116
12907684-3	2003	Disruption of the actin cytoskeleton by cytochalasin D (CD) inhibited NO-induced apoptosis, dedifferentiation, COX-2 expression, and prostaglandin E2 production in chondrocytes cultured on plastic or during cartilage explants culture.	Cytochalasin D	56-58	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	111-116
12907684-4	2003	CD treatment did not affect ERK-1/-2 activation but blocked the signaling events necessary for NO-induced dedifferentiation, apoptosis, and COX-2 expression such as activation of p38 kinase and inhibition of PKCalpha and -zeta.	Cytochalasin D	0-2	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	140-145
12907684-4	2003	CD treatment did not affect ERK-1/-2 activation but blocked the signaling events necessary for NO-induced dedifferentiation, apoptosis, and COX-2 expression such as activation of p38 kinase and inhibition of PKCalpha and -zeta.	Cytochalasin D	0-2	mitogen-activated protein kinase 1	Homo sapiens	179-182
12907684-4	2003	CD treatment did not affect ERK-1/-2 activation but blocked the signaling events necessary for NO-induced dedifferentiation, apoptosis, and COX-2 expression such as activation of p38 kinase and inhibition of PKCalpha and -zeta.	Cytochalasin D	0-2	protein kinase C alpha	Homo sapiens	208-226
12907684-5	2003	CD also suppressed activation of downstream signaling of p38 kinase and PKC, such as NF-kappaB activation, p53 accumulation, and caspase-3 activation, which are necessary for NO-induced apoptosis.	Cytochalasin D	0-2	mitogen-activated protein kinase 1	Homo sapiens	57-60
12907684-5	2003	CD also suppressed activation of downstream signaling of p38 kinase and PKC, such as NF-kappaB activation, p53 accumulation, and caspase-3 activation, which are necessary for NO-induced apoptosis.	Cytochalasin D	0-2	protein kinase C alpha	Homo sapiens	72-75
12907684-5	2003	CD also suppressed activation of downstream signaling of p38 kinase and PKC, such as NF-kappaB activation, p53 accumulation, and caspase-3 activation, which are necessary for NO-induced apoptosis.	Cytochalasin D	0-2	tumor protein p53	Homo sapiens	107-110
12907684-5	2003	CD also suppressed activation of downstream signaling of p38 kinase and PKC, such as NF-kappaB activation, p53 accumulation, and caspase-3 activation, which are necessary for NO-induced apoptosis.	Cytochalasin D	0-2	caspase 3	Homo sapiens	129-138
12907684-7	2003	The down-regulation of PI 3-kinase and Akt was blocked by CD treatment, and the CD effects on apoptosis, p38 kinase, and PKCalpha and -zeta were abolished by the inhibition of PI 3-kinase with LY294002.	Cytochalasin D	58-60	AKT serine/threonine kinase 1	Homo sapiens	39-42
12907684-7	2003	The down-regulation of PI 3-kinase and Akt was blocked by CD treatment, and the CD effects on apoptosis, p38 kinase, and PKCalpha and -zeta were abolished by the inhibition of PI 3-kinase with LY294002.	Cytochalasin D	80-82	mitogen-activated protein kinase 1	Homo sapiens	105-108
12907684-7	2003	The down-regulation of PI 3-kinase and Akt was blocked by CD treatment, and the CD effects on apoptosis, p38 kinase, and PKCalpha and -zeta were abolished by the inhibition of PI 3-kinase with LY294002.	Cytochalasin D	80-82	protein kinase C alpha	Homo sapiens	121-129
12746290-7	2003	Stretch-induced phosphorylation of ERK1/2 was inhibited by EGTA and an inhibitor of the Src kinase family [4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine], but not by cytochalasin D, to disrupt actin polymerization.	Cytochalasin D	184-198	mitogen activated protein kinase 3	Rattus norvegicus	35-41
12874450-5	2003	Disrupting the actin cytoskeleton with cytochalasin D (Cyto D) selectively decreased basal and TGF-beta1-induced cell-layer collagen I and IV accumulation.	Cytochalasin D	39-53	transforming growth factor beta 1	Homo sapiens	95-104
12799187-4	2003	Accordingly, direct disruption of the actin cytoskeleton by cytochalasin D, latrunculin B, or jasplakinolide enhanced cytokine-induced iNOS expression.	Cytochalasin D	60-74	nitric oxide synthase 2	Homo sapiens	135-139
14522909-10	2003	IGF-I induces a 1.7-2.2 (MM.1S) and 2-2.5-fold (OPM6) increase in migration, whereas blocking anti-IGF-I and anti-beta1 integrin monoclonal antibodies, PI3-K inhibitors, as well as cytochalasin D abrogate IGF-I-induced MM cell transmigration.	Cytochalasin D	181-195	insulin like growth factor 1	Homo sapiens	0-5
12761229-7	2003	Cytochalasin D, which inhibits protein I/II-induced phosphorylation of FAK (Tyr-397), had no effect either on activation of ERK 1/2 and JNKs or on IL-6 and IL-8 release.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	71-74
12616543-7	2003	The induction of cell death was not the result of direct cytoskeletal collapse, since treatment of the cells with cytochalasin D in the presence of IL-2 did not promote death.	Cytochalasin D	114-128	interleukin 2	Homo sapiens	148-152
12704650-5	2003	pp60(c-src) kinase activity was elevated fourfold within 15 min after CD addition to quiescent R22 smooth muscle cells and declined quickly thereafter.	Cytochalasin D	70-72	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	5-10
12704650-6	2003	CD-induced increases in the phosphorylation levels of both pp60(c-src) and IgG heavy chain (a substrate target in the coupled immunoprecipitation/in vitro pp60(c-src) kinase assay) were ablated completely by pretreatment with the src-type kinase inhibitor PP1.	Cytochalasin D	0-2	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	64-69
12704650-6	2003	CD-induced increases in the phosphorylation levels of both pp60(c-src) and IgG heavy chain (a substrate target in the coupled immunoprecipitation/in vitro pp60(c-src) kinase assay) were ablated completely by pretreatment with the src-type kinase inhibitor PP1.	Cytochalasin D	0-2	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	160-165
12704650-6	2003	CD-induced increases in the phosphorylation levels of both pp60(c-src) and IgG heavy chain (a substrate target in the coupled immunoprecipitation/in vitro pp60(c-src) kinase assay) were ablated completely by pretreatment with the src-type kinase inhibitor PP1.	Cytochalasin D	0-2	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	66-69
12704650-6	2003	CD-induced increases in the phosphorylation levels of both pp60(c-src) and IgG heavy chain (a substrate target in the coupled immunoprecipitation/in vitro pp60(c-src) kinase assay) were ablated completely by pretreatment with the src-type kinase inhibitor PP1.	Cytochalasin D	0-2	neuropeptide Y receptor Y4	Rattus norvegicus	256-259
12704650-7	2003	Prior PP1 exposure similarly repressed CD-stimulated PAI-1 transcript accumulation.	Cytochalasin D	39-41	neuropeptide Y receptor Y4	Rattus norvegicus	6-9
12704650-7	2003	Prior PP1 exposure similarly repressed CD-stimulated PAI-1 transcript accumulation.	Cytochalasin D	39-41	serpin family E member 1	Rattus norvegicus	53-58
12704650-8	2003	Consistent with the pharmacologic findings, transfection of a dominant-negative pp60(c-src) expression construct (DN-Src) effectively suppressed (in a concentration-dependent manner) CD-induced PAI-1 synthesis in R22 cells.	Cytochalasin D	183-185	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	85-90
12704650-8	2003	Consistent with the pharmacologic findings, transfection of a dominant-negative pp60(c-src) expression construct (DN-Src) effectively suppressed (in a concentration-dependent manner) CD-induced PAI-1 synthesis in R22 cells.	Cytochalasin D	183-185	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	117-120
12704650-8	2003	Consistent with the pharmacologic findings, transfection of a dominant-negative pp60(c-src) expression construct (DN-Src) effectively suppressed (in a concentration-dependent manner) CD-induced PAI-1 synthesis in R22 cells.	Cytochalasin D	183-185	serpin family E member 1	Rattus norvegicus	194-199
12704650-9	2003	To more specifically address the potential involvement of src kinases in CD-initiated ERK mobilization, R22 cells were transiently co-transfected with DN-Src and Myc-tagged ERK2 expression constructs, serum-deprived then stimulated with CD.	Cytochalasin D	73-75	Eph receptor B1	Rattus norvegicus	86-89
12850472-8	2003	Cytochalasin D, an inhibitor of actin polymerization, blocked phosphorylation of FAK and paxillin as well as cell motility induced by the cytokine.	Cytochalasin D	0-14	protein tyrosine kinase 2	Rattus norvegicus	81-84
12850472-8	2003	Cytochalasin D, an inhibitor of actin polymerization, blocked phosphorylation of FAK and paxillin as well as cell motility induced by the cytokine.	Cytochalasin D	0-14	paxillin	Rattus norvegicus	89-97
12393736-5	2003	Cytochalasin D, which inhibits translocation of Src kinases to the cytoskeleton, further increased Src and GPIb association.	Cytochalasin D	0-14	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	48-51
12393736-5	2003	Cytochalasin D, which inhibits translocation of Src kinases to the cytoskeleton, further increased Src and GPIb association.	Cytochalasin D	0-14	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	99-102
12827288-4	2003	We also show that CD-induced actin aggregates bind the F-actin-selective drug phalloidin and associate with proteins involved in cell signaling as well as with receptors and endosomal markers (active MAP kinases, paxillin, erbB2, transferrin, Rab-5), but not with clathrin, protein kinase A, protein tyrosine phosphatase 1B, or tubulin.	Cytochalasin D	18-20	paxillin	Homo sapiens	213-221
12827288-4	2003	We also show that CD-induced actin aggregates bind the F-actin-selective drug phalloidin and associate with proteins involved in cell signaling as well as with receptors and endosomal markers (active MAP kinases, paxillin, erbB2, transferrin, Rab-5), but not with clathrin, protein kinase A, protein tyrosine phosphatase 1B, or tubulin.	Cytochalasin D	18-20	erb-b2 receptor tyrosine kinase 2	Homo sapiens	223-228
12827288-4	2003	We also show that CD-induced actin aggregates bind the F-actin-selective drug phalloidin and associate with proteins involved in cell signaling as well as with receptors and endosomal markers (active MAP kinases, paxillin, erbB2, transferrin, Rab-5), but not with clathrin, protein kinase A, protein tyrosine phosphatase 1B, or tubulin.	Cytochalasin D	18-20	transferrin	Homo sapiens	230-241
12827288-4	2003	We also show that CD-induced actin aggregates bind the F-actin-selective drug phalloidin and associate with proteins involved in cell signaling as well as with receptors and endosomal markers (active MAP kinases, paxillin, erbB2, transferrin, Rab-5), but not with clathrin, protein kinase A, protein tyrosine phosphatase 1B, or tubulin.	Cytochalasin D	18-20	RAB5A, member RAS oncogene family	Homo sapiens	243-248
12480544-6	2003	The expression of Fas receptor ligand (FasL) is specifically detected in cells under suspension conditions or treated with cytochalasin-D.	Cytochalasin D	123-137	Fas cell surface death receptor	Rattus norvegicus	18-30
12584244-2	2003	By laser tweezer application we demonstrated that the strength of adhesion of VE-cadherin-coated microspheres to the surface of cultured endothelial monolayers is significantly reduced by treatment with two well-established permeability-increasing compounds, cytochalasin D and the Ca(2+)-ionophore A23187, which shows that both compounds directly affect cadherin-mediated adhesion.	Cytochalasin D	259-273	cadherin 5	Homo sapiens	78-89
12577305-6	2003	In addition, inhibition of p38 MAP kinase did not alter CD-induced increased expression and activity of PKC alpha, whereas down-regulation of PKC by prolonged exposure of cells to phorbol ester inhibited CD-induced p38 MAP kinase activation.	Cytochalasin D	204-206	adapter molecule crk	Gallus gallus	215-218
12480544-6	2003	The expression of Fas receptor ligand (FasL) is specifically detected in cells under suspension conditions or treated with cytochalasin-D.	Cytochalasin D	123-137	Fas ligand	Rattus norvegicus	39-43
12480544-7	2003	We present here the first report that FasL expression is up-regulated by the cytoskeletal disruption directed by cytochalasin-D treatment or cell detachment from ECM.	Cytochalasin D	113-127	Fas ligand	Rattus norvegicus	38-42
12393569-7	2003	However, cytochalasin D-induced inhibition of CD8(+) cytoskeletal rearrangements abrogated CD34(+) transendothelial migration and impaired CD34(+) cell homing in vivo.	Cytochalasin D	9-23	CD8a molecule	Homo sapiens	46-49
12417182-7	2003	Expression of PCNA was suppressed in the presence of Cytochalasin B, Cytochalasin D, Aphidicolin, and AraC.	Cytochalasin D	69-83	proliferating cell nuclear antigen	Ovis aries	14-18
12393569-7	2003	However, cytochalasin D-induced inhibition of CD8(+) cytoskeletal rearrangements abrogated CD34(+) transendothelial migration and impaired CD34(+) cell homing in vivo.	Cytochalasin D	9-23	CD34 molecule	Homo sapiens	91-95
12393569-7	2003	However, cytochalasin D-induced inhibition of CD8(+) cytoskeletal rearrangements abrogated CD34(+) transendothelial migration and impaired CD34(+) cell homing in vivo.	Cytochalasin D	9-23	CD34 molecule	Homo sapiens	139-143
14504039-6	2003	Disruption of the actin cytoskeleton with cytochalasin D abolished all inhibitory effects of cyclic strain on MMP-1 expression.	Cytochalasin D	42-56	matrix metallopeptidase 1	Rattus norvegicus	110-115
12351399-8	2002	Cytochalasin D, an inhibitor of actin polymerization, and antimycin A, an inhibitor of mitochondrial electron transfer, completely suppressed CD47-induced phosphatidylserine exposure.	Cytochalasin D	0-14	CD47 molecule	Homo sapiens	142-146
12443832-6	2002	Treatment of HUVEC with cytochalasin D, an inhibitor of endocytosis, prevented MCP-1 mRNA up-regulation by P. gingivalis 381, suggesting that internalization of P. gingivalis is necessary for MCP-1 induction.	Cytochalasin D	24-38	chemokine (C-C motif) ligand 2	Mus musculus	79-84
12443832-6	2002	Treatment of HUVEC with cytochalasin D, an inhibitor of endocytosis, prevented MCP-1 mRNA up-regulation by P. gingivalis 381, suggesting that internalization of P. gingivalis is necessary for MCP-1 induction.	Cytochalasin D	24-38	chemokine (C-C motif) ligand 2	Mus musculus	192-197
12480917-7	2002	MT1-MMP function at the cell surface was also accelerated by treatment of cells with cytochalasin D, an inhibitor of actin filaments, PMA, a stimulator of protein kinase C, and bafilomycin A(1), an inhibitor of lysosome/endosome function.	Cytochalasin D	85-99	matrix metallopeptidase 14	Homo sapiens	0-7
12495677-4	2002	Inhibition of bacterial internalization by cytochalasin D resulted in lower levels of nuclear NF-kappaB at 30 min and 1h of infection, however, it did not affect the initial nuclear translocation of NF-kappaB observed at 15 min postinfection.	Cytochalasin D	43-57	nuclear factor kappa B subunit 1	Homo sapiens	94-103
12441137-5	2002	Concentrations of cytochalasin D, which abolished FAK tyrosine phosphorylation, also blocked LPA- and PDGF-induced migration.	Cytochalasin D	18-32	protein tyrosine kinase 2	Homo sapiens	50-53
12371961-11	2002	The effects of simvastatin on t-PA and PAI-1 expression as well as on cell shape were completely mimicked by cytochalasin D, a disrupter of cellular actin filaments, but not by colchicine, a disrupter of microtubules.	Cytochalasin D	109-123	plasminogen activator, tissue type	Homo sapiens	30-34
12371961-11	2002	The effects of simvastatin on t-PA and PAI-1 expression as well as on cell shape were completely mimicked by cytochalasin D, a disrupter of cellular actin filaments, but not by colchicine, a disrupter of microtubules.	Cytochalasin D	109-123	serpin family E member 1	Homo sapiens	39-44
12372334-6	2002	MMP-9 activation required cytoskeleton integrity since this effect was abolished by cytochalasin D.	Cytochalasin D	84-98	matrix metallopeptidase 9	Homo sapiens	0-5
12594849-6	2003	Cytochalasin D, an inhibitor of actin polymerization, inhibited ZAP-70, MAP kinase activation, or IL-4/IL-10 secretion.	Cytochalasin D	0-14	zeta-chain (TCR) associated protein kinase	Mus musculus	64-70
12594849-6	2003	Cytochalasin D, an inhibitor of actin polymerization, inhibited ZAP-70, MAP kinase activation, or IL-4/IL-10 secretion.	Cytochalasin D	0-14	interleukin 4	Mus musculus	98-102
12594849-6	2003	Cytochalasin D, an inhibitor of actin polymerization, inhibited ZAP-70, MAP kinase activation, or IL-4/IL-10 secretion.	Cytochalasin D	0-14	interleukin 10	Mus musculus	103-108
12205089-10	2002	By contrast, disruption of the F-actin cytoskeleton with cytochalasin D increased cell surface NHE5 activity and abundance.	Cytochalasin D	57-71	solute carrier family 9 member A5	Homo sapiens	95-99
12445471-4	2002	Depolymerization of stress-fibre systems with cytochalasin D leads to the translocation of actin-bound annexin 2 from the cytoplasm to the plasma membrane at high intracellular levels of Ca(2+).	Cytochalasin D	46-60	annexin A2	Homo sapiens	103-112
12379227-4	2002	Furthermore, TSA inhibits cytochalasin D-induced activation of gelatinase A, but TSA does not affect other members of the gelatinase A activation complex, MT1-MMP and TIMP-2.	Cytochalasin D	26-40	matrix metallopeptidase 2	Mus musculus	63-75
12372346-7	2002	In addition, the EGF-induced phosphorylation of caveolin-1 in A431 cells was blocked by the Src kinase antagonists PP1 and PP2, but not by the MEK inhibitor PD98059, the phosphoinositide 3-kinase inhibitors LY294002 and wortmannin, or cytoskeleton-disrupting agents, such as cytochalasin D, colchicine, and nocadazole.	Cytochalasin D	275-289	caveolin 1	Homo sapiens	48-58
12372346-7	2002	In addition, the EGF-induced phosphorylation of caveolin-1 in A431 cells was blocked by the Src kinase antagonists PP1 and PP2, but not by the MEK inhibitor PD98059, the phosphoinositide 3-kinase inhibitors LY294002 and wortmannin, or cytoskeleton-disrupting agents, such as cytochalasin D, colchicine, and nocadazole.	Cytochalasin D	275-289	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	92-95
12126956-3	2002	ROCK-II-induced membrane blebbing, however, is reversed by the myosin light chain kinase inhibitor ML-7 or cytochalasin D.	Cytochalasin D	107-121	Rho associated coiled-coil containing protein kinase 2	Homo sapiens	0-7
12372346-7	2002	In addition, the EGF-induced phosphorylation of caveolin-1 in A431 cells was blocked by the Src kinase antagonists PP1 and PP2, but not by the MEK inhibitor PD98059, the phosphoinositide 3-kinase inhibitors LY294002 and wortmannin, or cytoskeleton-disrupting agents, such as cytochalasin D, colchicine, and nocadazole.	Cytochalasin D	275-289	neuropeptide Y receptor Y6 (pseudogene)	Homo sapiens	123-126
12399107-3	2002	Such strong co-localisation was maintained following treatment of cells with cytochalasin D, which inhibits actin polymerization and which is capable of inhibiting ICAM-1-induced signalling.	Cytochalasin D	77-91	intercellular adhesion molecule 1	Homo sapiens	164-170
12105199-6	2002	We found that the disruption of actin filaments by cytochalasin D prevented the peripheral accumulation of MLC kinase and that inhibition of myosin-mediated contractility by 2,3-butanedione monoxime induced FAK(-/-) cells to spread.	Cytochalasin D	51-65	megalencephalic leukoencephalopathy with subcortical cysts 1 homolog (human)	Mus musculus	107-110
12198653-10	2002	Induction of apoptosis by cytochalasin D and C(2)-ceramide upregulated MT1-MMP protein expression and MT1-MMP mRNA expression.	Cytochalasin D	26-40	matrix metallopeptidase 14	Homo sapiens	71-78
12198653-10	2002	Induction of apoptosis by cytochalasin D and C(2)-ceramide upregulated MT1-MMP protein expression and MT1-MMP mRNA expression.	Cytochalasin D	26-40	matrix metallopeptidase 14	Homo sapiens	102-109
12193698-7	2002	RhoA kinase inhibitor effects on de-adhesion and spreading were reversed by treatment with the cytoskeletal-disrupting agent cytochalasin D.	Cytochalasin D	125-139	ras homolog family member A	Homo sapiens	0-4
11969294-4	2002	Use of PD98059 to inhibit MAPK/Erk and cytochalasin D (Cyto D) to disrupt the actin CSK at progressive time points in G(1) revealed that the requirement for MAPK/Erk activation lasts only to mid-G(1), while the actin CSK must remain intact up to late G(1) restriction point, R, in order for capillary endothelial cells to enter S phase.	Cytochalasin D	39-53	mitogen-activated protein kinase 1	Homo sapiens	162-165
12118065-4	2002	PAI-1 transcript levels in quiescent R22 cells increased rapidly and in a CD-concentration-dependent fashion, with kinetics of expression paralleling the morphological changes.	Cytochalasin D	74-76	serpin family E member 1	Rattus norvegicus	0-5
12118065-5	2002	Colchicine concentrations that effectively disrupted microtubule structure and reduced the cellular "footprint" area (to approximately that of CD treatment) also stimulated PAI-1 synthesis.	Cytochalasin D	143-145	serpin family E member 1	Rattus norvegicus	173-178
12118065-7	2002	Unlike the mechanism of induction in growth-factor-stimulated cells, CD- and colchicine-induced PAI-1 expression required on-going protein synthesis (i.e. it was a secondary response).	Cytochalasin D	69-71	serpin family E member 1	Rattus norvegicus	96-101
12118065-12	2002	Reduced PAI-1 mRNA levels upon exposure to genistein prior to CD addition correlated with inhibition of ERK1/2 activity, implicating a tyrosine kinase in shape-dependent MEK activation.	Cytochalasin D	62-64	serpin family E member 1	Rattus norvegicus	8-13
12118065-13	2002	Src-family kinases, moreover, appeared to be specific upstream elements in the CD- and colchicine-dependent pathways of PAI-1 transcription since both agents effectively activated pp60(c-src) kinase activity in quiescent R22 cells.	Cytochalasin D	79-81	serpin family E member 1	Rattus norvegicus	120-125
12118065-13	2002	Src-family kinases, moreover, appeared to be specific upstream elements in the CD- and colchicine-dependent pathways of PAI-1 transcription since both agents effectively activated pp60(c-src) kinase activity in quiescent R22 cells.	Cytochalasin D	79-81	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	185-190
12118065-16	2002	In contrast to the rapid and transient kinetics of ERK activity typical of serum-stimulated cells, the ERK1/2 response to CD and colchicine is both delayed and relatively sustained.	Cytochalasin D	122-124	mitogen activated protein kinase 3	Rattus norvegicus	103-109
12093770-8	2002	Indeed, disruption of the actin cytoskeleton, the downstream target of Rho-kinase, by cytochalasin D also upregulated eNOS expression.	Cytochalasin D	86-100	nitric oxide synthase 3	Homo sapiens	118-122
12061792-7	2002	The disorganization of cellular cytoskeleton by cytochalasin D, colchicine, or acrylamide treatment disrupts CAS-stimulated HT-29 cell polarization.	Cytochalasin D	48-62	chromosome segregation 1 like	Homo sapiens	109-112
12093473-10	2002	Cytochalasin D, an inhibitor of actin polymerization, suppressed the zymosan-induced increases in iPLA2 activity and protein in the membranes and the release of arachidonic acid.	Cytochalasin D	0-14	phospholipase A2, group VI	Mus musculus	98-103
12093473-11	2002	These results suggest that zymosan stimulates an increase in iPLA2 in the membranes of P388D1 cells probably through activation of PKCalpha in concert with cytochalasin D-sensitive events.	Cytochalasin D	156-170	phospholipase A2, group VI	Mus musculus	61-66
12123836-3	2002	The effect of neurotensin was found to result from an increase in cell surface expression of EAAC1 and accordingly, cytochalasin D and colchicine were shown to block the effect of neurotensin on aspartate uptake, suggesting that the cytoskeleton participates in this regulation.	Cytochalasin D	116-130	neurotensin	Homo sapiens	14-25
12123836-3	2002	The effect of neurotensin was found to result from an increase in cell surface expression of EAAC1 and accordingly, cytochalasin D and colchicine were shown to block the effect of neurotensin on aspartate uptake, suggesting that the cytoskeleton participates in this regulation.	Cytochalasin D	116-130	solute carrier family 1 member 1	Homo sapiens	93-98
12123836-3	2002	The effect of neurotensin was found to result from an increase in cell surface expression of EAAC1 and accordingly, cytochalasin D and colchicine were shown to block the effect of neurotensin on aspartate uptake, suggesting that the cytoskeleton participates in this regulation.	Cytochalasin D	116-130	neurotensin	Homo sapiens	180-191
11994301-5	2002	The Rap1b effect was cell-autonomous and was prevented by pre-treating cells with cytochalasin D or latrunculin A to inhibit actin polymerization.	Cytochalasin D	82-96	RAS related protein 1b	Mus musculus	4-9
12470617-0	2002	Hexokinase translocation during neutrophil activation, chemotaxis, and phagocytosis: disruption by cytochalasin D, dexamethasone, and indomethacin.	Cytochalasin D	99-113	hexokinase 1	Homo sapiens	0-10
12470617-8	2002	Further studies noted that cytochalasin D, dexamethasone, and indomethacin blocked hexokinase translocation.	Cytochalasin D	27-41	hexokinase 1	Homo sapiens	83-93
12107753-11	2002	Cytochalasin D prevented loss of CD11b ( p<0.001).	Cytochalasin D	0-14	integrin subunit alpha M	Homo sapiens	33-38
11741921-8	2002	The export of SK-1 is constitutive and is inhibited by cytochalasin D and treatment at 4 degrees C but not by brefeldin A or nocodazole, suggesting that a nonclassical secretory pathway that requires the actin cytoskeleton dynamics is involved.	Cytochalasin D	55-69	sphingosine kinase 1	Homo sapiens	14-18
11880329-10	2002	However, cytochalasin D treatment abolished the effect of vasopressin on the SK channels.	Cytochalasin D	9-23	arginine vasopressin	Rattus norvegicus	58-69
11903054-3	2002	The effects of cytochalasin D (0.1 microM) on vasopressin-induced Ca(2+) inflow were similar to those on thapsigargin-induced Ca(2+) inflow, except that cytochalasin D did inhibit vasopressin-induced release of Ca(2+) from the ER.	Cytochalasin D	15-29	arginine vasopressin	Rattus norvegicus	46-57
11903054-4	2002	Cytochalasin D (0.1 microM) inhibited vasopressin-induced Mn(2+) inflow (predominantly through intracellular messenger-activated non-selective cation channels), but the degree of inhibition was less than that of vasopressin-induced Ca(2+) inflow (predominantly through Ca(2+)-selective SOCs).	Cytochalasin D	0-14	arginine vasopressin	Rattus norvegicus	38-49
11920577-2	2002	The specific and dose-dependent induction of IFN-gamma release and cytotoxicity in CTL by metabolically active DC did not depend on antigenic peptides contaminating the particles, was cytochalasin D resistant, independent of the maturation state of DC, and blocked by primaquine, amiloride and NH(4)Cl (indicating involvement of acid proteolysis).	Cytochalasin D	184-198	interferon gamma	Mus musculus	45-54
12039062-6	2002	Interestingly, TNFalpha reversed FSH- and cytochalasin D-induced effects both on cell shape and on MMP-2 and TIMP-2.	Cytochalasin D	42-56	tumor necrosis factor	Rattus norvegicus	15-23
12039062-6	2002	Interestingly, TNFalpha reversed FSH- and cytochalasin D-induced effects both on cell shape and on MMP-2 and TIMP-2.	Cytochalasin D	42-56	matrix metallopeptidase 2	Rattus norvegicus	99-104
12039062-6	2002	Interestingly, TNFalpha reversed FSH- and cytochalasin D-induced effects both on cell shape and on MMP-2 and TIMP-2.	Cytochalasin D	42-56	TIMP metallopeptidase inhibitor 2	Rattus norvegicus	109-115
11837785-5	2002	Disrupting the actin cytoskeleton with cytochalasin D (CD) in adherent monocytes inhibited LPS-induced TNFalpha production by 55%, thereby abrogating adherence-induced priming.	Cytochalasin D	39-53	tumor necrosis factor	Homo sapiens	103-111
11786928-2	2002	In the present study, cytochalasin D, which failed to affect D-glucose uptake and metabolism by isolated islets, also augmented glucose-stimulated insulin release, but unexpectedly to a lesser extent than cytochalasin B.	Cytochalasin D	22-36	insulin	Homo sapiens	147-154
11786928-5	2002	Nevertheless, even in the presence of forskolin, cytochalasin B was more efficient than cytochalasin D in augmenting glucose-stimulated insulin secretion.	Cytochalasin D	88-102	insulin	Homo sapiens	136-143
11849381-9	2002	Disruption of the actin cytoskeleton by treatment with cytochalasin D or latrunculin A blocked beta2m up-regulation of VCAM-1 and COX-2.	Cytochalasin D	55-69	beta-2-microglobulin	Homo sapiens	95-101
11849381-9	2002	Disruption of the actin cytoskeleton by treatment with cytochalasin D or latrunculin A blocked beta2m up-regulation of VCAM-1 and COX-2.	Cytochalasin D	55-69	vascular cell adhesion molecule 1	Homo sapiens	119-125
11849381-9	2002	Disruption of the actin cytoskeleton by treatment with cytochalasin D or latrunculin A blocked beta2m up-regulation of VCAM-1 and COX-2.	Cytochalasin D	55-69	prostaglandin-endoperoxide synthase 2	Homo sapiens	130-135
11677248-10	2002	PP2, a Src family kinase inhibitor, or cytochalasin D, which selectively disrupts the network of actin filaments, inhibited both FAK phosphorylation and NO production induced by FN-f, but the phosphatidylinositol 3-kinase inhibitor wortmannin had no effect.	Cytochalasin D	39-53	protein tyrosine kinase 2	Homo sapiens	129-132
11837785-5	2002	Disrupting the actin cytoskeleton with cytochalasin D (CD) in adherent monocytes inhibited LPS-induced TNFalpha production by 55%, thereby abrogating adherence-induced priming.	Cytochalasin D	55-57	tumor necrosis factor	Homo sapiens	103-111
11837785-6	2002	Moreover, CD pretreatment abrogated adherence-induced activation of Pyk2, a major focal adhesion kinase, and ERK 1/2, a component of the mitogen-activated protein kinase (MAPK) signaling pathway, and it completely inhibited LPS-induced ERK 1/2 activation.	Cytochalasin D	10-12	protein tyrosine kinase 2 beta	Homo sapiens	68-72
11837785-6	2002	Moreover, CD pretreatment abrogated adherence-induced activation of Pyk2, a major focal adhesion kinase, and ERK 1/2, a component of the mitogen-activated protein kinase (MAPK) signaling pathway, and it completely inhibited LPS-induced ERK 1/2 activation.	Cytochalasin D	10-12	mitogen-activated protein kinase 3	Homo sapiens	109-116
11837785-6	2002	Moreover, CD pretreatment abrogated adherence-induced activation of Pyk2, a major focal adhesion kinase, and ERK 1/2, a component of the mitogen-activated protein kinase (MAPK) signaling pathway, and it completely inhibited LPS-induced ERK 1/2 activation.	Cytochalasin D	10-12	mitogen-activated protein kinase 3	Homo sapiens	171-175
11779164-6	2002	The blockade of Jo2-induced apoptosis by cytochalasin D occurred upstream of caspase-8 activation.	Cytochalasin D	41-55	caspase 8	Mus musculus	77-86
11837785-6	2002	Moreover, CD pretreatment abrogated adherence-induced activation of Pyk2, a major focal adhesion kinase, and ERK 1/2, a component of the mitogen-activated protein kinase (MAPK) signaling pathway, and it completely inhibited LPS-induced ERK 1/2 activation.	Cytochalasin D	10-12	mitogen-activated protein kinase 3	Homo sapiens	236-243
11751256-8	2002	Disruption of actin cytoskeleton in endometrial stromal cells by treatment with cytochalasin D blocked the increase of FasL protein expression that occurred in response to adhesion to the extracellular matrix.	Cytochalasin D	80-94	Fas ligand	Homo sapiens	119-123
11749662-8	2002	Cytoskeletal disruption with cytochalasin D had an effect on CD11b and CD69 exocytosis similar to that of BIM and E64d.	Cytochalasin D	29-43	integrin subunit alpha M	Homo sapiens	61-66
11749662-8	2002	Cytoskeletal disruption with cytochalasin D had an effect on CD11b and CD69 exocytosis similar to that of BIM and E64d.	Cytochalasin D	29-43	CD69 molecule	Homo sapiens	71-75
11813255-14	2002	Depolymerization of microfilaments with cytochalasin D had no effect on the overall expression of any of these genes in response to cell adhesion and only blocked the induction of opn expression in response to mechanical perturbation.	Cytochalasin D	40-54	secreted phosphoprotein 1	Homo sapiens	180-183
12112011-12	2002	In contrast, parallel increases in mRNA expression and transcription of Class I Pgp gene were observed upon culturing of hepatocytes, in the collagen sandwich system, and treatment with some drugs (cytochalasin D, colchicine, and phalloidin).	Cytochalasin D	198-212	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	80-83
11740863-7	2002	Treatment of chondrocytes with cytochalasin D (an agent that disrupts the actin cytoskeleton) inhibited BMP 7-induced upregulation of tensin, talin, paxillin, and FAK, and blocked the effect of BMP 7 on chondrocyte phenotype.	Cytochalasin D	31-45	bone morphogenetic protein 7	Mus musculus	104-109
11740863-7	2002	Treatment of chondrocytes with cytochalasin D (an agent that disrupts the actin cytoskeleton) inhibited BMP 7-induced upregulation of tensin, talin, paxillin, and FAK, and blocked the effect of BMP 7 on chondrocyte phenotype.	Cytochalasin D	31-45	paxillin	Mus musculus	149-157
11740863-7	2002	Treatment of chondrocytes with cytochalasin D (an agent that disrupts the actin cytoskeleton) inhibited BMP 7-induced upregulation of tensin, talin, paxillin, and FAK, and blocked the effect of BMP 7 on chondrocyte phenotype.	Cytochalasin D	31-45	PTK2 protein tyrosine kinase 2	Mus musculus	163-166
11740863-7	2002	Treatment of chondrocytes with cytochalasin D (an agent that disrupts the actin cytoskeleton) inhibited BMP 7-induced upregulation of tensin, talin, paxillin, and FAK, and blocked the effect of BMP 7 on chondrocyte phenotype.	Cytochalasin D	31-45	bone morphogenetic protein 7	Mus musculus	194-199
11787054-7	2002	In addition, blocking the cytoskeleton rearrangement with inhibitors (colchicine, cytochalasin D, or chlerythrine (a specific PKC inhibitor)) inhibited cyclin expression and cell proliferation.	Cytochalasin D	82-96	proliferating cell nuclear antigen	Homo sapiens	152-158
11748592-10	2001	Experiments using cycloheximide to inhibit protein synthesis demonstrated that recycling of the PTHR-GFP back to the plasma membrane was complete within 1-2 h of ligand removal and was partially blocked by pretreatment with cytochalasin D, but not nocodazole.	Cytochalasin D	224-238	parathyroid hormone 1 receptor	Homo sapiens	96-100
11518778-7	2001	Inhibition of RhoA depolymerized the actin cytoskeleton, as did treatment with cytochalasin D. Preincubation of the human renal fibroblasts with cytochalasin D prevented induction of CTGF by LPA, indicating a strong contribution of an intact cytoskeleton.	Cytochalasin D	79-93	cellular communication network factor 2	Homo sapiens	183-187
11731584-10	2001	Disrupting rafts by removal of cholesterol with methyl-beta-cyclodextrin (MbetaCD) or destabilizing the actin cytoskeleton with cytochalasin D decreased the amount of NHE3 in early endosomes isolated by OptiPrep gradient fractionation.	Cytochalasin D	128-142	sodium/hydrogen exchanger 3	Oryctolagus cuniculus	167-171
11731584-11	2001	Specifically, NHE3 was shown to associate with endosomal vesicles immunoisolated by anti-EEA1 (early endosomal autoantigen 1) antibody-coated magnetic beads and the endosome-associated NHE3 was decreased by cytochalasin D and MbetaCD treatment.	Cytochalasin D	207-221	sodium/hydrogen exchanger 3	Oryctolagus cuniculus	14-18
11731584-11	2001	Specifically, NHE3 was shown to associate with endosomal vesicles immunoisolated by anti-EEA1 (early endosomal autoantigen 1) antibody-coated magnetic beads and the endosome-associated NHE3 was decreased by cytochalasin D and MbetaCD treatment.	Cytochalasin D	207-221	LOW QUALITY PROTEIN: early endosome antigen 1	Oryctolagus cuniculus	89-93
11731584-11	2001	Specifically, NHE3 was shown to associate with endosomal vesicles immunoisolated by anti-EEA1 (early endosomal autoantigen 1) antibody-coated magnetic beads and the endosome-associated NHE3 was decreased by cytochalasin D and MbetaCD treatment.	Cytochalasin D	207-221	sodium/hydrogen exchanger 3	Oryctolagus cuniculus	185-189
11691539-13	2001	Cytochalasin D, AG1478 and dominant-negative EGFR strongly inhibited the phosphorylation of ERK, whereas calphostin C, calmidazolium and KN62 did not.	Cytochalasin D	0-14	Eph receptor B1	Rattus norvegicus	92-95
11691580-4	2001	Disruption of the actin stress fibers by CD induced a moderate increase of MMP-2 mRNA and a much larger stimulation of MMP-3, -9, -13 and -14 mRNAs.	Cytochalasin D	41-43	matrix metallopeptidase 2	Homo sapiens	75-80
11691580-4	2001	Disruption of the actin stress fibers by CD induced a moderate increase of MMP-2 mRNA and a much larger stimulation of MMP-3, -9, -13 and -14 mRNAs.	Cytochalasin D	41-43	matrix metallopeptidase 3	Homo sapiens	119-141
11691580-5	2001	In RCG, a significant up-regulation of these MMPs was also observed although to a lower extent than in CD-treated monolayers.	Cytochalasin D	103-105	matrix metallopeptidase 1	Homo sapiens	45-49
11691580-8	2001	The CD-induced up-regulation of gene expression was largely repressed by blocking protein synthesis by cycloheximide for all the MMPs, by inhibiting the tyrosine-kinases of the src family by herbimycin A for all MMPs, except MMP-2, and by inhibiting the TPA-inducible PKC isoforms by bisindoyl maleimide for all MMPs, except MMP-14.	Cytochalasin D	4-6	matrix metallopeptidase 1	Homo sapiens	129-133
11691580-8	2001	The CD-induced up-regulation of gene expression was largely repressed by blocking protein synthesis by cycloheximide for all the MMPs, by inhibiting the tyrosine-kinases of the src family by herbimycin A for all MMPs, except MMP-2, and by inhibiting the TPA-inducible PKC isoforms by bisindoyl maleimide for all MMPs, except MMP-14.	Cytochalasin D	4-6	matrix metallopeptidase 1	Homo sapiens	212-216
11691580-8	2001	The CD-induced up-regulation of gene expression was largely repressed by blocking protein synthesis by cycloheximide for all the MMPs, by inhibiting the tyrosine-kinases of the src family by herbimycin A for all MMPs, except MMP-2, and by inhibiting the TPA-inducible PKC isoforms by bisindoyl maleimide for all MMPs, except MMP-14.	Cytochalasin D	4-6	matrix metallopeptidase 2	Homo sapiens	225-230
11691580-8	2001	The CD-induced up-regulation of gene expression was largely repressed by blocking protein synthesis by cycloheximide for all the MMPs, by inhibiting the tyrosine-kinases of the src family by herbimycin A for all MMPs, except MMP-2, and by inhibiting the TPA-inducible PKC isoforms by bisindoyl maleimide for all MMPs, except MMP-14.	Cytochalasin D	4-6	proline rich transmembrane protein 2	Homo sapiens	268-271
11691580-8	2001	The CD-induced up-regulation of gene expression was largely repressed by blocking protein synthesis by cycloheximide for all the MMPs, by inhibiting the tyrosine-kinases of the src family by herbimycin A for all MMPs, except MMP-2, and by inhibiting the TPA-inducible PKC isoforms by bisindoyl maleimide for all MMPs, except MMP-14.	Cytochalasin D	4-6	matrix metallopeptidase 1	Homo sapiens	212-216
11691580-8	2001	The CD-induced up-regulation of gene expression was largely repressed by blocking protein synthesis by cycloheximide for all the MMPs, by inhibiting the tyrosine-kinases of the src family by herbimycin A for all MMPs, except MMP-2, and by inhibiting the TPA-inducible PKC isoforms by bisindoyl maleimide for all MMPs, except MMP-14.	Cytochalasin D	4-6	matrix metallopeptidase 14	Homo sapiens	325-331
11594774-2	2001	Insulin but not IGF-I or PDGF-induced ERK activation was abrogated by Ras inhibition, either by treatment with the farnesyl transferase inhibitor FTP III, or by actin disassembly by cytochalasin D, previously shown to inhibit Ras activation.	Cytochalasin D	182-196	insulin	Homo sapiens	0-7
11727833-7	2001	Activation of MMP-2 in HRSF could be induced by treatment with concanavalin A (ConA) or cytochalasin D, as was shown for other cell types.	Cytochalasin D	88-102	matrix metallopeptidase 2	Homo sapiens	14-19
11466321-9	2001	A second inhibitor of endocytosis, cytochalasin D, also blocked insulin-dependent MAPK phosphorylation.	Cytochalasin D	35-49	insulin	Homo sapiens	64-71
11553610-7	2001	Collagen or FN-induced tyrosine phosphorylation of VEGFR-3 was inhibited by treatment with cytochalasin D, an inhibitor of actin polymerization.	Cytochalasin D	91-105	fms related receptor tyrosine kinase 4	Homo sapiens	51-58
11413143-5	2001	Cytochalasin D inhibited the adhesion of cells expressing non-myristoylated MARCKS, but did not further decrease the adhesion of cells expressing adhesion-inhibitory proteins.	Cytochalasin D	0-14	myristoylated alanine rich protein kinase C substrate	Mus musculus	76-82
11278380-4	2001	Cytochalasin D (CD) that depolymerizes actin also enhances vWF binding to wild type GPIb-IX.	Cytochalasin D	0-14	von Willebrand factor	Homo sapiens	59-62
11406462-10	2001	In the second group of experiments, 2 microl of cytochalasin D injected subdermally into rats with intact circulation increased the total tissue water (TTW) and albumin extravasation rate (E(ALB)) by 0.7 +/- 0.2 and 0.4 +/- 0.3 ml/g dry wt, respectively (P < 0.05 compared with vehicle).	Cytochalasin D	48-62	albumin	Rattus norvegicus	191-194
11507676-3	2001	Inhibition of actin polymerization by cytochalasin D significantly decreased the tyrosine phosphorylation of paxillin, p130Cas, PYK2 and FAK but not Gab1, but had no effect on 2-deoxyglucose (DOG) uptake, suggesting a role for Gab1 in osmotic shock-induced glucose transport.	Cytochalasin D	38-52	GRB2 associated binding protein 1	Canis lupus familiaris	227-231
11397002-5	2001	The synthesis of PECAM-1 is independent of compaction, cytokinesis, and DNA replication, as it is detected in embryos that are chronologically at the blastocyst stage following culture of 8-cell embryos in Ca2+-free medium, or medium containing cytochalasin D or aphidicolin, respectively.	Cytochalasin D	245-259	platelet/endothelial cell adhesion molecule 1	Mus musculus	17-24
11389769-6	2001	Cytochalasin D-treatment dramatically reduced the rate of internalization of BCR, and blocked the movement of the BCR from early endosomes to late endosomes/lysosomes, without affecting BCR-signaling.	Cytochalasin D	0-14	BCR activator of RhoGEF and GTPase	Homo sapiens	77-80
11389769-6	2001	Cytochalasin D-treatment dramatically reduced the rate of internalization of BCR, and blocked the movement of the BCR from early endosomes to late endosomes/lysosomes, without affecting BCR-signaling.	Cytochalasin D	0-14	BCR activator of RhoGEF and GTPase	Homo sapiens	114-117
11389769-6	2001	Cytochalasin D-treatment dramatically reduced the rate of internalization of BCR, and blocked the movement of the BCR from early endosomes to late endosomes/lysosomes, without affecting BCR-signaling.	Cytochalasin D	0-14	BCR activator of RhoGEF and GTPase	Homo sapiens	114-117
11406493-6	2001	PYK2 phosphorylation was inhibited by treatment with cytochalasin D but with neither botulinum C3 transferase nor overexpression of a dominant negative mutant of Rho A.	Cytochalasin D	53-67	protein tyrosine kinase 2 beta	Bos taurus	0-4
11399050-2	2001	We observed extension formation when neutrophils were plated to fibronectin-coated substrata in Na(+)-free extracellular medium or in the presence of drugs capable of inhibiting spreading: 4-bromophenacyl bromide, N-ethylmaleimide, 7-chloro-4-nitrobenz-2-oxa-1,3-diazole, and cytochalasin D.	Cytochalasin D	276-290	fibronectin 1	Homo sapiens	64-75
11309409-6	2001	Elk-1 phosphorylation was dependent on an intact actin cytoskeleton, as discerned by treatment with cytochalasin D (CCD).	Cytochalasin D	100-114	ETS transcription factor ELK1	Homo sapiens	0-5
11313461-7	2001	Upon disruption of the F-actin network with phalloidin or cytochalasin D, wild-type hPKCalpha translocates but did not accumulate at the plasma membrane and beta-catenin did not accumulate at the cell-cell contacts.	Cytochalasin D	58-72	protein kinase C alpha	Homo sapiens	84-93
11358485-5	2001	Activation of caspase-3, a crucial step in apoptosis, could be inhibited by cytochalasin D, a substance that counteracts the actin-modulating activity of Rho GTPases, indicating that Rho proteins may have impact on injury-initiated neuronal signal transduction.	Cytochalasin D	76-90	caspase 3	Mus musculus	14-23
11249854-4	2001	Furthermore, pretreatment of cells with exogenous ET-1 obviously prevented cytochalasin D-elicited activation of MMP-2, an effect that was completely abolished by ET(A) receptor antagonist, FR139317.	Cytochalasin D	75-89	endothelin 1	Rattus norvegicus	50-54
11323024-9	2001	Pretreatment of platelets with cytochalasin D resulted in the inhibition of actin binding to GpIbalpha in sheared platelets and in an increase in the rate and magnitude of platelet disaggregation.	Cytochalasin D	31-45	glycoprotein Ib platelet subunit alpha	Homo sapiens	93-102
11249854-4	2001	Furthermore, pretreatment of cells with exogenous ET-1 obviously prevented cytochalasin D-elicited activation of MMP-2, an effect that was completely abolished by ET(A) receptor antagonist, FR139317.	Cytochalasin D	75-89	matrix metallopeptidase 2	Rattus norvegicus	113-118
11249854-6	2001	The addition of recombinant TIMP-2 into the culture abrogated dose-dependently the cytochalasin D-elicited activation of MMP-2.	Cytochalasin D	83-97	TIMP metallopeptidase inhibitor 2	Rattus norvegicus	28-34
11249854-6	2001	The addition of recombinant TIMP-2 into the culture abrogated dose-dependently the cytochalasin D-elicited activation of MMP-2.	Cytochalasin D	83-97	matrix metallopeptidase 2	Rattus norvegicus	121-126
11287749-2	2001	However, when cells are in suspension or in the presence of cytochalasin D which disrupts the intracellular network of actin microfilaments, TPA loses its ability to stimulate tyrosine phosphorylation of FAK and paxillin but it still activates mitogen-activated protein kinase (MAPK) and induces PKC translocation from cytosol to the membrane in HepG2 cells.	Cytochalasin D	60-74	protein tyrosine kinase 2	Homo sapiens	204-207
11310855-6	2001	In both cell lines, the enhancement of MCP-1 binding by stimulation with MCP-1 was blocked by cytochalasin D, an inhibitor of actin polymerization.	Cytochalasin D	94-108	C-C motif chemokine ligand 2	Homo sapiens	39-44
11310855-6	2001	In both cell lines, the enhancement of MCP-1 binding by stimulation with MCP-1 was blocked by cytochalasin D, an inhibitor of actin polymerization.	Cytochalasin D	94-108	C-C motif chemokine ligand 2	Homo sapiens	73-78
11287749-2	2001	However, when cells are in suspension or in the presence of cytochalasin D which disrupts the intracellular network of actin microfilaments, TPA loses its ability to stimulate tyrosine phosphorylation of FAK and paxillin but it still activates mitogen-activated protein kinase (MAPK) and induces PKC translocation from cytosol to the membrane in HepG2 cells.	Cytochalasin D	60-74	paxillin	Homo sapiens	212-220
11087735-6	2001	In contrast, disruption of the actin cytoskeleton with cytochalasin D stimulated ACK-1 phosphorylation, and moreover, addition of Oxo-M to cells preincubated with this agent elicited a further increase in phosphorylation, indicating that an intact cytoskeleton is not required for mAChR signaling to ACK-1.	Cytochalasin D	55-69	tyrosine kinase non receptor 2	Homo sapiens	81-86
11251083-6	2001	Thus, blockade of cell spreading by cytochalasin D or PD98059 treatment resulted in inhibition of EGF-dependent DNA replication.	Cytochalasin D	36-50	epidermal growth factor	Homo sapiens	98-101
11332608-5	2001	Cytochalasin D, actin microfilament disrupting reagent, also abolished the stress activation of JNK/SAPK.	Cytochalasin D	0-14	mitogen-activated protein kinase 8	Homo sapiens	96-104
11121866-7	2001	Cytochalasin D (0.3 microM), which inhibits actin polymerization, reduced the ability of BB to stimulate tyrosine phosphorylation of p125(FAK) and paxillin.	Cytochalasin D	0-14	SEC23 interacting protein	Homo sapiens	133-137
11121866-7	2001	Cytochalasin D (0.3 microM), which inhibits actin polymerization, reduced the ability of BB to stimulate tyrosine phosphorylation of p125(FAK) and paxillin.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	138-141
11121866-7	2001	Cytochalasin D (0.3 microM), which inhibits actin polymerization, reduced the ability of BB to stimulate tyrosine phosphorylation of p125(FAK) and paxillin.	Cytochalasin D	0-14	paxillin	Homo sapiens	147-155
11292176-6	2001	Depolymerization of actin filaments with cytochalasin D blocked the force-induced reduction of SMA.	Cytochalasin D	41-55	immunoglobulin mu binding protein 2	Mus musculus	95-98
11145710-4	2001	Cytochalasin D significantly inhibited the recycling of both CXCR1 and CXCR2 following IL-8-induced internalization, the inhibition being more pronounced for CXCR2 than for CXCR1.	Cytochalasin D	0-14	C-X-C motif chemokine receptor 1	Homo sapiens	61-66
11145710-4	2001	Cytochalasin D significantly inhibited the recycling of both CXCR1 and CXCR2 following IL-8-induced internalization, the inhibition being more pronounced for CXCR2 than for CXCR1.	Cytochalasin D	0-14	C-X-C motif chemokine receptor 2	Homo sapiens	71-76
11145710-4	2001	Cytochalasin D significantly inhibited the recycling of both CXCR1 and CXCR2 following IL-8-induced internalization, the inhibition being more pronounced for CXCR2 than for CXCR1.	Cytochalasin D	0-14	C-X-C motif chemokine ligand 8	Homo sapiens	87-91
11145710-4	2001	Cytochalasin D significantly inhibited the recycling of both CXCR1 and CXCR2 following IL-8-induced internalization, the inhibition being more pronounced for CXCR2 than for CXCR1.	Cytochalasin D	0-14	C-X-C motif chemokine receptor 2	Homo sapiens	158-163
11145710-4	2001	Cytochalasin D significantly inhibited the recycling of both CXCR1 and CXCR2 following IL-8-induced internalization, the inhibition being more pronounced for CXCR2 than for CXCR1.	Cytochalasin D	0-14	C-X-C motif chemokine receptor 1	Homo sapiens	173-178
10984494-11	2000	Strain increased ERK-dependent AP-1 nuclear protein binding, which was attenuated by cytochalasin D and 8-Br-cGMP.	Cytochalasin D	85-99	mitogen-activated protein kinase 1	Homo sapiens	17-20
11845308-6	2001	Partial disruption of the actin cytoskeleton of CFTR-expressing cells with cytochalasin D (CD) induced CFTR activation in the absence of an activated PKA.	Cytochalasin D	75-89	CF transmembrane conductance regulator	Homo sapiens	48-52
11845308-6	2001	Partial disruption of the actin cytoskeleton of CFTR-expressing cells with cytochalasin D (CD) induced CFTR activation in the absence of an activated PKA.	Cytochalasin D	75-89	CF transmembrane conductance regulator	Homo sapiens	103-107
11113628-7	2000	Polycystin-1 multiprotein complexes can be disrupted by cytochalasin D but not by colchicine, suggesting involvement of the actin cytoskeleton.	Cytochalasin D	56-70	polycystin 1, transient receptor potential channel interacting	Homo sapiens	0-12
11078719-3	2000	In contrast, cells pretreated with cytochalasin D showed minimal inhibition of bombesin/GRP receptor internalization.	Cytochalasin D	35-49	gastrin releasing peptide	Mus musculus	88-91
11095944-4	2000	The beta1 integrin antibody and several inhibitors of signaling molecules such as herbimycin A, U73122, LY294002, as well as cytochalasin D, an actin depolymerizing agent, remarkably decreased tyrosine phosphorylation of FAK and its association with fibronectin and paxillin during condensation.	Cytochalasin D	125-139	protein tyrosine kinase 2	Gallus gallus	221-224
11090165-5	2000	The secretion of NSP4 aa112-175 was not affected by treatment of cells with brefeldin A but was abolished by treatment with nocodazole and cytochalasin D, indicating that secretion of this protein occurs via a nonclassical, Golgi apparatus-independent mechanism that utilizes the microtubule and actin microfilament network.	Cytochalasin D	139-153	serine protease 57	Homo sapiens	17-21
10976102-2	2000	We show that disruption of the actin cytoskeleton by cytochalasin D causes a complete inhibition of FAK but does not inhibit Shc signaling and activation of ERK.	Cytochalasin D	53-67	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
11104665-1	2000	We show here that cytochalasin D-induced depolymerization of actin filaments markedly reduces the stimulus-dependent activation of protein kinase B (PKB) in four different cell types (HEK-293 cells, L6 myotubes, 3T3-L1 adipocytes and U87MG cells).	Cytochalasin D	18-32	protein tyrosine kinase 2 beta	Homo sapiens	131-147
11104665-1	2000	We show here that cytochalasin D-induced depolymerization of actin filaments markedly reduces the stimulus-dependent activation of protein kinase B (PKB) in four different cell types (HEK-293 cells, L6 myotubes, 3T3-L1 adipocytes and U87MG cells).	Cytochalasin D	18-32	protein tyrosine kinase 2 beta	Homo sapiens	149-152
11104665-5	2000	Withdrawal of cytochalasin D from the extracellular medium induced actin filament repolymerization, and reinstated both the recruitment of PH-GFP fusion proteins to the plasma membrane and PKB activation in response to insulin and PDGF.	Cytochalasin D	14-28	protein tyrosine kinase 2 beta	Homo sapiens	189-192
11104665-5	2000	Withdrawal of cytochalasin D from the extracellular medium induced actin filament repolymerization, and reinstated both the recruitment of PH-GFP fusion proteins to the plasma membrane and PKB activation in response to insulin and PDGF.	Cytochalasin D	14-28	insulin	Homo sapiens	219-226
11095956-4	2000	Treatment with cytochalasin D, an inhibitor of actin polymerization, could mimic the effects of expression of Rnd1, in that this inhibitor disrupted the cortical actin filaments and induced the formation of many thin processes containing microtubules.	Cytochalasin D	15-29	Rho family GTPase 1	Rattus norvegicus	110-114
11095944-4	2000	The beta1 integrin antibody and several inhibitors of signaling molecules such as herbimycin A, U73122, LY294002, as well as cytochalasin D, an actin depolymerizing agent, remarkably decreased tyrosine phosphorylation of FAK and its association with fibronectin and paxillin during condensation.	Cytochalasin D	125-139	fibronectin 1	Gallus gallus	250-261
11095944-4	2000	The beta1 integrin antibody and several inhibitors of signaling molecules such as herbimycin A, U73122, LY294002, as well as cytochalasin D, an actin depolymerizing agent, remarkably decreased tyrosine phosphorylation of FAK and its association with fibronectin and paxillin during condensation.	Cytochalasin D	125-139	paxillin	Gallus gallus	266-274
11071645-2	2000	This study demonstrated that pretreating human platelets with inhibitors of actin polymerization, cytochalasin D or latrunculin B, dramatically enhances platelet aggregation induced by vWf.	Cytochalasin D	98-112	von Willebrand factor	Homo sapiens	185-188
11056521-13	2000	Microfilaments in NIH 3T3 cells containing Tm 5NM isoforms were more resistant to cytochalasin D-mediated actin depolymerisation than filaments containing isoforms from the alpha Tm(fast) and beta-Tm genes.	Cytochalasin D	82-96	tropomyosin 3, gamma	Mus musculus	43-49
11050044-3	2000	Disruption of F-actin by treatment of cultured hepatocytes with cytochalasin D recovered the EGF-induced IP(3) formation and Ca(2+) mobilization to the same level and with the same dose-response relationship as was obtained in freshly isolated cells.	Cytochalasin D	64-78	epidermal growth factor like 1	Rattus norvegicus	93-96
11035913-6	2000	Treatment of cells with cytochalasin D, which disrupts actin filaments but not cell-substrate adhesion, causes only a slight increase in c-Src PTK activity.	Cytochalasin D	24-38	SRC proto-oncogene, non-receptor tyrosine kinase	Gallus gallus	137-142
11074594-8	2000	Similar cell cycle defects and the loss of microtubules were observed after a cytochalasin D treatment, indicating that the ability of RhoA to regulate the integrity of actin cytoskeleton may be critical for the cell cycle transition through both the G(1)/S and M phase checkpoints.	Cytochalasin D	78-92	ras homolog family member A	Homo sapiens	135-139
11001174-6	2000	In addition, calphostin C as well as cytochalasin D effectively inhibited A23187-induced EPO release.	Cytochalasin D	37-51	eosinophil peroxidase	Cavia porcellus	89-92
10915788-5	2000	Translocation of PYK2 to focal adhesions, as well as its tyrosine phosphorylation in response to histamine treatment, was abolished in the presence of protein kinase C inhibitors or cytochalasin D treatment, whereas activation of protein kinase C by phorbol ester resulted in focal adhesion targeting of PYK2 and its tyrosine phosphorylation in an integrin-clustering dependent manner.	Cytochalasin D	182-196	protein tyrosine kinase 2 beta	Homo sapiens	17-21
10942579-2	2000	A decrease in mitochondrial transmembrane potential, release of cytochrome c into the cytosol, and cleavage of procaspase-9 to its active form preceded the activation of caspase-3 and, moreover, all of these events began earlier and/or proceeded faster in cells treated with AD plus CL or CD than in cells treated with AD only.	Cytochalasin D	289-291	caspase-3	Macaca fascicularis	170-179
10804218-9	2000	Cytochalasin D, an actin depolymerizing agent, decreases tyrosine phosphorylation of FAK and paxillin and their association with beta1 integrin and causes a dose-dependent increase in the abundance of insoluble FAK and paxillin complexes.	Cytochalasin D	0-14	paxillin	Homo sapiens	93-101
10809726-11	2000	Additionally, cytochalasin D, an agent that inhibits actin polymerization, stimulated COX-2 transcription by the same signaling pathway as MIAs.	Cytochalasin D	14-28	prostaglandin-endoperoxide synthase 2	Homo sapiens	86-91
10880044-3	2000	Mice treated with the Rho inhibitor Clostridium botulinum C3 transferase (10 microgram/d) or the actin cytoskeleton disrupter cytochalasin D (1 mg/kg) showed a two- to fourfold increase in vascular eNOS expression and activity.	Cytochalasin D	126-140	nitric oxide synthase 3, endothelial cell	Mus musculus	198-202
10880044-6	2000	Inhibition of vascular Rho guanosine-5"-triphosphate binding activity by the 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor simvastatin increased cerebral blood flow to ischemic regions of the brain, and mice treated with simvastatin, C3 transferase, or cytochalasin D showed smaller cerebral infarctions following MCA occlusion.	Cytochalasin D	265-279	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	Mus musculus	77-124
10888925-5	2000	In monocytes, the transfer of CCR5 could be inhibited by cytochalasin D, and transferred CCR5 could be downmodulated by chemokines.	Cytochalasin D	57-71	C-C motif chemokine receptor 5	Homo sapiens	30-34
10860814-6	2000	The increased expression of MMP-9 by the cytokines was inhibited by cytochalasin D or colchicine but not by PI3 kinase inhibitor wortmannin.	Cytochalasin D	68-82	matrix metallopeptidase 9	Homo sapiens	28-33
10804218-9	2000	Cytochalasin D, an actin depolymerizing agent, decreases tyrosine phosphorylation of FAK and paxillin and their association with beta1 integrin and causes a dose-dependent increase in the abundance of insoluble FAK and paxillin complexes.	Cytochalasin D	0-14	integrin subunit beta 1	Homo sapiens	129-143
10804218-9	2000	Cytochalasin D, an actin depolymerizing agent, decreases tyrosine phosphorylation of FAK and paxillin and their association with beta1 integrin and causes a dose-dependent increase in the abundance of insoluble FAK and paxillin complexes.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	211-214
10804218-9	2000	Cytochalasin D, an actin depolymerizing agent, decreases tyrosine phosphorylation of FAK and paxillin and their association with beta1 integrin and causes a dose-dependent increase in the abundance of insoluble FAK and paxillin complexes.	Cytochalasin D	0-14	paxillin	Homo sapiens	219-227
10662836-12	2000	Furthermore, BDNF/NO-induced growth cone stabilization correlated with the appearance of a cytochalasin D-resistant population of actin filaments.	Cytochalasin D	91-105	brain derived neurotrophic factor	Homo sapiens	13-17
10804218-9	2000	Cytochalasin D, an actin depolymerizing agent, decreases tyrosine phosphorylation of FAK and paxillin and their association with beta1 integrin and causes a dose-dependent increase in the abundance of insoluble FAK and paxillin complexes.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	85-88
10720417-5	2000	The NADPH inhibitor diphenylene iodonium and the superoxide dismutase mimetic manganese (III) tetrakis(1-methyl-4-pyridyl)porphyrin (MnTMPyP) virtually abolished cytochalasin D-inhibitable actin monomer incorporation at the fast-growing barbed ends of filaments.	Cytochalasin D	162-176	2,4-dienoyl-CoA reductase 1	Homo sapiens	4-9
10772825-9	2000	Treatment of cells with Cytochalasin D leads to redistribution of p65 into the actin-containing aggregates.	Cytochalasin D	24-38	synaptotagmin 1	Rattus norvegicus	66-69
10682859-1	2000	Pretreatment of intact platelets with cytochalasin D prevented actin polymerization and cytoskeleton reorganization induced by thrombin, but did not affect platelet aggregation.	Cytochalasin D	38-52	coagulation factor II, thrombin	Homo sapiens	127-135
10652253-4	2000	The "gap" disappeared when cells were treated for 10 minutes with anti-actin drugs (cytochalasin D, latrunculin B, swinholide A), or with the anti-myosin drug 2,3-butanedione 2-monoxime.	Cytochalasin D	84-98	Actin 79B	Drosophila melanogaster	71-76
10652253-8	2000	Spindle F-actin was no longer seen after cells were treated with cytochalasin D, swinholide A or a high concentration of latrunculin B, whereas a low concentration of latrunculin B, which did not completely remove the "gap", caused reduced staining of spindle actin.	Cytochalasin D	65-79	spn-F	Drosophila melanogaster	0-9
10652253-8	2000	Spindle F-actin was no longer seen after cells were treated with cytochalasin D, swinholide A or a high concentration of latrunculin B, whereas a low concentration of latrunculin B, which did not completely remove the "gap", caused reduced staining of spindle actin.	Cytochalasin D	65-79	Actin 79B	Drosophila melanogaster	10-15
10654625-5	2000	In addition, Lat B and CD inhibited vasopressin-induced endocytosis of horseradish peroxidase (HRP), a fluid endocytotic marker.	Cytochalasin D	23-25	arginine vasopressin	Homo sapiens	36-47
10682859-3	2000	The inhibitory effect of cytochalasin D was not observed when platelet aggregation was prevented by the RGDS peptide.	Cytochalasin D	25-39	ral guanine nucleotide dissociation stimulator	Homo sapiens	104-108
10623819-7	2000	Up-regulated adhesion to ICAM-1 was abolished by cytochalasin D, an inhibitor of cytoskeletal rearrangement.	Cytochalasin D	49-63	intercellular adhesion molecule 1	Homo sapiens	25-31
10620493-7	2000	Latrunculin B treatment results in rapid relocalization of GFP-neurabin-II to the cytosol, whereas cytochalasin D treatment causes the collapse of GFP-neurabin-II fluorescence to intensely fluorescent foci of F-actin within the cell body.	Cytochalasin D	99-113	protein phosphatase 1, regulatory subunit 9B	Rattus norvegicus	151-162
11113337-11	2000	Indeed, when growth-cone collapse was induced in hippocampal neurons after cytochalasin D treatment, which depolymerizes microfilaments, the ratio MAP2-P:MAP2 in these growing regions decreased down to 1.	Cytochalasin D	75-89	microtubule-associated protein 2	Rattus norvegicus	147-151
11315093-9	2000	However, disruption of the cellular cytoskeleton by cytochalasin D prevented FAK activation, but did not block genistein-induced complex formation.	Cytochalasin D	52-66	protein tyrosine kinase 2	Homo sapiens	77-80
11113363-6	2000	zDEVD-fmk, an irreversible inhibitor of caspase-3-like enzymes, and cytochalasin D, an actin depolymerizing agent, blocked caspase-3 cleavage and delayed cell death.	Cytochalasin D	68-82	caspase 3	Homo sapiens	123-132
10645887-8	2000	In addition, cytochalasin D, which inhibits the phagocytosis of DEPs, reduced the increase in GM-CSF release after DEP treatment.	Cytochalasin D	13-27	colony stimulating factor 2	Homo sapiens	94-100
10600813-9	1999	Cytochalasin D, an inhibitor of actin filament formation, inhibited the ability of cAMP to stimulate TC uptake and Ntcp translocation.	Cytochalasin D	0-14	solute carrier family 10 member 1	Rattus norvegicus	115-119
10575001-6	1999	The binding interactions of ZO-2, ZO-3, and occludin were corroborated in vivo by immunofluorescence colocalization experiments which showed that all three proteins colocalized with actin aggregates at cell borders in cytochalasin D-treated Madin-Darby canine kidney cells.	Cytochalasin D	218-232	tight junction protein 2	Canis lupus familiaris	28-38
10575001-6	1999	The binding interactions of ZO-2, ZO-3, and occludin were corroborated in vivo by immunofluorescence colocalization experiments which showed that all three proteins colocalized with actin aggregates at cell borders in cytochalasin D-treated Madin-Darby canine kidney cells.	Cytochalasin D	218-232	occludin	Canis lupus familiaris	44-52
10600776-8	1999	Cytochalasin D also induced MARCKS translocation and enhanced PMA-stimulated translocation of MARCKS.	Cytochalasin D	0-14	myristoylated alanine rich protein kinase C substrate	Homo sapiens	28-34
10600776-8	1999	Cytochalasin D also induced MARCKS translocation and enhanced PMA-stimulated translocation of MARCKS.	Cytochalasin D	0-14	myristoylated alanine rich protein kinase C substrate	Homo sapiens	94-100
10535385-5	1999	Cytochalasin D pretreatment of liver cells reduced the vasopressin-stimulated elevation of [Ca2+]i by 60% and of glucagon by 50%.	Cytochalasin D	0-14	arginine vasopressin	Rattus norvegicus	55-66
10587368-6	1999	Disruption of the actin cytoskeleton by treating ESC with cytochalasin D completely blocked the increase of IL-8 that was induced in response to integrin activation.	Cytochalasin D	58-72	C-X-C motif chemokine ligand 8	Homo sapiens	108-112
10535385-10	1999	The reduced [Ca2+]i response may be the mechanism by which cytochalasin D pretreatment inhibits vasopressin-induced metabolic effects.	Cytochalasin D	59-73	arginine vasopressin	Rattus norvegicus	96-107
10464255-2	1999	We found that inhibiting actin polymerization in unstimulated platelets with cytochalasin D or latrunculin A mimics the effects of platelet agonists by inducing fibrinogen binding to alpha(IIb)beta(3).	Cytochalasin D	77-91	fibrinogen beta chain	Homo sapiens	161-171
10464255-3	1999	By contrast, stabilizing actin filaments with jasplakinolide prevented cytochalasin D-, latrunculin A-, and ADP-induced fibrinogen binding.	Cytochalasin D	71-85	fibrinogen beta chain	Homo sapiens	120-130
10464255-4	1999	Cytochalasin D- and latrunculin A-induced fibrinogen was inhibited by ADP scavengers, suggesting that subthreshold concentrations of ADP provided the stimulus for the actin filament turnover required to see cytochalasin D and latrunculin A effects.	Cytochalasin D	207-221	fibrinogen beta chain	Homo sapiens	42-52
10455189-12	1999	Pretreatment with cytochalasin D, which disrupts actin microfilaments, prevented the calcitonin-induced HEF1 and paxillin phosphorylation.	Cytochalasin D	18-32	neural precursor cell expressed, developmentally down-regulated 9	Homo sapiens	104-108
10484469-2	1999	Disrupting microfilaments or microtubules with cytochalasin D (CytoD) or colchicine can suppress LPS-induced tumor necrosis factor-alpha (TNF-alpha) gene expression and protein production from these cells.	Cytochalasin D	47-61	tumor necrosis factor	Rattus norvegicus	109-136
10484469-2	1999	Disrupting microfilaments or microtubules with cytochalasin D (CytoD) or colchicine can suppress LPS-induced tumor necrosis factor-alpha (TNF-alpha) gene expression and protein production from these cells.	Cytochalasin D	47-61	tumor necrosis factor	Rattus norvegicus	138-147
10496324-10	1999	Localization of PAK1 and F-actin in cytoskeletal structures was abolished by the actin polymerization inhibitor cytochalasin D and the phosphatidylinositol 3-kinase inhibitor wortmannin.	Cytochalasin D	112-126	p21 (RAC1) activated kinase 1	Homo sapiens	16-20
10455189-12	1999	Pretreatment with cytochalasin D, which disrupts actin microfilaments, prevented the calcitonin-induced HEF1 and paxillin phosphorylation.	Cytochalasin D	18-32	paxillin	Homo sapiens	113-121
10446931-10	1999	These calcitonin effects on endocytotic and re-exocytotic pathways were inhibited by 100 nM cytochalasin D, 100 nM nocodazole, 0.1 to 1 microM bafilomycin A1, or 0.1 mM monodansyl cadaverine.	Cytochalasin D	92-106	Calcitonin gene-related peptide	Sus scrofa	6-16
10411539-8	1999	Disruption of the actin cytoskeleton by treating ESC with cytochalasin D completely blocked the increase of MCP-1 induced in response to integrin activation.	Cytochalasin D	58-72	C-C motif chemokine ligand 2	Homo sapiens	108-113
10400706-5	1999	Rephosphorylation of PTP36 seemed to depend on actin polymerization since it was inhibited by cytochalasin D.	Cytochalasin D	94-108	protein tyrosine phosphatase, non-receptor type 14	Mus musculus	21-26
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	292-306	catenin delta 1	Homo sapiens	106-110
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	292-306	cadherin 1	Homo sapiens	125-135
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	292-306	cadherin 1	Homo sapiens	178-188
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	292-306	cadherin 1	Homo sapiens	178-188
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	292-306	cadherin 1	Homo sapiens	178-188
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	322-336	catenin delta 1	Homo sapiens	106-110
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	322-336	cadherin 1	Homo sapiens	125-135
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	322-336	cadherin 1	Homo sapiens	178-188
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	322-336	cadherin 1	Homo sapiens	178-188
10409703-7	1999	Finally, we show that staurosporine, a kinase inhibitor, induces an increased electrophoretic mobility of p120(ctn) bound to E-cadherin polypeptides, activates the nonfunctional E-cadherin protein, and converts the wild-type E-cadherin and an E-cadherin-alpha-catenin chimeric protein from a cytochalasin D-sensitive to a cytochalasin D-insensitive state.	Cytochalasin D	322-336	cadherin 1	Homo sapiens	178-188
10391917-11	1999	Phosphatidylinositol 3,4, 5-trisphosphate-mediated membrane translocation of Btk was enhanced in cytochalasin D-pretreated, FcepsilonRI-stimulated mast cells.	Cytochalasin D	97-111	Bruton tyrosine kinase	Homo sapiens	77-80
10391917-11	1999	Phosphatidylinositol 3,4, 5-trisphosphate-mediated membrane translocation of Btk was enhanced in cytochalasin D-pretreated, FcepsilonRI-stimulated mast cells.	Cytochalasin D	97-111	Fc epsilon receptor Ia	Homo sapiens	124-135
10399827-9	1999	IGF-1, PMA and dibutyryl cAMP modified the peritubular cell morphology, cytoskeletal organization and proteoglycan production; the cytoskeleton disrupting drugs such as vinblastine, colchicine and cytochalasin D mimicked some of these effects.	Cytochalasin D	197-211	insulin-like growth factor 1	Rattus norvegicus	0-5
10406836-11	1999	The pressure-induced expression of c-fos was not inhibited by nitrendipine (10 micromol/L), a calcium-free Krebs" solution containing EGTA (1 to 2 mmol/L), calphostin C (0.1 micromol/L), or cytochalasin D (0.4 micromol/L) but was inhibited by genistein (30 micromol/L).	Cytochalasin D	190-204	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	35-40
10400905-8	1999	Cytochalasin D, which selectively disrupts the network of actin filaments, markedly inhibited stretch-induced ERK activation.	Cytochalasin D	0-14	Eph receptor B1	Rattus norvegicus	110-113
10333493-3	1999	In contrast, cytochalasin D (2 microM) completely abolished the stimulatory effect of insulin and dexamethasone on both heparin-releasable LPL and total cellular LPL activities.	Cytochalasin D	13-27	lipoprotein lipase	Rattus norvegicus	139-142
10333493-3	1999	In contrast, cytochalasin D (2 microM) completely abolished the stimulatory effect of insulin and dexamethasone on both heparin-releasable LPL and total cellular LPL activities.	Cytochalasin D	13-27	lipoprotein lipase	Rattus norvegicus	162-165
10333493-4	1999	The potential role of the actin cytoskeleton in the stimulation of LPL activity by insulin and dexamethasone appears to be distal to the initial signalling events since cytochalasin D is still effective in preventing the stimulation when added 2 h after the hormones.	Cytochalasin D	169-183	lipoprotein lipase	Rattus norvegicus	67-70
10224142-3	1999	Association of Rap2B with the cytoskeleton was very rapid, while translocation of Rap1B occurred in a later phase of platelet activation and was totally inhibited by cytochalasin D.	Cytochalasin D	166-180	RAP1B, member of RAS oncogene family	Homo sapiens	82-87
10208419-6	1999	Tyrosine phosphorylation of FAK, paxillin and p130Cas was inhibited by cytochalasin D or two specific inhibitors of phosphatidylinositol-3" kinase (PI-3" kinase), wortmannin and LY294002, indicating that their tyrosine phosphorylation depends on the formation of actin stress fiber and activation of PI-3" kinase.	Cytochalasin D	71-85	protein tyrosine kinase 2	Homo sapiens	28-31
10208419-6	1999	Tyrosine phosphorylation of FAK, paxillin and p130Cas was inhibited by cytochalasin D or two specific inhibitors of phosphatidylinositol-3" kinase (PI-3" kinase), wortmannin and LY294002, indicating that their tyrosine phosphorylation depends on the formation of actin stress fiber and activation of PI-3" kinase.	Cytochalasin D	71-85	paxillin	Homo sapiens	33-41
10208419-6	1999	Tyrosine phosphorylation of FAK, paxillin and p130Cas was inhibited by cytochalasin D or two specific inhibitors of phosphatidylinositol-3" kinase (PI-3" kinase), wortmannin and LY294002, indicating that their tyrosine phosphorylation depends on the formation of actin stress fiber and activation of PI-3" kinase.	Cytochalasin D	71-85	BCAR1 scaffold protein, Cas family member	Homo sapiens	46-53
10066433-5	1999	In contrast to GPVI-mediated platelet activation, most of these phenomena induced by GPIa/IIa activation were markedly suppressed by acetylsalicylic acid (ASA) or cytochalasin D.	Cytochalasin D	163-177	multimerin 1	Homo sapiens	85-89
9927495-5	1999	In addition, treatment with cytochalasin D, a fungal toxin that depolymerizes actin filaments, reduced the infarct size of both gelsolin-null and control mice to the same final volume.	Cytochalasin D	28-42	gelsolin	Mus musculus	128-136
10096665-17	1999	Zyxin, vinculin, and other associated proteins were disrupted in the CD-treated tissues and do not colocalize with each other or CD-induced actin aggregates.	Cytochalasin D	69-71	zyxin	Homo sapiens	0-5
10096665-17	1999	Zyxin, vinculin, and other associated proteins were disrupted in the CD-treated tissues and do not colocalize with each other or CD-induced actin aggregates.	Cytochalasin D	69-71	vinculin	Homo sapiens	7-15
10094466-3	1999	Gastrin-induced PI 3-kinase activity was coprecipitated with p60Src and p125FAK and was inhibited by herbimycin A, the selective Src inhibitor PP-2 or cytochalasin D, which disrupts the actin cytoskeleton and prevents p125FAK activity.	Cytochalasin D	151-165	gastrin	Homo sapiens	0-7
10094466-3	1999	Gastrin-induced PI 3-kinase activity was coprecipitated with p60Src and p125FAK and was inhibited by herbimycin A, the selective Src inhibitor PP-2 or cytochalasin D, which disrupts the actin cytoskeleton and prevents p125FAK activity.	Cytochalasin D	151-165	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	61-67
10094466-3	1999	Gastrin-induced PI 3-kinase activity was coprecipitated with p60Src and p125FAK and was inhibited by herbimycin A, the selective Src inhibitor PP-2 or cytochalasin D, which disrupts the actin cytoskeleton and prevents p125FAK activity.	Cytochalasin D	151-165	protein tyrosine kinase 2	Homo sapiens	72-79
10094466-3	1999	Gastrin-induced PI 3-kinase activity was coprecipitated with p60Src and p125FAK and was inhibited by herbimycin A, the selective Src inhibitor PP-2 or cytochalasin D, which disrupts the actin cytoskeleton and prevents p125FAK activity.	Cytochalasin D	151-165	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	64-67
10094466-3	1999	Gastrin-induced PI 3-kinase activity was coprecipitated with p60Src and p125FAK and was inhibited by herbimycin A, the selective Src inhibitor PP-2 or cytochalasin D, which disrupts the actin cytoskeleton and prevents p125FAK activity.	Cytochalasin D	151-165	protein tyrosine kinase 2	Homo sapiens	218-225
9931015-9	1999	Disruption of the actin cytoskeleton with cytochalasin D, but not the microtubule network with colchicine, completely inhibited CCK-8-stimulated p130(Cas) phosphorylation.	Cytochalasin D	42-56	cholecystokinin	Rattus norvegicus	128-131
9931015-9	1999	Disruption of the actin cytoskeleton with cytochalasin D, but not the microtubule network with colchicine, completely inhibited CCK-8-stimulated p130(Cas) phosphorylation.	Cytochalasin D	42-56	phospholipase C-like 1	Rattus norvegicus	145-149
9950820-2	1999	In separate experiments, EGF or EGF concurrent with cytochalasin D, an inhibitor of actin polymerization, was administered to the experimental loop and compared with its vehicle control.	Cytochalasin D	52-66	actin	Oryctolagus cuniculus	84-89
9927334-6	1999	Furthermore, the addition of cycloheximide inhibited expression of IGFBP-1 in cytochalasin D-treated cells.	Cytochalasin D	78-92	insulin-like growth factor-binding protein 1	Papio anubis	67-74
10098935-2	1999	Induced transcription of the plasminogen activator inhibitor type-1 (PAI-1) gene in serum-free cultures of normal rat kidney (NRK-52E) cells following disruption of actin microfilament structures with cytochalasin D (CD) provides a simple model to probe mechanisms underlying shape-related expression control.	Cytochalasin D	201-215	serpin family E member 2	Rattus norvegicus	29-67
10098935-2	1999	Induced transcription of the plasminogen activator inhibitor type-1 (PAI-1) gene in serum-free cultures of normal rat kidney (NRK-52E) cells following disruption of actin microfilament structures with cytochalasin D (CD) provides a simple model to probe mechanisms underlying shape-related expression control.	Cytochalasin D	201-215	serpin family E member 2	Rattus norvegicus	69-74
10098935-2	1999	Induced transcription of the plasminogen activator inhibitor type-1 (PAI-1) gene in serum-free cultures of normal rat kidney (NRK-52E) cells following disruption of actin microfilament structures with cytochalasin D (CD) provides a simple model to probe mechanisms underlying shape-related expression control.	Cytochalasin D	217-219	serpin family E member 2	Rattus norvegicus	29-67
10401576-3	1999	An immediate effect of 10-100 microM CD at late diakinesis was the formation of highly refractile, actin-containing cables within the nonchromosomal nucleoplasm.	Cytochalasin D	37-39	Actin 79B	Drosophila melanogaster	99-104
10098935-2	1999	Induced transcription of the plasminogen activator inhibitor type-1 (PAI-1) gene in serum-free cultures of normal rat kidney (NRK-52E) cells following disruption of actin microfilament structures with cytochalasin D (CD) provides a simple model to probe mechanisms underlying shape-related expression control.	Cytochalasin D	217-219	serpin family E member 2	Rattus norvegicus	69-74
10098935-4	1999	Stimulated expression occurred rapidly (i.e., within 2 h of CD addition), involved increases in both PAI-1 mRNA abundance and de novo protein synthesis, and was dependent upon the concentration of CD used.	Cytochalasin D	60-62	serpin family E member 2	Rattus norvegicus	101-106
10401576-7	1999	Rhodamine-conjugates of phalloidin and DNase I were used to assess the status of actin in untreated cells as well as the effect of CD on actin distribution.	Cytochalasin D	131-133	Actin 79B	Drosophila melanogaster	137-142
10098935-4	1999	Stimulated expression occurred rapidly (i.e., within 2 h of CD addition), involved increases in both PAI-1 mRNA abundance and de novo protein synthesis, and was dependent upon the concentration of CD used.	Cytochalasin D	197-199	serpin family E member 2	Rattus norvegicus	101-106
10098935-5	1999	A series of culture conditions were designed (e.g., use of bacteriological surfaces, poly-HEMA coated surfaces, maintenance in suspension on agarose) to discriminate cell shape from adhesive influences on CD-stimulated PAI-1 expression.	Cytochalasin D	205-207	serpin family E member 2	Rattus norvegicus	219-224
10098935-6	1999	Cytoskeletal disruption, and not simply changes in cell shape, was a critical aspect of CD-mediated PAI-1 expression in NRK cells cultured under serum-free conditions; induced expression was independent of substrate anchorage.	Cytochalasin D	88-90	serpin family E member 2	Rattus norvegicus	100-105
10098935-7	1999	Low concentrations of CD (1-2 microM) failed to cause cell arborization or increase either relative PAI-1 mRNA/protein abundance levels suggesting, however, that cell rounding may be a necessary but not sufficient aspect in CD-mediated PAI-1 induction.	Cytochalasin D	224-226	serpin family E member 2	Rattus norvegicus	236-241
10098935-8	1999	Transfection of PAI-1 promoter-CAT reporter constructs into NRK cells followed by stimulation with CD or serum additionally indicated that CD-induced PAI-1 expression did not utilize the same functional complement of serum-responsive promoter sequences, thus, further defining differences in the growth factor- and cytoskeletal-mediated pathways of PAI-1 gene regulation.	Cytochalasin D	139-141	serpin family E member 2	Rattus norvegicus	16-21
10098935-8	1999	Transfection of PAI-1 promoter-CAT reporter constructs into NRK cells followed by stimulation with CD or serum additionally indicated that CD-induced PAI-1 expression did not utilize the same functional complement of serum-responsive promoter sequences, thus, further defining differences in the growth factor- and cytoskeletal-mediated pathways of PAI-1 gene regulation.	Cytochalasin D	139-141	serpin family E member 2	Rattus norvegicus	150-155
10098935-8	1999	Transfection of PAI-1 promoter-CAT reporter constructs into NRK cells followed by stimulation with CD or serum additionally indicated that CD-induced PAI-1 expression did not utilize the same functional complement of serum-responsive promoter sequences, thus, further defining differences in the growth factor- and cytoskeletal-mediated pathways of PAI-1 gene regulation.	Cytochalasin D	139-141	myotrophin	Rattus norvegicus	296-309
10098935-8	1999	Transfection of PAI-1 promoter-CAT reporter constructs into NRK cells followed by stimulation with CD or serum additionally indicated that CD-induced PAI-1 expression did not utilize the same functional complement of serum-responsive promoter sequences, thus, further defining differences in the growth factor- and cytoskeletal-mediated pathways of PAI-1 gene regulation.	Cytochalasin D	139-141	serpin family E member 2	Rattus norvegicus	150-155
9832561-8	1998	The responsiveness to the survival factor activities of VEGF and FGF-2 was not dependent on cell shape changes since it was retained after cytochalasin D treatment.	Cytochalasin D	139-153	vascular endothelial growth factor A	Homo sapiens	56-60
10919716-12	1999	Cytochalasin D and acrylamide were found to inhibit Tyr-phosphorylation of FAK and paxillin, whereas microtubule disrupting agents at low but not high concentrations increased phosphorylation of these focal adhesion proteins.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	75-78
9832561-8	1998	The responsiveness to the survival factor activities of VEGF and FGF-2 was not dependent on cell shape changes since it was retained after cytochalasin D treatment.	Cytochalasin D	139-153	fibroblast growth factor 2	Homo sapiens	65-70
9756930-4	1998	In particular, CD146 cross-linking induces the tyrosine phosphorylation of the protein tyrosine kinase p125(FAK) as well as p125(FAK) association with paxillin, both events being inhibited by cytochalasin D.	Cytochalasin D	192-206	melanoma cell adhesion molecule	Homo sapiens	15-20
9765250-7	1998	The activation of wild-type and mutant Raf proteins was ablated by cytochalasin D, demonstrating that cytoskeletal organization is required for activation of Raf, even when targeted to the membrane.	Cytochalasin D	67-81	zinc fingers and homeoboxes 2	Homo sapiens	39-42
9765250-7	1998	The activation of wild-type and mutant Raf proteins was ablated by cytochalasin D, demonstrating that cytoskeletal organization is required for activation of Raf, even when targeted to the membrane.	Cytochalasin D	67-81	zinc fingers and homeoboxes 2	Homo sapiens	158-161
9758637-13	1998	A disrupter of actin filaments, cytochalasin D, induced the same effect as lovastatin on tPA, whereas a disrupter of microtubules, nocodazole, did not.	Cytochalasin D	32-46	plasminogen activator, tissue type	Rattus norvegicus	89-92
9860134-10	1998	The expression of cyclin D1 was slightly more suppressed than total protein synthesis after addition of CD during that reactivation process.	Cytochalasin D	104-106	cyclin D1	Homo sapiens	18-27
9756930-4	1998	In particular, CD146 cross-linking induces the tyrosine phosphorylation of the protein tyrosine kinase p125(FAK) as well as p125(FAK) association with paxillin, both events being inhibited by cytochalasin D.	Cytochalasin D	192-206	SEC23 interacting protein	Homo sapiens	103-107
9722543-1	1998	The integrin-mediated stress relaxation as it occurs in a retracting three-dimensional collagen gel (RCG) is accompanied by a large up-regulation of the interstitial collagenase, matrix metalloproteinase 1 ((MMP-1), EC 3.4.24.7), regulated notably by interleukin-1 (IL-1), phorbol esters, and cytoskeleton-disrupting drugs as cytochalasin D (CD).	Cytochalasin D	326-340	matrix metallopeptidase 1	Homo sapiens	208-213
9739170-8	1998	Pretreatment with different concentrations of cytochalasin D, an actin cytoskeleton assembly inhibitor, completely inhibited CCK-8-stimulated tyrosine phosphorylation of p125FAK and paxillin without having any effect on either the potency or efficacy of CCK-8 at stimulating amylase release.	Cytochalasin D	46-60	cholecystokinin	Rattus norvegicus	125-128
9739170-8	1998	Pretreatment with different concentrations of cytochalasin D, an actin cytoskeleton assembly inhibitor, completely inhibited CCK-8-stimulated tyrosine phosphorylation of p125FAK and paxillin without having any effect on either the potency or efficacy of CCK-8 at stimulating amylase release.	Cytochalasin D	46-60	protein tyrosine kinase 2	Rattus norvegicus	170-177
9739170-8	1998	Pretreatment with different concentrations of cytochalasin D, an actin cytoskeleton assembly inhibitor, completely inhibited CCK-8-stimulated tyrosine phosphorylation of p125FAK and paxillin without having any effect on either the potency or efficacy of CCK-8 at stimulating amylase release.	Cytochalasin D	46-60	paxillin	Rattus norvegicus	182-190
9739170-8	1998	Pretreatment with different concentrations of cytochalasin D, an actin cytoskeleton assembly inhibitor, completely inhibited CCK-8-stimulated tyrosine phosphorylation of p125FAK and paxillin without having any effect on either the potency or efficacy of CCK-8 at stimulating amylase release.	Cytochalasin D	46-60	cholecystokinin	Rattus norvegicus	254-257
9722543-3	1998	We demonstrate here that culture of human skin fibroblasts in RCG or in CD- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated monolayers resulted in the activation of an IL-1 autocrine feedback loop that was switched off by the naturally occurring IL-1 receptor antagonist (IL-1RA), a blocker of the common IL-1 receptor.	Cytochalasin D	72-74	interleukin 1 alpha	Homo sapiens	175-179
9722543-3	1998	We demonstrate here that culture of human skin fibroblasts in RCG or in CD- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated monolayers resulted in the activation of an IL-1 autocrine feedback loop that was switched off by the naturally occurring IL-1 receptor antagonist (IL-1RA), a blocker of the common IL-1 receptor.	Cytochalasin D	72-74	interleukin 1 receptor antagonist	Homo sapiens	253-277
9722543-3	1998	We demonstrate here that culture of human skin fibroblasts in RCG or in CD- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated monolayers resulted in the activation of an IL-1 autocrine feedback loop that was switched off by the naturally occurring IL-1 receptor antagonist (IL-1RA), a blocker of the common IL-1 receptor.	Cytochalasin D	72-74	interleukin 1 receptor antagonist	Homo sapiens	279-285
9781725-9	1998	MEASUREMENTS AND MAIN RESULTS: Exposure to TNF-alpha and IL-1beta led to significant decreases in neutrophil filterability, which was attenuated by cytochalasin D pretreatment.	Cytochalasin D	148-162	tumor necrosis factor	Homo sapiens	43-52
9781725-9	1998	MEASUREMENTS AND MAIN RESULTS: Exposure to TNF-alpha and IL-1beta led to significant decreases in neutrophil filterability, which was attenuated by cytochalasin D pretreatment.	Cytochalasin D	148-162	interleukin 1 beta	Homo sapiens	57-65
9731041-6	1998	Collagen-induced tyrosine phosphorylation of WASP was inhibited by cytochalasin D and wortmannin, respectively, suggesting that actin polymerization and phosphatidylinositol 3-kinase (PI3-kinase) play a role in the induction of tyrosine phosphorylation of WASP.	Cytochalasin D	67-81	WASP actin nucleation promoting factor	Homo sapiens	45-49
9722543-3	1998	We demonstrate here that culture of human skin fibroblasts in RCG or in CD- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-treated monolayers resulted in the activation of an IL-1 autocrine feedback loop that was switched off by the naturally occurring IL-1 receptor antagonist (IL-1RA), a blocker of the common IL-1 receptor.	Cytochalasin D	72-74	interleukin 1 alpha	Homo sapiens	253-257
9722543-1	1998	The integrin-mediated stress relaxation as it occurs in a retracting three-dimensional collagen gel (RCG) is accompanied by a large up-regulation of the interstitial collagenase, matrix metalloproteinase 1 ((MMP-1), EC 3.4.24.7), regulated notably by interleukin-1 (IL-1), phorbol esters, and cytoskeleton-disrupting drugs as cytochalasin D (CD).	Cytochalasin D	342-344	matrix metallopeptidase 1	Homo sapiens	208-213
9722543-5	1998	The RCG- as well as the TPA-, IL-1-, and CD-induced up-regulation of both MMP-1 and IL-1 was totally suppressed by protein tyrosine kinases inhibitors.	Cytochalasin D	41-43	interleukin 1 alpha	Homo sapiens	30-34
9739461-7	1998	A calpain inhibitor peptide (CIP, 10(-2) mM) reduced the proteolysis of fodrin, opacity, and enzyme leakage in glucose-treated lenses but only partially retarded them in CD-treated lenses.	Cytochalasin D	170-172	calpastatin	Homo sapiens	2-19
9722543-5	1998	The RCG- as well as the TPA-, IL-1-, and CD-induced up-regulation of both MMP-1 and IL-1 was totally suppressed by protein tyrosine kinases inhibitors.	Cytochalasin D	41-43	matrix metallopeptidase 1	Homo sapiens	74-79
9722543-5	1998	The RCG- as well as the TPA-, IL-1-, and CD-induced up-regulation of both MMP-1 and IL-1 was totally suppressed by protein tyrosine kinases inhibitors.	Cytochalasin D	41-43	interleukin 1 alpha	Homo sapiens	84-88
9722543-6	1998	In contrast bisindoylmaleimide, at a concentration (5 microM) that inhibits the TPA-induced protein kinase C activity, suppressed the CD-induced MMP-1 expression but did not or barely altered that induced in RCG or by IL-1.	Cytochalasin D	134-136	matrix metallopeptidase 1	Homo sapiens	145-150
9722543-7	1998	None of the other tested inhibitors of a variety of signaling pathways including those used by integrins was able to suppress the RCG or CD-induced MMP-1.	Cytochalasin D	137-139	matrix metallopeptidase 1	Homo sapiens	148-153
9685378-12	1998	The microfilament-disrupting, macropinocytosis blocking agent cytochalasin D inhibited LPS and CD14 internalization but did not prevent LPS-dependent activation, indicating that these two processes are dissociated.	Cytochalasin D	62-76	CD14 molecule	Homo sapiens	95-99
9721762-4	1998	Treatment of SH-SY5Y cells with cytochalasin D disrupted the actin cytoskeleton and prevented any morphological changes induced by IGF-I.	Cytochalasin D	32-46	insulin like growth factor 1	Homo sapiens	131-136
9721762-7	1998	In parallel with effects on the actin cytoskeleton, cytochalasin D and PI 3-K inhibitors blocked IGF-I-induced FAK tyrosine phosphorylation, whereas PD98059 had no effect.	Cytochalasin D	52-66	insulin like growth factor 1	Homo sapiens	97-102
9721762-7	1998	In parallel with effects on the actin cytoskeleton, cytochalasin D and PI 3-K inhibitors blocked IGF-I-induced FAK tyrosine phosphorylation, whereas PD98059 had no effect.	Cytochalasin D	52-66	protein tyrosine kinase 2	Homo sapiens	111-114
9716023-8	1998	Cytoskeleton reorganization following cytochalasin D treatment caused an induction of Wnt5a, which was associated with changes in cell morphology.	Cytochalasin D	38-52	Wnt family member 5A	Homo sapiens	86-91
9688570-0	1998	Disruption of actin microfilaments by cytochalasin D leads to activation of p53.	Cytochalasin D	38-52	tumor protein p53	Homo sapiens	76-79
9648916-3	1998	Treatment with 1-10 microM CD resulted in an increased 1) incidence of rounded cells, 2) relative PAI-1 mRNA content, and 3) fraction of PAI-1 protein-expressing cells.	Cytochalasin D	27-29	serpin family E member 2	Rattus norvegicus	98-103
9648916-3	1998	Treatment with 1-10 microM CD resulted in an increased 1) incidence of rounded cells, 2) relative PAI-1 mRNA content, and 3) fraction of PAI-1 protein-expressing cells.	Cytochalasin D	27-29	serpin family E member 2	Rattus norvegicus	137-142
9648916-5	1998	Maximal levels of induced PAI-1 transcripts (18-fold that of control) occurred 4 hours post-CD addition and declined thereafter but remained elevated (by at least tenfold) for 24 hours.	Cytochalasin D	92-94	serpin family E member 2	Rattus norvegicus	26-31
9648916-6	1998	Assessment of the metabolic requirements for CD-induced PAI-1 expression by using the protein synthesis inhibitors puromycin and cycloheximide indicated that PAI-1 transcripts were regulated in a complex manner in response to CD.	Cytochalasin D	45-47	serpin family E member 2	Rattus norvegicus	56-61
9648916-6	1998	Assessment of the metabolic requirements for CD-induced PAI-1 expression by using the protein synthesis inhibitors puromycin and cycloheximide indicated that PAI-1 transcripts were regulated in a complex manner in response to CD.	Cytochalasin D	45-47	serpin family E member 2	Rattus norvegicus	158-163
9648916-6	1998	Assessment of the metabolic requirements for CD-induced PAI-1 expression by using the protein synthesis inhibitors puromycin and cycloheximide indicated that PAI-1 transcripts were regulated in a complex manner in response to CD.	Cytochalasin D	226-228	serpin family E member 2	Rattus norvegicus	56-61
9648916-6	1998	Assessment of the metabolic requirements for CD-induced PAI-1 expression by using the protein synthesis inhibitors puromycin and cycloheximide indicated that PAI-1 transcripts were regulated in a complex manner in response to CD.	Cytochalasin D	226-228	serpin family E member 2	Rattus norvegicus	158-163
9648916-9	1998	Relative abundance of PAI-1 transcripts in suspended cells cultured in the presence of CD, however, closely approximated that of plastic-adherent, CD-treated cells (13-fold over control).	Cytochalasin D	87-89	serpin family E member 2	Rattus norvegicus	22-27
9648916-12	1998	A protein tyrosine kinase is likely involved in the CD-mediated signal-transduction cascade, since induced PAI-1 expression can be down-regulated by genistein and herbimycin A but not by calphostin C or tyrphostin B46.	Cytochalasin D	52-54	serpin family E member 2	Rattus norvegicus	107-112
9684857-3	1998	The inhibitory effect of thrombin required actin polymerisation and was not observed when interaction of CD38 with the cytoskeleton was prevented by cytochalasin D.	Cytochalasin D	149-163	coagulation factor II, thrombin	Homo sapiens	25-33
9668122-7	1998	Bombesin-induced FAK activation is not dependent either on protein kinase C or Ca2+ mobilization but was completely blocked by treatment with cytochalasin D or by placing the cells in suspension.	Cytochalasin D	142-156	PTK2 protein tyrosine kinase 2	Mus musculus	17-20
9688570-2	1998	We investigated whether p53 is activated upon disruption of actin microfilaments, caused by cytochalasin D (CD).	Cytochalasin D	92-106	tumor protein p53	Homo sapiens	24-27
9637734-4	1998	However, the early onset of Cvx-induced PTP is not sensitive to cAMP (including PLCgamma2), and it also occurs in the presence of integrin alphaIIb beta3-antagonist (RGDS peptide, RGDS) or inhibitors of actin polymerization (cytochalasin D, CD) and tyrosine-phosphatases (phenylarsine oxide, PAO).	Cytochalasin D	225-239	protein tyrosine phosphatase receptor type U	Homo sapiens	40-43
9800350-10	1998	Treatment of the starved cells with either demecolcine or cytochalasin D had an only moderately disturbing effect on vimentin IF distribution and the ribosomes stayed in contact with the vimentin IFs.	Cytochalasin D	58-72	vimentin	Mus musculus	117-125
9648724-2	1998	This ligand induced a transient increase in p130Cas tyrosine phosphorylation, which was sensitive to the actin polymerization inhibitor cytochalasin D and to the intracellular Ca2+ chelator BAPTA-AM but not the Ca2+ channel blocker verapamil.	Cytochalasin D	136-150	BCAR1 scaffold protein, Cas family member	Homo sapiens	44-51
9593690-4	1998	Cytochalasin-D treatment of SNB19 cells resulted in the loss of phorbol 12-myristate 13-acetate-induced matrix metalloproteinase-9 (also known as gelatinase-B) expression and coincided with inhibition of actin polymerization, resulting in cell rounding.	Cytochalasin D	0-14	matrix metallopeptidase 9	Homo sapiens	104-130
10192526-7	1998	The disruption of N-CAM accumulation appeared to be rapid and occurred within 5 h of cytochalasin D treatment.	Cytochalasin D	85-99	neural cell adhesion molecule 1	Mus musculus	18-23
10192526-8	1998	These results indicate that the restricted localization of N-CAM, but not of L1, is sensitive to cytochalasin D treatment, suggesting a dependence on the integrity of the actin network.	Cytochalasin D	97-111	neural cell adhesion molecule 1	Mus musculus	59-64
9605168-8	1998	While alpha V beta 3- and alpha L beta 2-mediated cell adhesion was significantly reduced by cytochalasin D, alpha 4 beta 7-mediated adhesion was enhanced.	Cytochalasin D	93-107	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	34-40
9553116-7	1998	Cytochalasin D inhibition suggests a role for the actin cytoskeleton in immune complex activation of alphaM beta2, but cytochalasin has no effect on fMLP-induced activation.	Cytochalasin D	0-14	tubulin beta 4B class IVb	Homo sapiens	108-113
9545257-7	1998	In contrast, monocyte adherence to tissue culture plastic-stimulated CADTK tyrosine phosphorylation, a process that was enhanced by thapsigargin, phorbol 12-myristate 13-acetate, and RANTES but that was completely blocked by preincubation with cytochalasin D.	Cytochalasin D	244-258	protein tyrosine kinase 2 beta	Homo sapiens	69-74
9654134-3	1998	The interaction of CD38 with the cytoskeleton was a specific and reversible process, mediated by the binding to the actin-rich filaments and was inhibited by treatment of platelets with cytochalasin D.	Cytochalasin D	186-200	CD38 molecule	Homo sapiens	19-23
9601640-8	1998	Treatment of lymphocytes with cytochalasin D, which blocks actin polymerization, inhibited cap formation and produced defects in signaling and IL-2 transcriptional induction in response to antigen-receptor signaling that were nearly identical to those seen in vav-/- cells.	Cytochalasin D	30-44	interleukin 2	Mus musculus	143-147
9601640-8	1998	Treatment of lymphocytes with cytochalasin D, which blocks actin polymerization, inhibited cap formation and produced defects in signaling and IL-2 transcriptional induction in response to antigen-receptor signaling that were nearly identical to those seen in vav-/- cells.	Cytochalasin D	30-44	vav 1 oncogene	Mus musculus	260-263
9607310-5	1998	We further show that wortmannin and the cytoskeleton disruptors cytochalasin D and latrunculin B completely blocked these insulin effects.	Cytochalasin D	64-78	insulin	Homo sapiens	122-129
9566877-4	1998	Cytochalasin D treatment of fibroblasts inhibited FN-induced FAK in vitro kinase activity and signaling to ERK2, but it only partially inhibited c-Src activation.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	61-64
9566877-4	1998	Cytochalasin D treatment of fibroblasts inhibited FN-induced FAK in vitro kinase activity and signaling to ERK2, but it only partially inhibited c-Src activation.	Cytochalasin D	0-14	mitogen-activated protein kinase 1	Homo sapiens	107-111
9536039-5	1998	Treatment of aerobic tubers with cytochalasin D, an agent that disrupts actin filaments, reduced wound-induced protein synthesis in vivo.	Cytochalasin D	34-48	actin-66	Solanum tuberosum	73-78
9515168-5	1998	cAMP, PDE-4, and PKA were localized at sites of zymosan adherence in cells treated with cytochalasin D to inhibit phagosome formation, suggesting that zymosan engagement to Fc/CR3 receptors triggers cAMP elevations at sites of phagocytosis.	Cytochalasin D	88-102	cathelicidin antimicrobial peptide	Homo sapiens	0-4
9515718-3	1998	As demonstrated in 13 well-characterized MDR cell models (20 resistant sublines), there is a significant correlation between cytokinesis-blocking CD doses, as well as responsiveness to chemosensitizers and MDR1 gene expression (mRNA and P-gp) allowing discrimination between different levels of P-gp-MDR.	Cytochalasin D	146-148	ATP binding cassette subfamily B member 1	Homo sapiens	237-241
9515718-3	1998	As demonstrated in 13 well-characterized MDR cell models (20 resistant sublines), there is a significant correlation between cytokinesis-blocking CD doses, as well as responsiveness to chemosensitizers and MDR1 gene expression (mRNA and P-gp) allowing discrimination between different levels of P-gp-MDR.	Cytochalasin D	146-148	ATP binding cassette subfamily B member 1	Homo sapiens	295-299
9515718-5	1998	A modulation of CD activity was confined exclusively to both P-gp-expressing cell lines and P-gp chemosensitizers.	Cytochalasin D	16-18	ATP binding cassette subfamily B member 1	Homo sapiens	61-65
9515718-5	1998	A modulation of CD activity was confined exclusively to both P-gp-expressing cell lines and P-gp chemosensitizers.	Cytochalasin D	16-18	ATP binding cassette subfamily B member 1	Homo sapiens	92-96
9515718-6	1998	CD cytoskeletal activity measured by FACS is a specific and sensitive tool with which to detect functional P-gp and related chemosensitizers.	Cytochalasin D	0-2	ATP binding cassette subfamily B member 1	Homo sapiens	107-111
9489713-3	1998	In contrast, the increased tyrosine phosphorylations of FAK and paxillin were inhibited by inclusion of either cytochalasin D or mevastatin, agents that disrupt the cytoskeleton.	Cytochalasin D	111-125	protein tyrosine kinase 2	Homo sapiens	56-59
9489713-3	1998	In contrast, the increased tyrosine phosphorylations of FAK and paxillin were inhibited by inclusion of either cytochalasin D or mevastatin, agents that disrupt the cytoskeleton.	Cytochalasin D	111-125	paxillin	Homo sapiens	64-72
9515168-5	1998	cAMP, PDE-4, and PKA were localized at sites of zymosan adherence in cells treated with cytochalasin D to inhibit phagosome formation, suggesting that zymosan engagement to Fc/CR3 receptors triggers cAMP elevations at sites of phagocytosis.	Cytochalasin D	88-102	phosphodiesterase 4A	Homo sapiens	6-11
9515168-5	1998	cAMP, PDE-4, and PKA were localized at sites of zymosan adherence in cells treated with cytochalasin D to inhibit phagosome formation, suggesting that zymosan engagement to Fc/CR3 receptors triggers cAMP elevations at sites of phagocytosis.	Cytochalasin D	88-102	cathelicidin antimicrobial peptide	Homo sapiens	199-203
16793707-0	1998	GPIIb-IIIa antagonists cause rapid disaggregation of platelets pre-treated with cytochalasin D.	Cytochalasin D	80-94	integrin subunit alpha 2b	Homo sapiens	0-5
9510034-2	1998	The function of both the actin and microtubule cytoskeletons appears to be required for the growth of wing hairs, as treatment of cultured pupal wings with either cytochalasin D or vinblastine was able to slow prehair extension.	Cytochalasin D	163-177	Actin 79B	Drosophila melanogaster	25-30
9405068-13	1997	Cytochalasin D, an agent which disrupts actin microfilaments, inhibited BN- and TPA-induced tyrosine phosphorylation of p125(FAK) completely.	Cytochalasin D	0-14	protein tyrosine kinase 2	Rattus norvegicus	125-128
9464835-4	1997	The inhibition of bacterial invasion by cytochalasin D, a specific inhibitor of actin polymerization, led to a reduction in the expression of IL-7R.	Cytochalasin D	40-54	interleukin 7 receptor	Homo sapiens	142-147
9395506-7	1997	Tyrosine phosphorylation of FAK is pertussis toxin-insensitive, can be mimicked by calcium ionophore, and is inhibited by treatment with cytochalasin D, which depolymerizes the actin cytoskeleton.	Cytochalasin D	137-151	protein tyrosine kinase 2	Rattus norvegicus	28-31
9366409-7	1997	TNF-alpha-induced hepatocyte spreading was blocked by cytochalasin D, Arg-Gly-Asp peptides, cycloheximide, or anti-integrin beta1 Ab.	Cytochalasin D	54-68	tumor necrosis factor	Mus musculus	0-9
9421230-5	1997	Pretreatment of MC3T3-E1 cells with cytochalasin D completely prevented FAK and paxillin tyr phos without any alteration in the tyr phos of Shc proteins and activation of ERK2 induced by AlFx.	Cytochalasin D	36-50	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
9421230-5	1997	Pretreatment of MC3T3-E1 cells with cytochalasin D completely prevented FAK and paxillin tyr phos without any alteration in the tyr phos of Shc proteins and activation of ERK2 induced by AlFx.	Cytochalasin D	36-50	mitogen-activated protein kinase 1	Mus musculus	171-175
9421907-6	1997	Prevention of invasion of salmonellae with cytochalasin D inhibited spvA induction within tissue culture cells, indicating that salmonellae must be internalized for spvA to be induced.	Cytochalasin D	43-57	Salmonella plasmid virulence outer membrane protein A	Salmonella enterica subsp. enterica serovar Typhimurium	68-72
9351824-4	1997	Firstly, unlike alpha IIb beta 3-mediated activation of pp125FAK, Syk activation could be triggered by the binding of soluble fibrinogen and abolished by truncation of the alpha IIb or beta 3 cytoplasmic tail, and it was resistant to inhibition by cytochalasin D.	Cytochalasin D	248-262	tyrosine-protein kinase SYK	Cricetulus griseus	66-69
9361011-7	1997	Inhibition of tyrosine kinase by herbimycin A, destruction of focal adhesion by cytochalasin D, or overexpression of antisense FAK mRNA prevented the activation of ERK/MAPK and the increase in alkaline phosphatase (ALP) activity.	Cytochalasin D	80-94	mitogen-activated protein kinase 1	Mus musculus	164-167
9418045-7	1997	After cytochalasin D treatment which disrupts actin filaments, short rods of ZmADF3 and actin appear in the nucleus suggesting that ZmADF3 may function by guiding actin to sites of actin polymerization.	Cytochalasin D	6-20	actin-depolymerizing factor 3	Zea mays	77-83
9418045-7	1997	After cytochalasin D treatment which disrupts actin filaments, short rods of ZmADF3 and actin appear in the nucleus suggesting that ZmADF3 may function by guiding actin to sites of actin polymerization.	Cytochalasin D	6-20	actin-depolymerizing factor 3	Zea mays	132-138
9342235-4	1997	Relocated Syk is associated with the actin filament network, and the early phase (10-90 s) of this association can be partially inhibited by the pretreatment of platelets with cytochalasin D, an inhibitor of actin polymerization.	Cytochalasin D	176-190	spleen associated tyrosine kinase	Homo sapiens	10-13
9359417-11	1997	Cytochalasin D, but not colchicine, completely inhibited CCK-8- and PMA-induced p125(FAK) and paxillin phosphorylation.	Cytochalasin D	0-14	cholecystokinin	Rattus norvegicus	57-60
9359417-11	1997	Cytochalasin D, but not colchicine, completely inhibited CCK-8- and PMA-induced p125(FAK) and paxillin phosphorylation.	Cytochalasin D	0-14	protein tyrosine kinase 2	Rattus norvegicus	80-89
9359417-11	1997	Cytochalasin D, but not colchicine, completely inhibited CCK-8- and PMA-induced p125(FAK) and paxillin phosphorylation.	Cytochalasin D	0-14	paxillin	Rattus norvegicus	94-102
9314528-3	1997	Here we show that cytochalasin D (CD) treatment inhibited formation of the AlF-induced protrusions and shifted the distribution of ARF6 to a tubular membrane compartment emanating from the juxtanuclear region of cells, which resembled the compartment where the GTP-binding defective mutant of ARF6 localized.	Cytochalasin D	18-32	ADP ribosylation factor 6	Homo sapiens	131-135
9314528-3	1997	Here we show that cytochalasin D (CD) treatment inhibited formation of the AlF-induced protrusions and shifted the distribution of ARF6 to a tubular membrane compartment emanating from the juxtanuclear region of cells, which resembled the compartment where the GTP-binding defective mutant of ARF6 localized.	Cytochalasin D	18-32	ADP ribosylation factor 6	Homo sapiens	293-297
9314528-3	1997	Here we show that cytochalasin D (CD) treatment inhibited formation of the AlF-induced protrusions and shifted the distribution of ARF6 to a tubular membrane compartment emanating from the juxtanuclear region of cells, which resembled the compartment where the GTP-binding defective mutant of ARF6 localized.	Cytochalasin D	34-36	ADP ribosylation factor 6	Homo sapiens	131-135
9314528-3	1997	Here we show that cytochalasin D (CD) treatment inhibited formation of the AlF-induced protrusions and shifted the distribution of ARF6 to a tubular membrane compartment emanating from the juxtanuclear region of cells, which resembled the compartment where the GTP-binding defective mutant of ARF6 localized.	Cytochalasin D	34-36	ADP ribosylation factor 6	Homo sapiens	293-297
9314528-6	1997	Whereas AlF treatment blocked internalization, CD treatment blocked the recycling of wild-type ARF6 and Tac back to the PM; these blocks were mimicked by expression of ARF6 mutants Q67L and T27N, which were predicted to be in either the GTP- or GDP-bound state, respectively.	Cytochalasin D	47-49	ADP ribosylation factor 6	Homo sapiens	95-99
9314528-6	1997	Whereas AlF treatment blocked internalization, CD treatment blocked the recycling of wild-type ARF6 and Tac back to the PM; these blocks were mimicked by expression of ARF6 mutants Q67L and T27N, which were predicted to be in either the GTP- or GDP-bound state, respectively.	Cytochalasin D	47-49	ADP ribosylation factor 6	Homo sapiens	168-172
9334374-5	1997	Notably, low doses of cytochalasin D partially restored the deficiency in cell adhesion seen upon alpha4 tail deletion.	Cytochalasin D	22-36	immunoglobulin binding protein 1	Homo sapiens	98-104
9099734-5	1997	Cytochalasin D, which disrupts the cytoskeleton, abolished the phosphorylation of RAFTK upon phorbol myristate acetate and stem cell factor stimulation, indicating that RAFTK association with the actin cytoskeleton appears to be critical for its phosphorylation.	Cytochalasin D	0-14	protein tyrosine kinase 2 beta	Homo sapiens	82-87
9200693-6	1997	Treatment of RBL-2H3 cells with cytochalasin D, an inhibitor of actin polymerization, enhances downstream signaling and enables the less readily dissociable aggregates to stimulate Ca2+ and degranulation responses.	Cytochalasin D	32-46	RB transcriptional corepressor like 2	Rattus norvegicus	13-18
9182576-7	1997	The effect of VEGF on p125(FAK) tyrosine phosphorylation was completely inhibited by the actin filament-disrupting agent cytochalasin D and was partially inhibited by the protein kinase C inhibitor GF109203X.	Cytochalasin D	121-135	vascular endothelial growth factor A	Homo sapiens	14-18
9182576-7	1997	The effect of VEGF on p125(FAK) tyrosine phosphorylation was completely inhibited by the actin filament-disrupting agent cytochalasin D and was partially inhibited by the protein kinase C inhibitor GF109203X.	Cytochalasin D	121-135	SEC23 interacting protein	Homo sapiens	22-26
9182576-7	1997	The effect of VEGF on p125(FAK) tyrosine phosphorylation was completely inhibited by the actin filament-disrupting agent cytochalasin D and was partially inhibited by the protein kinase C inhibitor GF109203X.	Cytochalasin D	121-135	protein tyrosine kinase 2	Homo sapiens	27-30
9176243-5	1997	The focal contacts contained latent MMP-2, and stimulation of the cells with cytochalasin D or with 8-bromoadenosine 3",5"-cyclic monophosphate with 3-isobutyl-1-methylxanthine increased both latent and activated MMP-9 in the focal contacts.	Cytochalasin D	77-91	matrix metallopeptidase 9	Bos taurus	213-218
9150270-6	1997	Staurosporine inhibited the phorbol ester-induced translocation of MARCKS but not of PKC alpha in both CD pretreated and untreated cells.	Cytochalasin D	103-105	myristoylated alanine rich protein kinase C substrate	Homo sapiens	67-73
9199415-3	1997	Hp150 phosphorylation was specifically inhibited by the addition of cytochalasin D, an inhibitor of actin polymerization, although this appeared to be an indirect effect preventing interaction of intimin with its receptor, tyrosine-phosphorylated Hp90, and thus triggering Hp150 phosphorylation.	Cytochalasin D	68-82	chromatin assembly factor 1 subunit A	Homo sapiens	0-5
9199415-3	1997	Hp150 phosphorylation was specifically inhibited by the addition of cytochalasin D, an inhibitor of actin polymerization, although this appeared to be an indirect effect preventing interaction of intimin with its receptor, tyrosine-phosphorylated Hp90, and thus triggering Hp150 phosphorylation.	Cytochalasin D	68-82	chromatin assembly factor 1 subunit A	Homo sapiens	273-278
9150270-3	1997	CD treatment for 1 h disrupted F-actin filaments, increased membrane bound immunoreactive MARCKS (from 51% to 62% of total), yet markedly enhanced the amount of MARCKS translocated to the cytosolic fraction in response to the phorbol ester 4beta-12-O-tetradecanoylphorbol 13-acetate.	Cytochalasin D	0-2	myristoylated alanine rich protein kinase C substrate	Homo sapiens	90-96
9150270-3	1997	CD treatment for 1 h disrupted F-actin filaments, increased membrane bound immunoreactive MARCKS (from 51% to 62% of total), yet markedly enhanced the amount of MARCKS translocated to the cytosolic fraction in response to the phorbol ester 4beta-12-O-tetradecanoylphorbol 13-acetate.	Cytochalasin D	0-2	myristoylated alanine rich protein kinase C substrate	Homo sapiens	161-167
9099753-11	1997	Phosphorylation of RAFTK is dependent upon the formation of actin cytoskeleton as disruption of actin polymerization by cytochalasin D significantly inhibited this phosphorylation.	Cytochalasin D	120-134	protein tyrosine kinase 2 beta	Homo sapiens	19-24
9099734-5	1997	Cytochalasin D, which disrupts the cytoskeleton, abolished the phosphorylation of RAFTK upon phorbol myristate acetate and stem cell factor stimulation, indicating that RAFTK association with the actin cytoskeleton appears to be critical for its phosphorylation.	Cytochalasin D	0-14	KIT ligand	Homo sapiens	123-139
9099734-5	1997	Cytochalasin D, which disrupts the cytoskeleton, abolished the phosphorylation of RAFTK upon phorbol myristate acetate and stem cell factor stimulation, indicating that RAFTK association with the actin cytoskeleton appears to be critical for its phosphorylation.	Cytochalasin D	0-14	protein tyrosine kinase 2 beta	Homo sapiens	169-174
9131007-6	1997	Cytochalasin D, a compound that prevents actin polymerization, prevented not only alpha 4 receptor capping, but also the inhibition of CFC proliferation observed following alpha 4 crosslinking.	Cytochalasin D	0-14	immunoglobulin binding protein 1	Homo sapiens	82-89
9131007-6	1997	Cytochalasin D, a compound that prevents actin polymerization, prevented not only alpha 4 receptor capping, but also the inhibition of CFC proliferation observed following alpha 4 crosslinking.	Cytochalasin D	0-14	immunoglobulin binding protein 1	Homo sapiens	172-179
9091579-7	1997	The tyrosine phosphorylation of RAFTK after T cell receptor-mediated stimulation was reduced by the pretreatment of cells with cytochalasin D, suggesting the role of the cytoskeleton in this process.	Cytochalasin D	127-141	protein tyrosine kinase 2 beta	Homo sapiens	32-37
9012782-5	1997	The egr-1 gene elevation was not blocked by prior exposure to indomethacin, saralasin, Rp-cAMP, A23187, and colchicine, and it was blocked partially by cytochalasin D, H-7, and prolonged exposure to TPA.	Cytochalasin D	152-166	early growth response 1	Mus musculus	4-9
9008226-4	1997	Cytochalasin D reversed the effect of fibronectin on the suppression of apoptosis in melanocytes, suggesting that an intact cytoskeleton is required for transduction of survival signals.	Cytochalasin D	0-14	fibronectin 1	Homo sapiens	38-49
8929456-4	1996	Cytochalasin D, an inhibitor of actin polymerization, inhibited both PMA-induced and anti-CD44 Mab-induced binding.	Cytochalasin D	0-14	CD44 molecule (Indian blood group)	Homo sapiens	90-94
8968108-6	1996	Induction was also inhibited by cytochalasin D, staurosporine, or dexamethasone, suggesting the need, respectively, for an organized actin cytoskeleton, protein kinase C, and AP-1-driven gene transcription.	Cytochalasin D	32-46	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	175-179
8946288-8	1996	Phalloidin labeling intensified in the ciliary stalk with increasing CD concentration, indicating F-actin aggregation.	Cytochalasin D	69-71	actin like 6A S homeolog	Xenopus laevis	100-105
8970151-2	1996	We found that tyrosine phosphorylation of p125FAK in response to these growth factors is completely abolished in cells treated with cytochalasin D or in cells that were suspended in serum-free medium for 30 min.	Cytochalasin D	132-146	PTK2 protein tyrosine kinase 2	Mus musculus	42-49
8937988-7	1996	The response to EGF can be blocked with cytochalasin D indicating that the binding of EF1 alpha to the cytoskeleton is mediated by F-actin.	Cytochalasin D	40-54	Transcription factor EF1(a)	Rattus norvegicus	86-95
8816918-7	1996	Colchicine (a microtubule-disrupting agent) enhanced, whereas cytochalasin-D (a microfilament inhibitor) inhibited bacterial phagocytosis; cytochalasin-D completely abrogated the effect of anti-CD44 on this PMN function.	Cytochalasin D	139-153	CD44 molecule (Indian blood group)	Homo sapiens	194-198
8918923-2	1996	If infection takes place in the presence of cytochalasin D (CD), however, host actin synthesis is transiently stimulated and continues to be synthesized until approximately 30 hpi, and the hyperexpression of polyhedrin is delayed from about 20 hpi until about 36 hpi (S. N. Talhouk and L. E. Volkman, Virology 182, 626-634, 1991; N. Wei and L. E. Volkman, Virology 191, 42-48, 1992).	Cytochalasin D	44-58	major occlusion body protein	Autographa californica nucleopolyhedrovirus	208-218
8918923-2	1996	If infection takes place in the presence of cytochalasin D (CD), however, host actin synthesis is transiently stimulated and continues to be synthesized until approximately 30 hpi, and the hyperexpression of polyhedrin is delayed from about 20 hpi until about 36 hpi (S. N. Talhouk and L. E. Volkman, Virology 182, 626-634, 1991; N. Wei and L. E. Volkman, Virology 191, 42-48, 1992).	Cytochalasin D	60-62	major occlusion body protein	Autographa californica nucleopolyhedrovirus	208-218
12239373-3	1996	Actin and EF-1[alpha] appear to exist in a complex, because we observed that the two are colocalized, and treatment with cytochalasin D resulted in the redistribution of EF-1[alpa].	Cytochalasin D	121-135	actin-7	Zea mays	0-5
12239373-3	1996	Actin and EF-1[alpha] appear to exist in a complex, because we observed that the two are colocalized, and treatment with cytochalasin D resulted in the redistribution of EF-1[alpa].	Cytochalasin D	121-135	elongation factor 1-alpha	Zea mays	10-20
8647278-7	1996	Upregulation of FAK-YP by activation of G-proteins and PKC was dependent upon intact F-actin, as cytochalasin D abolished stimulation by Mas-7 and by phorbol ester.	Cytochalasin D	97-111	protein tyrosine kinase 2	Rattus norvegicus	16-19
8938986-3	1996	Both cytochalasin D, an inhibitor of microfilament formation, and W7, an inhibitor of calmodulin, inhibited capping of CD3.	Cytochalasin D	5-19	CD3 antigen, epsilon polypeptide	Mus musculus	119-122
8681792-1	1996	We have investigated the role of the actin cytoskeleton during mid-oogenesis and have found that disrupting the actin cytoskeleton with cytochalasin D induces microtubule bundling and microtubule-based cytoplasmic streaming within the oocyte, similar to that which occurs prematurely in cappuccino and spire mutant oocytes.	Cytochalasin D	136-150	cappuccino	Drosophila melanogaster	287-297
8883284-2	1996	Incubation of gel-filtered platelets with increasing concentrations of cytochalasin D resulted in a dose-dependent inhibition of actin polymerization and association of actin-binding proteins with the Triton X-100-insoluble material induced by the thromboxane analogue, U46619, and the thrombin receptor activating peptide, TRAP.	Cytochalasin D	71-85	TRAP	Homo sapiens	324-328
8682873-10	1996	Inhibition of microfilament assembly with cytochalasin D precluded spreading and concomitantly abolished superoxide production and the associated pHi changes, indicating that cytoskeletal reorganization and/or an increase in the number of adherence receptors engaged are required for the responses.	Cytochalasin D	42-56	glucose-6-phosphate isomerase	Homo sapiens	146-149
8737083-4	1996	Acute changes in the actin cytoskeleton by addition of cytochalasin D (CD) activated whole-cell currents in CFTR cells and NRVM.	Cytochalasin D	55-69	CF transmembrane conductance regulator	Homo sapiens	108-112
8645141-5	1996	Cytochalasin D, which selectively disrupts the network of actin filaments, inhibited sphingomyelinase-induced tyrosine phosphorylation of p125FAK and elevation of tyrosine kinase activity in the anti-p125FAK immunoprecipitates.	Cytochalasin D	0-14	PTK2 protein tyrosine kinase 2	Mus musculus	138-145
8645141-5	1996	Cytochalasin D, which selectively disrupts the network of actin filaments, inhibited sphingomyelinase-induced tyrosine phosphorylation of p125FAK and elevation of tyrosine kinase activity in the anti-p125FAK immunoprecipitates.	Cytochalasin D	0-14	PTK2 protein tyrosine kinase 2	Mus musculus	200-207
8737083-4	1996	Acute changes in the actin cytoskeleton by addition of cytochalasin D (CD) activated whole-cell currents in CFTR cells and NRVM.	Cytochalasin D	71-73	CF transmembrane conductance regulator	Homo sapiens	108-112
8737083-7	1996	Incubation of CFTR cells and NRVM with CD for over 6 h prevented CFTR activation either by the cAMP pathway under whole-cell conditions or by PKA under excised inside-out conditions.	Cytochalasin D	39-41	CF transmembrane conductance regulator	Homo sapiens	14-18
8737083-7	1996	Incubation of CFTR cells and NRVM with CD for over 6 h prevented CFTR activation either by the cAMP pathway under whole-cell conditions or by PKA under excised inside-out conditions.	Cytochalasin D	39-41	CF transmembrane conductance regulator	Homo sapiens	65-69
8609175-7	1996	When a mechanical stress was applied to H18/7-coated ferromagnetic beads bound to the surface of IL-1 beta-activated HUVEC, using a magnetical twisting cytometer, the observed resistance to the applied stress was inhibited by cytochalasin D, thus demonstrating transmembrane cytoskeletal mechanical linkage.	Cytochalasin D	226-240	interleukin 1 beta	Homo sapiens	97-106
8735589-15	1996	It resembles cytochalasin D in selectively inducing an activated form of gelatinase A in peritubular cells.	Cytochalasin D	13-27	matrix metallopeptidase 2	Rattus norvegicus	73-85
8612695-5	1996	Interestingly, culture conditions which indirectly perturb cell-cell contacts, such as low Ca2+ or incubation with cytoskeleton disrupting agents such as nocodazole or cytochalasin D, prevented the expression of stathmin in C2 cells even at high density.	Cytochalasin D	168-182	stathmin 1	Mus musculus	212-220
8743194-6	1996	Cytochalasin D completely inhibited protein tyrosine phosphorylation and p72syk activation.	Cytochalasin D	0-14	spleen associated tyrosine kinase	Homo sapiens	73-79
8626373-8	1996	In contrast, cytochalasin D eliminated neurite outgrowth, cell spreading, and the tyrosine phosphorylation of paxillin and focal adhesion kinase.	Cytochalasin D	13-27	paxillin	Homo sapiens	110-118
8631492-9	1996	The decrease in eIF-4C expression, however, does not require cytokinesis or mitosis, since it occurs when 2-cell embryos are cultured in the presence of cytochalasin D or nocodazole, respectively.	Cytochalasin D	153-167	eukaryotic translation initiation factor 1A, X-linked	Mus musculus	16-22
8704107-9	1996	Cytochalasin D blocked the ability of thrombin to restore focal adhesions and phosphorylate p125FAK.	Cytochalasin D	0-14	coagulation factor II, thrombin	Homo sapiens	38-46
8704107-9	1996	Cytochalasin D blocked the ability of thrombin to restore focal adhesions and phosphorylate p125FAK.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	92-99
8852373-3	1996	After subsequent treatment with 5 micrograms/ml cytochalasin D (a reagent that depolymerizes actin filaments), MTI-5 cells maintained their shape, while cells of a drebrin-negative cell line, MTI-11, formed retraction processes.	Cytochalasin D	48-62	drebrin 1	Mus musculus	164-171
8852373-6	1996	In MTI-5 cells, adhesion plaques that were resistant to treatment with cytochalasin D appeared upon expression of drebrin.	Cytochalasin D	71-85	drebrin 1	Mus musculus	114-121
8611170-2	1996	Rat kidney mesangial cells secrete predominantly latent gelatinase A that can be activated following treatment with cytochalasin D.	Cytochalasin D	116-130	matrix metallopeptidase 2	Rattus norvegicus	56-68
8741843-2	1996	We report here that disrupting the cytoskeleton in normal human fibroblasts causes the same cell cycle phenotype that is observed after blocking cell adhesion: suspended cells and cytochalasin D-treated monolayers fail to progress through G1 despite normal mitogen-induced expression of c-myc mRNA.	Cytochalasin D	180-194	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	287-292
8620337-7	1996	Cytochalasin D, an inhibitor of actin polymerization, inhibited the inhomogeneous increase or redistribution of F-actin and GPIIb-IIIa but did not inhibit the rise in mean [Ca2+]i.	Cytochalasin D	0-14	integrin subunit alpha 2b	Homo sapiens	124-129
8913639-13	1996	Anti-p73 Western blotting reveals that nanomolar concentrations of CD are capable of selectively eluting p73 and ezrin from beta actin Sepharose 4B, indicating that p73 binds beta actin via the barbed end.	Cytochalasin D	67-69	transformation related protein 73	Mus musculus	5-8
8913639-13	1996	Anti-p73 Western blotting reveals that nanomolar concentrations of CD are capable of selectively eluting p73 and ezrin from beta actin Sepharose 4B, indicating that p73 binds beta actin via the barbed end.	Cytochalasin D	67-69	transformation related protein 73	Mus musculus	105-108
8913639-13	1996	Anti-p73 Western blotting reveals that nanomolar concentrations of CD are capable of selectively eluting p73 and ezrin from beta actin Sepharose 4B, indicating that p73 binds beta actin via the barbed end.	Cytochalasin D	67-69	transformation related protein 73	Mus musculus	105-108
8647902-4	1996	Tyrosine phosphorylation of PDGF beta-receptors induced by plating on collagen type I was inhibited by cytochalasin D and herbimycin A, unaffected by cycloheximide and enhanced by orthovanadate.	Cytochalasin D	103-117	platelet derived growth factor subunit B	Homo sapiens	28-32
7589239-8	1995	Downregulation of p125FAK tyrosine phosphorylation is observed by treating cells with cytochalasin D (CD), a drug known to rapidly disrupt the actin cytoskeleton.	Cytochalasin D	86-100	protein tyrosine kinase 2	Homo sapiens	18-25
8788939-2	1995	Cytochalasin D (CD; 5 microM) readily stimulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel activity in cell-attached and whole-cell patch recordings from 3T3 fibroblasts expressing recombinant CFTR but not in mock-transfected cells.	Cytochalasin D	0-14	cystic fibrosis transmembrane conductance regulator	Mus musculus	49-100
8788939-2	1995	Cytochalasin D (CD; 5 microM) readily stimulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel activity in cell-attached and whole-cell patch recordings from 3T3 fibroblasts expressing recombinant CFTR but not in mock-transfected cells.	Cytochalasin D	0-14	cystic fibrosis transmembrane conductance regulator	Mus musculus	102-106
8788939-2	1995	Cytochalasin D (CD; 5 microM) readily stimulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel activity in cell-attached and whole-cell patch recordings from 3T3 fibroblasts expressing recombinant CFTR but not in mock-transfected cells.	Cytochalasin D	0-14	cystic fibrosis transmembrane conductance regulator	Mus musculus	222-226
8788939-2	1995	Cytochalasin D (CD; 5 microM) readily stimulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel activity in cell-attached and whole-cell patch recordings from 3T3 fibroblasts expressing recombinant CFTR but not in mock-transfected cells.	Cytochalasin D	16-18	cystic fibrosis transmembrane conductance regulator	Mus musculus	49-100
8788939-2	1995	Cytochalasin D (CD; 5 microM) readily stimulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel activity in cell-attached and whole-cell patch recordings from 3T3 fibroblasts expressing recombinant CFTR but not in mock-transfected cells.	Cytochalasin D	16-18	cystic fibrosis transmembrane conductance regulator	Mus musculus	102-106
8788939-2	1995	Cytochalasin D (CD; 5 microM) readily stimulated cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channel activity in cell-attached and whole-cell patch recordings from 3T3 fibroblasts expressing recombinant CFTR but not in mock-transfected cells.	Cytochalasin D	16-18	cystic fibrosis transmembrane conductance regulator	Mus musculus	222-226
8788939-6	1995	To elucidate the mechanism of action of CD we tested its effects on cAMP, protein kinase A, and the CFTR itself during CD stimulation.	Cytochalasin D	40-42	cystic fibrosis transmembrane conductance regulator	Mus musculus	100-104
8788939-15	1995	We conclude that the stimulatory effect of CD is cAMP independent, but needs a functional protein kinase A in order to activate the CFTR.	Cytochalasin D	43-45	cystic fibrosis transmembrane conductance regulator	Mus musculus	132-136
8788939-16	1995	We propose that cytochalasin D activates CFTR by releasing a cellular inhibitor, e.g. a phosphatase, that is held in place by F-actin.	Cytochalasin D	16-30	cystic fibrosis transmembrane conductance regulator	Mus musculus	41-45
7589239-8	1995	Downregulation of p125FAK tyrosine phosphorylation is observed by treating cells with cytochalasin D (CD), a drug known to rapidly disrupt the actin cytoskeleton.	Cytochalasin D	102-104	protein tyrosine kinase 2	Homo sapiens	18-25
7589239-9	1995	When PTPase inhibitors are added in combination to CD, the level of tyrosine phosphorylation of p125FAK remains high and focal adhesions and actin stress fibers are preserved from the CD-mediated disruption.	Cytochalasin D	51-53	protein tyrosine kinase 2	Homo sapiens	96-103
7643084-3	1995	We now report that cytochalasin D, a compound that depolymerizes actin microfilaments selectively, protects cultured rat hippocampal neurons against A beta neurotoxicity.	Cytochalasin D	19-33	amyloid beta precursor protein	Rattus norvegicus	149-155
7556524-7	1995	FAK phosphorylation in BCR-ABL-expressing cells was inhibited in a dose-dependent manner by cytochalasin D, a reagent that disrupts the intracellular network of actin filaments.	Cytochalasin D	92-106	protein tyrosine kinase 2	Homo sapiens	0-3
7556524-7	1995	FAK phosphorylation in BCR-ABL-expressing cells was inhibited in a dose-dependent manner by cytochalasin D, a reagent that disrupts the intracellular network of actin filaments.	Cytochalasin D	92-106	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	23-30
8575462-7	1995	Disintegration of microfilaments by cytochalasin D hampered this specific cell surface rearrangement of neurothelin, whereas depolymerization of microtubules by demecolcine had no effect.	Cytochalasin D	36-50	basigin (Ok blood group)	Gallus gallus	104-115
23282387-8	1995	The action of GROa was independent of cytochalasin D, staurosporine, and pertussis toxin but was inhibited by sodium azide and cycloheximide.	Cytochalasin D	38-52	C-X-C motif chemokine ligand 1	Homo sapiens	14-18
7667304-8	1995	Disorganization of F-actin filaments with cytochalasin D preserved G alpha q/G alpha 11 and F-actin colocalization but partially inhibited vasopressin- and fluoroaluminate-sensitive phospholipase C activity, suggesting that actin-associated G alpha q/G alpha 11 proteins play a role in signal transduction.	Cytochalasin D	42-56	G protein subunit alpha q	Rattus norvegicus	67-76
7667304-8	1995	Disorganization of F-actin filaments with cytochalasin D preserved G alpha q/G alpha 11 and F-actin colocalization but partially inhibited vasopressin- and fluoroaluminate-sensitive phospholipase C activity, suggesting that actin-associated G alpha q/G alpha 11 proteins play a role in signal transduction.	Cytochalasin D	42-56	G protein subunit alpha 11	Rattus norvegicus	77-87
7667304-8	1995	Disorganization of F-actin filaments with cytochalasin D preserved G alpha q/G alpha 11 and F-actin colocalization but partially inhibited vasopressin- and fluoroaluminate-sensitive phospholipase C activity, suggesting that actin-associated G alpha q/G alpha 11 proteins play a role in signal transduction.	Cytochalasin D	42-56	G protein subunit alpha q	Rattus norvegicus	241-250
7667304-8	1995	Disorganization of F-actin filaments with cytochalasin D preserved G alpha q/G alpha 11 and F-actin colocalization but partially inhibited vasopressin- and fluoroaluminate-sensitive phospholipase C activity, suggesting that actin-associated G alpha q/G alpha 11 proteins play a role in signal transduction.	Cytochalasin D	42-56	G protein subunit alpha 11	Rattus norvegicus	251-261
7541794-8	1995	In adhering cells, pre-treatment with cytochalasin D suppresses tyrosine phosphorylation of FAK and paxillin but not of Syk, while IL-1 beta message induction is unaffected.	Cytochalasin D	38-52	protein tyrosine kinase 2	Homo sapiens	92-95
7541942-3	1995	The actin filament disrupter cytochalasin D (CD; approximately 5 micrograms/ml) readily activated whole cell currents in CFTR but not in mock-transfected (MOCK) cells.	Cytochalasin D	29-43	CF transmembrane conductance regulator	Homo sapiens	121-125
7542276-11	1995	Pretreating PMNs with cytochalasin D before activation prevented the change in cell shape, the redistribution of binding sites for P-selectin-coated beads, and the decrease in cellular adhesiveness for P-selectin.	Cytochalasin D	22-36	selectin P	Homo sapiens	131-141
7542276-11	1995	Pretreating PMNs with cytochalasin D before activation prevented the change in cell shape, the redistribution of binding sites for P-selectin-coated beads, and the decrease in cellular adhesiveness for P-selectin.	Cytochalasin D	22-36	selectin P	Homo sapiens	202-212
7631807-8	1995	NKA-stimulated migration was both chemokinetic and chemotactic, and it could be blocked by inhibition of protein synthesis with cyclohexamide, inhibition of microtubular function with colchicine, or inhibition of actin microfilament elongation with cytochalasin D.	Cytochalasin D	249-263	tachykinin precursor 1	Homo sapiens	0-3
7541942-3	1995	The actin filament disrupter cytochalasin D (CD; approximately 5 micrograms/ml) readily activated whole cell currents in CFTR but not in mock-transfected (MOCK) cells.	Cytochalasin D	45-47	CF transmembrane conductance regulator	Homo sapiens	121-125
7541942-7	1995	Incubation of CFTR cells with CD (approximately 15 micrograms/ml) for > 6 h prevented CFTR activation by the addition of either 8-bromoadenosine 3",5"-cyclic monophosphate plus forskolin under whole cell conditions or PKA under excised inside-out conditions.	Cytochalasin D	30-32	CF transmembrane conductance regulator	Homo sapiens	14-18
7541942-7	1995	Incubation of CFTR cells with CD (approximately 15 micrograms/ml) for > 6 h prevented CFTR activation by the addition of either 8-bromoadenosine 3",5"-cyclic monophosphate plus forskolin under whole cell conditions or PKA under excised inside-out conditions.	Cytochalasin D	30-32	CF transmembrane conductance regulator	Homo sapiens	89-93
7790902-8	1995	Depolymerization of microfilaments by cytochalasin D in contrast generated smaller clusters of increased gephyrin density.	Cytochalasin D	38-52	gephyrin	Rattus norvegicus	105-113
7538126-7	1995	Cytochalasin D blocked relocation of both PTP1B and PTP1C but not PTP1B cleavage.	Cytochalasin D	0-14	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	42-47
7538126-7	1995	Cytochalasin D blocked relocation of both PTP1B and PTP1C but not PTP1B cleavage.	Cytochalasin D	0-14	protein tyrosine phosphatase non-receptor type 6	Homo sapiens	52-57
7799959-9	1995	Moreover, in cells treated with cytochalasin D, wild-type HSP27 but not the phosphorylated form of HSP27 accelerated the reappearance of actin filaments.	Cytochalasin D	32-46	heat shock protein family B (small) member 1	Homo sapiens	58-63
7887903-1	1995	Expression of the rat p52(PAI-1) gene is positively regulated by agents that influence cellular microfilament organization and/or cell-to-substrate adhesion [e.g. cytochalasin D (CD) and sodium n-butyrate (NaB)] [Higgins, Chaudhari and Ryan (1991) Biochem.	Cytochalasin D	163-177	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	22-25
7887903-1	1995	Expression of the rat p52(PAI-1) gene is positively regulated by agents that influence cellular microfilament organization and/or cell-to-substrate adhesion [e.g. cytochalasin D (CD) and sodium n-butyrate (NaB)] [Higgins, Chaudhari and Ryan (1991) Biochem.	Cytochalasin D	163-177	serpin family E member 1	Rattus norvegicus	26-31
7887903-1	1995	Expression of the rat p52(PAI-1) gene is positively regulated by agents that influence cellular microfilament organization and/or cell-to-substrate adhesion [e.g. cytochalasin D (CD) and sodium n-butyrate (NaB)] [Higgins, Chaudhari and Ryan (1991) Biochem.	Cytochalasin D	179-181	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	22-25
7887903-1	1995	Expression of the rat p52(PAI-1) gene is positively regulated by agents that influence cellular microfilament organization and/or cell-to-substrate adhesion [e.g. cytochalasin D (CD) and sodium n-butyrate (NaB)] [Higgins, Chaudhari and Ryan (1991) Biochem.	Cytochalasin D	179-181	serpin family E member 1	Rattus norvegicus	26-31
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	Cytochalasin D	11-13	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	37-40
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	Cytochalasin D	11-13	serpin family E member 1	Rattus norvegicus	41-46
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	Cytochalasin D	11-13	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	92-95
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	Cytochalasin D	11-13	serpin family E member 1	Rattus norvegicus	96-101
7769014-7	1995	Treatment with cytochalasin D drastically increased the shock sensitivity of myotubes and abolished the difference between dystrophin-less and control cells.	Cytochalasin D	15-29	dystrophin, muscular dystrophy	Mus musculus	123-133
7738118-8	1995	Treatment of Pam cells with cytochalasin D caused aggregation of caveolae where PM InsP3R-L as well as F-actin and fodrin were localized.	Cytochalasin D	28-42	inositol 1,4,5-trisphosphate receptor 1	Mus musculus	83-89
7733965-6	1995	Pretreatment of the B cells with cytochalasin D or botulinum C2 toxin, microfilament-disrupting agents, prevented the increases in F-actin content as well as MAPK and p90rsk activation.	Cytochalasin D	33-47	ribosomal protein S6 kinase A1	Homo sapiens	167-173
7542259-9	1995	However, cytochalasin D pretreatment blocks both the EGF-induced ZO-1 rearrangement and tyrosine phosphorylation, suggesting that these responses are dependent on an intact actin microfilament system.	Cytochalasin D	9-23	tight junction protein 1	Homo sapiens	65-69
7887903-9	1995	Pretreatment with cycloheximide (CX) markedly attenuated NaB- and/or CD-stimulated p52(PAI-1) expression.	Cytochalasin D	69-71	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	83-86
7887903-9	1995	Pretreatment with cycloheximide (CX) markedly attenuated NaB- and/or CD-stimulated p52(PAI-1) expression.	Cytochalasin D	69-71	serpin family E member 1	Rattus norvegicus	87-92
7887903-12	1995	Full stimulation of p52(PAI-1) expression in KNRK cells in response to the shape modulators NaB and/or CD involves transcriptional activation of the p52(PAI-1) gene, requires de novo RNA synthesis and occurs through a secondary-response (i.e. protein-synthesis-dependent) pathway.	Cytochalasin D	103-105	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	20-23
7887903-12	1995	Full stimulation of p52(PAI-1) expression in KNRK cells in response to the shape modulators NaB and/or CD involves transcriptional activation of the p52(PAI-1) gene, requires de novo RNA synthesis and occurs through a secondary-response (i.e. protein-synthesis-dependent) pathway.	Cytochalasin D	103-105	serpin family E member 1	Rattus norvegicus	24-29
7887903-12	1995	Full stimulation of p52(PAI-1) expression in KNRK cells in response to the shape modulators NaB and/or CD involves transcriptional activation of the p52(PAI-1) gene, requires de novo RNA synthesis and occurs through a secondary-response (i.e. protein-synthesis-dependent) pathway.	Cytochalasin D	103-105	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	149-152
7887903-12	1995	Full stimulation of p52(PAI-1) expression in KNRK cells in response to the shape modulators NaB and/or CD involves transcriptional activation of the p52(PAI-1) gene, requires de novo RNA synthesis and occurs through a secondary-response (i.e. protein-synthesis-dependent) pathway.	Cytochalasin D	103-105	serpin family E member 1	Rattus norvegicus	153-158
7612963-6	1995	Cytochalasin D blocked the activation of MAP kinase activity that was induced by the binding of cells to fibronectin.	Cytochalasin D	0-14	fibronectin 1	Mus musculus	105-116
8608610-9	1995	Despite morphologically similar perturbations of actin organization in follicular cultures treated with cytochalasin D, junctional staining of ZO-1 and E-cadherin was preserved and cells remained adherent to one another.	Cytochalasin D	104-118	cadherin 1	Homo sapiens	152-162
7806502-4	1994	Furthermore, the early phase of p72syk translocation (within 60 s) was significantly inhibited with cytochalasin D, whereas the late phase of p72syk translocation (after 90 s) was completely inhibited with RGDS tetrapeptide treatment.	Cytochalasin D	100-114	spleen associated tyrosine kinase	Homo sapiens	32-38
7862107-2	1994	We investigated the effects of cytochalasin D, a fungal metabolite that binds to actin and disrupts the microfilament structure, on insulin-induced expression of glucokinase mRNA in rat hepatocyte cultures.	Cytochalasin D	31-45	glucokinase	Rattus norvegicus	162-173
7961991-8	1994	The inhibitory effect of cytochalasin D treatment on the insulin stimulation of glucose transport occurred downstream of tyrosine phosphorylation of the insulin receptor substrate-1 and of binding of phosphatidylinositol 3-kinase to the insulin receptor substrate-1.	Cytochalasin D	25-39	insulin receptor substrate 1	Rattus norvegicus	153-181
7961991-8	1994	The inhibitory effect of cytochalasin D treatment on the insulin stimulation of glucose transport occurred downstream of tyrosine phosphorylation of the insulin receptor substrate-1 and of binding of phosphatidylinositol 3-kinase to the insulin receptor substrate-1.	Cytochalasin D	25-39	insulin receptor substrate 1	Rattus norvegicus	237-265
7862107-3	1994	Cytochalasin-D significantly potentiates insulin-induced glucokinase mRNA expression at 100 nM concentration but counteracts glucokinase expression at 2-20 microM.	Cytochalasin D	0-14	glucokinase	Rattus norvegicus	57-68
7862107-3	1994	Cytochalasin-D significantly potentiates insulin-induced glucokinase mRNA expression at 100 nM concentration but counteracts glucokinase expression at 2-20 microM.	Cytochalasin D	0-14	glucokinase	Rattus norvegicus	125-136
7512933-2	1994	Translocation of the enzyme became maximal within 1-2 min of thrombin stimulation and was suppressed by cytochalasin D or upon inhibition of aggregation.	Cytochalasin D	104-118	coagulation factor II, thrombin	Homo sapiens	61-69
7816555-6	1994	Similar changes were produced in the absence of a transmembrane osmotic gradient by 500 nM intracellular cytochalasin D (gCl = 34.3 +/- 10.3 microS/cm2; n = 6) or 12.5 microM colchicine (gCl = 15.4 +/- 1.4 microS/cm2; n = 5).	Cytochalasin D	105-119	germ cell-less 2, spermatogenesis associated	Homo sapiens	121-124
7913666-0	1994	Cytochalasin D modulates CD4 crosslinking sensitive mitogenic signal in T lymphocytes.	Cytochalasin D	0-14	CD4 molecule	Homo sapiens	25-28
7514181-11	1994	Cytochalasin D, an inhibitor of actin polymerization, blocked FAK phosphorylation under all these conditions.	Cytochalasin D	0-14	protein tyrosine kinase 2	Homo sapiens	62-65
8290249-7	1994	The redistribution of neurofibromin coincided both spatially and temporally with the relocalization of crosslinked slg and was inhibited by the cytoskeletal disrupting agents colchicine and cytochalasin D.	Cytochalasin D	190-204	neurofibromin 1	Homo sapiens	22-35
7514713-6	1994	Furthermore, the increase in rG-CSF binding sites due to histamine treatment seemed to take place in association with the externalization of G-CSF receptors, because 1) the binding increase was observed in the presence of cycloheximide, 2) no concomitant increase in [3H]leucine uptake was elicited, and 3) colchicine and cytochalasin D effectively prevented the increase in rG-CSF binding due to histamine.	Cytochalasin D	322-336	colony stimulating factor 3	Rattus norvegicus	29-35
7514713-6	1994	Furthermore, the increase in rG-CSF binding sites due to histamine treatment seemed to take place in association with the externalization of G-CSF receptors, because 1) the binding increase was observed in the presence of cycloheximide, 2) no concomitant increase in [3H]leucine uptake was elicited, and 3) colchicine and cytochalasin D effectively prevented the increase in rG-CSF binding due to histamine.	Cytochalasin D	322-336	colony stimulating factor 3	Rattus norvegicus	30-35
8138587-0	1994	Induced expression of p52(PAI-1) in normal rat kidney cells by the microfilament-disrupting agent cytochalasin D. In established normal rat kidney (NRK) cells, synthesis of the 52 kDa type-1 inhibitor of plasminogen activator [p52(PAI-1)] is stimulated by the cell shape-modulating fungal metabolite cytochalasin D (CD).	Cytochalasin D	98-112	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	22-25
8138587-0	1994	Induced expression of p52(PAI-1) in normal rat kidney cells by the microfilament-disrupting agent cytochalasin D. In established normal rat kidney (NRK) cells, synthesis of the 52 kDa type-1 inhibitor of plasminogen activator [p52(PAI-1)] is stimulated by the cell shape-modulating fungal metabolite cytochalasin D (CD).	Cytochalasin D	98-112	serpin family E member 1	Rattus norvegicus	26-31
8138587-0	1994	Induced expression of p52(PAI-1) in normal rat kidney cells by the microfilament-disrupting agent cytochalasin D. In established normal rat kidney (NRK) cells, synthesis of the 52 kDa type-1 inhibitor of plasminogen activator [p52(PAI-1)] is stimulated by the cell shape-modulating fungal metabolite cytochalasin D (CD).	Cytochalasin D	316-318	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	22-25
8138587-0	1994	Induced expression of p52(PAI-1) in normal rat kidney cells by the microfilament-disrupting agent cytochalasin D. In established normal rat kidney (NRK) cells, synthesis of the 52 kDa type-1 inhibitor of plasminogen activator [p52(PAI-1)] is stimulated by the cell shape-modulating fungal metabolite cytochalasin D (CD).	Cytochalasin D	316-318	serpin family E member 1	Rattus norvegicus	26-31
8138587-4	1994	CD-induced p52(PAI-1) expression occurred efficiently in quiescent NRK cells maintained under serum-free conditions as well as in fully serum-supplemented actively growing cultures.	Cytochalasin D	0-2	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	11-14
8138587-4	1994	CD-induced p52(PAI-1) expression occurred efficiently in quiescent NRK cells maintained under serum-free conditions as well as in fully serum-supplemented actively growing cultures.	Cytochalasin D	0-2	serpin family E member 1	Rattus norvegicus	15-20
8138587-6	1994	Long-term (24 h) exposure of NRK/CD cells to 8-bromo-cAMP did result in an approximately 34% reduction in stimulated p52(PAI-1) expression, however, levels expressed by NRK/CD+cAMP populations remained markedly elevated relative to control values.	Cytochalasin D	33-35	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	117-120
8138587-6	1994	Long-term (24 h) exposure of NRK/CD cells to 8-bromo-cAMP did result in an approximately 34% reduction in stimulated p52(PAI-1) expression, however, levels expressed by NRK/CD+cAMP populations remained markedly elevated relative to control values.	Cytochalasin D	33-35	serpin family E member 1	Rattus norvegicus	121-126
8077255-7	1994	Furthermore, cytochalasin D, which inhibits actin polymerization, showed a marked inhibitory effect on oxygen consumption in the RGDS-carrying microsphere system, as compared with those in other systems.	Cytochalasin D	13-27	ral guanine nucleotide dissociation stimulator	Homo sapiens	129-133
7508894-7	1994	The microfilament-disrupter cytochalasin D was shown to enhance the basal and calcitonin-induced production of PTHrP.	Cytochalasin D	28-42	parathyroid hormone like hormone	Homo sapiens	111-116
8068874-7	1994	Cytochalasin D treatment of mesangial cells reduces TIMP-2 expression.	Cytochalasin D	0-14	TIMP metallopeptidase inhibitor 2	Rattus norvegicus	52-58
8068874-9	1994	It was concluded that cytochalasin D-induced cytoskeletal disruption in mesangial cells may activate procollagenase IV by inhibiting TIMP-2 expression and that there is a concanavalin A-binding site on mesangial cells that is part of a transmembrane signaling system altering mesangial cell cytoskeletal organization and metalloproteinase secretion and activation.	Cytochalasin D	22-36	TIMP metallopeptidase inhibitor 2	Rattus norvegicus	133-139
8290249-7	1994	The redistribution of neurofibromin coincided both spatially and temporally with the relocalization of crosslinked slg and was inhibited by the cytoskeletal disrupting agents colchicine and cytochalasin D.	Cytochalasin D	190-204	sialic acid binding Ig like lectin 12	Homo sapiens	115-118
8276872-7	1994	Cytochalasin D, which disrupts the actin cytoskeleton, completely inhibited the tyrosine phosphorylation of p125FAK and paxillin by PDGF.	Cytochalasin D	0-14	PTK2 protein tyrosine kinase 2	Mus musculus	108-115
8308054-13	1993	In cells cultured with cytochalasin D (CD) and laminin the actin cortical mat was not reorganized.	Cytochalasin D	23-37	actin, beta	Gallus gallus	59-64
7954857-0	1994	Coordinated expression of five tropomyosin isoforms and beta-actin in astrocytes treated with dibutyryl cAMP and cytochalasin D.	Cytochalasin D	113-127	POTE ankyrin domain family member F	Homo sapiens	56-66
7954857-7	1994	The decrease in beta-actin mRNA concentration was not blocked by cycloheximide, whereas down-regulation of tropomyosin transcripts was completely reversed when protein synthesis was inhibited, and (3) cytochalasin D induced an increase in the concentration of tropomyosin transcripts (+69 to 185%) which was cumulative with serum stimulation.	Cytochalasin D	201-215	POTE ankyrin domain family member F	Homo sapiens	16-26
7954857-8	1994	Cytochalasin D induction of both beta-actin and TM-4 operated through transcriptional activation, independent of protein synthesis.	Cytochalasin D	0-14	POTE ankyrin domain family member F	Homo sapiens	33-43
7901227-10	1993	In rat liver hepatocytes, different culture conditions, as well as drugs such as cytochalasin D and colchicine, appear to affect the level of the class II Pgp gene expression.	Cytochalasin D	81-95	ATP-binding cassette, subfamily B (MDR/TAP), member 1B	Rattus norvegicus	155-158
8308054-18	1993	This study is the first to demonstrate that CD-aggregated F-actin does not capture the alpha-actinin.	Cytochalasin D	44-46	actin, beta	Gallus gallus	60-65
8104997-6	1993	Cytoskeletal interactions also regulate CD4/class II adhesion as treatment with the microtubule and microfilament inhibitors colchicine, cytochalasin-D, and nocodazole rapidly dissociates even preformed cell conjugates.	Cytochalasin D	137-151	CD4 molecule	Homo sapiens	40-43
7904268-6	1993	Cytochalasin D (10(-4) M) stimulated CD18 expression even though it inhibited shape changes.	Cytochalasin D	0-14	integrin subunit beta 2	Homo sapiens	37-41
7904268-8	1993	Experiments with colchicine, nocodazole, 2H2O and cytochalasin D suggest that microtubules as well as microfilaments modulate surface expression of CD18.	Cytochalasin D	50-64	integrin subunit beta 2	Homo sapiens	148-152
8409756-7	1993	The suppressive effect of CD on TNF production was confirmed by the observation that TNF-alpha mRNA expression was also inhibited by CD.	Cytochalasin D	26-28	tumor necrosis factor	Mus musculus	85-94
8409756-7	1993	The suppressive effect of CD on TNF production was confirmed by the observation that TNF-alpha mRNA expression was also inhibited by CD.	Cytochalasin D	133-135	tumor necrosis factor	Mus musculus	32-35
8409756-0	1993	Cytochalasin D inhibits lipopolysaccharide-induced tumor necrosis factor production in macrophages.	Cytochalasin D	0-14	tumor necrosis factor	Mus musculus	51-72
8409756-7	1993	The suppressive effect of CD on TNF production was confirmed by the observation that TNF-alpha mRNA expression was also inhibited by CD.	Cytochalasin D	133-135	tumor necrosis factor	Mus musculus	85-94
8409756-9	1993	These effects of CD were observed only when CD was added within the first 20 min after LPS stimulation.	Cytochalasin D	17-19	toll-like receptor 4	Mus musculus	87-90
8409756-4	1993	To investigate this, we studied the effect of cytochalasin D (CD), which inhibits reorganization of microfilaments, on LPS-induced tumor necrosis factor (TNF) production.	Cytochalasin D	46-60	toll-like receptor 4	Mus musculus	119-122
8409756-4	1993	To investigate this, we studied the effect of cytochalasin D (CD), which inhibits reorganization of microfilaments, on LPS-induced tumor necrosis factor (TNF) production.	Cytochalasin D	46-60	tumor necrosis factor	Mus musculus	131-152
8409756-9	1993	These effects of CD were observed only when CD was added within the first 20 min after LPS stimulation.	Cytochalasin D	44-46	toll-like receptor 4	Mus musculus	87-90
8409756-10	1993	These results suggest that the CD-sensitive microfilament response is essential in the signaling pathway for the production of certain monokines in LPS-stimulated macrophages.	Cytochalasin D	31-33	toll-like receptor 4	Mus musculus	148-151
8409756-4	1993	To investigate this, we studied the effect of cytochalasin D (CD), which inhibits reorganization of microfilaments, on LPS-induced tumor necrosis factor (TNF) production.	Cytochalasin D	46-60	tumor necrosis factor	Mus musculus	154-157
8509453-4	1993	The cytoskeletal association of GPIIb-IIIa is independent of platelet aggregation and fibrin sedimentation and is sensitive to cytochalasin D treatment.	Cytochalasin D	127-141	integrin subunit alpha 2b	Homo sapiens	32-37
8409756-4	1993	To investigate this, we studied the effect of cytochalasin D (CD), which inhibits reorganization of microfilaments, on LPS-induced tumor necrosis factor (TNF) production.	Cytochalasin D	62-64	toll-like receptor 4	Mus musculus	119-122
8409756-4	1993	To investigate this, we studied the effect of cytochalasin D (CD), which inhibits reorganization of microfilaments, on LPS-induced tumor necrosis factor (TNF) production.	Cytochalasin D	62-64	tumor necrosis factor	Mus musculus	131-152
8409756-4	1993	To investigate this, we studied the effect of cytochalasin D (CD), which inhibits reorganization of microfilaments, on LPS-induced tumor necrosis factor (TNF) production.	Cytochalasin D	62-64	tumor necrosis factor	Mus musculus	154-157
8409756-6	1993	When this concentration of CD was added after LPS stimulation, microfilament reorganization and TNF production were inhibited.	Cytochalasin D	27-29	toll-like receptor 4	Mus musculus	46-49
8409756-6	1993	When this concentration of CD was added after LPS stimulation, microfilament reorganization and TNF production were inhibited.	Cytochalasin D	27-29	tumor necrosis factor	Mus musculus	96-99
8409756-7	1993	The suppressive effect of CD on TNF production was confirmed by the observation that TNF-alpha mRNA expression was also inhibited by CD.	Cytochalasin D	26-28	tumor necrosis factor	Mus musculus	32-35
8314789-9	1993	In contrast, cytochalasin D, an agent which selectively disrupts the network of actin microfilaments, completely inhibited bombesin- and PDB-induced p125FAK tyrosine phosphorylation.	Cytochalasin D	13-27	PTK2 protein tyrosine kinase 2	Mus musculus	149-156
8243205-8	1993	Cytochalasin D efficiently inhibited the disappearance of electroinserted glycophorin A during the first 2 h after electroinsertion only.	Cytochalasin D	0-14	glycophorin A (MNS blood group)	Homo sapiens	74-87
8223720-4	1993	Cytochalasin D, known to inhibit the increase in F-actin after thrombin, also inhibits the fall in T beta 4-actin complex and the increase in nucleation sites.	Cytochalasin D	0-14	coagulation factor II, thrombin	Homo sapiens	63-71
8223720-4	1993	Cytochalasin D, known to inhibit the increase in F-actin after thrombin, also inhibits the fall in T beta 4-actin complex and the increase in nucleation sites.	Cytochalasin D	0-14	thymosin beta 4 X-linked	Homo sapiens	99-107
7680961-5	1993	Treatment with cytochalasin D (an agent that inhibits microfilament polymerization) but not colchicine (an agent that inhibits microtubule polymerization) reproduced the effect of TPA on the mAb-induced modulation of CD2, CD3, and CD5.	Cytochalasin D	15-29	CD2 molecule	Homo sapiens	217-220
7680961-5	1993	Treatment with cytochalasin D (an agent that inhibits microfilament polymerization) but not colchicine (an agent that inhibits microtubule polymerization) reproduced the effect of TPA on the mAb-induced modulation of CD2, CD3, and CD5.	Cytochalasin D	15-29	CD5 molecule	Homo sapiens	231-234
8318952-4	1993	At the same time, the disassembly of actin microfilaments by cytochalasin D results also in the disappearance of eEF-2- carrying threads.	Cytochalasin D	61-75	eukaryotic translation elongation factor 2	Homo sapiens	113-118
1471975-1	1992	The microfilament-disrupting agent cytochalasin D (CD) increased (by 10-22-fold) the synthesis de novo and extracellular matrix deposition of plasminogen-activator inhibitor type-1 [p52(PAI-1)] in normal rat kidney (NRK) cells.	Cytochalasin D	35-49	serpin family E member 2	Rattus norvegicus	142-180
8482333-2	1993	We have previously shown that disruption of MFs with cytochalasin D (CD) induced beta-actin gene transcription, resulting in elevated levels of beta-actin mRNA and protein synthesis.	Cytochalasin D	53-67	actin, beta	Mus musculus	81-91
8482333-2	1993	We have previously shown that disruption of MFs with cytochalasin D (CD) induced beta-actin gene transcription, resulting in elevated levels of beta-actin mRNA and protein synthesis.	Cytochalasin D	53-67	actin, beta	Mus musculus	144-154
8482333-2	1993	We have previously shown that disruption of MFs with cytochalasin D (CD) induced beta-actin gene transcription, resulting in elevated levels of beta-actin mRNA and protein synthesis.	Cytochalasin D	69-71	actin, beta	Mus musculus	81-91
8482333-2	1993	We have previously shown that disruption of MFs with cytochalasin D (CD) induced beta-actin gene transcription, resulting in elevated levels of beta-actin mRNA and protein synthesis.	Cytochalasin D	69-71	actin, beta	Mus musculus	144-154
8482333-4	1993	These CD-induced responses were reversible since recovering cells progressed through the G2 phase and resumed normal growth while beta-actin mRNA and protein synthesis rapidly returned to control levels.	Cytochalasin D	6-8	actin, beta	Mus musculus	130-140
8482333-6	1993	CD induces beta- and gamma-actin mRNA in a dose-dependent manner, reaching a maximum of 20-fold over control mRNA levels at 30 microM.	Cytochalasin D	0-2	actin, beta	Mus musculus	11-32
8482333-7	1993	beta- and gamma-Actin gene expression was also induced 5-fold by serum stimulation of quiescent murine erythroleukemia (MEL) cells, while combined treatment with serum and CD had an additive effect.	Cytochalasin D	172-174	actin, beta	Mus musculus	0-21
8482333-8	1993	Two protein synthesis inhibitors, cycloheximide and puromycin, blocked the CD-induced increase in beta-actin mRNA, in contrast to the serum-induced increase which is insensitive to inhibitors of protein synthesis.	Cytochalasin D	75-77	actin, beta	Mus musculus	98-108
8482333-9	1993	The rapid return of beta-actin mRNA to basal levels following CD removal did not require protein synthesis nor did it require progression through the G2 phase of the cell cycle.	Cytochalasin D	62-64	actin, beta	Mus musculus	20-30
8482333-10	1993	A vector containing the 5" end of the beta-actin gene linked to a CAT reporter responded to CD when transfected into MEL cells, localizing the responsive element to the 5" portion of the beta-actin gene.	Cytochalasin D	92-94	actin, beta	Mus musculus	38-48
8482333-10	1993	A vector containing the 5" end of the beta-actin gene linked to a CAT reporter responded to CD when transfected into MEL cells, localizing the responsive element to the 5" portion of the beta-actin gene.	Cytochalasin D	92-94	actin, beta	Mus musculus	187-197
1471975-1	1992	The microfilament-disrupting agent cytochalasin D (CD) increased (by 10-22-fold) the synthesis de novo and extracellular matrix deposition of plasminogen-activator inhibitor type-1 [p52(PAI-1)] in normal rat kidney (NRK) cells.	Cytochalasin D	35-49	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	182-185
1471975-1	1992	The microfilament-disrupting agent cytochalasin D (CD) increased (by 10-22-fold) the synthesis de novo and extracellular matrix deposition of plasminogen-activator inhibitor type-1 [p52(PAI-1)] in normal rat kidney (NRK) cells.	Cytochalasin D	35-49	serpin family E member 1	Rattus norvegicus	186-191
1471975-1	1992	The microfilament-disrupting agent cytochalasin D (CD) increased (by 10-22-fold) the synthesis de novo and extracellular matrix deposition of plasminogen-activator inhibitor type-1 [p52(PAI-1)] in normal rat kidney (NRK) cells.	Cytochalasin D	51-53	serpin family E member 2	Rattus norvegicus	142-180
1471975-1	1992	The microfilament-disrupting agent cytochalasin D (CD) increased (by 10-22-fold) the synthesis de novo and extracellular matrix deposition of plasminogen-activator inhibitor type-1 [p52(PAI-1)] in normal rat kidney (NRK) cells.	Cytochalasin D	51-53	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	182-185
1471975-1	1992	The microfilament-disrupting agent cytochalasin D (CD) increased (by 10-22-fold) the synthesis de novo and extracellular matrix deposition of plasminogen-activator inhibitor type-1 [p52(PAI-1)] in normal rat kidney (NRK) cells.	Cytochalasin D	51-53	serpin family E member 1	Rattus norvegicus	186-191
1471975-4	1992	CD-associated increases in p52(PAI-1) mRNA abundance and protein biosynthesis were maximal between 6 and 8 h of continuous CD exposure, declined by 50% thereafter, but remained elevated (by at least 6-21-fold respectively over control values) for 24 h. Changes in p52(PAI-1) mRNA abundance at this 24 h point reflected an approx.	Cytochalasin D	0-2	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	27-30
1471975-4	1992	CD-associated increases in p52(PAI-1) mRNA abundance and protein biosynthesis were maximal between 6 and 8 h of continuous CD exposure, declined by 50% thereafter, but remained elevated (by at least 6-21-fold respectively over control values) for 24 h. Changes in p52(PAI-1) mRNA abundance at this 24 h point reflected an approx.	Cytochalasin D	0-2	serpin family E member 1	Rattus norvegicus	31-36
1471975-4	1992	CD-associated increases in p52(PAI-1) mRNA abundance and protein biosynthesis were maximal between 6 and 8 h of continuous CD exposure, declined by 50% thereafter, but remained elevated (by at least 6-21-fold respectively over control values) for 24 h. Changes in p52(PAI-1) mRNA abundance at this 24 h point reflected an approx.	Cytochalasin D	0-2	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	264-267
1471975-4	1992	CD-associated increases in p52(PAI-1) mRNA abundance and protein biosynthesis were maximal between 6 and 8 h of continuous CD exposure, declined by 50% thereafter, but remained elevated (by at least 6-21-fold respectively over control values) for 24 h. Changes in p52(PAI-1) mRNA abundance at this 24 h point reflected an approx.	Cytochalasin D	0-2	serpin family E member 1	Rattus norvegicus	268-273
1471975-4	1992	CD-associated increases in p52(PAI-1) mRNA abundance and protein biosynthesis were maximal between 6 and 8 h of continuous CD exposure, declined by 50% thereafter, but remained elevated (by at least 6-21-fold respectively over control values) for 24 h. Changes in p52(PAI-1) mRNA abundance at this 24 h point reflected an approx.	Cytochalasin D	123-125	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	27-30
1471975-4	1992	CD-associated increases in p52(PAI-1) mRNA abundance and protein biosynthesis were maximal between 6 and 8 h of continuous CD exposure, declined by 50% thereafter, but remained elevated (by at least 6-21-fold respectively over control values) for 24 h. Changes in p52(PAI-1) mRNA abundance at this 24 h point reflected an approx.	Cytochalasin D	123-125	serpin family E member 1	Rattus norvegicus	31-36
1471975-8	1992	284, 433-439], that CD-mediated increases in p52(PAI-1) expression are at least partly due to transcription-level events.	Cytochalasin D	20-22	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	45-48
1471975-8	1992	284, 433-439], that CD-mediated increases in p52(PAI-1) expression are at least partly due to transcription-level events.	Cytochalasin D	20-22	serpin family E member 1	Rattus norvegicus	49-54
1471975-10	1992	Induction of p52(PAI-1) synthesis and matrix deposition in CD-stimulated quiescent NRK cells was as efficient under growth-factor-deficient conditions as when CD was added simultaneously with serum.	Cytochalasin D	59-61	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	13-16
1471975-10	1992	Induction of p52(PAI-1) synthesis and matrix deposition in CD-stimulated quiescent NRK cells was as efficient under growth-factor-deficient conditions as when CD was added simultaneously with serum.	Cytochalasin D	59-61	serpin family E member 1	Rattus norvegicus	17-22
1471975-10	1992	Induction of p52(PAI-1) synthesis and matrix deposition in CD-stimulated quiescent NRK cells was as efficient under growth-factor-deficient conditions as when CD was added simultaneously with serum.	Cytochalasin D	59-61	myotrophin	Rattus norvegicus	116-129
1471975-10	1992	Induction of p52(PAI-1) synthesis and matrix deposition in CD-stimulated quiescent NRK cells was as efficient under growth-factor-deficient conditions as when CD was added simultaneously with serum.	Cytochalasin D	159-161	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	13-16
1471975-10	1992	Induction of p52(PAI-1) synthesis and matrix deposition in CD-stimulated quiescent NRK cells was as efficient under growth-factor-deficient conditions as when CD was added simultaneously with serum.	Cytochalasin D	159-161	serpin family E member 1	Rattus norvegicus	17-22
1471975-11	1992	CD alone is thus a complete inducer of p52(PAI-1) expression in NRK cells, an observation that supports the contention that cell shape is an important regulatory element in p52(PAI-1)-gene control.	Cytochalasin D	0-2	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	39-42
1471975-11	1992	CD alone is thus a complete inducer of p52(PAI-1) expression in NRK cells, an observation that supports the contention that cell shape is an important regulatory element in p52(PAI-1)-gene control.	Cytochalasin D	0-2	serpin family E member 1	Rattus norvegicus	43-48
1471975-11	1992	CD alone is thus a complete inducer of p52(PAI-1) expression in NRK cells, an observation that supports the contention that cell shape is an important regulatory element in p52(PAI-1)-gene control.	Cytochalasin D	0-2	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	173-176
1471975-11	1992	CD alone is thus a complete inducer of p52(PAI-1) expression in NRK cells, an observation that supports the contention that cell shape is an important regulatory element in p52(PAI-1)-gene control.	Cytochalasin D	0-2	serpin family E member 1	Rattus norvegicus	177-182
1385445-7	1992	The induction of tyrosine phosphorylation of pp125FAK was inhibited in thrombin- and collagen-treated platelets preincubated with cytochalasin D, which prevents actin polymerization following activation.	Cytochalasin D	130-144	protein tyrosine kinase 2	Homo sapiens	45-53
1334976-9	1992	Cytoskeletal disruption with colchicine or cytochalasin D also prevented apical AII-induced IP3 generation.	Cytochalasin D	43-57	angiotensinogen	Rattus norvegicus	80-83
1385445-7	1992	The induction of tyrosine phosphorylation of pp125FAK was inhibited in thrombin- and collagen-treated platelets preincubated with cytochalasin D, which prevents actin polymerization following activation.	Cytochalasin D	130-144	coagulation factor II, thrombin	Homo sapiens	71-79
1599429-11	1992	Like actin, CD-induced p52(PAI-1) synthesis, cellular content, and partitioning to the detergent-insoluble cytoskeletal compartment reflected a corresponding increase in p52(PAI-1) mRNA.	Cytochalasin D	12-14	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	23-26
1443108-8	1992	Vasopressin plus 1 microM CD produced a striking increase in microvillar length, direct evidence of the polymerizing action of CD in the cell.	Cytochalasin D	127-129	arginine vasopressin	Homo sapiens	0-11
1397084-5	1992	Three different cytochalasans, cytochalasin B, cytochalasin D, and chaetoglobosin C, all of which bind to cellular actin with different affinities and only one of which affects glucose transport, induced IL-2 receptors in combination with PMA.	Cytochalasin D	47-61	interleukin 2	Homo sapiens	204-208
1418986-13	1992	It was found that the number of cells with calmodulin in the equatorial region increased in the presence of cytochalasin D while the number of cells with calmodulin in the postacrosomal region decreased.	Cytochalasin D	108-122	calmodulin-3	Cavia porcellus	43-53
1599429-11	1992	Like actin, CD-induced p52(PAI-1) synthesis, cellular content, and partitioning to the detergent-insoluble cytoskeletal compartment reflected a corresponding increase in p52(PAI-1) mRNA.	Cytochalasin D	12-14	serpin family E member 2	Rattus norvegicus	27-32
1599429-11	1992	Like actin, CD-induced p52(PAI-1) synthesis, cellular content, and partitioning to the detergent-insoluble cytoskeletal compartment reflected a corresponding increase in p52(PAI-1) mRNA.	Cytochalasin D	12-14	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	170-173
1599429-11	1992	Like actin, CD-induced p52(PAI-1) synthesis, cellular content, and partitioning to the detergent-insoluble cytoskeletal compartment reflected a corresponding increase in p52(PAI-1) mRNA.	Cytochalasin D	12-14	serpin family E member 2	Rattus norvegicus	174-179
1599429-13	1992	p52(PAI-1) expression in the NRK-cell system is thus responsive to CD-mediated shape changes and requires ongoing RNA synthesis for its induction.	Cytochalasin D	67-69	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	0-3
1599429-13	1992	p52(PAI-1) expression in the NRK-cell system is thus responsive to CD-mediated shape changes and requires ongoing RNA synthesis for its induction.	Cytochalasin D	67-69	serpin family E member 2	Rattus norvegicus	4-9
1547340-9	1992	Pretreatment with cytochalasin D 1 mumol/L, which inhibits clot retraction, also abolished the platelet-induced inhibition of lysis and t-PA binding by platelets.	Cytochalasin D	18-32	plasminogen activator, tissue type	Homo sapiens	136-140
1562729-6	1992	Preincubation of platelets with cytochalasin D (30 micrograms/mL) also inhibited the decrease in platelet aggregation after exposure of ADP-treated platelets to fibrinogen over a 60-minute time course.	Cytochalasin D	32-46	fibrinogen beta chain	Homo sapiens	161-171
1577858-9	1992	The role of the actin cytoskeleton in mediating this feedback-regulation was evaluated by disruption of the actin network with Cytochalasin D. We found that treatment with Cytochalasin D abolished the down-regulation of mouse gamma-actin in both the gamma- and beta sm-actin transfectants.	Cytochalasin D	127-141	actin, gamma, cytoplasmic 1	Mus musculus	226-237
1371960-0	1992	Induction of tyrosinase in human melanoma cells by L-tyrosine phosphate and cytochalasin D.	Cytochalasin D	76-90	tyrosinase	Homo sapiens	13-23
1371960-4	1992	In contrast, in the presence of cytochalasin D or L-tyrosine phosphate, the increase in amount of tyrosinase mRNA is not sufficient to account for the increase in enzyme activity, indicating that these compounds act mainly at a post-transcriptional level.	Cytochalasin D	32-46	tyrosinase	Homo sapiens	98-108
1311317-7	1992	Depolymerization of actin with DNase I, or inhibition of ligand binding to GPIIb/IIIa by RGDS, however, in combination with cytochalasin D, further depletes actin and significantly decreases sedimentability of GPIIb/IIIa as well as phosphoinositide 3-kinase, pp60c-src, and PKC, without inhibiting total 3-kinase activity.	Cytochalasin D	124-138	integrin subunit alpha 2b	Homo sapiens	75-80
1311317-7	1992	Depolymerization of actin with DNase I, or inhibition of ligand binding to GPIIb/IIIa by RGDS, however, in combination with cytochalasin D, further depletes actin and significantly decreases sedimentability of GPIIb/IIIa as well as phosphoinositide 3-kinase, pp60c-src, and PKC, without inhibiting total 3-kinase activity.	Cytochalasin D	124-138	integrin subunit alpha 2b	Homo sapiens	210-215
1916664-7	1991	Cytochalasin D, which depolymerizes actin filaments, inhibited ATP-induced canalicular contraction, but not the increase in [Ca2+]i. Microdialysis of myosin light chain kinase and its Ca(2+)-independent fragment (but not the heat-denatured fragment, albumin, trypsin plus soybean inhibitor or buffer) into one hepatocyte of a doublet resulted in canalicular contraction in 86% of doublets.	Cytochalasin D	0-14	myosin light chain kinase	Rattus norvegicus	150-175
1737100-6	1992	(3) Platelets treated at 4 degrees C contained more F-actin than did platelets kept at 37 degrees C. (4) Cytochalasin D (10 mumol/L) inhibited the increase of phallacidin binding to individual platelets stimulated by either ADP or U46619.	Cytochalasin D	105-119	actin	Oryctolagus cuniculus	54-59
1536899-6	1992	By electron microscopic and immunohistochemical examinations, it became clear that CD also affected formation of the basal lamina and accumulation of vimentin filaments in Sertoli cells.	Cytochalasin D	83-85	vimentin	Mus musculus	150-158
1358992-10	1992	This patching and capping of CR3 required the actin cytoskeleton, as it was inhibited by cytochalasin D.	Cytochalasin D	89-103	teratocarcinoma-derived growth factor 1 pseudogene 3	Homo sapiens	29-32
1719004-7	1991	Permeability coefficients for cyanocobalamin (9.66 x 10(-5) cm/s) and insulin (4.18 x 10(-5) cm/s) increased significantly during perfusion with thrombin (10 U/ml) or cytochalasin D (1 microgram/ml), whereas permeability to albumin (0.39 x 10(-5) cm/s) remained unchanged.	Cytochalasin D	167-181	insulin	Homo sapiens	70-77
1353539-4	1992	Cells treated with colcemid (0.05 micrograms/ml) or cytochalasin D (2 micrograms/ml), which limit microtubule (MT) and microfilament (MF) formation, respectively, displayed an increased NGFR-IR in terms of gold labeling.	Cytochalasin D	52-66	nerve growth factor receptor	Rattus norvegicus	186-190
1353539-6	1992	Cells treated simultaneously with cytochalasin D and taxol had a dramatically augmented NGFR-IR on their surfaces, which exceeded levels obtained with either agent alone.	Cytochalasin D	34-48	nerve growth factor receptor	Rattus norvegicus	88-92
1629252-7	1992	Disruption of the actin network with cytochalasin D revealed a differential interaction of alpha-actinin and vinculin with the actin network.	Cytochalasin D	37-51	actinin alpha 1	Homo sapiens	91-104
1629252-7	1992	Disruption of the actin network with cytochalasin D revealed a differential interaction of alpha-actinin and vinculin with the actin network.	Cytochalasin D	37-51	vinculin	Homo sapiens	109-117
1907805-6	1991	The authors have studied the effect of DHCB and CD on IFN-gamma-induced MHC gene expression in 143 B cells, a human osteosarcoma-derived cell line.	Cytochalasin D	48-50	interferon gamma	Homo sapiens	54-63
1907805-7	1991	Herein the authors demonstrate that alterations in the cytoskeleton induced by DHCB and CD can lead to increases in IFN-gamma-induced MHC gene expression.	Cytochalasin D	88-90	interferon gamma	Homo sapiens	116-125
1910809-7	1991	Cytochalasin D (CD), which disrupted the cytoarchitecture as assessed by confocal microscopy but did not affect cell volume or adherence, decreased the stiffness of undifferentiated and FMLP-stimulated differentiated cells, thus suggesting the importance of microfilament organization in the stiffness of these cells.	Cytochalasin D	0-14	formyl peptide receptor 1	Homo sapiens	186-190
1910809-7	1991	Cytochalasin D (CD), which disrupted the cytoarchitecture as assessed by confocal microscopy but did not affect cell volume or adherence, decreased the stiffness of undifferentiated and FMLP-stimulated differentiated cells, thus suggesting the importance of microfilament organization in the stiffness of these cells.	Cytochalasin D	16-18	formyl peptide receptor 1	Homo sapiens	186-190
1910809-9	1991	Differentiated cells exposed to FMLP exhibited a concentration-dependent increase in retention in 8-microns pores that was abolished by CD.	Cytochalasin D	136-138	formyl peptide receptor 1	Homo sapiens	32-36
1907805-11	1991	Studies using 125I-IFN-gamma demonstrate that the occupied IFN-gamma receptor associates with a Triton X-100 insoluble fraction of 143 B cells and that DHCB and CD markedly inhibit this association.	Cytochalasin D	161-163	interferon gamma	Homo sapiens	19-28
2120590-8	1990	The redistribution of p21ras is apparent at the early stages (patching) of immunoglobulin capping and is inhibited by metabolic inhibitors and the cytoskeleton-disrupting agents colchicine and cytochalasin D.	Cytochalasin D	193-207	HRas proto-oncogene, GTPase	Homo sapiens	22-28
1907805-11	1991	Studies using 125I-IFN-gamma demonstrate that the occupied IFN-gamma receptor associates with a Triton X-100 insoluble fraction of 143 B cells and that DHCB and CD markedly inhibit this association.	Cytochalasin D	161-163	interferon gamma	Homo sapiens	59-68
1898594-0	1991	Disruption of the cytoskeleton with cytochalasin D induces c-fos gene expression.	Cytochalasin D	36-50	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	59-64
1898594-1	1991	The treatment of exponentially growing HeLa cells and quiescent WI-38 cells with cytochalasin D, which disrupts the cytoskeletal microfilaments, results in a rapid and marked increase in the transcription of the c-fos protooncogene with a concomitant increase in c-fos mRNA steady-state levels.	Cytochalasin D	81-95	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	212-217
1898594-1	1991	The treatment of exponentially growing HeLa cells and quiescent WI-38 cells with cytochalasin D, which disrupts the cytoskeletal microfilaments, results in a rapid and marked increase in the transcription of the c-fos protooncogene with a concomitant increase in c-fos mRNA steady-state levels.	Cytochalasin D	81-95	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	263-268
2119831-8	1990	Cytochalasin D (CD) and monobromobimane (MB) enhanced agglutination and prevented the inhibitory action of ADP on bovine vWf-induced platelet agglutination.	Cytochalasin D	0-14	von Willebrand factor	Bos taurus	121-124
2119831-8	1990	Cytochalasin D (CD) and monobromobimane (MB) enhanced agglutination and prevented the inhibitory action of ADP on bovine vWf-induced platelet agglutination.	Cytochalasin D	16-18	von Willebrand factor	Bos taurus	121-124
2332454-0	1990	p52 induction by cytochalasin D in rat kidney fibroblasts: homologies between p52 and plasminogen activator inhibitor type-1.	Cytochalasin D	17-31	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	0-3
2168179-3	1990	Cytochalasin D potentiated insulin secretion in a dose-dependent manner, and the combination of theophylline and cytochalasin D resulted in an insulin secretory response no greater than that produced by either agent alone.	Cytochalasin D	0-14	insulin	Homo sapiens	27-34
2118557-0	1990	Effects of cytochalasin D on actin and vinculin in cultured corneal epithelial cells.	Cytochalasin D	11-25	vinculin	Rattus norvegicus	39-47
2332454-0	1990	p52 induction by cytochalasin D in rat kidney fibroblasts: homologies between p52 and plasminogen activator inhibitor type-1.	Cytochalasin D	17-31	serpin family E member 2	Rattus norvegicus	86-124
2332454-3	1990	A threshold of 2-4 microM CD was found to be necessary to augment p52 deposition into both the secreted protein- and saponin-resistant cytomatrix (SAP) fractions of NRK cells.	Cytochalasin D	26-28	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	66-69
2332454-5	1990	Augmented p52 production in CD-treated NRK (NRK/CD) cells provided a means to assess the identity of this protein.	Cytochalasin D	28-30	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	10-13
2332454-8	1990	CD-augmented p52(rPAI-1) synthesis and SAP deposition was blocked by actinomycin D, implicating a need for RNA synthesis during the period of CD exposure to effect induction.	Cytochalasin D	0-2	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	13-16
2332454-8	1990	CD-augmented p52(rPAI-1) synthesis and SAP deposition was blocked by actinomycin D, implicating a need for RNA synthesis during the period of CD exposure to effect induction.	Cytochalasin D	0-2	serpin family E member 1	Rattus norvegicus	17-23
2332454-8	1990	CD-augmented p52(rPAI-1) synthesis and SAP deposition was blocked by actinomycin D, implicating a need for RNA synthesis during the period of CD exposure to effect induction.	Cytochalasin D	142-144	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	13-16
1969411-3	1990	Cytochalasin D also reduced the endocytosis of ricin in cells where uptake of transferrin from coated pits was blocked by low cytosolic pH.	Cytochalasin D	0-14	serotransferrin	Chlorocebus sabaeus	78-89
2182648-6	1990	Adhesion mediated by either CAM was inhibited by treatment with cytochalasin D that disrupted the actin network of the transfected cells.	Cytochalasin D	64-78	calmodulin 2	Mus musculus	28-31
34568340-7	2021	However, 24 h of treatment with cytochalasin D decreases the amounts of TRPM7 only in macrovascular endothelial cells, suggesting that the regulation and the role of TRPM7 in microvascular cells are more complex than expected.	Cytochalasin D	32-46	transient receptor potential cation channel subfamily M member 7	Homo sapiens	72-77
34657240-4	2022	And we found that when cells were treated with different vesicles uptake inhibitors (chlorpromazine, methyl-beta-cyclodextrin (MbetaCD), cytochalasin D, chloroquine and heparin) and heparinase (HSPE), only heparin and HSPE counteracted the uptake enhancement effect caused by DAL-1/4.1B.	Cytochalasin D	137-151	erythrocyte membrane protein band 4.1 like 3	Homo sapiens	282-286
34620239-5	2021	Y-15, cytochalasin D and verteporfin were used to inhibit phosphorylation of FAK, polymerization of microfilament and function of nuclear YAP, respectively.	Cytochalasin D	6-20	protein tyrosine kinase 2	Homo sapiens	77-80
34620239-5	2021	Y-15, cytochalasin D and verteporfin were used to inhibit phosphorylation of FAK, polymerization of microfilament and function of nuclear YAP, respectively.	Cytochalasin D	6-20	Yes1 associated transcriptional regulator	Homo sapiens	138-141
34568340-7	2021	However, 24 h of treatment with cytochalasin D decreases the amounts of TRPM7 only in macrovascular endothelial cells, suggesting that the regulation and the role of TRPM7 in microvascular cells are more complex than expected.	Cytochalasin D	32-46	transient receptor potential cation channel subfamily M member 7	Homo sapiens	166-171
34239547-8	2021	During the study of cellular uptake on A2780 ovarian cancer cells pretreated with cytochalasin D, a statistically significant inhibition of endocytosis was observed for Oct.	Cytochalasin D	82-96	plexin A2	Homo sapiens	169-172
2529923-11	1989	When platelet shape change was prevented by the addition of cytochalasin D, ADP-induced platelet-vWf surface expression on ASA-treated platelets was reduced by more than 80%.	Cytochalasin D	60-74	von Willebrand factor	Homo sapiens	97-100
35300996-9	2022	Co-treatment of SFN with CD increased more tyrosinase expression than SFN alone whereas with JAS, slightly reduced the expression.	Cytochalasin D	25-27	tyrosinase	Mus musculus	43-53
2630560-7	1989	A high dose of CD caused the absence of actin as well as the complete inhibition of cell wall formation.	Cytochalasin D	15-17	actin	Saccharomyces cerevisiae S288C	40-45
2630560-8	1989	A low dose of CD caused weakly stained unlocalized actin, which induced grossly aberrant cell wall deposition as well as substantial changes in the morphology of the reverting protoplasts.	Cytochalasin D	14-16	actin	Saccharomyces cerevisiae S288C	51-56
2715193-0	1989	Cytochalasin D-mediated hyperinduction of the substrate-associated 52-kilodalton protein p52 in rat kidney fibroblasts.	Cytochalasin D	0-14	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	89-92
2681516-8	1989	Second, both rM-CSF- and PMA-stimulated LY accumulation could be inhibited by treatment of cells with the cytoskeleton destabilizing drugs nocodazole, colchicine, or cytochalasin D.	Cytochalasin D	166-180	colony stimulating factor 1	Rattus norvegicus	13-19
2715193-7	1989	The matrix p52 content of CD-induced and uninduced cells, however, was significantly greater (by 200-500-fold) than the corresponding medium levels.	Cytochalasin D	26-28	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	11-14
2715193-10	1989	Morphologic rounding (seen in 10-100 microM CD) coincided with augmented p52 production.	Cytochalasin D	44-46	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	73-76
2715193-11	1989	Transition from a flat to a round phenotype in NRK cells, or at least the generation of sufficient microfilament fragmentation to compromise cell-substrate adhesivity, appears to be an essential aspect of CD-mediated p52 hyperinduction.	Cytochalasin D	205-207	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	217-220
2492187-6	1989	In contrast, stimulation of t-PA synthesis was completely inhibited by actinomycin D and cycloheximide; partially inhibited by cytochalasin D, vinblastine, and trifluoperazine; and not affected by indomethacin.	Cytochalasin D	127-141	plasminogen activator, tissue type	Homo sapiens	28-32
2522483-6	1989	This inhibition appeared to be due to the blockade of the interaction of Fc gamma 2bR with various cytoskeletal components, because the association of Fc gamma 2bR and these cytoskeletal components, which could be eliminated by cytochalasin D, was found to be increased by the inhibition of phospholipase A2 activity.	Cytochalasin D	228-242	phospholipase A2, group IB, pancreas	Mus musculus	291-307
2642389-2	1989	Cytochalasin D, which inhibits actin assembly at the fast-exchanging ends of filaments (barbed with respect to heavy meromyosin decorated filaments), only partially inhibits the increased assembly rate, demonstrating that pyrene-actin monomers add to both ends of filaments present in the cytoskeletons.	Cytochalasin D	0-14	actin	Oryctolagus cuniculus	31-36
2642389-2	1989	Cytochalasin D, which inhibits actin assembly at the fast-exchanging ends of filaments (barbed with respect to heavy meromyosin decorated filaments), only partially inhibits the increased assembly rate, demonstrating that pyrene-actin monomers add to both ends of filaments present in the cytoskeletons.	Cytochalasin D	0-14	actin	Oryctolagus cuniculus	229-234
3366789-4	1988	Treatment with cytochalasin D or colchicine for 24 h inhibits the accumulation of alpha-casein, transferrin, and alpha-lactalbumin without significant effect on general protein synthesis.	Cytochalasin D	15-29	casein alpha s1	Rattus norvegicus	82-94
3169039-8	1988	Neurite extensions of F11 cells on either pFN or CTB were comparably sensitive to low concentrations of cytochalasin D, revealing the mediation of microfilament reorganization in these processes.	Cytochalasin D	104-118	phosphate cytidylyltransferase 1B, choline	Homo sapiens	49-52
3135294-4	1988	Further analysis indicates that hormone receptor capping is inhibited by (1) cytochalasin D, suggesting the involvement of microfilaments; (2) sodium azide, indicating a requirement for ATP production; and (3) W-5, W-7, and W-12 drugs, implying a need for Ca2+/calmodulin activity.	Cytochalasin D	77-91	nuclear receptor subfamily 4, group A, member 1	Mus musculus	32-48
3198692-6	1988	Incubation in cytochalasin D produced a clustering of both actin and gp135, and double-label fluorescence microscopy demonstrated that these proteins were colocalized.	Cytochalasin D	14-28	podocalyxin like	Canis lupus familiaris	69-74
3366789-4	1988	Treatment with cytochalasin D or colchicine for 24 h inhibits the accumulation of alpha-casein, transferrin, and alpha-lactalbumin without significant effect on general protein synthesis.	Cytochalasin D	15-29	transferrin	Rattus norvegicus	96-107
3366789-4	1988	Treatment with cytochalasin D or colchicine for 24 h inhibits the accumulation of alpha-casein, transferrin, and alpha-lactalbumin without significant effect on general protein synthesis.	Cytochalasin D	15-29	lactalbumin, alpha	Rattus norvegicus	113-130
3366789-6	1988	Additionally, treatment with cytochalasin D causes an early (within 1 h) increase in secretion of alpha-casein and transferrin suggesting that the actin cytoskeleton provides a meshwork for secretory vesicles.	Cytochalasin D	29-43	casein alpha s1	Rattus norvegicus	98-110
3366789-6	1988	Additionally, treatment with cytochalasin D causes an early (within 1 h) increase in secretion of alpha-casein and transferrin suggesting that the actin cytoskeleton provides a meshwork for secretory vesicles.	Cytochalasin D	29-43	transferrin	Rattus norvegicus	115-126
3366789-9	1988	Northern blot analysis indicates that treatment with cytochalasin D or colchicine inhibits the laminin induced increase in alpha-casein, alpha-lactalbumin, and transferrin mRNAs.	Cytochalasin D	53-67	casein alpha s1	Rattus norvegicus	123-135
3366789-9	1988	Northern blot analysis indicates that treatment with cytochalasin D or colchicine inhibits the laminin induced increase in alpha-casein, alpha-lactalbumin, and transferrin mRNAs.	Cytochalasin D	53-67	lactalbumin, alpha	Rattus norvegicus	137-154
3366789-9	1988	Northern blot analysis indicates that treatment with cytochalasin D or colchicine inhibits the laminin induced increase in alpha-casein, alpha-lactalbumin, and transferrin mRNAs.	Cytochalasin D	53-67	transferrin	Rattus norvegicus	160-171
3120594-6	1987	Finally, vasopressin-induced tubular invaginations of the apical plasma membrane were visualized in stereomicrographs, and the number and size of such invaginations were altered in the presence of cytochalasin D.	Cytochalasin D	197-211	arginine vasopressin	Homo sapiens	9-20
3285181-8	1988	In contrast, CD alone was sufficient to produce changes in gamma-actin gene expression.	Cytochalasin D	13-15	actin, gamma, cytoplasmic 1	Mus musculus	59-70
3257187-6	1988	Cytochalasin D and colchicine caused significantly greater increases in hCG mobility to 22.0 and 22.5 X 10(-11) cm2 sec-1, respectively, although the mobile fraction remained at about 25-30%.	Cytochalasin D	0-14	secretory blood group 1, pseudogene	Homo sapiens	116-121
3208716-4	1988	No increase in transport occurred following disruption of microtubules by vinblastine, but disruption of microfilaments with cytochalasin D resulted in increased transport of radiolabeled tracers [99mTc- and 111In-labeled diethylenetriamine-pentacetate (DTPA) and 125I-labeled bovine serum albumin (BSA)].	Cytochalasin D	125-139	albumin	Rattus norvegicus	284-297
4043251-6	1985	These effects of cycloheximide, which resemble observations on "super-induction", suggest that actin synthesis in CD-treated and recovering HEp-2 cells may be regulated by a repressor protein.	Cytochalasin D	114-116	DNL-type zinc finger	Homo sapiens	140-143
3527817-6	1986	However, cytochalasin D treatment of subconfluent cultures on plastic substrates, another treatment known to promote chondrogenesis, induces the production of type II collagen, but not type X collagen.	Cytochalasin D	9-23	collagen type II alpha 1 chain	Gallus gallus	159-175
3096573-2	1986	Cytochalasin D-induced retraction and disappearance of stress fibers is followed, with a brief delay, by the dissolution of vinculin-containing patches and the coordinated redistribution of both actin and vinculin into newly formed amorphous aggregates or foci.	Cytochalasin D	0-14	vinculin	Homo sapiens	124-132
3096573-2	1986	Cytochalasin D-induced retraction and disappearance of stress fibers is followed, with a brief delay, by the dissolution of vinculin-containing patches and the coordinated redistribution of both actin and vinculin into newly formed amorphous aggregates or foci.	Cytochalasin D	0-14	vinculin	Homo sapiens	205-213
3085282-12	1986	The characteristic CD-induced distribution of actin filament aggregates and redistribution of vimentin in these cell types also occur when cells are allowed to respread from the rounded state in the presence of CD.	Cytochalasin D	19-21	vimentin	Rattus norvegicus	94-102
3085282-12	1986	The characteristic CD-induced distribution of actin filament aggregates and redistribution of vimentin in these cell types also occur when cells are allowed to respread from the rounded state in the presence of CD.	Cytochalasin D	211-213	vimentin	Rattus norvegicus	94-102
4043251-0	1985	Evidence for regulation of actin synthesis in cytochalasin D-treated HEp-2 cells.	Cytochalasin D	46-60	DNL-type zinc finger	Homo sapiens	69-72
4043251-1	1985	In HEp-2 cells treated with 0.2 or 2.0 microM cytochalasin D (CD), the relative rate of actin synthesis increased for about 12 h and then reached a plateau; this increase was suppressed by actinomycin D (AD).	Cytochalasin D	46-60	DNL-type zinc finger	Homo sapiens	3-6
4043251-1	1985	In HEp-2 cells treated with 0.2 or 2.0 microM cytochalasin D (CD), the relative rate of actin synthesis increased for about 12 h and then reached a plateau; this increase was suppressed by actinomycin D (AD).	Cytochalasin D	62-64	DNL-type zinc finger	Homo sapiens	3-6
4043251-5	1985	In HEp-2 cells treated with cycloheximide during exposure to CD for 20 h, the relative rate of actin synthesis measured after removal of cycloheximide was twofold higher than with CD alone and such cells exhibited a twofold slower decline in the rate of actin synthesis during recovery from CD in the continued presence of cycloheximide.	Cytochalasin D	61-63	DNL-type zinc finger	Homo sapiens	3-6
3115801-0	1987	Early stimulation by EGF plus insulin of rRNA, c-fos, and actin mRNA expression: inhibition by cytochalasin D.	Cytochalasin D	95-109	insulin	Homo sapiens	30-37
3115801-3	1987	We observed that CD slightly increased rRNA synthesis in nonstimulated cells; conversely, it decreased rRNA synthesis in cells stimulated by EGF + insulin.	Cytochalasin D	17-19	insulin	Homo sapiens	147-154
3115801-5	1987	The c-fos mRNA was not expressed in control cells and was accumulated in cells stimulated by the mixture of EGF + insulin; this accumulation was inhibited by CD.	Cytochalasin D	158-160	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	4-9
3115801-5	1987	The c-fos mRNA was not expressed in control cells and was accumulated in cells stimulated by the mixture of EGF + insulin; this accumulation was inhibited by CD.	Cytochalasin D	158-160	insulin	Homo sapiens	114-121
2420586-6	1986	Synthesis of alpha-actinin, the higher-molecular-mass pair of tropomyosins and actin were similarly increased with cytochalasin D treatment, suggesting coordinate induction.	Cytochalasin D	115-129	actinin alpha 1	Homo sapiens	13-26
3949737-8	1986	However, the addition of cytochalasin D to actin in the presence of 50 microM Mg2+ rapidly induces the formation of dimers, presumably related to cytochalasin"s ability to nucleate actin polymerization.	Cytochalasin D	25-39	mucin 7, secreted	Homo sapiens	78-81
3955635-2	1986	Cytochalasin D (CD) was used to induce the known actin-based sequence of events in a culture of an endothelial-cell line (XTH-2) derived from hearts from tadpoles of Xenopus laevis.	Cytochalasin D	0-14	apurinic/apyrimidinic endodeoxyribonuclease 2 L homeolog	Xenopus laevis	122-127
3955635-2	1986	Cytochalasin D (CD) was used to induce the known actin-based sequence of events in a culture of an endothelial-cell line (XTH-2) derived from hearts from tadpoles of Xenopus laevis.	Cytochalasin D	16-18	apurinic/apyrimidinic endodeoxyribonuclease 2 L homeolog	Xenopus laevis	122-127
6321655-2	1984	Specifically, we investigated the effect of the cytoskeletal perturbants, colchicine and cytochalasin D, on the induction of the oligodendroglial marker enzyme, 2",3"-cyclic nucleotide 3"-phosphohydrolase (CNP), caused by removal of serum from the culture medium.	Cytochalasin D	89-103	2',3'-cyclic nucleotide 3' phosphodiesterase	Homo sapiens	161-204
4040915-11	1985	The rate of actin polymerization (3.8 +/- 0.3-4.4 +/- 0.6% increase in F-actin/s) is the same for 10(-10) - 10(-6) M fMLP and the polymerization is inhibited by cytochalasin D.	Cytochalasin D	161-175	formyl peptide receptor 1	Homo sapiens	117-121
3016950-6	1985	Cytochalasin D, a microfilament perturbing agent, inhibited steroid-stimulated 20-DHP production, suggesting that ACTH and steroid stimulation mechanisms were similar.	Cytochalasin D	0-14	dihydropyrimidinase	Mus musculus	82-85
6233366-4	1984	The redistribution of cross-linked C3b receptors was inhibited by pretreatment of the neutrophils with either cytochalasin D or chlorpromazine.	Cytochalasin D	110-124	endogenous retrovirus group K member 3	Homo sapiens	35-38
4040866-5	1985	In cultures treated with cytochalasin D (0.2 microgram/ml) or dihydrocytochalasin B (5.0 micrograms/ml) (to disrupt microfilaments), 35 and 65% decreases in cell surface AChR number were seen after 48 h. However, in cultures treated with CBE and cytochalasin D, the same total number of AChRs was found as in cultures treated with CBE alone.	Cytochalasin D	25-39	cholinergic receptor nicotinic delta subunit	Gallus gallus	170-174
6317543-6	1984	Both cytochalasin B, cytochalasin D and hydrocortisone reduced the release of ECP.	Cytochalasin D	21-35	ribonuclease A family member 3	Homo sapiens	78-81
6982901-5	1982	Trifluoperazine, W-7, cytochalasin D, and taxol also block DNA synthesis in response to EGF as measured by autoradiography using [3H]thymidine.	Cytochalasin D	22-36	epidermal growth factor	Homo sapiens	88-91
6686086-6	1983	The inhibitory effects of fibronectin can be reversed by keeping cells in a rounded configuration or by exposing cells to either cytochalasin D, which disrupts the actin cytoskeleton, or insulin, a key lipogenic hormone.	Cytochalasin D	129-143	fibronectin 1	Mus musculus	26-37
6444302-4	1980	In 0.5 mM MgCl2, cytochalasin D uncoupled the actin ATPase activity from actin polymerization, increasing the ATPase rate by at least 20 times while inhibiting polymerization.	Cytochalasin D	17-31	dynein axonemal heavy chain 8	Homo sapiens	52-58
7088173-0	1982	Effect of cytochalasin D on thrombin-induced actin filaments in platelets.	Cytochalasin D	10-24	coagulation factor II, thrombin	Homo sapiens	28-36
7024999-6	1981	Neuraminidase removal of the sialic acid component of the glomerular glycocalyx and exposure to either cytochalasin B (25 microgram/ml) or cytochalasin D (2 microgram/ml), prevent the in vitro formation of podocyte microprojections.	Cytochalasin D	139-153	neuraminidase 1	Homo sapiens	0-13
6444302-4	1980	In 0.5 mM MgCl2, cytochalasin D uncoupled the actin ATPase activity from actin polymerization, increasing the ATPase rate by at least 20 times while inhibiting polymerization.	Cytochalasin D	17-31	dynein axonemal heavy chain 8	Homo sapiens	110-116
6444302-8	1980	Cytochalasin D also stimulated the ATPase activity of monomeric actin in the absence of MgCl2 and KCl and, to a much greater extent, stimulated the ATPase activity of monomeric actin below its critical concentration in 0.5 mM MgCl2.	Cytochalasin D	0-14	dynein axonemal heavy chain 8	Homo sapiens	35-41
6444302-8	1980	Cytochalasin D also stimulated the ATPase activity of monomeric actin in the absence of MgCl2 and KCl and, to a much greater extent, stimulated the ATPase activity of monomeric actin below its critical concentration in 0.5 mM MgCl2.	Cytochalasin D	0-14	dynein axonemal heavy chain 8	Homo sapiens	148-154
6444302-9	1980	Both above and below its critical concentration and in the presence and absence of cytochalasin D, the initial rate of actin ATPase activity, when little or no polymerization had occurred, was directly proportional to the actin concentration and, therefore, apparently was independent of actin-actin interactions.	Cytochalasin D	83-97	dynein axonemal heavy chain 8	Homo sapiens	125-131
33603366-12	2021	After treatment with cytochalasin D and MAPK signaling pathway inhibitors, differences in the TAZ subcellular localization and transcriptional activity were no longer observed among the different titanium surfaces.	Cytochalasin D	21-35	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	94-97
33922367-5	2021	Cell-attached patch-clamp experiments revealed that cytochalasin D increases the activity of TRPC6 channels in CHO (Chinese Hamster Ovary) cells overexpressing the channel and in podocytes from freshly isolated glomeruli.	Cytochalasin D	52-66	short transient receptor potential channel 6	Cricetulus griseus	93-98
32437028-3	2020	Our data highlighted that compared with control, ECE1 was continuously downregulated in ARPE-19 cells treated by MS or CD + MS from 6 to 24 hr.	Cytochalasin D	119-123	endothelin converting enzyme 1	Homo sapiens	49-53
32437028-7	2020	Overexpression of ATAD2 and AHSG were also shown to reverse the apoptosis of ARPE-19 cells induced by MS or CD + MS, with significantly decreased apoptotic rates and caspase-3 activities.	Cytochalasin D	108-112	ATPase family AAA domain containing 2	Homo sapiens	18-23
32437028-7	2020	Overexpression of ATAD2 and AHSG were also shown to reverse the apoptosis of ARPE-19 cells induced by MS or CD + MS, with significantly decreased apoptotic rates and caspase-3 activities.	Cytochalasin D	108-112	alpha 2-HS glycoprotein	Homo sapiens	28-32
31209295-7	2019	Potentiation or disruption of the G-actin/ArhGAP12 interaction, by treatment with the actin-binding drugs latrunculin B or cytochalasin D, has corresponding effects on Rac GTP loading.	Cytochalasin D	123-137	Rho GTPase activating protein 12	Mus musculus	42-50
32513915-9	2020	Inhibition of the NMMHC IIA-actin interaction using blebbistatin and the F-actin polymerization inhibitor cytochalasin D significantly suppressed ATG9A trafficking and autophagy induction.	Cytochalasin D	106-120	myosin heavy chain 9-like 1	Rattus norvegicus	18-27
32513915-9	2020	Inhibition of the NMMHC IIA-actin interaction using blebbistatin and the F-actin polymerization inhibitor cytochalasin D significantly suppressed ATG9A trafficking and autophagy induction.	Cytochalasin D	106-120	autophagy related 9A	Rattus norvegicus	146-151
32636813-7	2020	The endocytosis of the biomarker MCP is dependent on low pH and cytoskeletal actin filaments, as shown with various inhibitors (chloroquine, ammonia chloride, cytochalasin D).	Cytochalasin D	159-173	capping actin protein, gelsolin like	Homo sapiens	33-36
31401177-8	2019	Further examination of the effect of actin manipulation reveals that actin depolymerisation by cytochalasin D results in sustained syndecan-1 reduction.	Cytochalasin D	95-109	syndecan 1	Homo sapiens	131-141
31255721-5	2019	Inhibition of actin polymerisation with cytochalasin-D, latrunculin-B or the ROCK inhibitor, Y-27632, mimicked effects of cAMP on EPAC1 mRNA and protein levels.	Cytochalasin D	40-54	Rap guanine nucleotide exchange factor 3	Homo sapiens	130-135
31116579-12	2019	Cytochalasin D prevented oxidative stress and Nrf2 nuclear translocation after OD.	Cytochalasin D	0-14	nuclear factor, erythroid derived 2, like 2	Mus musculus	46-50
31209295-7	2019	Potentiation or disruption of the G-actin/ArhGAP12 interaction, by treatment with the actin-binding drugs latrunculin B or cytochalasin D, has corresponding effects on Rac GTP loading.	Cytochalasin D	123-137	thymoma viral proto-oncogene 1	Mus musculus	168-171
31011633-6	2019	Even in the presence of endocytosis inhibitors, cytochalasin D or dynasore, K3C16 continued to activate the NLRP3 inflammasomes and to induce IL-1beta release.	Cytochalasin D	48-62	NLR family pyrin domain containing 3	Homo sapiens	108-113
30809816-6	2019	The response to ET-1 was inhibited by the Rho/ROCK kinase antagonist, Y27632 and by cytochalasin D, an inhibitor of actin polymerization but the ET-1-mediated pSmad2C was not inhibited by the matrix metalloproteinase (MMP) inhibitor, GM6001.	Cytochalasin D	84-98	endothelin 1	Bos taurus	16-20
30809816-7	2019	ET-1 increased CHSY-1 protein level, which was inhibited in the presence of BQ788, cytochalasin D and Y27632.	Cytochalasin D	83-97	endothelin 1	Bos taurus	0-4
30809816-7	2019	ET-1 increased CHSY-1 protein level, which was inhibited in the presence of BQ788, cytochalasin D and Y27632.	Cytochalasin D	83-97	chondroitin sulfate synthase 1	Bos taurus	15-21
29242135-3	2018	In this paper, we describe the use of iMSD to obtain quantitative data of the diffusion dynamics of a small cytoskeletal protein, profilin 1 (pfn1), at the membrane of live cells and how its diffusion is perturbed when the cells are treated with Cytochalasin D and/or the interactions of pfn1 are modified when its actin and polyphosphoinositide binding sites are mutated (pfn1-R88A).	Cytochalasin D	246-260	profilin 1	Homo sapiens	130-140
30350968-7	2018	Intracellular material transport by TNTs was tested in MSC spheroids treated with cytochalasin D (CytoD), a known actin polymerization inhibitor for disrupting TNT formation.	Cytochalasin D	82-96	chromosome 16 open reading frame 82	Homo sapiens	36-39
30350968-7	2018	Intracellular material transport by TNTs was tested in MSC spheroids treated with cytochalasin D (CytoD), a known actin polymerization inhibitor for disrupting TNT formation.	Cytochalasin D	98-103	chromosome 16 open reading frame 82	Homo sapiens	36-39
30058115-12	2018	Cytoskeleton inhibitor, cytochalasin D, obviously inhibited the nuclear localization of YAP/TAZ.	Cytochalasin D	24-38	Yes1 associated transcriptional regulator	Homo sapiens	88-91
30058115-12	2018	Cytoskeleton inhibitor, cytochalasin D, obviously inhibited the nuclear localization of YAP/TAZ.	Cytochalasin D	24-38	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	92-95
29720549-4	2018	Furthermore, palladin-knockdown podocytes were more susceptible to disruption of the actin cytoskeleton with cytochalasin D, latrunculin A, or jasplakinolide and showed altered migration dynamics.	Cytochalasin D	109-123	palladin, cytoskeletal associated protein	Mus musculus	13-21
30628700-4	2019	Subsequently, the EPCs were treated with anti-integrin beta1 or beta3 antibodies to block integrin beta1 and beta3, respectively, or cytochalasin D to destroy F-actin, and the subsequent expression levels of KLF2 in EPCs were measured.	Cytochalasin D	133-147	Kruppel-like factor 2	Rattus norvegicus	208-212
29964013-3	2018	In a whole-cell patch clamp recording of ANO6 current (IANO6,w-c), disruption of the actin cytoskeleton with cytochalasin-D (cytoD) significantly accelerated the activation kinetics, while actin filament-stabilizing agents (phalloidin and jasplakinolide) commonly inhibited IANO6,w-c. Inside-out patch clamp recording of ANO6 (IANO6,i-o) showed immediate activation by raising [Ca2+]i.	Cytochalasin D	109-123	anoctamin 6	Homo sapiens	41-45
29964013-3	2018	In a whole-cell patch clamp recording of ANO6 current (IANO6,w-c), disruption of the actin cytoskeleton with cytochalasin-D (cytoD) significantly accelerated the activation kinetics, while actin filament-stabilizing agents (phalloidin and jasplakinolide) commonly inhibited IANO6,w-c. Inside-out patch clamp recording of ANO6 (IANO6,i-o) showed immediate activation by raising [Ca2+]i.	Cytochalasin D	109-123	anoctamin 6	Homo sapiens	56-60
29492987-6	2018	When cellular uptake of SPIONs was inhibited by the actin polymerization inhibitor, cytochalasin D, SPION-induced IL-1beta release was suppressed in BMMs.	Cytochalasin D	84-98	interleukin 1 alpha	Mus musculus	114-122
29754473-4	2018	We observed that de-polymerization of actin with cytochalasin D (CD) constitutively activated ribosomal S6 kinase (RSK) and induced inhibitory phosphorylation of Cdc2 (Tyr 15) in IMR-90 cells.	Cytochalasin D	49-63	ribosomal protein S6 kinase A2	Homo sapiens	115-118
29754473-4	2018	We observed that de-polymerization of actin with cytochalasin D (CD) constitutively activated ribosomal S6 kinase (RSK) and induced inhibitory phosphorylation of Cdc2 (Tyr 15) in IMR-90 cells.	Cytochalasin D	49-63	cyclin dependent kinase 1	Homo sapiens	162-166
29242135-3	2018	In this paper, we describe the use of iMSD to obtain quantitative data of the diffusion dynamics of a small cytoskeletal protein, profilin 1 (pfn1), at the membrane of live cells and how its diffusion is perturbed when the cells are treated with Cytochalasin D and/or the interactions of pfn1 are modified when its actin and polyphosphoinositide binding sites are mutated (pfn1-R88A).	Cytochalasin D	246-260	profilin 1	Homo sapiens	142-146
29242135-3	2018	In this paper, we describe the use of iMSD to obtain quantitative data of the diffusion dynamics of a small cytoskeletal protein, profilin 1 (pfn1), at the membrane of live cells and how its diffusion is perturbed when the cells are treated with Cytochalasin D and/or the interactions of pfn1 are modified when its actin and polyphosphoinositide binding sites are mutated (pfn1-R88A).	Cytochalasin D	246-260	profilin 1	Homo sapiens	288-292
29242135-3	2018	In this paper, we describe the use of iMSD to obtain quantitative data of the diffusion dynamics of a small cytoskeletal protein, profilin 1 (pfn1), at the membrane of live cells and how its diffusion is perturbed when the cells are treated with Cytochalasin D and/or the interactions of pfn1 are modified when its actin and polyphosphoinositide binding sites are mutated (pfn1-R88A).	Cytochalasin D	246-260	profilin 1	Homo sapiens	288-292
29242135-6	2018	We could also see changes in the modes of diffusion between the different conditions and changes in the size of the zones of pfn1 confinements for the pfn1 treated with Cytochalasin D.	Cytochalasin D	169-183	profilin 1	Homo sapiens	125-129
29242135-6	2018	We could also see changes in the modes of diffusion between the different conditions and changes in the size of the zones of pfn1 confinements for the pfn1 treated with Cytochalasin D.	Cytochalasin D	169-183	profilin 1	Homo sapiens	151-155
29605806-8	2018	Moreover, treating hMSCs by Cytochalasin D inhibited ERK and Smad2 signaling and this was associated with enhanced adipocyte differentiation.	Cytochalasin D	28-42	SMAD family member 2	Homo sapiens	61-66
29605806-8	2018	Moreover, treating hMSCs by Cytochalasin D inhibited ERK and Smad2 signaling and this was associated with enhanced adipocyte differentiation.	Cytochalasin D	28-42	mitogen-activated protein kinase 1	Homo sapiens	53-56
29428600-12	2018	Abrogation of TGF-beta activation by contraction inhibitors cytochalasin D and formoterol prevents the thrombin-induced effects.	Cytochalasin D	60-74	transforming growth factor beta 1	Homo sapiens	14-22
29329985-5	2018	P2X7-mediated phagocytosis was found to account for about half of Latrunculin (or Cytochalasin D)-sensitive bead engulfment by fresh human monocytes.	Cytochalasin D	82-96	purinergic receptor P2X 7	Homo sapiens	0-4
29274784-11	2018	Treatment of the cells with cytochalasin D, an inhibitor of actin polymerization, significantly reduced PD-L1 protein levels.	Cytochalasin D	28-42	CD274 molecule	Homo sapiens	104-109
29278699-6	2018	Treatment of the tongue epithelium with cytochalasin D (CytD), which disturbs ACTIN polymerization in the microvilli, resulted in the loss of TAS2R119 localization at the microvilli and the loss of BAB for quinine and thiamine.	Cytochalasin D	40-54	taste receptor, type 2, member 119	Mus musculus	142-150
29293453-6	2018	The destruction of the actin cytoskeleton of endothelial cells by cytochalasin D inhibits PDI release.	Cytochalasin D	66-80	prolyl 4-hydroxylase subunit beta	Homo sapiens	90-93
28798145-4	2018	Inhibition of actin polymerization by cytochalasin D significantly diminished TNF-induced human neutrophil adhesion in vitro and abolished TNF-induced membrane alterations and cell spreading.	Cytochalasin D	38-52	tumor necrosis factor	Homo sapiens	78-81
28798145-4	2018	Inhibition of actin polymerization by cytochalasin D significantly diminished TNF-induced human neutrophil adhesion in vitro and abolished TNF-induced membrane alterations and cell spreading.	Cytochalasin D	38-52	tumor necrosis factor	Homo sapiens	139-142
29395289-5	2018	Cytochalasin D, an inhibitor of actin filament polymerization prevented uptake of S. Typhimurium.	Cytochalasin D	0-14	actin, beta	Gallus gallus	32-37
29106958-6	2017	We found that cytochalasin H (CH), CD, and especially CE could induce the up-regulation of autophagy-related protein (LC3-II) and SQSTM1/p62.	Cytochalasin D	35-37	sequestosome 1	Homo sapiens	130-136
29106958-6	2017	We found that cytochalasin H (CH), CD, and especially CE could induce the up-regulation of autophagy-related protein (LC3-II) and SQSTM1/p62.	Cytochalasin D	35-37	sequestosome 1	Homo sapiens	137-140
28101059-4	2016	The actin cytoskeleton inhibitors cytochalasin D (10 muM, 5 h) and latrunculin A (10 muM, 5 h) reduced the targeting of KCa3.1 to the BLM by 88 +- 4 and 70 +- 5%, respectively.	Cytochalasin D	34-48	potassium calcium-activated channel subfamily N member 4	Rattus norvegicus	120-126
28943429-8	2017	However, shear stress-induced CD59 expression was reduced when the F-actin stress fiber formation process was delayed by Gly-Arg-Gly-Asp-Ser-Pro (GRGDSP) or destroyed by cytochalasin D (Cyto D), while Jasplakinolide (JAS) reversed the expression of CD59 through promotion of F-actin polymerization and its stabilizing capacities.	Cytochalasin D	170-184	CD59 molecule (CD59 blood group)	Homo sapiens	30-34
28469768-9	2017	Besides, rapamycin was found to destruct the granular pattern of mTORC1, while dissociation between F-actin and mTORC1 was noted after cytochalasin D administration.	Cytochalasin D	135-149	CREB regulated transcription coactivator 1	Mus musculus	112-118
28388885-9	2017	After pre-treatment with Cytochalasin D alone, IL-8 expression and JNK phosphorylation levels were not significantly different at 6 h but were significantly increased by approximately 1.2-fold (1.18 +- 0.05; P<0.01) and 3.0-fold (3.01 +- 0.02; P<0.01) at 24 h, respectively.	Cytochalasin D	25-39	mitogen-activated protein kinase 8	Homo sapiens	67-70
28179028-7	2017	Furthermore, VLP entry is dependent on low pH and cytoskeleton, demonstrated by inhibitor (chloroquine, ammonia chloride, cytochalasin D, wiskostatin, and nocodazole) perturbation.	Cytochalasin D	122-136	VHL like	Homo sapiens	13-16
27212030-5	2017	Treatment with cytochalasin D, an actin polymerization inhibitor, significantly reduced the FMOD-induced glioma cell migration.	Cytochalasin D	15-29	fibromodulin	Homo sapiens	92-96
28804558-3	2017	Here, we found that the classic NOX2 inhibitor diphenyleneiodonium (DPI) induced uptake of E. coli by murine peritoneal macrophages through enhancing phagocytosis, and this effect was temperature-sensitive and attenuated by cytochalasin D as well as chemical inhibition of Syk and PLCgamma, two downstream kinases involved in actin polymerization during phagocytosis.	Cytochalasin D	224-238	cytochrome b-245, beta polypeptide	Mus musculus	32-36
28388885-9	2017	After pre-treatment with Cytochalasin D alone, IL-8 expression and JNK phosphorylation levels were not significantly different at 6 h but were significantly increased by approximately 1.2-fold (1.18 +- 0.05; P<0.01) and 3.0-fold (3.01 +- 0.02; P<0.01) at 24 h, respectively.	Cytochalasin D	25-39	C-X-C motif chemokine ligand 8	Homo sapiens	47-51
27986631-8	2017	As for the complex, the internalization of alpha-LA-OA was completely blocked at 4 C and significantly decreased in the presence of cytochalasin D, an inhibitor of phagocytosis (p<0.01).	Cytochalasin D	132-146	lactalbumin alpha	Homo sapiens	43-51
29238726-8	2017	When either ROS production/ROCK activation was blocked or cells were treated with Cytochalasin D (actin depolymerizer), H9c2 cells were protected against AGEs-induced cardiac myocyte abnormalities, concomitantly with downregulated expression of PFN-1 and improved actin cytoskeleton alteration.	Cytochalasin D	82-96	profilin 1	Rattus norvegicus	245-250
27721022-0	2017	Synergistic induction of CTGF by cytochalasin D and TGFbeta-1 in primary human renal epithelial cells: Role of transcriptional regulators MKL1, YAP/TAZ and Smad2/3.	Cytochalasin D	33-47	cellular communication network factor 2	Homo sapiens	25-29
27590529-5	2016	FIB significantly enhanced cell elongation even in presence of actin polymerization blockers cytochalasin D (CytoD) and ROCK inhibitor Y-27632, which generally caused more rounded cells.	Cytochalasin D	93-107	fibronectin 1	Homo sapiens	0-3
28740333-0	2017	Mold Alkaloid Cytochalasin D Modifies the Morphology and Secretion of fMLP-, LPS-, or PMA-Stimulated Neutrophils upon Adhesion to Fibronectin.	Cytochalasin D	14-28	formyl peptide receptor 1	Homo sapiens	70-74
28740333-0	2017	Mold Alkaloid Cytochalasin D Modifies the Morphology and Secretion of fMLP-, LPS-, or PMA-Stimulated Neutrophils upon Adhesion to Fibronectin.	Cytochalasin D	14-28	fibronectin 1	Homo sapiens	130-141
27682586-5	2016	We show that cultured hippocampal neurons treated with cytochalasin D or latrunculin B contained dense accumulations of branched actin filaments at ~50% of neurite tips at all tested drug concentrations (1-10 muM).	Cytochalasin D	55-69	latexin	Homo sapiens	209-212
27288050-7	2016	Interestingly, pretreatment with inhibitors of actin polymerization, cytochalasin D or latrunculin A, substantially restores both RE and lysosome exocytosis in cells expressing S25N Rab11.	Cytochalasin D	69-83	RAB11A, member RAS oncogene family	Homo sapiens	182-187
26493329-6	2016	RESULTS: IFT88(orpk) cells exhibited a significant increase in acto-myosin stress fibre organisation relative to wild-type (WT) cells in monolayer and an altered response to cytochalasin D.	Cytochalasin D	174-188	intraflagellar transport 88	Homo sapiens	9-14
27226736-8	2016	The ConA-mediated reduction in LRP-1 expression was emulated by the actin cytoskeleton-disrupting agent cytochalasin-D, but not by the microtubule inhibitor nocodazole, and required both lysosomal- and ubiquitin-proteasome system-mediated degradation.	Cytochalasin D	104-118	LDL receptor related protein 1	Homo sapiens	31-36
30189125-2	2016	In the presence of an inhibitor of polymerization microfilaments cytochalasin D additional release of Ca2+ not detected in oocytes treated by theophylline and guanosine diphosphate, but treatment of oocyte by prolactin with guanosine triphosphate leads to the additional release of Ca2+ from intracellular stores.	Cytochalasin D	65-79	carbonic anhydrase 2	Homo sapiens	282-285
25906316-12	2016	In vitro, antibodies from Ro52-immune sera were internalised by a SG cell line and this uptake was inhibited by cytochalasin D treatment.	Cytochalasin D	112-126	tripartite motif-containing 21	Mus musculus	26-30
27164414-8	2016	In addition, inhibition of actin polymerization with cytochalasin D completely blocked C1P-induced MMP-2 and -9 expression as well as C1P-stimulated macrophage migration.	Cytochalasin D	53-67	matrix metallopeptidase 9	Homo sapiens	99-111
30189125-2	2016	In the presence of an inhibitor of polymerization microfilaments cytochalasin D additional release of Ca2+ not detected in oocytes treated by theophylline and guanosine diphosphate, but treatment of oocyte by prolactin with guanosine triphosphate leads to the additional release of Ca2+ from intracellular stores.	Cytochalasin D	65-79	carbonic anhydrase 2	Homo sapiens	102-105
26493329-6	2016	RESULTS: IFT88(orpk) cells exhibited a significant increase in acto-myosin stress fibre organisation relative to wild-type (WT) cells in monolayer and an altered response to cytochalasin D.	Cytochalasin D	174-188	intraflagellar transport 88	Homo sapiens	15-19
27825172-7	2016	Pre-exposure to either the actin-depolymerizing agent cytochalasin D or the actin-polymerizing agent jasplakinolide inhibited CyPA secretion induced by ox-LDL.	Cytochalasin D	54-68	peptidylprolyl isomerase A	Rattus norvegicus	126-130
27033446-9	2016	The cytoskeleton disruptor cytochalasin D (1 mumol/L) decreased flow-induced Nox4 translocation by 0.3 +- 0.01 (P < 0.01); however, it did not reduce flow-induced O2 (-) Flow did not alter Poldip2 localization.	Cytochalasin D	27-41	NADPH oxidase 4	Homo sapiens	77-81
27033446-9	2016	The cytoskeleton disruptor cytochalasin D (1 mumol/L) decreased flow-induced Nox4 translocation by 0.3 +- 0.01 (P < 0.01); however, it did not reduce flow-induced O2 (-) Flow did not alter Poldip2 localization.	Cytochalasin D	27-41	DNA polymerase delta interacting protein 2	Homo sapiens	192-199
26320605-10	2015	Epithelial cells treatment with cytochalasin D caused the inhibition of B182 internalisation and caspase 3 activation.	Cytochalasin D	32-46	caspase 3	Homo sapiens	97-106
26557089-5	2015	Stretching the RPV for 1 or 24 h significantly increased leptin protein level and ROS formation in VSMCs, which was prevented by 1 h pretreatment with the ROCK inhibitor Y-27632 and the actin cytoskeleton depolymerization agent cytochalasin D.	Cytochalasin D	228-242	leptin	Rattus norvegicus	57-63
26557089-10	2015	Pretreating VSMC with leptin for 1 h significantly activated GATA-4 nuclear translocation, which was potently attenuated by the NADPH oxidase inhibitor apocynin, Y-27632, and cytochalasin D.	Cytochalasin D	175-189	leptin	Rattus norvegicus	22-28
26557089-10	2015	Pretreating VSMC with leptin for 1 h significantly activated GATA-4 nuclear translocation, which was potently attenuated by the NADPH oxidase inhibitor apocynin, Y-27632, and cytochalasin D.	Cytochalasin D	175-189	GATA binding protein 4	Rattus norvegicus	61-67
26057877-5	2015	We confirmed that the binding occurs through endocytosis mediated by ASGPR via inhibition studies with cytochalasin D; fluorescence microscopy studies display the uptake of the carrier peptides inside the cell.	Cytochalasin D	103-117	asialoglycoprotein receptor 1	Homo sapiens	69-74
25652011-8	2015	Furthermore, the cytoskeletal disorganization stimulated by cytochalasin D in COS7 cells was recovered by cotransfection with wild-type IQGAP1 and nephrin plasmids but was not recovered either by single transfection of the wild-type IQGAP1 plasmid or by cotransfection of mutant IQGAP1 [ 1443(S A)] and wild-type nephrin plasmids.	Cytochalasin D	60-74	IQ motif containing GTPase activating protein 1	Homo sapiens	233-239
25990946-5	2015	Cytochalasin D treatment resulted in RelA/p65 redistribution to actin-containing aggregates, with the number of cells with RelA/p65-containing clusters in the cytoplasm increasing under the effect of EGF.	Cytochalasin D	0-14	RELA proto-oncogene, NF-kB subunit	Homo sapiens	37-41
25990946-5	2015	Cytochalasin D treatment resulted in RelA/p65 redistribution to actin-containing aggregates, with the number of cells with RelA/p65-containing clusters in the cytoplasm increasing under the effect of EGF.	Cytochalasin D	0-14	RELA proto-oncogene, NF-kB subunit	Homo sapiens	42-45
25990946-5	2015	Cytochalasin D treatment resulted in RelA/p65 redistribution to actin-containing aggregates, with the number of cells with RelA/p65-containing clusters in the cytoplasm increasing under the effect of EGF.	Cytochalasin D	0-14	RELA proto-oncogene, NF-kB subunit	Homo sapiens	123-127
25990946-5	2015	Cytochalasin D treatment resulted in RelA/p65 redistribution to actin-containing aggregates, with the number of cells with RelA/p65-containing clusters in the cytoplasm increasing under the effect of EGF.	Cytochalasin D	0-14	RELA proto-oncogene, NF-kB subunit	Homo sapiens	128-131
25652011-8	2015	Furthermore, the cytoskeletal disorganization stimulated by cytochalasin D in COS7 cells was recovered by cotransfection with wild-type IQGAP1 and nephrin plasmids but was not recovered either by single transfection of the wild-type IQGAP1 plasmid or by cotransfection of mutant IQGAP1 [ 1443(S A)] and wild-type nephrin plasmids.	Cytochalasin D	60-74	IQ motif containing GTPase activating protein 1	Homo sapiens	136-142
26028560-7	2015	HSP27(Asp) overexpression also rendered the monolayer more resistant to barrier disruption caused by Cytochalasin D, a chemical reagent that depolymerizes F-actin specifically.	Cytochalasin D	101-115	heat shock protein family B (small) member 1	Homo sapiens	0-10
25055182-7	2015	Inhibition of actin polymerization with cytochalasin D obviously abolished the effects of visfatin on the migration of Caov-3 cells.	Cytochalasin D	40-54	nicotinamide phosphoribosyltransferase	Homo sapiens	90-98
25652011-8	2015	Furthermore, the cytoskeletal disorganization stimulated by cytochalasin D in COS7 cells was recovered by cotransfection with wild-type IQGAP1 and nephrin plasmids but was not recovered either by single transfection of the wild-type IQGAP1 plasmid or by cotransfection of mutant IQGAP1 [ 1443(S A)] and wild-type nephrin plasmids.	Cytochalasin D	60-74	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	313-320
25652011-8	2015	Furthermore, the cytoskeletal disorganization stimulated by cytochalasin D in COS7 cells was recovered by cotransfection with wild-type IQGAP1 and nephrin plasmids but was not recovered either by single transfection of the wild-type IQGAP1 plasmid or by cotransfection of mutant IQGAP1 [ 1443(S A)] and wild-type nephrin plasmids.	Cytochalasin D	60-74	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	147-154
25652011-8	2015	Furthermore, the cytoskeletal disorganization stimulated by cytochalasin D in COS7 cells was recovered by cotransfection with wild-type IQGAP1 and nephrin plasmids but was not recovered either by single transfection of the wild-type IQGAP1 plasmid or by cotransfection of mutant IQGAP1 [ 1443(S A)] and wild-type nephrin plasmids.	Cytochalasin D	60-74	IQ motif containing GTPase activating protein 1	Homo sapiens	233-239
25387906-3	2014	A polarized Src activation was observed with higher activity at the side facing the flow, which was enhanced by a cytochalasin D-mediated disruption of actin filaments but inhibited by a benzyl alcohol-mediated enhancement of membrane fluidity.	Cytochalasin D	114-128	SRC proto-oncogene, non-receptor tyrosine kinase	Bos taurus	12-15
25756282-2	2015	Here we show that depolymerization of the actin cytoskeleton of various metastatic cancer cell lines with Cytochalasin D (Cyt D) reduces cell size and F-actin levels and induces E-cadherin expression at both the protein and mRNA level.	Cytochalasin D	106-120	cadherin 1	Homo sapiens	178-188
25187968-5	2014	Chemical inhibition of actin polymerization using cytochalasin D rescued the loss of SSH1.	Cytochalasin D	50-64	slingshot protein phosphatase 1	Homo sapiens	85-89
25142580-4	2014	We found that macropinocytosis inhibitor cytochalasin D blocked rAAV transduction of HeLa cells (>2-fold) but enhanced (10-fold) transduction in HepG2 and Huh7 lines.	Cytochalasin D	41-55	MIR7-3 host gene	Homo sapiens	158-162
24880063-10	2014	Regulation of mFPR2-induced respiratory response by ROCK was impossible under the cytoskeleton disruption by cytochalasin D, whereas it persisted in the case of mFPR1 activation.	Cytochalasin D	109-123	formyl peptide receptor 2	Mus musculus	14-19
24625812-7	2014	NTHi-induced beta-defensin 2 up-regulation was attenuated by cytochalasin D, an inhibitor of actin polymerization and was enhanced by alpha-hemolysin, a pore-forming toxin.	Cytochalasin D	61-75	defensin beta 4B	Homo sapiens	13-28
24969778-6	2014	PECAM-1-mediated internalization of GPIbalpha was reduced in the presence of both EGTA and cytochalasin D or latrunculin, but not either individually, and was reduced in mice in which tyrosines 747 and 759 of the cytoplasmic tail of beta3 integrin were mutated to phenylalanine.	Cytochalasin D	91-105	platelet/endothelial cell adhesion molecule 1	Mus musculus	0-7
24969778-6	2014	PECAM-1-mediated internalization of GPIbalpha was reduced in the presence of both EGTA and cytochalasin D or latrunculin, but not either individually, and was reduced in mice in which tyrosines 747 and 759 of the cytoplasmic tail of beta3 integrin were mutated to phenylalanine.	Cytochalasin D	91-105	glycoprotein 1b, alpha polypeptide	Mus musculus	36-45
25072322-3	2014	In addition, we show that both chronic administration of D-Asp and deletion of the gene coding for the catabolic enzyme D-aspartate oxidase (DDO) trigger plastic modifications of neuronal cytoarchitecture in the prefrontal cortex and CA1 subfield of the hippocampus and promote a cytochalasin D-sensitive form of synaptic plasticity in adult mouse brains.	Cytochalasin D	280-294	D-aspartate oxidase	Mus musculus	141-144
24956930-5	2014	We also carry out live-cell imaging of N19-OLGs co-transfected with fluorescent MBP and actin, and show that when actin filaments re-assemble after recovery from cytochalasin D treatment, MBP and actin are rapidly enriched and co-localized at certain sites at the plasma membrane and in newly-formed membrane ruffles.	Cytochalasin D	162-176	myelin basic protein	Homo sapiens	188-191
24901433-4	2014	These two processes appear to regulate different stages of exocytosis; whereas the inhibition of actin polymerization with the N-WASP inhibitor wiskostatin restricts fusion pore expansion, thus limiting the release of transmitters, the disruption of the cortical actin network with cytochalasin D increases the amount of transmitter released per event.	Cytochalasin D	282-296	WASP like actin nucleation promoting factor	Bos taurus	127-133
24901433-6	2014	Finally, the isolated SH3 domain of c-Src prevents both the disruption of the actin network and the increase in the quantal release induced by cytochalasin D.	Cytochalasin D	143-157	SRC proto-oncogene, non-receptor tyrosine kinase	Bos taurus	38-41
25155506-7	2014	Previous work showed that treating Chlamydomonas cells with the actin-depolymerizing compound cytochalasin D resulted in reversible flagellar shortening [5], but how actin is related to flagellar length or assembly remains unknown.	Cytochalasin D	94-108	uncharacterized protein	Chlamydomonas reinhardtii	64-69
25155506-7	2014	Previous work showed that treating Chlamydomonas cells with the actin-depolymerizing compound cytochalasin D resulted in reversible flagellar shortening [5], but how actin is related to flagellar length or assembly remains unknown.	Cytochalasin D	94-108	uncharacterized protein	Chlamydomonas reinhardtii	166-171
24952458-6	2014	Although, molecular mechanisms of actin and vimentin disruption by the applied cytoskeletal drugs, Cytochalasin-D and Withaferin-A, are different, cell softening in both cases can be attributed to reduction of the effective density and stiffness of filament networks.	Cytochalasin D	99-113	vimentin	Homo sapiens	44-52
24331979-6	2014	Moreover, the treatments of PF573228, Y27632 and cytochalasin D promoted p38 and ERK1/2 phosphorylations, and the treatments of U0126 and SB203580 decreased p38 and ERK1/2 phosphorylations, respectively.	Cytochalasin D	49-63	mitogen-activated protein kinase 1	Homo sapiens	73-76
24331979-6	2014	Moreover, the treatments of PF573228, Y27632 and cytochalasin D promoted p38 and ERK1/2 phosphorylations, and the treatments of U0126 and SB203580 decreased p38 and ERK1/2 phosphorylations, respectively.	Cytochalasin D	49-63	mitogen-activated protein kinase 3	Homo sapiens	81-87
24331979-6	2014	Moreover, the treatments of PF573228, Y27632 and cytochalasin D promoted p38 and ERK1/2 phosphorylations, and the treatments of U0126 and SB203580 decreased p38 and ERK1/2 phosphorylations, respectively.	Cytochalasin D	49-63	mitogen-activated protein kinase 3	Homo sapiens	165-171
24133214-7	2013	Inhibiting F-actin assembly with cytochalasin D enhanced secretion in WT platelets and further increased TGF-beta1 release in WASp(-/-) platelets, indicating that WASp and actin assembly independently regulate TGF-beta1 release.	Cytochalasin D	33-47	transforming growth factor beta 1	Homo sapiens	105-114
24036211-6	2014	Disruption of actin cytoskeletal polymerization with cytochalasin D inhibited HRG induced MTK1/HER3 association.	Cytochalasin D	53-67	mitogen-activated protein kinase kinase kinase 4	Homo sapiens	90-94
24036211-6	2014	Disruption of actin cytoskeletal polymerization with cytochalasin D inhibited HRG induced MTK1/HER3 association.	Cytochalasin D	53-67	erb-b2 receptor tyrosine kinase 3	Homo sapiens	95-99
24097312-5	2014	Inhibitors of MPC, Cytochalasin D and amiloride, decreased P27-mediated uptake of soluble dextran and inhibited P27-induced virus uptake by >60%, which provides further evidence that P27 induces MPC.	Cytochalasin D	19-33	interferon alpha inducible protein 27	Homo sapiens	59-62
24097312-5	2014	Inhibitors of MPC, Cytochalasin D and amiloride, decreased P27-mediated uptake of soluble dextran and inhibited P27-induced virus uptake by >60%, which provides further evidence that P27 induces MPC.	Cytochalasin D	19-33	interferon alpha inducible protein 27	Homo sapiens	112-115
24097312-5	2014	Inhibitors of MPC, Cytochalasin D and amiloride, decreased P27-mediated uptake of soluble dextran and inhibited P27-induced virus uptake by >60%, which provides further evidence that P27 induces MPC.	Cytochalasin D	19-33	interferon alpha inducible protein 27	Homo sapiens	112-115
23670201-11	2013	Regarding the mechanism of PM2.5 uptake, in both THP-1 and A549 cells, cytochalasin D prevented PM2.5-induced IL-8 mRNA expression and cytokine release, indicating a key role for actin polymerization in particles uptake and that the production of IL-8 correlated with particle phagocytosis.	Cytochalasin D	71-85	GLI family zinc finger 2	Homo sapiens	49-54
23670201-11	2013	Regarding the mechanism of PM2.5 uptake, in both THP-1 and A549 cells, cytochalasin D prevented PM2.5-induced IL-8 mRNA expression and cytokine release, indicating a key role for actin polymerization in particles uptake and that the production of IL-8 correlated with particle phagocytosis.	Cytochalasin D	71-85	C-X-C motif chemokine ligand 8	Homo sapiens	110-114
23670201-11	2013	Regarding the mechanism of PM2.5 uptake, in both THP-1 and A549 cells, cytochalasin D prevented PM2.5-induced IL-8 mRNA expression and cytokine release, indicating a key role for actin polymerization in particles uptake and that the production of IL-8 correlated with particle phagocytosis.	Cytochalasin D	71-85	C-X-C motif chemokine ligand 8	Homo sapiens	247-251
24312378-6	2013	Finally, we noted that albumin uptake in RPMEC was in part sensitive to pharmacological agents (amiloride [sodium transport inhibitor], Go6976 [protein kinase C inhibitor], and cytochalasin D [inhibitor of actin polymerization]) consistent with a macropinocytosis-like process.	Cytochalasin D	177-191	albumin	Mus musculus	23-30
23831868-8	2013	Incubation of chondrocytes with cytochalasin D, an actin microfilament-disrupting reagent, blocked the induction of PTHrP expression in response to strain.	Cytochalasin D	32-46	parathyroid hormone-like hormone	Rattus norvegicus	116-121
24135874-5	2013	Treatment of cells with cytochalasin D resulted in a loss of the microvilli projections and concomitantly abrogated CD44-mediated adhesion to its ligand hyaluronan.	Cytochalasin D	24-38	CD44 molecule (Indian blood group)	Homo sapiens	116-120
23850690-6	2013	However, treatment with cytochalasin D also increased the protein level of p62 under starvation conditions, suggesting that depolymerization of F-actin impaired autophagosome maturation and that the intact F-actin network is required for basal and starvation-induced autophagy.	Cytochalasin D	24-38	nucleoporin 62	Mus musculus	75-78
24040268-12	2013	Intriguingly, cytochalasin D induced relocalization of both PIP2 and EHD2 to actin aggregates, supporting a role of PIP2 in controlling EHD2 subcellular localization.	Cytochalasin D	14-28	EH domain containing 2	Homo sapiens	69-73
24040268-12	2013	Intriguingly, cytochalasin D induced relocalization of both PIP2 and EHD2 to actin aggregates, supporting a role of PIP2 in controlling EHD2 subcellular localization.	Cytochalasin D	14-28	EH domain containing 2	Homo sapiens	136-140
22961094-8	2013	Cd-stimulated Trx1 nuclear translocation and NF-kappaB activation were inhibited by cytochalasin D, an inhibitor of actin polymerization, suggesting that actin regulates Trx1 nuclear translocation and NF-kappaB activation by Cd.	Cytochalasin D	84-98	thioredoxin 1	Mus musculus	14-18
23838354-9	2013	Reducing cytoskeletal tension through the use of chemical inhibitors, either cytochalasin D or blebbistatin, resulted in an up-regulation of adipogenic gene expression (peroxisome proliferator-activated receptor gamma (PPARgamma), lipoprotein lipase (LPL) and fatty acid binding protein 4 (FABP4)) and metabolic markers, regardless of oxygen levels.	Cytochalasin D	77-91	peroxisome proliferator activated receptor gamma	Homo sapiens	169-217
23838354-9	2013	Reducing cytoskeletal tension through the use of chemical inhibitors, either cytochalasin D or blebbistatin, resulted in an up-regulation of adipogenic gene expression (peroxisome proliferator-activated receptor gamma (PPARgamma), lipoprotein lipase (LPL) and fatty acid binding protein 4 (FABP4)) and metabolic markers, regardless of oxygen levels.	Cytochalasin D	77-91	peroxisome proliferator activated receptor gamma	Homo sapiens	219-228
23838354-9	2013	Reducing cytoskeletal tension through the use of chemical inhibitors, either cytochalasin D or blebbistatin, resulted in an up-regulation of adipogenic gene expression (peroxisome proliferator-activated receptor gamma (PPARgamma), lipoprotein lipase (LPL) and fatty acid binding protein 4 (FABP4)) and metabolic markers, regardless of oxygen levels.	Cytochalasin D	77-91	lipoprotein lipase	Homo sapiens	231-249
23838354-9	2013	Reducing cytoskeletal tension through the use of chemical inhibitors, either cytochalasin D or blebbistatin, resulted in an up-regulation of adipogenic gene expression (peroxisome proliferator-activated receptor gamma (PPARgamma), lipoprotein lipase (LPL) and fatty acid binding protein 4 (FABP4)) and metabolic markers, regardless of oxygen levels.	Cytochalasin D	77-91	lipoprotein lipase	Homo sapiens	251-254
23838354-9	2013	Reducing cytoskeletal tension through the use of chemical inhibitors, either cytochalasin D or blebbistatin, resulted in an up-regulation of adipogenic gene expression (peroxisome proliferator-activated receptor gamma (PPARgamma), lipoprotein lipase (LPL) and fatty acid binding protein 4 (FABP4)) and metabolic markers, regardless of oxygen levels.	Cytochalasin D	77-91	fatty acid binding protein 4	Homo sapiens	260-288
23838354-9	2013	Reducing cytoskeletal tension through the use of chemical inhibitors, either cytochalasin D or blebbistatin, resulted in an up-regulation of adipogenic gene expression (peroxisome proliferator-activated receptor gamma (PPARgamma), lipoprotein lipase (LPL) and fatty acid binding protein 4 (FABP4)) and metabolic markers, regardless of oxygen levels.	Cytochalasin D	77-91	fatty acid binding protein 4	Homo sapiens	290-295
23615686-0	2013	Cytochalasin D promotes pulmonary metastasis of B16 melanoma through expression of tissue factor.	Cytochalasin D	0-14	coagulation factor III	Mus musculus	83-96
23481505-15	2013	alpha Angle was elevated, and clotting time was shortened over the 4 h. Treatment with cytochalasin D (platelet function inhibitor) eliminated the increases in clotting firmness and thrombin generation seen at 2 h with rising platelet count.	Cytochalasin D	87-101	coagulation factor II	Rattus norvegicus	182-190
23085402-6	2013	Disruption of the actin cytoskeleton, upon treatment of the cells with latrunculin B or cytochalasin D, caused severe changes in cell and membrane morphology, and concomitant changes in the subcellular distribution of ABCB1, as revealed by confocal laser scanning and electron microscopy.	Cytochalasin D	88-102	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	218-223
23441986-10	2013	Colocalization of GFP-labeled E. coli with cells positive for CD45, CD68, and F4/80 revealed time-dependent phagocytotic uptake, which was underlined by colocalization with the LysoTracker-Red( ) dye as well as preincubation with cytochalasin D.	Cytochalasin D	230-244	adhesion G protein-coupled receptor E1	Mus musculus	78-83
23411345-7	2013	EGF-induced relocalization of T-cad to cell-cell contacts could be abrogated by specific inhibitors of EGFR tyrosine kinase activity (gefitinib or lapatinib), lipid raft integrity (filipin), actin microfilament polymerization (cytochalasin D or cytochalasin B), p38MAPK (SB203580) or Rac1 (compound4).	Cytochalasin D	227-241	cadherin 13	Homo sapiens	30-35
23411345-7	2013	EGF-induced relocalization of T-cad to cell-cell contacts could be abrogated by specific inhibitors of EGFR tyrosine kinase activity (gefitinib or lapatinib), lipid raft integrity (filipin), actin microfilament polymerization (cytochalasin D or cytochalasin B), p38MAPK (SB203580) or Rac1 (compound4).	Cytochalasin D	227-241	epidermal growth factor receptor	Homo sapiens	103-107
23454239-6	2013	Cytochalasin D selectively inhibited the recycling of endocytosed B2R-GFP (B2R-GFP imaging, [3H]BK binding).	Cytochalasin D	0-14	bradykinin receptor B2	Homo sapiens	66-69
23454239-6	2013	Cytochalasin D selectively inhibited the recycling of endocytosed B2R-GFP (B2R-GFP imaging, [3H]BK binding).	Cytochalasin D	0-14	bradykinin receptor B2	Homo sapiens	75-78
22961094-8	2013	Cd-stimulated Trx1 nuclear translocation and NF-kappaB activation were inhibited by cytochalasin D, an inhibitor of actin polymerization, suggesting that actin regulates Trx1 nuclear translocation and NF-kappaB activation by Cd.	Cytochalasin D	84-98	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	45-54
22961094-8	2013	Cd-stimulated Trx1 nuclear translocation and NF-kappaB activation were inhibited by cytochalasin D, an inhibitor of actin polymerization, suggesting that actin regulates Trx1 nuclear translocation and NF-kappaB activation by Cd.	Cytochalasin D	84-98	thioredoxin 1	Mus musculus	170-174
22961094-8	2013	Cd-stimulated Trx1 nuclear translocation and NF-kappaB activation were inhibited by cytochalasin D, an inhibitor of actin polymerization, suggesting that actin regulates Trx1 nuclear translocation and NF-kappaB activation by Cd.	Cytochalasin D	84-98	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	201-210
22929165-10	2012	Disruption of cytoskeletal networks with 5-iodonaphthalene-1-sulfonyl homopiperazine and cytochalasin D abolished the effects of ZASP1-D117N on Na(v)1.5.	Cytochalasin D	89-103	immunoglobulin lambda variable 2-18	Homo sapiens	144-152
22956334-5	2012	Moreover, the inhibition of actin polymerization blocked the FSS-induced activation of Ccn2, whereas inducing F-actin formation using cytochalasin D and jasplakinolide enhanced Ccn2 expression in the same cells.	Cytochalasin D	134-148	cellular communication network factor 2	Mus musculus	177-181
22786771-8	2012	Inhibition of MMP-induced IFN-alpha secretion by cytochalasin D, chloroquine, and an inhibitory G-rich oligodeoxynucleotide identify TLR9 as the receptor for MMP-DNA.	Cytochalasin D	49-63	interferon alpha 1	Homo sapiens	26-35
22252987-5	2012	When the cells were subjected to hypotonic stress, the content of ACTN4 increased in a 100,000 x g pellet, which was sensitive to cytochalasin D pretreatment.	Cytochalasin D	130-144	actinin alpha 4	Homo sapiens	66-71
23026698-3	2012	Fibroblasts were harvested from the patellar tendon of a mature Japanese white rabbit and treated with cytochalasin D to depolymerize the actin filaments.	Cytochalasin D	103-117	actin	Oryctolagus cuniculus	138-143
22684244-7	2012	Cytochalasin D reduced the phosphorylation of cofilin, whereas staurosporine showed little effect on cofilin phosphorylation.	Cytochalasin D	0-14	cofilin 1	Homo sapiens	46-53
22798677-6	2012	Treatment of APCs with the actin filament depolymerizing agent, cytochalasin D, as well as knockdown of LIM kinase by short hairpin RNA, resulted in enhanced Ag presentation to NKT cells by CD1d, consistent with our ROCK inhibition data.	Cytochalasin D	64-78	amyloid P component, serum	Mus musculus	13-17
22798677-6	2012	Treatment of APCs with the actin filament depolymerizing agent, cytochalasin D, as well as knockdown of LIM kinase by short hairpin RNA, resulted in enhanced Ag presentation to NKT cells by CD1d, consistent with our ROCK inhibition data.	Cytochalasin D	64-78	CD1d1 antigen	Mus musculus	190-194
21984596-3	2012	Depolymerization of actin filaments with cytochalasin D or latrunculin A increased AFAP in the cytosolic fraction.	Cytochalasin D	41-55	actin filament associated protein 1	Homo sapiens	83-87
22683858-7	2012	Furthermore, cytochalasin D, an inhibitor of actin polymerization, also inhibited the mechanical strain-induced increase in phospho-Akt.	Cytochalasin D	13-27	thymoma viral proto-oncogene 1	Mus musculus	132-135
22728040-0	2012	Cytochalasin D acts as an inhibitor of the actin-cofilin interaction.	Cytochalasin D	0-14	cofilin 1	Homo sapiens	49-56
22728040-2	2012	In this study, cytochalasin D (CytoD), a widely used inhibitor of actin dynamics, was found to act as an inhibitor of the G-actin-cofilin interaction by binding to G-actin.	Cytochalasin D	15-29	cofilin 1	Homo sapiens	130-137
22088432-8	2012	Finally, we demonstrate that the increase in surface expression of NHE8 with acid media was blocked by colchicine and cytochalasin D and mediated by acid increasing the rate of exocytosis.	Cytochalasin D	118-132	solute carrier family 9 member A8	Homo sapiens	67-71
22131419-9	2011	Disruption of estradiol-induced beta-actin polymerization with cytochalasin D attenuated lordosis behavior, indicating the importance of estradiol-mediated spinogenesis for female sexual receptivity (81.43 +- 7.05 to 35.00 +- 11.76, p < 0.05).	Cytochalasin D	63-77	actin, beta	Rattus norvegicus	32-42
21809384-6	2012	Short exposure to IL-1alpha, IL-6, or IL-8 decreased endogenous GTP-Cdc42 and increased stress fibers, which were reversed with cytochalasin D treatment.	Cytochalasin D	128-142	interleukin 1 alpha	Homo sapiens	18-27
21809384-6	2012	Short exposure to IL-1alpha, IL-6, or IL-8 decreased endogenous GTP-Cdc42 and increased stress fibers, which were reversed with cytochalasin D treatment.	Cytochalasin D	128-142	interleukin 6	Homo sapiens	29-33
21809384-6	2012	Short exposure to IL-1alpha, IL-6, or IL-8 decreased endogenous GTP-Cdc42 and increased stress fibers, which were reversed with cytochalasin D treatment.	Cytochalasin D	128-142	C-X-C motif chemokine ligand 8	Homo sapiens	38-42
21898124-5	2012	The effects of PACAP at stimulating FAK and paxillin tyrosine phosphorylation were reversed by cytochalasin D and genistein which inhibit actin polymerization and tyrosine kinase activity, respectively.	Cytochalasin D	95-109	adenylate cyclase activating polypeptide 1	Homo sapiens	15-20
21898124-5	2012	The effects of PACAP at stimulating FAK and paxillin tyrosine phosphorylation were reversed by cytochalasin D and genistein which inhibit actin polymerization and tyrosine kinase activity, respectively.	Cytochalasin D	95-109	protein tyrosine kinase 2	Homo sapiens	36-39
21809384-6	2012	Short exposure to IL-1alpha, IL-6, or IL-8 decreased endogenous GTP-Cdc42 and increased stress fibers, which were reversed with cytochalasin D treatment.	Cytochalasin D	128-142	cell division cycle 42	Homo sapiens	68-73
21862582-9	2011	Inhibition of phagocytosis with cytochalasin D abolished the IL-1beta stimulatory activity of chitosan, offering an explanation for why the largest particles were nearly devoid of activity.	Cytochalasin D	32-46	interleukin 1 beta	Mus musculus	61-69
21921266-7	2011	Exposure to actin-targeting drugs (Cytochalasin D, Latrunculin B, Jasplakinolide) for 24 hours led to disruption of alpha-SMA containing stress fibers.	Cytochalasin D	35-49	actin gamma 2, smooth muscle	Rattus norvegicus	116-125
21918188-3	2011	LPS-induced tyrosine phosphorylation of MD-2 is specific; it is blocked by the tyrosine kinase inhibitor, herbimycin A, as well as by an inhibitor of endocytosis, cytochalasin D, suggesting that MD-2 phosphorylation occurs during trafficking of MD-2 and not on the cell surface.	Cytochalasin D	163-177	lymphocyte antigen 96	Homo sapiens	40-44
21827164-7	2011	At low concentrations (<5 muM), internalization of RNase A and these cell-penetrating peptides (CPPs) is inhibited by chlorpromazine as well as the macropinocytosis inhibitors cytochalasin D and 5-(N-ethyl-N-isopropyl)amiloride to a similar extent, indicative of common endocytic mechanism.	Cytochalasin D	179-193	ribonuclease A family member 1, pancreatic	Homo sapiens	54-61
21768101-8	2011	Treatment with either cytochalasin D or glyoxal, a cellular AGE, indicated that both actin depolymerization and AGE contribute to desmin disorganization.	Cytochalasin D	22-36	desmin	Mus musculus	130-136
21364884-2	2011	Here, we find that apoptosis induced by actin disruption via cytochalasin D and by the protein phosphatase 1/2A inhibitor okadaic acid also requires MEKK1 activation.	Cytochalasin D	61-75	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	149-154
21757694-3	2011	Disruption of the actin cytoskeleton with cytochalasin D inhibited P2X1 receptor currents with no effect on the time course of the response or surface expression of the receptor.	Cytochalasin D	42-56	purinergic receptor P2X 1	Homo sapiens	67-80
21207944-9	2011	Additionally, we have found that actin filaments are involved in the CD24-mediated cell rolling, as observed by the decreased rolling velocities of the MCF-7 cells upon treatment with cytochalasin D (an inhibitor of actin-filament dynamics) and the stationary binding of CD24-coated microspheres (the lack of actins) on the E-selectin-immobilized slides.	Cytochalasin D	184-198	CD24 molecule	Homo sapiens	69-73
21281570-7	2011	This tension-recovering activity was inhibited when cells were treated with cytochalasin D, an inhibitor of actin polymerization, or with (-)-blebbistatin, an inhibitor of myosin II ATPase activity, suggesting that the activity was driven by actin-myosin interaction.	Cytochalasin D	76-90	myosin heavy chain 14	Homo sapiens	172-178
21281570-7	2011	This tension-recovering activity was inhibited when cells were treated with cytochalasin D, an inhibitor of actin polymerization, or with (-)-blebbistatin, an inhibitor of myosin II ATPase activity, suggesting that the activity was driven by actin-myosin interaction.	Cytochalasin D	76-90	myosin heavy chain 14	Homo sapiens	248-254
21207944-9	2011	Additionally, we have found that actin filaments are involved in the CD24-mediated cell rolling, as observed by the decreased rolling velocities of the MCF-7 cells upon treatment with cytochalasin D (an inhibitor of actin-filament dynamics) and the stationary binding of CD24-coated microspheres (the lack of actins) on the E-selectin-immobilized slides.	Cytochalasin D	184-198	CD24 molecule	Homo sapiens	271-275
21207944-9	2011	Additionally, we have found that actin filaments are involved in the CD24-mediated cell rolling, as observed by the decreased rolling velocities of the MCF-7 cells upon treatment with cytochalasin D (an inhibitor of actin-filament dynamics) and the stationary binding of CD24-coated microspheres (the lack of actins) on the E-selectin-immobilized slides.	Cytochalasin D	184-198	selectin E	Homo sapiens	324-334
20961395-9	2011	A similar TAFI-dependent inhibition of fibrinolysis was observed when clot retraction was prevented by cytochalasin D or abciximab, or when platelet membranes were tested.	Cytochalasin D	103-117	carboxypeptidase B2	Homo sapiens	10-14
22216333-7	2011	(125)I-CXCL1 endocytosis was inhibited by amiloride, cytochalasin D, and the PKC inhibitor Go6976 whereas Platelet Derived Growth Factor (PDGF) enhanced ligand internalization through DARC.	Cytochalasin D	53-67	C-X-C motif chemokine ligand 1	Homo sapiens	7-12
21738583-6	2011	Our results show that cytochalasin D and jasplakinolide inhibit retinoschisin secretion, whereas Y-27632 and dibutyryl cGMP enhance secretion causing F-actin alterations.	Cytochalasin D	22-36	retinoschisin 1	Homo sapiens	64-77
20833776-9	2010	Actin depolymerization with cytochalasin D blocked the KGF-mediated increase in TER without significantly changing TER in control cells.	Cytochalasin D	28-42	fibroblast growth factor 7	Rattus norvegicus	55-58
21738688-6	2011	alpha(1A)-AR-induced activation of ERK1/2 but not p38 MAPK was sensitive to disruption of endocytosis, as demonstrated by 4 C chilling, dynamin mutation and treatment with cytochalasin D (actin depolymerizing agent).	Cytochalasin D	172-186	calcium voltage-gated channel subunit alpha1 A	Homo sapiens	0-8
21738688-6	2011	alpha(1A)-AR-induced activation of ERK1/2 but not p38 MAPK was sensitive to disruption of endocytosis, as demonstrated by 4 C chilling, dynamin mutation and treatment with cytochalasin D (actin depolymerizing agent).	Cytochalasin D	172-186	mitogen-activated protein kinase 3	Homo sapiens	35-41
20456692-0	2010	Anti-glycophorin C induces mitochondrial membrane  depolarization and a loss of extracellular regulated kinase 1/2  protein kinase activity that is prevented by pretreatment with  cytochalasin D: implications for hemolytic disease of the fetus  and newborn caused by anti-Ge3.	Cytochalasin D	180-194	glycophorin C (Gerbich blood group)	Homo sapiens	5-18
20814573-8	2010	Disrupting stress fiber contractile function with cytochalasin D or Y27632 decreased the levels of JNK and ERK phosphorylation.	Cytochalasin D	50-64	mitogen-activated protein kinase 8	Homo sapiens	99-102
20814573-8	2010	Disrupting stress fiber contractile function with cytochalasin D or Y27632 decreased the levels of JNK and ERK phosphorylation.	Cytochalasin D	50-64	mitogen-activated protein kinase 1	Homo sapiens	107-110
20338603-5	2010	This increased chemotactic activity of t10c12-CLA-treated porcine PMNs was inhibited by cytochalasin D, an F-actin polymerization inhibitor.	Cytochalasin D	88-102	selectin P ligand	Homo sapiens	46-49
20445173-8	2010	A simple explanation is that CD induces both clustering and integrin motion, fixation then stops motion on fixed cells, but integrins continue to diffuse on unfixed cells, increasing the kinetics of integrin/ICAM-1 interactions to enhance adhesion.	Cytochalasin D	29-31	intercellular adhesion molecule 1	Homo sapiens	208-214
20456692-7	2010	Both the ERK1/2 inhibition and the loss of mitochondrial potential were prevented by pretreatment with cytochalasin D.	Cytochalasin D	103-117	mitogen-activated protein kinase 3	Homo sapiens	9-15
20421639-7	2010	This beta-glucan triggered IL-1beta release was abolished by cytochalasin D, an inhibitor of phagocytosis, demonstrating that cytosolic recognition of beta-glucans is required for IL-1beta response in human macrophages.	Cytochalasin D	61-75	interleukin 1 beta	Homo sapiens	27-35
20376706-7	2010	Particularly, even if all methods tested allowed the production of blastocysts in vitro, the correct segregation of OCT4 occurred only in blastocysts developed from oocytes concomitantly treated for 4 h with Sr2+ and cytochalasin D.	Cytochalasin D	217-231	POU domain, class 5, transcription factor 1, related sequence 1	Mus musculus	116-120
20421639-7	2010	This beta-glucan triggered IL-1beta release was abolished by cytochalasin D, an inhibitor of phagocytosis, demonstrating that cytosolic recognition of beta-glucans is required for IL-1beta response in human macrophages.	Cytochalasin D	61-75	interleukin 1 beta	Homo sapiens	180-188
19647827-3	2009	Compared to untreated, maximally dilated controls, Cytochalasin D-treated arteries have shown a marked increase in compliance in the elastin-dominated pressure range.	Cytochalasin D	51-65	elastin	Homo sapiens	133-140
20393599-7	2010	Cytochalasin D decreased Cd2+-dependent ROS production, reduced the decline in mitochondrial membrane potential, and decreased phosphorylation of p38 kinase.	Cytochalasin D	0-14	mitogen-activated protein kinase 14	Mus musculus	146-149
20010439-0	2010	Cytochalasin D, LY294002 and olomoucine synergize in promoting death of melanoma cells through activation of caspase-3 and apoptosis.	Cytochalasin D	0-14	caspase 3	Homo sapiens	109-118
20010439-4	2010	We tested cell viability, terminal dUTP nick-end labeling and activation of caspase-3 upon exposure to cytochalasin D, LY294002 and olomoucine, added either alone or in various combinations.	Cytochalasin D	103-117	caspase 3	Homo sapiens	76-85
20010439-8	2010	In particular, the triple combination of cytochalasin D+LY294002+olomoucine was almost as effective as staurosporine in inducing caspase-3 activity and apoptosis.	Cytochalasin D	41-55	caspase 3	Homo sapiens	129-138
20196782-7	2009	Stimulation of Ror-alpha by cholesterol results in increased bone growth and enlarged, rounded cells, a phenotype similar to chondrocyte hypertrophy and to the changes induced by cytochalasin D, while inhibition of cholesterol synthesis by lovastatin inhibits cytochalasin D induced bone growth.	Cytochalasin D	179-193	RAR-related orphan receptor alpha	Mus musculus	15-24
19703961-11	2009	In LMN myocytes, cytochalasin D prevented inhibition of cAMP/PKA from enhancing zint-beta(2)-AR stimulation of I(Ca,L).	Cytochalasin D	17-31	adrenoceptor beta 2	Homo sapiens	85-95
20079271-5	2009	RESULTS: In control group and cytochalasin D group, fluid shear stress could significantly increase the expression levels of c-fos mRNA (0.1637 +/- 0.0303 and 0.0104 +/- 0.0070, respectively) and protein (177.14 +/- 9.37 and 150.95 +/- 6.17, respectively) in osteoblasts, compared with the unloaded osteoblasts of the control group and the cytochalasin D group (0.0057 +/- 0.0021 and 0.0032 +/- 0.0014, respectively for c-fos mRNA, and 117.96 +/- 4.11 and 119.77 +/- 5.19, respectively for protein, P < 0.05).	Cytochalasin D	30-44	FBJ osteosarcoma oncogene	Mus musculus	125-130
20079271-5	2009	RESULTS: In control group and cytochalasin D group, fluid shear stress could significantly increase the expression levels of c-fos mRNA (0.1637 +/- 0.0303 and 0.0104 +/- 0.0070, respectively) and protein (177.14 +/- 9.37 and 150.95 +/- 6.17, respectively) in osteoblasts, compared with the unloaded osteoblasts of the control group and the cytochalasin D group (0.0057 +/- 0.0021 and 0.0032 +/- 0.0014, respectively for c-fos mRNA, and 117.96 +/- 4.11 and 119.77 +/- 5.19, respectively for protein, P < 0.05).	Cytochalasin D	30-44	FBJ osteosarcoma oncogene	Mus musculus	420-425
20079271-6	2009	Induced by the fluid shear stress, the expression levels of c-fos mRNA and protein in cytochalasin D group were lower than control group, and the difference had statistical significance (P < 0.05).	Cytochalasin D	86-100	FBJ osteosarcoma oncogene	Mus musculus	60-65
20196782-7	2009	Stimulation of Ror-alpha by cholesterol results in increased bone growth and enlarged, rounded cells, a phenotype similar to chondrocyte hypertrophy and to the changes induced by cytochalasin D, while inhibition of cholesterol synthesis by lovastatin inhibits cytochalasin D induced bone growth.	Cytochalasin D	260-274	RAR-related orphan receptor alpha	Mus musculus	15-24
19372205-7	2009	Interestingly, ENC1 physically associated with actin and treatment with cytochalasin D, an actin-depolymerizing agent, abolished this association.	Cytochalasin D	72-86	ectodermal-neural cortex 1	Rattus norvegicus	15-19