PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33957118-8	2021	Notably, FAK knockout increased cellular sensitivity to the Stat3 inhibitor CPA7, while FAK reintroduction restored resistance to this drug.	cpa7	76-80	PTK2 protein tyrosine kinase 2	Mus musculus	9-12
2777903-1	1989	The effects of the protein kinase C inhibitor H-7 on the actin cytoskeleton of cultured cells (Swiss 3T3 and PTK2) are described.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	46-49	PTK2 protein tyrosine kinase 2	Mus musculus	109-113
2777903-2	1989	As documented by fluorescence microscopy and the higher-resolution technique of photoelectron microscopy, the effects are rapid and dramatic; exposure to 30 microM H-7 in culture medium for less than 6 min is sufficient to induce a significant reduction in the numbers and thickness of actin microfilament bundles and alterations in the morphology of cell-cell boundaries in PTK2 cells.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	164-167	PTK2 protein tyrosine kinase 2	Mus musculus	375-379
2594015-6	1989	Significant differences were observed between the effectiveness of synthetic polypeptides used as carrier: highest oxazolone-specific antibody titers were observed using the AK, LAK and FAK conjugates.	Oxazolone	115-124	PTK2 protein tyrosine kinase 2	Mus musculus	186-189
2594015-7	1989	The intensity and specificity of the DTH reaction and antibody response induced by the carrier-oxazolone conjugates suggested that the distinct effectiveness of L- and D-amino acid-containing conjugates (LAK vs D-LAK and FAK vs D-FAK) was dependent on altered B cell recognition of the haptenic group.	Oxazolone	95-104	PTK2 protein tyrosine kinase 2	Mus musculus	221-224
2594015-7	1989	The intensity and specificity of the DTH reaction and antibody response induced by the carrier-oxazolone conjugates suggested that the distinct effectiveness of L- and D-amino acid-containing conjugates (LAK vs D-LAK and FAK vs D-FAK) was dependent on altered B cell recognition of the haptenic group.	Oxazolone	95-104	PTK2 protein tyrosine kinase 2	Mus musculus	230-233
2941630-7	1986	PTK2 epithelial cells incubated with uroporphyrin I at either 40 micrograms/ml or 80 mu/ml and 10 J/cm2 (615 nm) showed no apparent damage and had 100% cell survival.	uroporphyrin I	37-51	PTK2 protein tyrosine kinase 2	Mus musculus	0-4
6572952-1	1983	Injection of the alpha, beta-nonhydrolyzable GTP analog, guanosine 5"-[alpha, beta-methylene]triphosphate (pp[CH2]pG) into PtK2, A549, and Swiss 3T3 cells produced dramatic changes in the normal pattern of long radiating microtubules displayed by the cells before injection.	guanosine 5'-(alpha,beta-methylene)triphosphate	57-105	PTK2 protein tyrosine kinase 2	Mus musculus	123-127
2594015-7	1989	The intensity and specificity of the DTH reaction and antibody response induced by the carrier-oxazolone conjugates suggested that the distinct effectiveness of L- and D-amino acid-containing conjugates (LAK vs D-LAK and FAK vs D-FAK) was dependent on altered B cell recognition of the haptenic group.	l- and d-amino acid	161-180	PTK2 protein tyrosine kinase 2	Mus musculus	221-224
2594015-7	1989	The intensity and specificity of the DTH reaction and antibody response induced by the carrier-oxazolone conjugates suggested that the distinct effectiveness of L- and D-amino acid-containing conjugates (LAK vs D-LAK and FAK vs D-FAK) was dependent on altered B cell recognition of the haptenic group.	l- and d-amino acid	161-180	PTK2 protein tyrosine kinase 2	Mus musculus	230-233
33617975-0	2021	Suppression of macrophage migration by down-regulating Src/FAK/P130Cas activation contributed to the anti-inflammatory activity of sinomenine.	sinomenine	131-141	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
33617975-17	2021	These results indicated that SIN significantly inhibited macrophage mesenchymal migration by down-regulating on Src/FAK/P130Cas axis activation.	sinomenine	29-32	PTK2 protein tyrosine kinase 2	Mus musculus	116-119
33846784-0	2021	Knockdown of lncRNA MIR4435-2HG and ST8SIA1 expression inhibits the proliferation, invasion and migration of prostate cancer cells in vitro and in vivo by blocking the activation of the FAK/AKT/beta-catenin signaling pathway.	mir4435	20-27	PTK2 protein tyrosine kinase 2	Mus musculus	186-189
33846784-2	2021	The present study aimed to examine the effects of long non-coding RNA (lncRNA) MIR4435-2HG binding with ST8SIA1 on the proliferation, invasion and migration of prostate cancer cells via the activation of the FAK/AKT/beta-catenin signaling pathway.	mir4435	79-86	PTK2 protein tyrosine kinase 2	Mus musculus	208-211
33846784-8	2021	Interference with MIR4435-2HG inhibited the proliferation, clone formation ability, and the invasion and migration of PC-3 cells, as well as tumor growth by suppressing the activation of the FAK/AKT/beta-catenin signaling pathway.	mir4435	18-25	PTK2 protein tyrosine kinase 2	Mus musculus	191-194
33846784-11	2021	Interference with ST8SIA1 inhibited the promoting effects of MIR4435-2HG on the proliferation, invasion and migration of PC-3 cells, as well as tumor growth by suppressing the activation of the FAK/AKT/beta-catenin signaling pathway.	mir4435	61-68	PTK2 protein tyrosine kinase 2	Mus musculus	194-197
33846784-12	2021	On the whole, the present study demonstrates that interference with MIR4435-2HG, combined with ST8SIA1, inhibits the proliferation, invasion and migration of prostate cancer cells in vitro and in vivo by blocking the activation of the FAK/AKT/beta-catenin signaling pathway.	mir4435	68-75	PTK2 protein tyrosine kinase 2	Mus musculus	235-238
33677375-8	2021	Inhibition of FAK using PF-573228 ablated the stiffness-dependent increase in NET formation and pro-inflammatory molecule secretion.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	24-33	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
33910400-8	2021	Moreover, AZD0530 blocked the Src signaling pathway by downregulating phospho-Src and its downstream mediators (p-Stat3, p-Akt, p-FAK, p-p44/42 MAPK, p-p38 MAPK) in post-ischemic brains.	saracatinib	10-17	PTK2 protein tyrosine kinase 2	Mus musculus	130-133
33920786-0	2021	ZINC40099027 Promotes Gastric Mucosal Repair in Ongoing Aspirin-Associated Gastric Injury by Activating Focal Adhesion Kinase.	SCHEMBL21467297	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	104-125
33920786-0	2021	ZINC40099027 Promotes Gastric Mucosal Repair in Ongoing Aspirin-Associated Gastric Injury by Activating Focal Adhesion Kinase.	Aspirin	56-63	PTK2 protein tyrosine kinase 2	Mus musculus	104-125
33920786-3	2021	ZINC40099027 (ZN27) activates focal adhesion kinase (FAK) and heals acute indomethacin-induced small bowel injury.	SCHEMBL21467297	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	30-51
33920786-3	2021	ZINC40099027 (ZN27) activates focal adhesion kinase (FAK) and heals acute indomethacin-induced small bowel injury.	SCHEMBL21467297	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
33920786-3	2021	ZINC40099027 (ZN27) activates focal adhesion kinase (FAK) and heals acute indomethacin-induced small bowel injury.	zn27	14-18	PTK2 protein tyrosine kinase 2	Mus musculus	30-51
33920786-3	2021	ZINC40099027 (ZN27) activates focal adhesion kinase (FAK) and heals acute indomethacin-induced small bowel injury.	zn27	14-18	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
33920786-11	2021	Blinded scoring of pFAK-Y-397 immunoreactivity at the edge of ZN27-treated lesions demonstrated increased FAK activation, compared to vehicle-treated lesions, confirming target activation in vivo.	zn27	62-66	PTK2 protein tyrosine kinase 2	Mus musculus	20-23
33920786-12	2021	These results suggest that ZN27 ameliorates ongoing aspirin-associated gastric mucosal injury by a pathway involving FAK activation.	zn27	27-31	PTK2 protein tyrosine kinase 2	Mus musculus	117-120
33920786-12	2021	These results suggest that ZN27 ameliorates ongoing aspirin-associated gastric mucosal injury by a pathway involving FAK activation.	Aspirin	52-59	PTK2 protein tyrosine kinase 2	Mus musculus	117-120
33739836-0	2021	Design, Synthesis, Biological Evaluation, and Molecular Docking of 2,4-Diaminopyrimidine Derivatives Targeting Focal Adhesion Kinase as Tumor Radiotracers.	2,4-diaminopyrimidine	67-88	PTK2 protein tyrosine kinase 2	Mus musculus	111-132
33900313-8	2021	Moreover, our data revealed that activation of the ROS-derived and AKT/FAK/PAK1 pathways is involved in the erinacine S-mediated transcriptional activation of Fas-L and TRAIL through H3K4 trimethylation on their promoters.	erinacine S	108-117	PTK2 protein tyrosine kinase 2	Mus musculus	71-74
33738062-4	2021	In our previous research, we found a lead compound with drug-like properties, ZINC40099027, which promotes FAK phosphorylation, inducing mucosal healing in murine models.	SCHEMBL21467297	78-90	PTK2 protein tyrosine kinase 2	Mus musculus	107-110
33715263-2	2021	ZINC40099027 (Zn27) activates cellular FAK and promotes intestinal epithelial wound closure in vitro and in mice.	SCHEMBL21467297	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
33715263-2	2021	ZINC40099027 (Zn27) activates cellular FAK and promotes intestinal epithelial wound closure in vitro and in mice.	zn27	14-18	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
33715263-3	2021	However, whether Zn27 activates FAK directly or indirectly remains unknown.	zn27	17-21	PTK2 protein tyrosine kinase 2	Mus musculus	32-35
33730293-1	2021	Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that is overexpressed in many cancer types and in vivo studies have shown that vascular endothelial cell FAK expression and FAK-phosphorylation at tyrosine (Y) 397, and subsequently FAK-Y861, are important in tumour angiogenesis.	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
33730293-1	2021	Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that is overexpressed in many cancer types and in vivo studies have shown that vascular endothelial cell FAK expression and FAK-phosphorylation at tyrosine (Y) 397, and subsequently FAK-Y861, are important in tumour angiogenesis.	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
33730293-1	2021	Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that is overexpressed in many cancer types and in vivo studies have shown that vascular endothelial cell FAK expression and FAK-phosphorylation at tyrosine (Y) 397, and subsequently FAK-Y861, are important in tumour angiogenesis.	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
33730293-1	2021	Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that is overexpressed in many cancer types and in vivo studies have shown that vascular endothelial cell FAK expression and FAK-phosphorylation at tyrosine (Y) 397, and subsequently FAK-Y861, are important in tumour angiogenesis.	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
33730293-1	2021	Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that is overexpressed in many cancer types and in vivo studies have shown that vascular endothelial cell FAK expression and FAK-phosphorylation at tyrosine (Y) 397, and subsequently FAK-Y861, are important in tumour angiogenesis.	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
33634976-17	2021	PF00562271, a specific FAK inhibitor, blocked MFG-E8-induced STAT3 phosphorylation.	PF-00562271	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
33643917-10	2020	Doxycycline inhibits the pancreatic cancer through the PAR1/FAK/PI3K/AKT pathway and enhances the therapeutic effect of 5-FU.	Doxycycline	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	60-63
32843133-3	2021	The kinase domain of FAK interacts with PLD2-PH and induces tyrosine phosphorylation and activation of PLD2.	Tyrosine	60-68	PTK2 protein tyrosine kinase 2	Mus musculus	21-24
32843133-4	2021	Furthermore, PLD2 increased tyrosine phosphorylation of FAK.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	56-59
32843133-5	2021	However, ectopic expression of the PLD2-PH competes for binding to FAK and reduces the interaction between PLD2 and FAK, thereby suppressing FAK-induced PLD activation and tyrosine phosphorylation of FAK.	Tyrosine	172-180	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
32843133-5	2021	However, ectopic expression of the PLD2-PH competes for binding to FAK and reduces the interaction between PLD2 and FAK, thereby suppressing FAK-induced PLD activation and tyrosine phosphorylation of FAK.	Tyrosine	172-180	PTK2 protein tyrosine kinase 2	Mus musculus	116-119
32843133-5	2021	However, ectopic expression of the PLD2-PH competes for binding to FAK and reduces the interaction between PLD2 and FAK, thereby suppressing FAK-induced PLD activation and tyrosine phosphorylation of FAK.	Tyrosine	172-180	PTK2 protein tyrosine kinase 2	Mus musculus	116-119
32843133-5	2021	However, ectopic expression of the PLD2-PH competes for binding to FAK and reduces the interaction between PLD2 and FAK, thereby suppressing FAK-induced PLD activation and tyrosine phosphorylation of FAK.	Tyrosine	172-180	PTK2 protein tyrosine kinase 2	Mus musculus	116-119
33577036-0	2021	Effects of PPARgamma agonist pioglitazone on cardiac fibrosis in diabetic mice by regulating PTEN/AKT/FAK pathway.	Pioglitazone	29-41	PTK2 protein tyrosine kinase 2	Mus musculus	102-105
33314143-0	2021	Adhesion-dependent Caveolin1 Tyrosine-14 phosphorylation is regulated by FAK in response to changing matrix stiffness.	Tyrosine	29-37	PTK2 protein tyrosine kinase 2	Mus musculus	73-76
33466636-11	2021	Also, 6,8-DG inhibited the activation of the lymphangiogenesis-related downstream signaling factors such as FAK, PI3K, AKT, p38, and ERK in rhVEGF-A-treated HLMECs.	6,8-diprenylgenistein	6-12	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
33488961-0	2021	Discovery of a Pyrimidothiazolodiazepinone as a Potent and Selective Focal Adhesion Kinase (FAK) Inhibitor.	pyrimidothiazolodiazepinone	15-42	PTK2 protein tyrosine kinase 2	Mus musculus	69-90
33488961-0	2021	Discovery of a Pyrimidothiazolodiazepinone as a Potent and Selective Focal Adhesion Kinase (FAK) Inhibitor.	pyrimidothiazolodiazepinone	15-42	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
33488961-4	2021	We report a novel series of small molecules based on a tricyclic pyrimidothiazolodiazepinone core that displays both high potency and selectivity for FAK.	pyrimidothiazolodiazepinone	65-92	PTK2 protein tyrosine kinase 2	Mus musculus	150-153
32534990-4	2020	Tablysin-15 binds to integrin alphavbeta3 and inhibits the activation of FAK-associated signaling pathways.	tablysin-15	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	73-76
32736683-8	2020	We further confirmed that inhibition of MEK/ERK signaling pathway is the mechanism of cobimetinib"s action in osteosarcoma, leading to inhibition of focal adhesion kinase (FAK) and anti-apoptotic pathway, as well as activation of pro-apoptotic pathway.	cobimetinib	86-97	PTK2 protein tyrosine kinase 2	Mus musculus	149-170
32736683-8	2020	We further confirmed that inhibition of MEK/ERK signaling pathway is the mechanism of cobimetinib"s action in osteosarcoma, leading to inhibition of focal adhesion kinase (FAK) and anti-apoptotic pathway, as well as activation of pro-apoptotic pathway.	cobimetinib	86-97	PTK2 protein tyrosine kinase 2	Mus musculus	172-175
32976654-7	2020	However, the precise role of ZF21 binding to FAK remains unclear.	zf21	29-33	PTK2 protein tyrosine kinase 2	Mus musculus	45-48
32827545-6	2020	V-L-R-H could inhibit the TNFalpha-mediated PI3K/AKT/NF-kappaB signal pathway and integrin alphavbeta3 correlative FAK focal adhesion signal pathway.	v-l-r-h	0-7	PTK2 protein tyrosine kinase 2	Mus musculus	115-118
32849915-12	2020	In addition, silencing of LINC00475 decreased the extent of FAK phosphorylation and reduced the expression of HIF-1alpha and AGAP2.	linc00475	26-35	PTK2 protein tyrosine kinase 2	Mus musculus	60-63
32618992-0	2020	Anti-osteosarcoma effect of hydroxyapatite nanoparticles both in vitro and in vivo by downregulating the FAK/PI3K/Akt signaling pathway.	Durapatite	28-42	PTK2 protein tyrosine kinase 2	Mus musculus	105-108
32605995-8	2020	These findings demonstrate that drug resistance is conferred by Annexin A6 in CAF-EV and provide a potential avenue for overcoming gastric cancer drug resistance through the inhibition of FAK-YAP signaling in combination with conventional chemotherapeutics.	caf-ev	78-84	PTK2 protein tyrosine kinase 2	Mus musculus	188-191
32605995-9	2020	SIGNIFICANCE: This study elucidates a novel molecular mechanism through which Annexin A6 in CAF-EV activates FAK-YAP by stabilizing beta1 integrin at the cell surface of gastric cancer cells and subsequently induces drug resistance.	caf-ev	92-98	PTK2 protein tyrosine kinase 2	Mus musculus	109-112
33210606-8	2020	MgD (with Ca:Mg ratios >1) elevated intracellular Ca levels, calpain activity and TRPM7 expression, as well as oxidative stress and cell migration, consistent with observed degradation of full-length E-cadherin, beta-catenin, and N-terminal FAK.	Magnesium	0-2	PTK2 protein tyrosine kinase 2	Mus musculus	241-244
32390845-0	2020	Ginsenoside Rg3 Alleviates ox-LDL Induced Endothelial Dysfunction and Prevents Atherosclerosis in ApoE-/- Mice by Regulating PPARgamma/FAK Signaling Pathway.	ginsenoside Rg3	0-15	PTK2 protein tyrosine kinase 2	Mus musculus	135-138
32585188-7	2020	Next, we showed that 75 muM 4HNE significantly decreased the intracellular mRNA levels of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), focal adhesion kinase (FAK) and other promigratory genes compared to control, which were further decreased by DSF pretreatment.	4-hydroxy-2-nonenal	28-32	PTK2 protein tyrosine kinase 2	Mus musculus	159-180
32585188-7	2020	Next, we showed that 75 muM 4HNE significantly decreased the intracellular mRNA levels of vascular endothelial growth factor (VEGF), VEGF receptor 2 (VEGFR2), focal adhesion kinase (FAK) and other promigratory genes compared to control, which were further decreased by DSF pretreatment.	4-hydroxy-2-nonenal	28-32	PTK2 protein tyrosine kinase 2	Mus musculus	182-185
32585188-8	2020	75 muM 4HNE also decreased the protein levels of VEGFR2, FAK, phospho-FAK, Src and paxillin in MCECs.	4-hydroxy-2-nonenal	7-11	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
32585188-8	2020	75 muM 4HNE also decreased the protein levels of VEGFR2, FAK, phospho-FAK, Src and paxillin in MCECs.	4-hydroxy-2-nonenal	7-11	PTK2 protein tyrosine kinase 2	Mus musculus	70-73
32198666-5	2020	Accordingly, in the presence of GM1-oligosaccharide, neurons show a higher phosphorylation rate of FAK and Src proteins, the intracellular key regulators of neuronal motility.	G(M1)-oligosaccharide	32-51	PTK2 protein tyrosine kinase 2	Mus musculus	99-102
32343611-8	2020	PGF2a downregulated SHP-1 via PLCbeta-PKC-NF-kB or PI3K-NF-kB pathways, suggesting the regenerative downregulation of SHP-1 enhances the uterine remodeling and plasticity by activating FAK and subsequent focal adhesion pathway, which eventually facilitates myometrium contraction and leads to labor.	Dinoprost	0-5	PTK2 protein tyrosine kinase 2	Mus musculus	185-188
32518750-4	2020	The aim of this study was to explore the correlation between H-type vessels and MSCs in OA pathogenesis through regulation of H-type vessel formation using defactinib (an FAK inhibitor).	defactinib	156-166	PTK2 protein tyrosine kinase 2	Mus musculus	171-174
32390845-6	2020	For in vivo assay, Rg3 significantly reduced atherosclerotic pathological changes in ApoE-/- mice fed with HFD, up-regulated PPARgamma, and inhibited activation FAK in aorta, thus inhibited expression of VCAM-1, ICAM-1 in intima.	ginsenoside Rg3	19-22	PTK2 protein tyrosine kinase 2	Mus musculus	161-164
32390845-7	2020	We conclude that Rg3 may protect endothelial cells and inhibit atherosclerosis by up-regulating PPARgamma via repressing FAK-mediated pathways, indicating that Rg3 have good potential in preventing dyslipidemia induced atherosclerosis.	ginsenoside Rg3	17-20	PTK2 protein tyrosine kinase 2	Mus musculus	121-124
32390845-7	2020	We conclude that Rg3 may protect endothelial cells and inhibit atherosclerosis by up-regulating PPARgamma via repressing FAK-mediated pathways, indicating that Rg3 have good potential in preventing dyslipidemia induced atherosclerosis.	ginsenoside Rg3	160-163	PTK2 protein tyrosine kinase 2	Mus musculus	121-124
31601793-7	2019	Matrine treatment retarded the cancer associated signaling transduction by decreasing the phosphorylation levels of ERK1/2, MEK1/2, PI3K, Akt, mTOR, FAK, RhoA, VEGFR2, and Tie2 in vitro and in vivo.	matrine	0-7	PTK2 protein tyrosine kinase 2	Mus musculus	149-152
31556111-6	2020	Similar results were found after treatment with PF573228, a FAK inhibitor.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	48-56	PTK2 protein tyrosine kinase 2	Mus musculus	60-63
31988451-6	2020	Lastly, profiling of miRs from CAF exosomes showed alterations of several exosomal miRs in FAK-null CAFs, and further analysis suggested that miR-16 and miR-148a enriched in exosomes from FAK-null CAFs contribute to the reduced tumor cell activities and metastasis.	CAF protocol	31-34	PTK2 protein tyrosine kinase 2	Mus musculus	91-94
32051399-11	2020	Saracatinib treatment abolished the activation of Fyn, downregulated the Fyn/FAK/N-WASP signaling in HSCs, and subsequently prevented the activation of HSCs.	saracatinib	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	77-80
32025610-7	2020	At the molecular and cellular level, active FAK (phosphorylated FAK at tyrosine 397) bound to TGFbetaR2 and kept TGFbetaR2 at the peripheral plasma membrane of HSCs, and it induced TGFbetaR2 phosphorylation at tyrosine 336.	Tyrosine	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	44-47
32025610-7	2020	At the molecular and cellular level, active FAK (phosphorylated FAK at tyrosine 397) bound to TGFbetaR2 and kept TGFbetaR2 at the peripheral plasma membrane of HSCs, and it induced TGFbetaR2 phosphorylation at tyrosine 336.	Tyrosine	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	64-67
32025610-7	2020	At the molecular and cellular level, active FAK (phosphorylated FAK at tyrosine 397) bound to TGFbetaR2 and kept TGFbetaR2 at the peripheral plasma membrane of HSCs, and it induced TGFbetaR2 phosphorylation at tyrosine 336.	Tyrosine	210-218	PTK2 protein tyrosine kinase 2	Mus musculus	44-47
32025610-7	2020	At the molecular and cellular level, active FAK (phosphorylated FAK at tyrosine 397) bound to TGFbetaR2 and kept TGFbetaR2 at the peripheral plasma membrane of HSCs, and it induced TGFbetaR2 phosphorylation at tyrosine 336.	Tyrosine	210-218	PTK2 protein tyrosine kinase 2	Mus musculus	64-67
31791326-8	2019	RESULTS: PTK2 was hyperphosphorylated in PC-9/PEM.	3-(2-phenylethyl)-4-methylsydnone	46-49	PTK2 protein tyrosine kinase 2	Mus musculus	9-13
31791326-9	2019	Defactinib (PTK2 inhibitor) and PD173074 (FGFR inhibitor) inhibited PTK2 phosphorylation.	defactinib	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	12-16
31791326-9	2019	Defactinib (PTK2 inhibitor) and PD173074 (FGFR inhibitor) inhibited PTK2 phosphorylation.	defactinib	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	68-72
31791326-9	2019	Defactinib (PTK2 inhibitor) and PD173074 (FGFR inhibitor) inhibited PTK2 phosphorylation.	PD 173074	32-40	PTK2 protein tyrosine kinase 2	Mus musculus	68-72
31791326-10	2019	Combination of PTK2 inhibitor and EGFR-TKI inhibited Akt and induced apoptosis in PC-9/PEM.	3-(2-phenylethyl)-4-methylsydnone	87-90	PTK2 protein tyrosine kinase 2	Mus musculus	15-19
31791326-12	2019	Furthermore, erlotinib-resistant NSCLC cell lines showed PTK2 hyperphosphorylation.	Erlotinib Hydrochloride	13-22	PTK2 protein tyrosine kinase 2	Mus musculus	57-61
31791326-13	2019	PTK2 inhibition in the PTK2 hyperphosphorylated erlotinib-resistant cell lines also recovered EGFR-TKI sensitivity.	Erlotinib Hydrochloride	48-57	PTK2 protein tyrosine kinase 2	Mus musculus	0-4
31791326-13	2019	PTK2 inhibition in the PTK2 hyperphosphorylated erlotinib-resistant cell lines also recovered EGFR-TKI sensitivity.	Erlotinib Hydrochloride	48-57	PTK2 protein tyrosine kinase 2	Mus musculus	23-27
31791326-15	2019	Combination of PTK2 inhibitor and EGFR-TKI (defactinib and osimertinib) recovered EGFR-TKI sensitivity in the EGFR-TKI-resistant NSCLC.	defactinib	44-54	PTK2 protein tyrosine kinase 2	Mus musculus	15-19
31791326-15	2019	Combination of PTK2 inhibitor and EGFR-TKI (defactinib and osimertinib) recovered EGFR-TKI sensitivity in the EGFR-TKI-resistant NSCLC.	osimertinib	59-70	PTK2 protein tyrosine kinase 2	Mus musculus	15-19
31483951-6	2019	Eucalyptol induces focal adhesion proteins of paxillin, vinculin, talin1, FAK, and Src in glucose-exposed podocytes and diabetic kidneys.	Eucalyptol	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
31604999-2	2019	The non-receptor tyrosine kinase focal adhesion kinase (FAK) stimulates epithelial motility.	Tyrosine	17-25	PTK2 protein tyrosine kinase 2	Mus musculus	56-59
31604999-3	2019	A virtual screen identified the small drug-like FAK mimic ZINC40099027, which activates FAK.	ZINC08254138	58-70	PTK2 protein tyrosine kinase 2	Mus musculus	48-51
31604999-3	2019	A virtual screen identified the small drug-like FAK mimic ZINC40099027, which activates FAK.	ZINC08254138	58-70	PTK2 protein tyrosine kinase 2	Mus musculus	88-91
31604999-4	2019	We assessed whether ZINC40099027 promotes FAK-Tyr-397 phosphorylation and wound healing in Caco-2 monolayers and two mouse intestinal injury models.	ZINC08254138	20-32	PTK2 protein tyrosine kinase 2	Mus musculus	42-45
31604999-4	2019	We assessed whether ZINC40099027 promotes FAK-Tyr-397 phosphorylation and wound healing in Caco-2 monolayers and two mouse intestinal injury models.	tyrosyltyrosine	46-49	PTK2 protein tyrosine kinase 2	Mus musculus	42-45
29945484-0	2019	Quercetin inhibits LPS-induced macrophage migration by suppressing the iNOS/FAK/paxillin pathway and modulating the cytoskeleton.	Quercetin	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
29945484-7	2019	Moreover, quercetin inhibited the LPS-induced expression of p-FAK, p-paxillin, FAK, and paxillin as well as the cytoskeletal adapter proteins vinculin and Tensin-2.	Quercetin	10-19	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
29945484-7	2019	Moreover, quercetin inhibited the LPS-induced expression of p-FAK, p-paxillin, FAK, and paxillin as well as the cytoskeletal adapter proteins vinculin and Tensin-2.	Quercetin	10-19	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
29945484-8	2019	Therefore, quercetin suppresses LPS-induced migration by inhibiting NO production, disrupting the F-actin cytoskeleton, and suppressing the FAK-paxillin pathway.	Quercetin	11-20	PTK2 protein tyrosine kinase 2	Mus musculus	140-143
31710352-9	2019	Mechanistically, CXCL13 induces the expression of PHLPP1, an Akt2 phosphatase, through FAK signaling; and correspondingly we show that CXCL13 and DFO-induced IL-6 and PAI-1 expression was blocked by Phlpp1 knockdown.	Deferoxamine	146-149	PTK2 protein tyrosine kinase 2	Mus musculus	87-90
31256326-13	2019	LXW7 may inhibit the activation of FAK and STAT3 signals in combination with integrin alphavbeta3 to restrain neuroinflammation and the antioxidative stress effect of cerium oxide; hence, CeO2@PAA-LXW7 can exert a more robust anti-inflammatory and neuroprotective effect via synergistically suppressing the ability of LXW7 to influence the integrin pathway and the free radical-scavenging ability of CeO2@PAA.	ceric oxide	188-192	PTK2 protein tyrosine kinase 2	Mus musculus	35-38
31450226-11	2019	Curcumolide also inhibited VEGF-induced phosphorylation of VEGFR-2 tyrosine kinase, and suppressed downstream protein kinases of VEGFR2, including Src, FAK, ERK, AKT, and mTOR in HRMECs.	curcumolide	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	152-155
31619255-7	2019	Au-NP exposure rapidly boosted the phosphorylation levels of focal adhesion kinase (FAK) and AKT, increased the accumulation of caveolin 1 (Cav1), and reduced the activity of extracellular regulated protein kinases (ERK).	au-np	0-5	PTK2 protein tyrosine kinase 2	Mus musculus	61-82
31619255-7	2019	Au-NP exposure rapidly boosted the phosphorylation levels of focal adhesion kinase (FAK) and AKT, increased the accumulation of caveolin 1 (Cav1), and reduced the activity of extracellular regulated protein kinases (ERK).	au-np	0-5	PTK2 protein tyrosine kinase 2	Mus musculus	84-87
31619255-8	2019	The inhibition of AKT (GDC-0068) or FAK (PF-573228) not only rescued ERK activity but also prevented AQP1 induction, whereas Au-NP-mediated Cav1 accumulation remained unaltered.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	41-50	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
31604999-7	2019	ZINC40099027 (10-1000 nM) dose-dependently activated FAK phosphorylation, without activating Pyk2-Tyr-402 or Src-Tyr-419.	ZINC08254138	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
31604999-9	2019	The FAK inhibitor PF-573228 prevented ZINC40099027-stimulated wound closure.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	18-27	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
31604999-9	2019	The FAK inhibitor PF-573228 prevented ZINC40099027-stimulated wound closure.	ZINC08254138	38-50	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
31478830-2	2019	Stem phenotypes involving Wnt-beta-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer.	Platinum	89-97	PTK2 protein tyrosine kinase 2	Mus musculus	196-199
31298744-6	2019	The authors found that many genes closely related to hepatocarcinogenesis were enriched in FAK/CAT-induced HCCs, including genes involved in oxidative phosphorylation, fatty acid metabolism, adipogenesis, mechanistic target of rapamycin complex 1 signaling, G2/M checkpoint, mitotic spindle formation, and cholesterol homeostasis.	Fatty Acids	168-178	PTK2 protein tyrosine kinase 2	Mus musculus	91-94
31298744-6	2019	The authors found that many genes closely related to hepatocarcinogenesis were enriched in FAK/CAT-induced HCCs, including genes involved in oxidative phosphorylation, fatty acid metabolism, adipogenesis, mechanistic target of rapamycin complex 1 signaling, G2/M checkpoint, mitotic spindle formation, and cholesterol homeostasis.	Cholesterol	306-317	PTK2 protein tyrosine kinase 2	Mus musculus	91-94
31189647-1	2019	Expression of focal adhesion kinase (FAK) in endothelial cells (EC) is essential for angiogenesis, but how FAK phosphorylation at tyrosine-(Y)397 and Y861 regulate tumor angiogenesis in vivo is unknown.	Tyrosine	130-138	PTK2 protein tyrosine kinase 2	Mus musculus	37-40
31189647-1	2019	Expression of focal adhesion kinase (FAK) in endothelial cells (EC) is essential for angiogenesis, but how FAK phosphorylation at tyrosine-(Y)397 and Y861 regulate tumor angiogenesis in vivo is unknown.	Tyrosine	130-138	PTK2 protein tyrosine kinase 2	Mus musculus	107-110
30887179-10	2019	Lidocaine suppressed VEGF-activated phosphorylation of VEGF receptor 2 (VEGFR2), PLCgamma-PKC-MAPK and FAK-paxillin in endothelial cells, demonstrating that VEGF, PLC, MAPK and FAK-paxillin suppression is associated with the antiangiogenic effect of lidocaine.	Lidocaine	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
31215459-0	2019	Pharmacological profiling of a dual FAK/IGF-1R kinase inhibitor TAE226 in cellular and in vivo tumor models.	TAE226	64-70	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
31215459-7	2019	In the MIA PaCa-2 model, TAE226 inhibited phosphorylation of Y397-FAK and phosphorylation of S473-Akt as IGF-1R signaling in the cell culture in vitro and the tumor in mice.	TAE226	25-31	PTK2 protein tyrosine kinase 2	Mus musculus	66-69
31215459-9	2019	Similarly in the 4T1 model, TAE226 inhibited phosphorylation of Y397-FAK and S473-Akt in the cell culture in vitro and the tumor in mice.	TAE226	28-34	PTK2 protein tyrosine kinase 2	Mus musculus	69-72
30887179-10	2019	Lidocaine suppressed VEGF-activated phosphorylation of VEGF receptor 2 (VEGFR2), PLCgamma-PKC-MAPK and FAK-paxillin in endothelial cells, demonstrating that VEGF, PLC, MAPK and FAK-paxillin suppression is associated with the antiangiogenic effect of lidocaine.	Lidocaine	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
31193808-9	2019	Interestingly, curcumol-treated IC mice showed that intracellular expressions of PTK2, p-PTK2Tyr397 in bladder samples were reduced, accompanied with lowered blood inflammatory cytokines of interleukin 6 (IL-6), TNF-alpha.	curcumol	15-23	PTK2 protein tyrosine kinase 2	Mus musculus	81-85
31171046-8	2019	FAK activity requires initial autophosphorylation of a tyrosine residue, Y397.	Tyrosine	55-63	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
29946167-5	2019	We further determined that the Gi/o protein, Gbetagamma subunits, phospholipase C, and focal adhesion kinase (FAK) were involved in the IGF-1R transactivation signaling axis, which further induced the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2) and cAMP response element-binding protein.	Cyclic AMP	274-278	PTK2 protein tyrosine kinase 2	Mus musculus	87-108
30879763-11	2019	Furthermore, FAK antagonism by PF562271(FAK antagonist) blocked the alleviating effect of Sox11 plasmid transfection on the VILI.	PF-562271	31-39	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
30879763-11	2019	Furthermore, FAK antagonism by PF562271(FAK antagonist) blocked the alleviating effect of Sox11 plasmid transfection on the VILI.	PF-562271	31-39	PTK2 protein tyrosine kinase 2	Mus musculus	40-43
29946167-5	2019	We further determined that the Gi/o protein, Gbetagamma subunits, phospholipase C, and focal adhesion kinase (FAK) were involved in the IGF-1R transactivation signaling axis, which further induced the phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2) and cAMP response element-binding protein.	Cyclic AMP	274-278	PTK2 protein tyrosine kinase 2	Mus musculus	110-113
30717276-2	2019	3"-deoxyadenosine (cordycepin) is known to suppress FAK expression, cell migration, and the epithelial-mesenchymal transition in hepatocellular carcinoma (HCC).	cordycepin	0-17	PTK2 protein tyrosine kinase 2	Mus musculus	52-55
30756417-11	2019	Blocking FAK and ERK1/2 pathways by selective inhibitors SCH772984 and PF573228, respectively, attenuated the CTGF-induced tenogenic differentiation and proliferation of ASCs.	SCH772984	57-66	PTK2 protein tyrosine kinase 2	Mus musculus	9-12
30756417-11	2019	Blocking FAK and ERK1/2 pathways by selective inhibitors SCH772984 and PF573228, respectively, attenuated the CTGF-induced tenogenic differentiation and proliferation of ASCs.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	9-12
30872746-4	2019	We previously showed that mice lacking FAK in the intestinal epithelium are phenotypically normal under homeostatic conditions but hypersensitive to experimental colitis induced by dextran sulfate sodium (DSS).	Dextran Sulfate	181-203	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
30872746-4	2019	We previously showed that mice lacking FAK in the intestinal epithelium are phenotypically normal under homeostatic conditions but hypersensitive to experimental colitis induced by dextran sulfate sodium (DSS).	Dextran Sulfate	205-208	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
30787865-6	2019	We then pharmacologically targeted focal adhesion (FAK) and extracellular-signal-regulated (ERK) kinases and determined that FAK and ERK activity are critical for the actions of citalopram.	Citalopram	178-188	PTK2 protein tyrosine kinase 2	Mus musculus	125-128
30717276-2	2019	3"-deoxyadenosine (cordycepin) is known to suppress FAK expression, cell migration, and the epithelial-mesenchymal transition in hepatocellular carcinoma (HCC).	cordycepin	19-29	PTK2 protein tyrosine kinase 2	Mus musculus	52-55
30699966-0	2019	Graphene-Induced Osteogenic Differentiation Is Mediated by the Integrin/FAK Axis.	Graphite	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
30699966-9	2019	In vitro, regardless of the stiffness of the underlying PDMS substrate, MSCs seeded onto graphene-coated PDMS substrates demonstrated higher expressions of all tested osteogenic and integrin/FAK proteins tested compared to MSCs seeded onto PDMS alone.	Graphite	89-97	PTK2 protein tyrosine kinase 2	Mus musculus	191-194
30699966-10	2019	Hence, graphene promotes osteogenesis via the activation of the mechanosensitive integrin/FAK axis.	Graphite	7-15	PTK2 protein tyrosine kinase 2	Mus musculus	90-93
30292831-0	2018	Inhibition of SRC/FAK cue: A novel pathway for the synergistic effect of rosuvastatin on the anti-cancer effect of dasatinib in hepatocellular carcinoma.	Rosuvastatin Calcium	73-85	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
30370649-9	2018	Importantly, we found that in HCC cell lines as well as c-Myc mouse HCC, Dasatinib treatment induced up regulation of activated/phosphorylated (p)-focal adhesion kinase(FAK).	Dasatinib	73-82	PTK2 protein tyrosine kinase 2	Mus musculus	169-172
30370649-10	2018	Concomitant treatment of HCC cell lines with Dasatinib and FAK inhibitor prevented Dasatinib-induced FAK activation, leading to stronger growth restraint.	Dasatinib	45-54	PTK2 protein tyrosine kinase 2	Mus musculus	101-104
30370649-10	2018	Concomitant treatment of HCC cell lines with Dasatinib and FAK inhibitor prevented Dasatinib-induced FAK activation, leading to stronger growth restraint.	Dasatinib	83-92	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
30370649-10	2018	Concomitant treatment of HCC cell lines with Dasatinib and FAK inhibitor prevented Dasatinib-induced FAK activation, leading to stronger growth restraint.	Dasatinib	83-92	PTK2 protein tyrosine kinase 2	Mus musculus	101-104
30370649-12	2018	Combined treatment with Dasatinib with FAK inhibitor might represent a novel therapeutic approach against HCC.	Dasatinib	24-33	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
30341186-9	2018	Analysis of the effects of FK506 and methylprednisolone, common immunosuppressive agents following organ transplantation, suggested a link between these immunosuppressive drugs and impaired macrophage migration via the Cx43/iNOS/Src/FAK pathway.	Tacrolimus	27-32	PTK2 protein tyrosine kinase 2	Mus musculus	233-236
30292831-0	2018	Inhibition of SRC/FAK cue: A novel pathway for the synergistic effect of rosuvastatin on the anti-cancer effect of dasatinib in hepatocellular carcinoma.	Dasatinib	115-124	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
30341186-9	2018	Analysis of the effects of FK506 and methylprednisolone, common immunosuppressive agents following organ transplantation, suggested a link between these immunosuppressive drugs and impaired macrophage migration via the Cx43/iNOS/Src/FAK pathway.	Methylprednisolone	37-55	PTK2 protein tyrosine kinase 2	Mus musculus	233-236
30292831-13	2018	CONCLUSION: Our results highlighted some of the signals involved in rosuvastatin antitumor effect and nominate it as an adds-on therapy with dasatinib to yield a better effect in HCC through inhibiting the FAK/Src cascade.	Rosuvastatin Calcium	68-80	PTK2 protein tyrosine kinase 2	Mus musculus	206-209
30292831-13	2018	CONCLUSION: Our results highlighted some of the signals involved in rosuvastatin antitumor effect and nominate it as an adds-on therapy with dasatinib to yield a better effect in HCC through inhibiting the FAK/Src cascade.	Dasatinib	141-150	PTK2 protein tyrosine kinase 2	Mus musculus	206-209
29737477-9	2018	We found that CTS increased the expression of genes encoding COX-2, IL-1beta, and TNF-alpha and activated the phosphorylation of FAK, p-38, ERK, and JNK.	castanospermine	14-17	PTK2 protein tyrosine kinase 2	Mus musculus	129-132
29737477-10	2018	Pretreatment with an FAK inhibitor for 2 h reduced the expression of genes encoding COX-2, IL-1beta, and TNF-alpha induced by CTS-associated inflammation and decreased phosphorylation of FAK, p-38, ERK, and JNK.	castanospermine	126-129	PTK2 protein tyrosine kinase 2	Mus musculus	21-24
30237500-0	2018	The FAK inhibitor BI 853520 exerts anti-tumor effects in breast cancer.	bi 853520	18-27	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
30237500-3	2018	We have assessed and characterized the therapeutic potential and the biological effects of BI 853520, a novel small chemical inhibitor of FAK, in several preclinical mouse models of breast cancer.	bi 853520	91-100	PTK2 protein tyrosine kinase 2	Mus musculus	138-141
30237500-6	2018	Together, the data demonstrate that the repression of FAK activity by the specific FAK inhibitor BI 853520 offers a promising anti-proliferative approach for cancer therapy.	bi 853520	97-106	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
30237500-6	2018	Together, the data demonstrate that the repression of FAK activity by the specific FAK inhibitor BI 853520 offers a promising anti-proliferative approach for cancer therapy.	bi 853520	97-106	PTK2 protein tyrosine kinase 2	Mus musculus	83-86
29528115-2	2018	Here we report that electrical field stimulation (EFS) of cholinergic motor neurons activates FAK in gastric fundus smooth muscles, and that FAK activation by EFS is atropine-sensitive but nicardipine-insensitive.	Atropine	166-174	PTK2 protein tyrosine kinase 2	Mus musculus	141-144
29966916-0	2018	Design, synthesis, in vitro and in silico evaluation of a new series of oxadiazole-based anticancer agents as potential Akt and FAK inhibitors.	Oxadiazoles	72-82	PTK2 protein tyrosine kinase 2	Mus musculus	128-131
30026862-9	2018	Indeed, RSV treatment recruited HDAC1 and DNMT3a to the promoter region of the focal adhesion kinase (FAK), a key factor involved in cell adhesion, enhanced the promoter methylation, and thus attenuated the protein expression.	Resveratrol	8-11	PTK2 protein tyrosine kinase 2	Mus musculus	79-100
30026862-9	2018	Indeed, RSV treatment recruited HDAC1 and DNMT3a to the promoter region of the focal adhesion kinase (FAK), a key factor involved in cell adhesion, enhanced the promoter methylation, and thus attenuated the protein expression.	Resveratrol	8-11	PTK2 protein tyrosine kinase 2	Mus musculus	102-105
30026862-10	2018	The inhibitory effect of RSV in cell migration was diminished once FAK expression was restored.	Resveratrol	25-28	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
30026862-11	2018	Thus, the mechanism of RSV in inhibiting cell migration could be largely accounted to epigenetically control of FAK expression.	Resveratrol	23-26	PTK2 protein tyrosine kinase 2	Mus musculus	112-115
29528115-2	2018	Here we report that electrical field stimulation (EFS) of cholinergic motor neurons activates FAK in gastric fundus smooth muscles, and that FAK activation by EFS is atropine-sensitive but nicardipine-insensitive.	Nicardipine	189-200	PTK2 protein tyrosine kinase 2	Mus musculus	141-144
29528115-13	2018	Electrical field stimulation in the presence of Nomega -nitro-l-arginine methyl ester and MRS2500 contracted gastric fundus smooth muscle strips and increased FAK Y397 phosphorylation (pY397).	NG-Nitroarginine Methyl Ester	48-85	PTK2 protein tyrosine kinase 2	Mus musculus	159-162
29528115-15	2018	The FAK inhibitor PF-431396 inhibited the contractions and the increase in pY397.	PF-431396	18-27	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
29528115-15	2018	The FAK inhibitor PF-431396 inhibited the contractions and the increase in pY397.	py397	75-80	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
29416084-2	2018	Here, we generated EC-specific tamoxifen-inducible FAK knockout and FAK kinase-defective (KD) mutant knockin mice to investigate the role of FAK and its kinase activity in angiogenesis of adult animals.	Tamoxifen	31-40	PTK2 protein tyrosine kinase 2	Mus musculus	51-54
29850504-5	2018	High glucose incubation led to a progressive increase of apelin-13, APJ, cytoskeleton, and tight junction proteins, including VE-Cadherin, FAK, Src, ZO-1, and occludin.	Glucose	5-12	PTK2 protein tyrosine kinase 2	Mus musculus	139-142
29351412-0	2018	Expression of CTGF/CCN2 in response to LPA is stimulated by fibrotic extracellular matrix via the integrin/FAK axis.	lysophosphatidic acid	39-42	PTK2 protein tyrosine kinase 2	Mus musculus	107-110
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	lysophosphatidic acid	114-135	PTK2 protein tyrosine kinase 2	Mus musculus	146-176
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	lysophosphatidic acid	114-135	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	lysophosphatidic acid	114-135	PTK2 protein tyrosine kinase 2	Mus musculus	328-331
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	lysophosphatidic acid	137-140	PTK2 protein tyrosine kinase 2	Mus musculus	146-176
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	lysophosphatidic acid	137-140	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	lysophosphatidic acid	137-140	PTK2 protein tyrosine kinase 2	Mus musculus	328-331
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Arginine	276-279	PTK2 protein tyrosine kinase 2	Mus musculus	146-176
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Arginine	276-279	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Glycine	280-283	PTK2 protein tyrosine kinase 2	Mus musculus	146-176
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Glycine	280-283	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Aspartic Acid	284-287	PTK2 protein tyrosine kinase 2	Mus musculus	146-176
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Aspartic Acid	284-287	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Serine	288-291	PTK2 protein tyrosine kinase 2	Mus musculus	146-176
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Serine	288-291	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Tyrosine	355-363	PTK2 protein tyrosine kinase 2	Mus musculus	146-176
29351412-4	2018	In this report, we present experimental evidence showing that ECM stimulates the synthesis of CTGF in response to lysophosphatidic acid (LPA).The integrin/focal adhesion kinase (FAK) signaling pathway mediates this effect, since CTGF expression is abolished by the use of the Arg-Gly-Asp-Ser peptide and also by an inhibitor of FAK autophosphorylation at tyrosine 397.	Tyrosine	355-363	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
29472531-0	2018	Efficacy of the highly selective focal adhesion kinase inhibitor BI 853520 in adenocarcinoma xenograft models is linked to a mesenchymal tumor phenotype.	bi 853520	65-74	PTK2 protein tyrosine kinase 2	Mus musculus	33-54
29447140-0	2018	Resveratrol Improves Endothelial Progenitor Cell Function through miR-138 by Targeting Focal Adhesion Kinase (FAK) and Promotes Thrombus Resolution In Vivo.	Resveratrol	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	87-108
29447140-0	2018	Resveratrol Improves Endothelial Progenitor Cell Function through miR-138 by Targeting Focal Adhesion Kinase (FAK) and Promotes Thrombus Resolution In Vivo.	Resveratrol	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	110-113
29447140-9	2018	Moreover, we demonstrated that FAK was a target of miR-138 and revealed that FAK knockdown downregulated migration and angiogenesis of RSV-treated EPCs.	Resveratrol	135-138	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
29447140-9	2018	Moreover, we demonstrated that FAK was a target of miR-138 and revealed that FAK knockdown downregulated migration and angiogenesis of RSV-treated EPCs.	Resveratrol	135-138	PTK2 protein tyrosine kinase 2	Mus musculus	77-80
29447140-12	2018	RSV exerted its role by reducing miR-138 expression and therefore upregulated FAK.	Resveratrol	0-3	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
29145097-0	2018	LC-ESI-MS/MS determination of defactinib, a novel FAK inhibitor in mice plasma and its application to a pharmacokinetic study in mice.	defactinib	30-40	PTK2 protein tyrosine kinase 2	Mus musculus	50-53
28759036-4	2017	Over-expression of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promoted FAK tyrosine phosphorylation.	Tyrosine	33-41	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
29090460-3	2017	When we treated RAW 264.7 macrophages with inhibitors of various oncogenic pathways, we found that the focal adhesion kinase (FAK) inhibitors PF573228 and TAE226 could induce cell multinucleation by suppressing furrowing and cytokinesis.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	142-150	PTK2 protein tyrosine kinase 2	Mus musculus	103-124
29090460-3	2017	When we treated RAW 264.7 macrophages with inhibitors of various oncogenic pathways, we found that the focal adhesion kinase (FAK) inhibitors PF573228 and TAE226 could induce cell multinucleation by suppressing furrowing and cytokinesis.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	142-150	PTK2 protein tyrosine kinase 2	Mus musculus	126-129
29090460-3	2017	When we treated RAW 264.7 macrophages with inhibitors of various oncogenic pathways, we found that the focal adhesion kinase (FAK) inhibitors PF573228 and TAE226 could induce cell multinucleation by suppressing furrowing and cytokinesis.	TAE226	155-161	PTK2 protein tyrosine kinase 2	Mus musculus	103-124
29090460-3	2017	When we treated RAW 264.7 macrophages with inhibitors of various oncogenic pathways, we found that the focal adhesion kinase (FAK) inhibitors PF573228 and TAE226 could induce cell multinucleation by suppressing furrowing and cytokinesis.	TAE226	155-161	PTK2 protein tyrosine kinase 2	Mus musculus	126-129
30043652-4	2018	Action mechanism studies manifested that DQA modified paclitaxel plus honokiol micelles could activate apoptotic enzymes caspase-3 and caspase-9 as well as down-regulate FAK, PI3K, MMP-2 and MMP-9.	Paclitaxel	54-64	PTK2 protein tyrosine kinase 2	Mus musculus	170-173
30043652-4	2018	Action mechanism studies manifested that DQA modified paclitaxel plus honokiol micelles could activate apoptotic enzymes caspase-3 and caspase-9 as well as down-regulate FAK, PI3K, MMP-2 and MMP-9.	honokiol	70-78	PTK2 protein tyrosine kinase 2	Mus musculus	170-173
28759036-4	2017	Over-expression of VHR decreased tyrosine phosphorylation of FAK and decreasing VHR promoted FAK tyrosine phosphorylation.	Tyrosine	97-105	PTK2 protein tyrosine kinase 2	Mus musculus	93-96
28832962-8	2017	CONCLUSIONS AND IMPLICATIONS: These findings suggest that rubiarbonone C inhibits the proliferation and migration of VSMCs by inhibiting the FAK, MAPK and STAT3 signalling pathways.	rubiarbonone C	58-72	PTK2 protein tyrosine kinase 2	Mus musculus	141-144
28444899-0	2017	Focal Adhesion Kinase (FAK) tyrosine 397E mutation restores the vascular leakage defect in endothelium-specific FAK-kinase dead mice.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
29048635-3	2017	In this study, we aimed to determine the effect of a novel synthetic FAK1 inhibitor 2-[2-(2-methoxy-4-morpholin-4-yl-phenylamino)-5-trifluoromethyl-pyrimidin-4-ylamino]-N-methyl-benzamide, (MPAP) on lung cancer cells.	mpap	190-194	PTK2 protein tyrosine kinase 2	Mus musculus	69-73
29048635-4	2017	MPAP suppressed cancer cell proliferation and the phosphorylation of FAK1.	mpap	0-4	PTK2 protein tyrosine kinase 2	Mus musculus	69-73
28444820-5	2017	Western blotting was used to examine the protein expression of B16F10 cells after exposed to casticin and the results showed that casticin decreased the expressions of MMP-9, MMP-2, MMP-1, FAK, 14-3-3, GRB2, Akt, NF-kappaB p65, SOS-1, p-EGFR, p-JNK 1/2, uPA, and Rho A in B16F10 cells.	casticin	130-138	PTK2 protein tyrosine kinase 2	Mus musculus	189-192
28495589-6	2017	Normal activation or phosphorylation of the upstream cytoplasmic FAK was also reduced, through mechanisms that involve tyrosine phosphatases and calcium signaling, as shown by pharmacological inhibitors, bisperoxovanadium (bpV) and 2-aminoethoxydiphenylborane (APB), respectively.	Calcium	145-152	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
28495589-6	2017	Normal activation or phosphorylation of the upstream cytoplasmic FAK was also reduced, through mechanisms that involve tyrosine phosphatases and calcium signaling, as shown by pharmacological inhibitors, bisperoxovanadium (bpV) and 2-aminoethoxydiphenylborane (APB), respectively.	bisperoxovanadium	204-221	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
28495589-6	2017	Normal activation or phosphorylation of the upstream cytoplasmic FAK was also reduced, through mechanisms that involve tyrosine phosphatases and calcium signaling, as shown by pharmacological inhibitors, bisperoxovanadium (bpV) and 2-aminoethoxydiphenylborane (APB), respectively.	bisperoxovanadium	223-226	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
28495589-6	2017	Normal activation or phosphorylation of the upstream cytoplasmic FAK was also reduced, through mechanisms that involve tyrosine phosphatases and calcium signaling, as shown by pharmacological inhibitors, bisperoxovanadium (bpV) and 2-aminoethoxydiphenylborane (APB), respectively.	2-aminoethoxydiphenylborane	232-259	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
28495589-6	2017	Normal activation or phosphorylation of the upstream cytoplasmic FAK was also reduced, through mechanisms that involve tyrosine phosphatases and calcium signaling, as shown by pharmacological inhibitors, bisperoxovanadium (bpV) and 2-aminoethoxydiphenylborane (APB), respectively.	2-aminoethoxydiphenylborane	261-264	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
28740192-4	2017	The in-vitro findings showed that CXB is involved in the inhibition of EMT and cell mobility through blocking transcription factors (Slug, Snail and ZEB1), cytoplasmic mediators (focal adhesion kinase (FAK), vimentin and beta-catenin), cell adhesion molecules (cadherins and integrins), and surface receptors (AMFR and EGFR).	Celecoxib	34-37	PTK2 protein tyrosine kinase 2	Mus musculus	179-200
28740192-4	2017	The in-vitro findings showed that CXB is involved in the inhibition of EMT and cell mobility through blocking transcription factors (Slug, Snail and ZEB1), cytoplasmic mediators (focal adhesion kinase (FAK), vimentin and beta-catenin), cell adhesion molecules (cadherins and integrins), and surface receptors (AMFR and EGFR).	Celecoxib	34-37	PTK2 protein tyrosine kinase 2	Mus musculus	202-205
28740192-7	2017	The expression levels of membrane EGFR, and nuclear FAK, Slug and ZEB1 were decreased in the xenograft tumours of CXB-treated mice.	Celecoxib	114-117	PTK2 protein tyrosine kinase 2	Mus musculus	52-55
28915654-0	2017	Daurinol blocks breast and lung cancer metastasis and development by inhibition of focal adhesion kinase (FAK).	daurinol	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	83-104
28915654-0	2017	Daurinol blocks breast and lung cancer metastasis and development by inhibition of focal adhesion kinase (FAK).	daurinol	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	106-109
28915654-4	2017	Daurinol selectively inhibited phosphorylation of FAK at Tyr925, Tyr576/577, and Tyr397 sites in a dose- and time-dependent manner.	daurinol	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	50-53
28915654-11	2017	Our results suggest that daurinol suppresses lung metastasis through inhibition of migration and survival via blockade of FAK activity.	daurinol	25-33	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
28832962-0	2017	Rubiarbonone C inhibits platelet-derived growth factor-induced proliferation and migration of vascular smooth muscle cells through the focal adhesion kinase, MAPK and STAT3 Tyr705 signalling pathways.	rubiarbonone C	0-14	PTK2 protein tyrosine kinase 2	Mus musculus	135-156
28639351-8	2017	The low PTP activity guarantees the phosphorylation of FAK at Y-residue, causing better pre-osteoblast adhesion in response to Ti-containing medium.	ti-containing medium	127-147	PTK2 protein tyrosine kinase 2	Mus musculus	55-58
28639351-9	2017	Altogether, these data indicate that ROS indirectly modulate FAK phosphorylation in response to Ti-released from dental implants.	Reactive Oxygen Species	37-40	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
29066893-5	2017	Action mechanism studies showed that multifunctional targeting epirubicin liposomes could downregulate PI3K, MMP-2, MMP-9, VE-Cadherin, and FAK and activate apoptotic enzyme caspase 3.	Epirubicin	63-73	PTK2 protein tyrosine kinase 2	Mus musculus	140-143
28583810-7	2017	Action mechanism studies indicated that Lf modified daunorubicin plus honokiol liposomes could activate apoptotic enzymes caspase 3 as well as down-regulate VM protein indicators (PI3K, MMP-2, MMP-9, VE-Cadherin and FAK).	Daunorubicin	52-64	PTK2 protein tyrosine kinase 2	Mus musculus	216-219
28583810-7	2017	Action mechanism studies indicated that Lf modified daunorubicin plus honokiol liposomes could activate apoptotic enzymes caspase 3 as well as down-regulate VM protein indicators (PI3K, MMP-2, MMP-9, VE-Cadherin and FAK).	honokiol	70-78	PTK2 protein tyrosine kinase 2	Mus musculus	216-219
28444899-0	2017	Focal Adhesion Kinase (FAK) tyrosine 397E mutation restores the vascular leakage defect in endothelium-specific FAK-kinase dead mice.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
28444899-0	2017	Focal Adhesion Kinase (FAK) tyrosine 397E mutation restores the vascular leakage defect in endothelium-specific FAK-kinase dead mice.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	112-115
28444899-2	2017	In vitro activation of the FAK kinase domain triggers autophosphorylation of Y397, Src activation, and subsequent phosphorylation of other FAK tyrosine residues.	Tyrosine	143-151	PTK2 protein tyrosine kinase 2	Mus musculus	27-30
28444899-2	2017	In vitro activation of the FAK kinase domain triggers autophosphorylation of Y397, Src activation, and subsequent phosphorylation of other FAK tyrosine residues.	Tyrosine	143-151	PTK2 protein tyrosine kinase 2	Mus musculus	139-142
28424421-5	2017	Mechanistic studies demonstrate that Lunasin reduced activating phosphorylations of the intracellular kinases FAK and AKT as well as reduced histone acetylation of lysine residues in H3 and H4 histones.	LUNASINE	37-44	PTK2 protein tyrosine kinase 2	Mus musculus	110-113
28283477-9	2017	Mice with AEC-specific deletion of FAK did not exhibit spontaneous lung injury but did have significantly greater terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling-positive cells (18.6 vs. 7.1) per x200 field, greater bronchoalveolar lavage protein (3.2 vs. 1.8 mg/ml), and significantly greater death (77 vs. 19%) after bleomycin injury compared with littermate control mice.	deoxyuridine triphosphate	152-156	PTK2 protein tyrosine kinase 2	Mus musculus	35-38
28283477-9	2017	Mice with AEC-specific deletion of FAK did not exhibit spontaneous lung injury but did have significantly greater terminal deoxynucleotidyl transferase dUTP-mediated nick-end labeling-positive cells (18.6 vs. 7.1) per x200 field, greater bronchoalveolar lavage protein (3.2 vs. 1.8 mg/ml), and significantly greater death (77 vs. 19%) after bleomycin injury compared with littermate control mice.	Bleomycin	341-350	PTK2 protein tyrosine kinase 2	Mus musculus	35-38
27939096-4	2017	In combination with gemcitabine and immune-checkpoint therapy, FAK inhibitor promotes long-term tumor stasis with extended survival in PDAC mouse models.	gemcitabine	20-31	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
28348210-0	2017	Myosin-1E interacts with FAK proline-rich region 1 to induce fibronectin-type matrix.	Proline	29-36	PTK2 protein tyrosine kinase 2	Mus musculus	25-28
27575453-5	2016	We found that Rb9 binds to and interferes with Hsp90 chaperone activity causing attenuation of FAK-Src signaling and downregulation of active Rac1 in B16F10-Nex2 melanoma cells.	N-Benzyl-2-({n-[2-(1h-Indol-3-Yl)ethyl]glycyl}amino)-4-Phenylthiophene-3-Carboxamide	14-17	PTK2 protein tyrosine kinase 2	Mus musculus	95-98
28011582-0	2017	Fluid shear stress induces upregulation of COX-2 and PGI2 release in endothelial cells via a pathway involving PECAM-1, PI3K, FAK, and p38.	Epoprostenol	53-57	PTK2 protein tyrosine kinase 2	Mus musculus	126-129
28011582-7	2017	Inhibition of integrin-associated FAK (PF573228) and MAPK p38 (SB203580) also inhibited the shear-induced upregulation of COX-2.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	39-47	PTK2 protein tyrosine kinase 2	Mus musculus	34-37
28004056-12	2017	Fc-saxatilin specifically bound to integrin alphavbeta3 of the endothelial cells and inhibited hypoxia-induced activation of FAK, a downstream signalling molecule in integrin-dependent signal transduction.	fc-saxatilin	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	125-128
28109944-0	2017	Synthesis, biological evaluation, and molecular dynamics (MD) simulation studies of three novel F-18 labeled and focal adhesion kinase (FAK) targeted 5-bromo pyrimidines as radiotracers for tumor.	5-bromopyrimidine	150-169	PTK2 protein tyrosine kinase 2	Mus musculus	113-134
28109944-0	2017	Synthesis, biological evaluation, and molecular dynamics (MD) simulation studies of three novel F-18 labeled and focal adhesion kinase (FAK) targeted 5-bromo pyrimidines as radiotracers for tumor.	5-bromopyrimidine	150-169	PTK2 protein tyrosine kinase 2	Mus musculus	136-139
28109944-2	2017	A series of F-18 labeled 5-bromo-N2-(4-(2-fluoro-pegylated (FPEG))-3,5-dimethoxyphenyl)-N4-(4-methoxyphenyl)pyrimidine-2,4-diamine derivatives were prepared and evaluated as the FAK targeted radiotracers for the early diagnoses of tumor.	Fluorine-18	12-16	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
28109944-2	2017	A series of F-18 labeled 5-bromo-N2-(4-(2-fluoro-pegylated (FPEG))-3,5-dimethoxyphenyl)-N4-(4-methoxyphenyl)pyrimidine-2,4-diamine derivatives were prepared and evaluated as the FAK targeted radiotracers for the early diagnoses of tumor.	5-bromo-n2-(4-(2-fluoro-pegylated	25-58	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
28109944-2	2017	A series of F-18 labeled 5-bromo-N2-(4-(2-fluoro-pegylated (FPEG))-3,5-dimethoxyphenyl)-N4-(4-methoxyphenyl)pyrimidine-2,4-diamine derivatives were prepared and evaluated as the FAK targeted radiotracers for the early diagnoses of tumor.	)-3,5-dimethoxyphenyl)-n4-(4-methoxyphenyl)pyrimidine-2,4-diamine	65-130	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
28109944-11	2017	Besides, for the [18F]2, both the biodistribution data and the micro-PET/CT imaging study showed significantly reduced uptake of the radiotracer in the tumor tissue at 30 min post-injection in mice that received PF-562,271 (one of the reported best selective FAK inhibitor which was developed by Pfitzer Inc. and inhibited the activity of FAK with IC50 value of 1.5 nM) at 1 h before the injection of radiotracer.	pf-562	212-218	PTK2 protein tyrosine kinase 2	Mus musculus	259-262
28109944-11	2017	Besides, for the [18F]2, both the biodistribution data and the micro-PET/CT imaging study showed significantly reduced uptake of the radiotracer in the tumor tissue at 30 min post-injection in mice that received PF-562,271 (one of the reported best selective FAK inhibitor which was developed by Pfitzer Inc. and inhibited the activity of FAK with IC50 value of 1.5 nM) at 1 h before the injection of radiotracer.	pf-562	212-218	PTK2 protein tyrosine kinase 2	Mus musculus	339-342
26420756-6	2016	Western blotting showed that triptolide markedly reduced CXCR4, SOS1, GRB2, p-ERK, FAK, p-AKT, Rho A, p-JNK, NF-kappaB, MMP-9, and MMP-2 but increased PI3K and p-p38 and COX2 after compared to the untreated (control) cells.	triptolide	29-39	PTK2 protein tyrosine kinase 2	Mus musculus	83-86
26420756-7	2016	Real time PCR indicated that triptolide inhibited the gene expression of MMP-2, FAK, ROCK-1, and NF-kappaB but did not significantly affect TIMP-1 and -2 gene expression in B16F10 cells in vitro.	triptolide	29-39	PTK2 protein tyrosine kinase 2	Mus musculus	80-83
28423510-0	2017	Genistein inhibits the growth and regulates the migration and invasion abilities of melanoma cells via the FAK/paxillin and MAPK pathways.	Genistein	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	107-110
28423510-8	2017	As a result, genistein is believed to strongly downregulate the migration and invasion abilities of B16F10 cells via the FAK/paxillin pathway.	Genistein	13-22	PTK2 protein tyrosine kinase 2	Mus musculus	121-124
28423510-11	2017	On the other hand, a lower concentration of genistein (12.5 muM) significantly promoted both invasion and migration by activating the FAK/paxillin and MAPK signaling cascades.	Genistein	44-53	PTK2 protein tyrosine kinase 2	Mus musculus	134-137
27978828-14	2016	FAK inhibition reduced pS727-STAT3 within mitochondria and reduced mitochondrial function in a non-transcriptional manner, as shown by co-treatment with actinomycin.	Dactinomycin	153-164	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
27978828-16	2016	FAK inhibition induced loss of mitochondrial membrane potential, which was counteracted by bryostatin, and increased superoxide and hydrogen peroxide production.	Bryostatins	91-101	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
27978828-16	2016	FAK inhibition induced loss of mitochondrial membrane potential, which was counteracted by bryostatin, and increased superoxide and hydrogen peroxide production.	Superoxides	117-127	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
27978828-16	2016	FAK inhibition induced loss of mitochondrial membrane potential, which was counteracted by bryostatin, and increased superoxide and hydrogen peroxide production.	Hydrogen Peroxide	132-149	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
27978828-17	2016	Bryostatin and HGF reduced the substantial cell death caused by FAK inhibition over a 24 h period.	Bryostatins	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	64-67
26890302-8	2016	Therefore, our results suggest that BMP2 can increase [Ca2+ ]i through extracellular calcium influx regulated by FAK and ALP and can deplete ER calcium through Src signaling simultaneously.	Calcium	85-92	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
27456486-7	2016	Examination of Pyk2 tyrosine phosphorylation in normal polarized cells demonstrated that Pyk2 phosphorylated at Y579 and Y580 preferentially localizes to the leading edge, whereas Y881-phosphorylated Pyk2 is enriched at the trailing edge, suggesting that the tyrosine phosphorylation of Pyk2 is spatially regulated in migrating CTL.	Tyrosine	20-28	PTK2 protein tyrosine kinase 2	Mus musculus	15-19
27463003-0	2016	alpha2-adrenoreceptor modulated FAK pathway induced by dexmedetomidine attenuates pulmonary microvascular hyper-permeability following kidney injury.	Dexmedetomidine	55-70	PTK2 protein tyrosine kinase 2	Mus musculus	32-35
27463003-10	2016	In vivo, dexmedetomidine remarkably attenuated lung injury and pulmonary microvascular hyper-permeability caused by rI/R injury, which was abolished by atipamezole or FAK inhibitor co-administration.	Dexmedetomidine	9-24	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
27463003-12	2016	Dexmedetomidine increased phospho-tyrosine397FAK in a time- and dose-dependent manner, which was correlated with the changes in trans-endothelial permeability.	Dexmedetomidine	0-15	PTK2 protein tyrosine kinase 2	Mus musculus	45-48
27463003-13	2016	Our data indicated that dexmedetomidine is able to ameliorate remote pulmonary microvascular hyper-permeability induced by rI/R, at least in part, via FAK modulation.	Dexmedetomidine	24-39	PTK2 protein tyrosine kinase 2	Mus musculus	151-154
27095850-9	2016	We found that glucose- and H2O2-induced activation of FAK, paxillin, ERK1/2 and Akt was significantly blocked by silencing SCGN.	Glucose	14-21	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
27286445-0	2016	MiR-7a is an important mediator in Fas-associated protein with death domain (FADD)-regulated expression of focal adhesion kinase (FAK).	mir-7a	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	107-128
27286445-0	2016	MiR-7a is an important mediator in Fas-associated protein with death domain (FADD)-regulated expression of focal adhesion kinase (FAK).	mir-7a	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	130-133
27286445-6	2016	Furthermore, we demonstrate that miR-7a was a necessary mediator in FADD-regulated FAK expression.	mir-7a	33-39	PTK2 protein tyrosine kinase 2	Mus musculus	83-86
27210504-0	2016	Cucurbitacin B inhibits breast cancer metastasis and angiogenesis through VEGF-mediated suppression of FAK/MMP-9 signaling axis.	cucurbitacin B	0-14	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
27374103-6	2016	In addition, roneparstat inhibited the activation of cell surface PDGFR and PDGFR-associated FAK, likely contributing to the reversion of NIH3T3COL1A1/PDGFB cell transformed and pro-invasive phenotype.	CHEMBL4280766	13-24	PTK2 protein tyrosine kinase 2	Mus musculus	93-96
27095850-9	2016	We found that glucose- and H2O2-induced activation of FAK, paxillin, ERK1/2 and Akt was significantly blocked by silencing SCGN.	Hydrogen Peroxide	27-31	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
26992741-4	2016	Herein, we showed that rLZ-8 effectively induced changes in EMT by interfering with cell adhesion and focal adhesion kinase (FAK) functions in lung cancer cells.	rlz-8	23-28	PTK2 protein tyrosine kinase 2	Mus musculus	102-123
26992741-4	2016	Herein, we showed that rLZ-8 effectively induced changes in EMT by interfering with cell adhesion and focal adhesion kinase (FAK) functions in lung cancer cells.	rlz-8	23-28	PTK2 protein tyrosine kinase 2	Mus musculus	125-128
23913855-10	2016	Furthermore, biochemical analysis indicated that short phenamil treatment of cells was accompanied by upregulation in protein expression of integrin alpha5, p125(FAK) and phosphorylation of CREB.	phenylamil	55-63	PTK2 protein tyrosine kinase 2	Mus musculus	162-165
27141946-7	2016	Treating FAK small interfering RNA (FAK siRNA) or specific inhibitor for JNK (SP600125) to iPSCs significantly reduced the phosphorylation of JNK and the expressions of Mef2c and Bcl-2.	pyrazolanthrone	78-86	PTK2 protein tyrosine kinase 2	Mus musculus	9-12
26477879-0	2016	In Vitro and In Vivo Anti-Melanoma Effects of Pituranthos tortuosus Essential Oil Via Inhibition of FAK and Src Activities.	pituranthos tortuosus essential oil	46-81	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
27009091-9	2016	CEP-37440 decreased the cell proliferation of FC-IBC02, SUM190, and KPL4 by blocking the autophosphorylation kinase activity of FAK1 (Tyr 397).	Tyrosine	134-137	PTK2 protein tyrosine kinase 2	Mus musculus	128-132
27009091-14	2016	CONCLUSIONS: CEP-37440 is effective against some IBC cells that express phospho-FAK1 (Tyr 397), and its antiproliferative activity is related to its ability to decrease phospho-FAK1.	Tyrosine	86-89	PTK2 protein tyrosine kinase 2	Mus musculus	80-84
26712802-9	2015	Furthermore, niacin induced phosphorylated focal adhesion kinase (FAK) and FAK inhibitor PF-573228 reduced the level of Bcl-2 and elevated the level of cleaved caspase-3 in VSMCs.	Niacin	13-19	PTK2 protein tyrosine kinase 2	Mus musculus	43-64
26886764-9	2016	Immunoblot analyses further revealed that the activities of focal adhesion proteins, such as FAK and c-Src, are upregulated by cisplatin through phosphorylation at tyrosine 397 and 530, respectively.	Cisplatin	127-136	PTK2 protein tyrosine kinase 2	Mus musculus	93-96
26886764-9	2016	Immunoblot analyses further revealed that the activities of focal adhesion proteins, such as FAK and c-Src, are upregulated by cisplatin through phosphorylation at tyrosine 397 and 530, respectively.	Tyrosine	164-172	PTK2 protein tyrosine kinase 2	Mus musculus	93-96
26886764-10	2016	Collectively, these results show that cisplatin-treated melanoma cells not only exhibit the upregulation of FAK-mediated signaling to enhance the cytoskeleton mechanical stretch, but also promote the cytoskeletal rearrangement resulting in 43% decrease in the cell modulus.	Cisplatin	38-47	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
26932297-0	2016	Hydrogen Sulfide Recruits Macrophage Migration by Integrin beta1-Src-FAK/Pyk2-Rac Pathway in Myocardial Infarction.	Hydrogen Sulfide	0-16	PTK2 protein tyrosine kinase 2	Mus musculus	69-72
26932297-7	2016	While, the inhibitors not only significantly diminished the migratory ability in response to NaHS, but also blocked the activation of phospho-Src, -Pyk2, -FAK(397), and -FAK(925).	sodium bisulfide	93-97	PTK2 protein tyrosine kinase 2	Mus musculus	170-173
26932297-9	2016	These results indicate that H2S may have the potential as an anti-infarct of MI by governing macrophage migration, which was achieved by accelerating internalization of integrin beta1 and activating downstream Src-FAK/Pyk2-Rac pathway.	Hydrogen Sulfide	28-31	PTK2 protein tyrosine kinase 2	Mus musculus	214-217
26627008-5	2016	In addition, penfluridol treatment significantly reduced the expression of integrin alpha6, integrin beta4, Fak, paxillin, Rac1/2/3, and ROCK1 in vitro.	Penfluridol	13-24	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
26830149-5	2016	Moreover, nifuroxazide markedly impaired melanoma cell migration and invasion by down-regulating phosphorylated-Src, phosphorylated-FAK, and expression of matrix metalloproteinase (MMP) -2, MMP-9 and vimentin.	nifuroxazide	10-22	PTK2 protein tyrosine kinase 2	Mus musculus	132-135
26517238-6	2015	Serum or fibronectin stimulation of focal adhesion kinase (FAK) autophosphorylation on tyrosine-397 was increased by either knockdown or ablation of RNase L.	Tyrosine	87-95	PTK2 protein tyrosine kinase 2	Mus musculus	36-57
26517238-6	2015	Serum or fibronectin stimulation of focal adhesion kinase (FAK) autophosphorylation on tyrosine-397 was increased by either knockdown or ablation of RNase L.	Tyrosine	87-95	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
26892465-8	2016	In addition, REH cell-injected NOD/SCID mice treated with rapamycin and a short-hairpin RNA (shRNA) to down-regulate FAK had significantly longer survival times and slower leukemia progression compared with mice injected with REH-empty vector cells and treated with rapamycin.	Sirolimus	58-67	PTK2 protein tyrosine kinase 2	Mus musculus	117-120
26892465-8	2016	In addition, REH cell-injected NOD/SCID mice treated with rapamycin and a short-hairpin RNA (shRNA) to down-regulate FAK had significantly longer survival times and slower leukemia progression compared with mice injected with REH-empty vector cells and treated with rapamycin.	Sirolimus	266-275	PTK2 protein tyrosine kinase 2	Mus musculus	117-120
26414708-13	2016	CONCLUSION: By regulating the phosphorylation of Src and FAK, RPTPalpha mediates proinflammatory and proinvasive signaling in RA FLS, correlating with the promotion of disease in an FLS-dependent model of RA.	CHEMBL1232769	129-132	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
26763945-9	2016	Importantly, FAK inhibitor protects bleomycin-induced lung fibrosis in mice.	Bleomycin	36-45	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
26763945-10	2016	FAK inhibitor blocks FAK activation and significantly reduces signaling cascade of fibroblast migration in bleomycin-challenged mice.	Bleomycin	107-116	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
26763945-10	2016	FAK inhibitor blocks FAK activation and significantly reduces signaling cascade of fibroblast migration in bleomycin-challenged mice.	Bleomycin	107-116	PTK2 protein tyrosine kinase 2	Mus musculus	21-24
26763945-11	2016	Furthermore, FAK inhibitor decreases lung fibrotic score, collagen accumulation, fibronectin production, and myofibroblast differentiation in in bleomycin-challenged mice.	Bleomycin	145-154	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
26712802-9	2015	Furthermore, niacin induced phosphorylated focal adhesion kinase (FAK) and FAK inhibitor PF-573228 reduced the level of Bcl-2 and elevated the level of cleaved caspase-3 in VSMCs.	Niacin	13-19	PTK2 protein tyrosine kinase 2	Mus musculus	66-69
26712802-9	2015	Furthermore, niacin induced phosphorylated focal adhesion kinase (FAK) and FAK inhibitor PF-573228 reduced the level of Bcl-2 and elevated the level of cleaved caspase-3 in VSMCs.	Niacin	13-19	PTK2 protein tyrosine kinase 2	Mus musculus	75-78
26712802-10	2015	CONCLUSIONS Niacin inhibits vascular inflammation and apoptosis of VSMCs via inhibiting the NF-kappaB signaling and the FAK signaling pathway, respectively, thus protecting ApoE-/- mice against atherosclerosis.	Niacin	12-18	PTK2 protein tyrosine kinase 2	Mus musculus	120-123
26340932-7	2015	mKL abolished STZ- and TNFalpha-induced inhibition of FAK and Akt phosphorylation, caspase 3 cleavage, and beta-cell apoptosis.	Streptozocin	14-17	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
26445848-1	2015	The present study sought to determine the anti-tumor effects of OXA-11, a potent, novel small-molecule amino pyrimidine inhibitor (1.2 pM biochemical IC(50)) of focal adhesion kinase (FAK).	oxa-11	64-70	PTK2 protein tyrosine kinase 2	Mus musculus	161-182
26445848-1	2015	The present study sought to determine the anti-tumor effects of OXA-11, a potent, novel small-molecule amino pyrimidine inhibitor (1.2 pM biochemical IC(50)) of focal adhesion kinase (FAK).	oxa-11	64-70	PTK2 protein tyrosine kinase 2	Mus musculus	184-187
26445848-1	2015	The present study sought to determine the anti-tumor effects of OXA-11, a potent, novel small-molecule amino pyrimidine inhibitor (1.2 pM biochemical IC(50)) of focal adhesion kinase (FAK).	2-aminopyrimidine	103-119	PTK2 protein tyrosine kinase 2	Mus musculus	161-182
26445848-1	2015	The present study sought to determine the anti-tumor effects of OXA-11, a potent, novel small-molecule amino pyrimidine inhibitor (1.2 pM biochemical IC(50)) of focal adhesion kinase (FAK).	2-aminopyrimidine	103-119	PTK2 protein tyrosine kinase 2	Mus musculus	184-187
26445848-9	2015	Together, these findings indicate that OXA-11 is a potent and selective inhibitor of FAK phosphorylation in vitro and in vivo.	oxa-11	39-45	PTK2 protein tyrosine kinase 2	Mus musculus	85-88
26445848-0	2015	Anti-metastatic action of FAK inhibitor OXA-11 in combination with VEGFR-2 signaling blockade in pancreatic neuroendocrine tumors.	oxa-11	40-46	PTK2 protein tyrosine kinase 2	Mus musculus	26-29
26098895-8	2015	A lower concentration of PF-562,271 that selectively inhibits FAK, but not Pyk2, did not have any effect on glioma cell migration.	pyrazofurin	25-27	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
26251180-10	2015	This work identifies FAK as a target of p110delta PI3K that links RhoA with PTEN and establishes for the first time that PTEN is a substrate of FAK-mediated Tyr phosphorylation.	Tyrosine	157-160	PTK2 protein tyrosine kinase 2	Mus musculus	21-24
26251180-10	2015	This work identifies FAK as a target of p110delta PI3K that links RhoA with PTEN and establishes for the first time that PTEN is a substrate of FAK-mediated Tyr phosphorylation.	Tyrosine	157-160	PTK2 protein tyrosine kinase 2	Mus musculus	144-147
26378057-7	2015	Further, overexpression of Syndecan-1 cCTF increased the basal activation of Src kinase, focal adhesion kinase (FAK) and Rho GTPase.	cctf	38-42	PTK2 protein tyrosine kinase 2	Mus musculus	89-110
26378057-7	2015	Further, overexpression of Syndecan-1 cCTF increased the basal activation of Src kinase, focal adhesion kinase (FAK) and Rho GTPase.	cctf	38-42	PTK2 protein tyrosine kinase 2	Mus musculus	112-115
26458186-5	2015	Furthermore, dasatinib treatment inhibited NTK activation (primarily Pyk2 and Fak) and reduced the level of FSP1 positive cells in the PO myocardium.	Dasatinib	13-22	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
25447223-3	2015	The neuroprotective effect of Ang1 was mediated by the integrin/focal adhesion kinase (FAK) signaling axis, as evidenced by the blocking effects of a pan-integrin inhibitory RGD peptide and PF-573228, a specific chemical inhibitor of FAK.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	190-199	PTK2 protein tyrosine kinase 2	Mus musculus	55-85
25447223-3	2015	The neuroprotective effect of Ang1 was mediated by the integrin/focal adhesion kinase (FAK) signaling axis, as evidenced by the blocking effects of a pan-integrin inhibitory RGD peptide and PF-573228, a specific chemical inhibitor of FAK.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	190-199	PTK2 protein tyrosine kinase 2	Mus musculus	87-90
25447223-3	2015	The neuroprotective effect of Ang1 was mediated by the integrin/focal adhesion kinase (FAK) signaling axis, as evidenced by the blocking effects of a pan-integrin inhibitory RGD peptide and PF-573228, a specific chemical inhibitor of FAK.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	190-199	PTK2 protein tyrosine kinase 2	Mus musculus	234-237
26090892-1	2015	TAE226, a bis-anilino pyrimidine compound, has been developed as an inhibitor of focal adhesion kinase (FAK) and insulin-like growth factor-I receptor (IGF-IR).	TAE226	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	81-102
26090892-1	2015	TAE226, a bis-anilino pyrimidine compound, has been developed as an inhibitor of focal adhesion kinase (FAK) and insulin-like growth factor-I receptor (IGF-IR).	TAE226	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
26090892-1	2015	TAE226, a bis-anilino pyrimidine compound, has been developed as an inhibitor of focal adhesion kinase (FAK) and insulin-like growth factor-I receptor (IGF-IR).	bis-anilino pyrimidine	10-32	PTK2 protein tyrosine kinase 2	Mus musculus	81-102
26090892-1	2015	TAE226, a bis-anilino pyrimidine compound, has been developed as an inhibitor of focal adhesion kinase (FAK) and insulin-like growth factor-I receptor (IGF-IR).	bis-anilino pyrimidine	10-32	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
25792283-7	2015	Importantly, pterostilbene suppressed tumor growth and metastasis in MDA-MB-231-bearing NOD/SCID mice by reducing Src/Fak signaling; this observation was consistent with the negative correlations between miR-205 and Src expression in both normal and malignant breast tissues.	pterostilbene	13-26	PTK2 protein tyrosine kinase 2	Mus musculus	118-121
25304155-9	2015	Taken together, these results suggest that interaction of alpha2,6-linked sialic acids with siglec-2 might modulate the adhesion of hepatocarcinoma cells to lymph nodes through the FAK signaling pathway.	alpha2,6-linked sialic acids	58-86	PTK2 protein tyrosine kinase 2	Mus musculus	181-184
25736483-4	2015	AC (2.5 muM) also significantly inhibited integrin beta1-mediated phosphorylation of focal adhesion kinase (FAK) which then decreased the phosphorylation of MAPK family.	alpha-carotene	0-2	PTK2 protein tyrosine kinase 2	Mus musculus	85-106
25736483-4	2015	AC (2.5 muM) also significantly inhibited integrin beta1-mediated phosphorylation of focal adhesion kinase (FAK) which then decreased the phosphorylation of MAPK family.	alpha-carotene	0-2	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
25736483-6	2015	AC treatment alone significantly decreased protein expression of integrin beta1 but increased protein expression of TIMP-1 and PAI-1 without affecting protein expression of TIMP-2 and phosphorylation of FAK in lung tissues, whereas taxol treatment alone significantly increased protein expression of TIMP-1, PAI-1 and TIMP-2 but decreased protein expression of integrin beta1 and phosphorylation of FAK.	alpha-carotene	0-2	PTK2 protein tyrosine kinase 2	Mus musculus	399-402
25870166-8	2015	Moreover, FAK knockdown suppressed LiCl-stimulated macrophage motility, suggesting the involvement of FAK in this process.	Lithium Chloride	35-39	PTK2 protein tyrosine kinase 2	Mus musculus	10-13
25870166-8	2015	Moreover, FAK knockdown suppressed LiCl-stimulated macrophage motility, suggesting the involvement of FAK in this process.	Lithium Chloride	35-39	PTK2 protein tyrosine kinase 2	Mus musculus	102-105
25870166-0	2015	The iNOS/Src/FAK axis contributes to lithium chloride-mediated macrophage migration.	Lithium Chloride	37-53	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
25250716-6	2014	Melatonin induced the phosphorylation of FAK and paxillin, which were concurrently downregulated by blocking of the PKC activity.	Melatonin	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	41-44
25377086-3	2015	FAK phosphorylation at Tyr397, Tyr576/577, and Tyr861 was increased rapidly after exposure to hypertonic (575 mOsm) saline, peaking after 10 (Tyr397, Tyr576/577) and 10-30 min (Tyr861).	Sodium Chloride	116-122	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
25377086-7	2015	The FAK inhibitor PF-573,228 augmented shrinkage-induced Src phosphorylation, and inhibited shrinkage-induced NKCC1 activity by ~15%.	pf-573	18-24	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
25047070-13	2015	Effects of QD232 on Src/FAK and STAT3 phosphorylation were blocked by N-acetylcysteine or glutathione.	Acetylcysteine	70-86	PTK2 protein tyrosine kinase 2	Mus musculus	24-27
25047070-13	2015	Effects of QD232 on Src/FAK and STAT3 phosphorylation were blocked by N-acetylcysteine or glutathione.	Glutathione	90-101	PTK2 protein tyrosine kinase 2	Mus musculus	24-27
26330161-4	2015	Thirty mice were surgically treated into Sham (n=7) and MI (n=23) groups; and FAK inhibitor PF-562271 was given to six survivor MI mice (as PF group, from 15 survivors).	pyrazofurin	92-94	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
26090090-0	2015	Proliferation of preosteoblasts on TiO2 nanotubes is FAK/RhoA related.	titanium dioxide	35-39	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
26090090-3	2015	Specifically, we hypothesize that TNTs can influence cell proliferation of preosteoblasts through cell adhesion and related modulation of FAK and RhoA.	tnts	34-38	PTK2 protein tyrosine kinase 2	Mus musculus	138-141
26090090-7	2015	The expression of FAK was 86.2% down regulated superimposition of TNTs topography.	tnts	66-70	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
25274988-9	2014	Inhibition of FAK increased the submembrane cAMP concentration, implicating FAK activity in the regulation of insulin exocytosis.	Cyclic AMP	44-48	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
25274988-9	2014	Inhibition of FAK increased the submembrane cAMP concentration, implicating FAK activity in the regulation of insulin exocytosis.	Cyclic AMP	44-48	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
25242698-3	2014	Focal adhesion kinase (FAK) activation involves the following: (1) ligand bound growth factors or clustered integrins activate FAK kinase domain; (2) FAK autophosphorylates tyrosine (Y) 397; (3) Src binds pY397 and phosphorylates FAK at various other sites including Y861; (4) downstream signaling of activated FAK elicits changes in cellular behavior.	Tyrosine	173-181	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
25242698-3	2014	Focal adhesion kinase (FAK) activation involves the following: (1) ligand bound growth factors or clustered integrins activate FAK kinase domain; (2) FAK autophosphorylates tyrosine (Y) 397; (3) Src binds pY397 and phosphorylates FAK at various other sites including Y861; (4) downstream signaling of activated FAK elicits changes in cellular behavior.	Tyrosine	173-181	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
25242698-3	2014	Focal adhesion kinase (FAK) activation involves the following: (1) ligand bound growth factors or clustered integrins activate FAK kinase domain; (2) FAK autophosphorylates tyrosine (Y) 397; (3) Src binds pY397 and phosphorylates FAK at various other sites including Y861; (4) downstream signaling of activated FAK elicits changes in cellular behavior.	Tyrosine	173-181	PTK2 protein tyrosine kinase 2	Mus musculus	127-130
25242698-3	2014	Focal adhesion kinase (FAK) activation involves the following: (1) ligand bound growth factors or clustered integrins activate FAK kinase domain; (2) FAK autophosphorylates tyrosine (Y) 397; (3) Src binds pY397 and phosphorylates FAK at various other sites including Y861; (4) downstream signaling of activated FAK elicits changes in cellular behavior.	Tyrosine	173-181	PTK2 protein tyrosine kinase 2	Mus musculus	127-130
25242698-3	2014	Focal adhesion kinase (FAK) activation involves the following: (1) ligand bound growth factors or clustered integrins activate FAK kinase domain; (2) FAK autophosphorylates tyrosine (Y) 397; (3) Src binds pY397 and phosphorylates FAK at various other sites including Y861; (4) downstream signaling of activated FAK elicits changes in cellular behavior.	Tyrosine	173-181	PTK2 protein tyrosine kinase 2	Mus musculus	127-130
25242698-3	2014	Focal adhesion kinase (FAK) activation involves the following: (1) ligand bound growth factors or clustered integrins activate FAK kinase domain; (2) FAK autophosphorylates tyrosine (Y) 397; (3) Src binds pY397 and phosphorylates FAK at various other sites including Y861; (4) downstream signaling of activated FAK elicits changes in cellular behavior.	Tyrosine	173-181	PTK2 protein tyrosine kinase 2	Mus musculus	127-130
25250716-9	2014	These results demonstrate that melatonin signaling via MT2 triggers FAK/paxillin phosphorylation to stimulate reorganization of the actin cytoskeleton, which is responsible for Cdc42/Arp2/3 activation to promote UCB-MSCs motility.	Melatonin	31-40	PTK2 protein tyrosine kinase 2	Mus musculus	68-71
25118939-7	2014	FAK deletion correlates with increased phosphorylation of Tks-5 (tyrosine kinase substrate with five SH3 domain) and reactive oxygen species production.	Reactive Oxygen Species	117-140	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
25319025-4	2014	Such an interaction requires FAK tyrosine 925 and is enhanced following its phosphorylation by Src, which occurs upon FAK stimulation.	Tyrosine	33-41	PTK2 protein tyrosine kinase 2	Mus musculus	29-32
25319025-4	2014	Such an interaction requires FAK tyrosine 925 and is enhanced following its phosphorylation by Src, which occurs upon FAK stimulation.	Tyrosine	33-41	PTK2 protein tyrosine kinase 2	Mus musculus	118-121
25079333-6	2014	Our study shows that deletion of FAK in endothelial cells has no apparent effect on blood vessel function per se, but induces increased apoptosis and decreased proliferation within perivascular tumour-cell compartments of doxorubicin- and radiotherapy-treated mice.	Doxorubicin	222-233	PTK2 protein tyrosine kinase 2	Mus musculus	33-36
24342076-8	2014	FAK was both necessary and sufficient for maintaining p21 levels following DOX treatment and depletion of p21 compromised FAK-dependent protection from DOX.	Doxorubicin	152-155	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
25036034-7	2014	Furthermore, carnosic acid suppressed phosphorylation of Src, FAK, and AKT.	salvin	13-26	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
24853558-4	2014	In this study, we compared FAK activation in the lungs of highly susceptible AKR mice and mildly susceptible C57BL/6 mice after exposure to CS for three weeks.	Cesium	140-142	PTK2 protein tyrosine kinase 2	Mus musculus	27-30
24853558-8	2014	These results suggest that FAK inhibition may contribute to CS-induced lung EC apoptosis and emphysema.	Cesium	60-62	PTK2 protein tyrosine kinase 2	Mus musculus	27-30
24853558-14	2014	Taken together, our data suggest that inhibition of eIF2alpha and FAK signaling may play an important role in CS-induced lung EC apoptosis and emphysema.	Cesium	110-112	PTK2 protein tyrosine kinase 2	Mus musculus	66-69
24915008-6	2014	Treatment of Alport mice with TAE226, a small molecule inhibitor of FAK activation, ameliorated fibrosis and glomerulosclerosis, significantly reduced proteinuria and blood urea nitrogen levels, and partially restored GBM ultrastructure.	TAE226	30-36	PTK2 protein tyrosine kinase 2	Mus musculus	68-71
24371135-9	2014	Furthermore, focal adhesion kinase (FAK), a nonreceptor tyrosine kinase important for regulating cell migration, was activated by LPA at a late time frame coinciding with Cyr61 accumulation.	lysophosphatidic acid	130-133	PTK2 protein tyrosine kinase 2	Mus musculus	13-34
24371135-9	2014	Furthermore, focal adhesion kinase (FAK), a nonreceptor tyrosine kinase important for regulating cell migration, was activated by LPA at a late time frame coinciding with Cyr61 accumulation.	lysophosphatidic acid	130-133	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
24371135-10	2014	Interestingly, knockdown of Cyr61 blocked LPA-induced FAK activation, indicating that an LPA-Cyr61-FAK axis leads to SMC migration.	lysophosphatidic acid	42-45	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
24371135-10	2014	Interestingly, knockdown of Cyr61 blocked LPA-induced FAK activation, indicating that an LPA-Cyr61-FAK axis leads to SMC migration.	lysophosphatidic acid	42-45	PTK2 protein tyrosine kinase 2	Mus musculus	99-102
24371135-11	2014	Our results further demonstrate that plasma membrane integrins alpha6beta1 and alphanubeta3 transduced the LPA-Cyr61 signal toward FAK activation and migration.	lysophosphatidic acid	107-110	PTK2 protein tyrosine kinase 2	Mus musculus	131-134
25063025-5	2014	We further demonstrated that PAI-1 induces phosphorylation of focal adhesion kinase (FAK) at Tyr(925), which, in turn, mediated the invasion of macrophages into the melanoma.	Tyrosine	93-96	PTK2 protein tyrosine kinase 2	Mus musculus	62-83
25063025-5	2014	We further demonstrated that PAI-1 induces phosphorylation of focal adhesion kinase (FAK) at Tyr(925), which, in turn, mediated the invasion of macrophages into the melanoma.	Tyrosine	93-96	PTK2 protein tyrosine kinase 2	Mus musculus	85-88
24755674-1	2014	This investigation describes the clinical significance of phosphorylated focal adhesion kinase (FAK) at the major activating tyrosine site (Y397) in epithelial ovarian cancer (EOC) cells and tumor-associated endothelial cells.	Tyrosine	125-133	PTK2 protein tyrosine kinase 2	Mus musculus	73-94
24755674-1	2014	This investigation describes the clinical significance of phosphorylated focal adhesion kinase (FAK) at the major activating tyrosine site (Y397) in epithelial ovarian cancer (EOC) cells and tumor-associated endothelial cells.	Tyrosine	125-133	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
24415158-7	2014	Interestingly, rOA stimulated-osteoblast adhesion promoted an increase in FAK and ERK activation, resulting in the formation of focal adhesions, cell spreading and enhanced actin cytoskeleton organization.	ROA	15-18	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
24860788-10	2014	We then treated mice xenografted with Ph+ leukemia cells with the FAK inhibitor TAE226 in combination with a BCR-ABL TKI nilotinib.	TAE226	80-86	PTK2 protein tyrosine kinase 2	Mus musculus	66-69
24342076-0	2014	Focal adhesion kinase antagonizes doxorubicin cardiotoxicity via p21(Cip1.).	Doxorubicin	34-45	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
24342076-3	2014	The objective of this study was to determine if targeted myocardial FAK activation could protect the heart from DOX-induced de-compensation and to characterize the underlying mechanisms.	Doxorubicin	112-115	PTK2 protein tyrosine kinase 2	Mus musculus	68-71
24342076-5	2014	FAK depletion enhanced susceptibility to DOX-induced myocyte apoptosis and cardiac dysfunction, while elevated FAK activity provided remarkable cardioprotection.	Doxorubicin	41-44	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
24342076-8	2014	FAK was both necessary and sufficient for maintaining p21 levels following DOX treatment and depletion of p21 compromised FAK-dependent protection from DOX.	Doxorubicin	75-78	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
24416452-7	2014	Moreover, niclosamide blocked breast cancer cells migration and invasion, and the reduction of phosphorylated STAT3(Tyr705), phosphorylated FAK(Tyr925) and phosphorylated Src(Tyr416) were also observed.	Niclosamide	10-21	PTK2 protein tyrosine kinase 2	Mus musculus	140-143
24446483-2	2014	In this paper, we show that vascular endothelial cadherin (VEC) tyrosine (Y) 658 is a target of FAK in tumor-associated endothelial cells (ECs).	Tyrosine	64-72	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
24446483-4	2014	Adherence of VEGF-expressing tumor cells to ECs triggered FAK-dependent VEC-Y658 phosphorylation.	y658	76-80	PTK2 protein tyrosine kinase 2	Mus musculus	58-61
24063814-9	2014	Both total MCP-1 levels and secreted MCP-1 levels were attenuated during the response to Cyr61 stimulation by pretreatment with integrin alphanubeta3-blocking antibodies, a FAK inhibitor (PF573228), a PI3K inhibitor (LY294002), and an Akt inhibitor (A6730).	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	188-196	PTK2 protein tyrosine kinase 2	Mus musculus	173-176
24528020-7	2014	Western blotting revealed that barbigerone inhibited phosphorylation of AKT, FAK and MAPK family members, including ERK, JNK, and p38 MAPKs, in B16F10 cells mainly through the MEK3/6/p38 MAPK signaling pathway.	barbigerone	31-42	PTK2 protein tyrosine kinase 2	Mus musculus	77-80
24359579-13	2013	A CD98hc/integrin interaction was required for adhesion-induced sustained FAK phosphorylation and activation of the major downstream signaling pathways PI3k/Akt and MEK/ERK, while overexpression of a constitutive active form of FAK rescued the CD98hc deficiency.	cd98hc	2-8	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
24359579-13	2013	A CD98hc/integrin interaction was required for adhesion-induced sustained FAK phosphorylation and activation of the major downstream signaling pathways PI3k/Akt and MEK/ERK, while overexpression of a constitutive active form of FAK rescued the CD98hc deficiency.	cd98hc	2-8	PTK2 protein tyrosine kinase 2	Mus musculus	228-231
24036212-0	2013	Activation of integrin beta1-focal adhesion kinase-RasGTP pathway plays a critical role in TGF beta1-induced podocyte injury.	rasgtp	51-57	PTK2 protein tyrosine kinase 2	Mus musculus	29-50
24194191-9	2013	The EDP-induced FAK and Akt phosphorylation was blocked by FAK- and Akt-specific inhibitors.	2-ethyl-3,5-dimethylpyrazine	4-7	PTK2 protein tyrosine kinase 2	Mus musculus	16-19
24194191-9	2013	The EDP-induced FAK and Akt phosphorylation was blocked by FAK- and Akt-specific inhibitors.	2-ethyl-3,5-dimethylpyrazine	4-7	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
24108461-7	2013	We demonstrate that Lyn association with focal adhesion kinase (FAK) and phosphorylation of FAK at tyrosine residues 576/577 and 925 were required for Lyn-dependent stabilization of endothelial adherens junctions.	Tyrosine	99-107	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
24036212-9	2013	The FAK inhibitor TAE226 and the specific knockdown of Grb2 remarkably alleviated TGFbeta1-induced podocyte apoptosis.	TAE226	18-24	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
24169345-8	2013	The inhibitory effect of reversine on FA turnover accounted for a large part on its capacity to interfere with FAK function on regulating its downstream targets.	2-(4-morpholinoanilino)-6-cyclohexylaminopurine	25-34	PTK2 protein tyrosine kinase 2	Mus musculus	111-114
24055813-4	2013	Over-expression of MARVELD1 in NIH3T3 cells decreased the expression level of integrin beta1 and vinculin, and further led to dephosphorylation of focal adhesion kinase (FAK) at Tyr 397.	Tyrosine	178-181	PTK2 protein tyrosine kinase 2	Mus musculus	147-168
24055813-4	2013	Over-expression of MARVELD1 in NIH3T3 cells decreased the expression level of integrin beta1 and vinculin, and further led to dephosphorylation of focal adhesion kinase (FAK) at Tyr 397.	Tyrosine	178-181	PTK2 protein tyrosine kinase 2	Mus musculus	170-173
24124594-1	2013	Several biological studies have indicated that hedgehog signaling plays an important role in osteoblast proliferation and differentiation, and sonic hedgehog (SHH) expression is positively correlated with phosphorylated focal adhesion kinase (FAK) Tyr(397).	Tyrosine	248-251	PTK2 protein tyrosine kinase 2	Mus musculus	220-241
24124594-1	2013	Several biological studies have indicated that hedgehog signaling plays an important role in osteoblast proliferation and differentiation, and sonic hedgehog (SHH) expression is positively correlated with phosphorylated focal adhesion kinase (FAK) Tyr(397).	Tyrosine	248-251	PTK2 protein tyrosine kinase 2	Mus musculus	243-246
23764511-8	2013	We report that beta1-integrin activity and FAK phosphorylation at tyrosine 397 (FAKpY397) are linked to neuronal polarization as well as neurite outgrowth and branching.	Tyrosine	66-74	PTK2 protein tyrosine kinase 2	Mus musculus	43-46
24080910-3	2013	METHODS AND RESULTS: The essential cytoskeletal signaling pathway member focal adhesion kinase (FAK) was selectively deleted in adult cardiac myocytes using a tamoxifen-inducible Cre-Lox system (alpha-MHC-MerCreMer).	Tamoxifen	159-168	PTK2 protein tyrosine kinase 2	Mus musculus	73-94
24080910-3	2013	METHODS AND RESULTS: The essential cytoskeletal signaling pathway member focal adhesion kinase (FAK) was selectively deleted in adult cardiac myocytes using a tamoxifen-inducible Cre-Lox system (alpha-MHC-MerCreMer).	Tamoxifen	159-168	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
24080910-7	2013	Control groups included wild-type (WT) and tamoxifen-treated alpha-MHC-MerCreMer+/-/FAK(WT/WT) (experimental control) mice.	Tamoxifen	43-52	PTK2 protein tyrosine kinase 2	Mus musculus	84-87
23642017-0	2013	Antifibrotic effects of focal adhesion kinase inhibitor in bleomycin-induced pulmonary fibrosis in mice.	Bleomycin	59-68	PTK2 protein tyrosine kinase 2	Mus musculus	24-45
23642017-3	2013	In the present study, we investigated whether the targeted inhibition of FAK by using a specific inhibitor, TAE226, has the potential to regulate pulmonary fibrosis.	TAE226	108-114	PTK2 protein tyrosine kinase 2	Mus musculus	73-76
23642017-4	2013	TAE226 showed inhibitory activity of autophosphorylation of FAK at tyrosine 397 in lung fibroblasts.	TAE226	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	60-63
23642017-4	2013	TAE226 showed inhibitory activity of autophosphorylation of FAK at tyrosine 397 in lung fibroblasts.	Tyrosine	67-75	PTK2 protein tyrosine kinase 2	Mus musculus	60-63
23707351-6	2013	Decreased phosphorylation of Src, CTTN, and FAK also followed EGCG treatment.	epigallocatechin gallate	62-66	PTK2 protein tyrosine kinase 2	Mus musculus	44-47
23664097-12	2013	The FAK phosphorylation induced by 12(S)-HETE was further inhibited by PD98059, indicating that FAK is the downstream target of ERK.	12-Hydroxy-5,8,10,14-eicosatetraenoic Acid	35-45	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
23571270-1	2013	Tyrosine phosphorylation (Tyr-P) of focal adhesion kinase (FAK) regulates FAK activation.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	36-57
23571270-1	2013	Tyrosine phosphorylation (Tyr-P) of focal adhesion kinase (FAK) regulates FAK activation.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
23571270-1	2013	Tyrosine phosphorylation (Tyr-P) of focal adhesion kinase (FAK) regulates FAK activation.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
23571270-1	2013	Tyrosine phosphorylation (Tyr-P) of focal adhesion kinase (FAK) regulates FAK activation.	tyr-p	26-31	PTK2 protein tyrosine kinase 2	Mus musculus	36-57
23571270-1	2013	Tyrosine phosphorylation (Tyr-P) of focal adhesion kinase (FAK) regulates FAK activation.	tyr-p	26-31	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
23571270-1	2013	Tyrosine phosphorylation (Tyr-P) of focal adhesion kinase (FAK) regulates FAK activation.	tyr-p	26-31	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
23571270-2	2013	Phosphorylated FAK Tyr 397 binds Src family kinases (Src), which in turn directly phosphorylate FAK Tyr 576/577 to produce maximal FAK enzymatic activity.	Tyrosine	19-22	PTK2 protein tyrosine kinase 2	Mus musculus	15-18
23571270-2	2013	Phosphorylated FAK Tyr 397 binds Src family kinases (Src), which in turn directly phosphorylate FAK Tyr 576/577 to produce maximal FAK enzymatic activity.	Tyrosine	19-22	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
23571270-2	2013	Phosphorylated FAK Tyr 397 binds Src family kinases (Src), which in turn directly phosphorylate FAK Tyr 576/577 to produce maximal FAK enzymatic activity.	Tyrosine	19-22	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
23571270-2	2013	Phosphorylated FAK Tyr 397 binds Src family kinases (Src), which in turn directly phosphorylate FAK Tyr 576/577 to produce maximal FAK enzymatic activity.	Tyrosine	100-103	PTK2 protein tyrosine kinase 2	Mus musculus	15-18
23571270-2	2013	Phosphorylated FAK Tyr 397 binds Src family kinases (Src), which in turn directly phosphorylate FAK Tyr 576/577 to produce maximal FAK enzymatic activity.	Tyrosine	100-103	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
23571270-2	2013	Phosphorylated FAK Tyr 397 binds Src family kinases (Src), which in turn directly phosphorylate FAK Tyr 576/577 to produce maximal FAK enzymatic activity.	Tyrosine	100-103	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
23571270-5	2013	Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2 min) maximal Tyr-P, Phase II (5-20 min) rapid decline in Tyr-P, and Phase III (>20 min) plateau in Tyr-P at submaximal levels.	Tyrosine	61-64	PTK2 protein tyrosine kinase 2	Mus musculus	49-52
23571270-5	2013	Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2 min) maximal Tyr-P, Phase II (5-20 min) rapid decline in Tyr-P, and Phase III (>20 min) plateau in Tyr-P at submaximal levels.	Tyrosine	81-84	PTK2 protein tyrosine kinase 2	Mus musculus	145-148
23571270-5	2013	Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2 min) maximal Tyr-P, Phase II (5-20 min) rapid decline in Tyr-P, and Phase III (>20 min) plateau in Tyr-P at submaximal levels.	tyr-p	157-162	PTK2 protein tyrosine kinase 2	Mus musculus	49-52
23571270-5	2013	Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2 min) maximal Tyr-P, Phase II (5-20 min) rapid decline in Tyr-P, and Phase III (>20 min) plateau in Tyr-P at submaximal levels.	tyr-p	157-162	PTK2 protein tyrosine kinase 2	Mus musculus	145-148
23571270-5	2013	Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2 min) maximal Tyr-P, Phase II (5-20 min) rapid decline in Tyr-P, and Phase III (>20 min) plateau in Tyr-P at submaximal levels.	tyr-p	215-220	PTK2 protein tyrosine kinase 2	Mus musculus	145-148
23571270-5	2013	Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2 min) maximal Tyr-P, Phase II (5-20 min) rapid decline in Tyr-P, and Phase III (>20 min) plateau in Tyr-P at submaximal levels.	tyr-p	215-220	PTK2 protein tyrosine kinase 2	Mus musculus	145-148
23571270-5	2013	Immunoblotting analyses using antibodies against FAK phospho-Tyr 397 and phospho-Tyr 576/577 demonstrated that the time-course of CB1-stimulated FAK 576/577 Tyr-P occurred in three phases: Phase I (0-2 min) maximal Tyr-P, Phase II (5-20 min) rapid decline in Tyr-P, and Phase III (>20 min) plateau in Tyr-P at submaximal levels.	tyr-p	215-220	PTK2 protein tyrosine kinase 2	Mus musculus	145-148
23571270-6	2013	In contrast, FAK 397 Tyr-P was monophasic and significantly lower in magnitude.	tyr-p	21-26	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
23571270-7	2013	FAK 397 Tyr-P and Phase I FAK 576/577 Tyr-P involved protein tyrosine phosphatase (PTP1B and Shp1/Shp2)-mediated Src activation, Protein Kinase A (PKA) inhibition, and integrin activation.	Tyrosine	8-11	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
23571270-7	2013	FAK 397 Tyr-P and Phase I FAK 576/577 Tyr-P involved protein tyrosine phosphatase (PTP1B and Shp1/Shp2)-mediated Src activation, Protein Kinase A (PKA) inhibition, and integrin activation.	Tyrosine	38-41	PTK2 protein tyrosine kinase 2	Mus musculus	26-29
23571270-8	2013	Phase I maximal FAK 576/577 Tyr-P also required cooperative signaling between receptor tyrosine kinases (RTKs) and integrins.	tyr-p	28-33	PTK2 protein tyrosine kinase 2	Mus musculus	16-19
23571270-11	2013	In contrast, cells grown on the integrin ligands fibronectin and laminin displayed increased FAK 576/577 Tyr-P that was augmented by CB1 agonists and blocked by the Src inhibitor PP2 and Flk-1 VEGFR antagonist SU5416.	tyr-p	105-110	PTK2 protein tyrosine kinase 2	Mus musculus	93-96
23571270-11	2013	In contrast, cells grown on the integrin ligands fibronectin and laminin displayed increased FAK 576/577 Tyr-P that was augmented by CB1 agonists and blocked by the Src inhibitor PP2 and Flk-1 VEGFR antagonist SU5416.	Semaxinib	210-216	PTK2 protein tyrosine kinase 2	Mus musculus	93-96
23571270-12	2013	Taken together, these studies have identified a complex integrative pathway utilized by CB1 to stimulate maximal FAK 576/577 Tyr-P in neuronal cells.	tyr-p	125-130	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
23664097-12	2013	The FAK phosphorylation induced by 12(S)-HETE was further inhibited by PD98059, indicating that FAK is the downstream target of ERK.	12-Hydroxy-5,8,10,14-eicosatetraenoic Acid	35-45	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
23664097-12	2013	The FAK phosphorylation induced by 12(S)-HETE was further inhibited by PD98059, indicating that FAK is the downstream target of ERK.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	71-78	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
23664097-12	2013	The FAK phosphorylation induced by 12(S)-HETE was further inhibited by PD98059, indicating that FAK is the downstream target of ERK.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	71-78	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
23936270-6	2013	Inhibition of the tyrosine kinases proline-rich tyrosine kinase (Pyk2) and focal adhesion kinase (FAK), kinases that are capable of mediating tyrosine phosphorylation of paxillin, also restored paxillin levels, indicating a role for these kinases in the CD45-dependent regulation of paxillin.	Tyrosine	18-26	PTK2 protein tyrosine kinase 2	Mus musculus	75-96
24187869-14	2013	In mice treated with JPJDF, the expression intensity of FAK was higher in the normal tissue and lower in the cancer tissue than those of the other treatment groups.	jpjdf	21-26	PTK2 protein tyrosine kinase 2	Mus musculus	56-59
23936270-6	2013	Inhibition of the tyrosine kinases proline-rich tyrosine kinase (Pyk2) and focal adhesion kinase (FAK), kinases that are capable of mediating tyrosine phosphorylation of paxillin, also restored paxillin levels, indicating a role for these kinases in the CD45-dependent regulation of paxillin.	Tyrosine	18-26	PTK2 protein tyrosine kinase 2	Mus musculus	98-101
23637231-3	2013	We show that cells stably depleted of LKB1 or its co-activator STRADalpha have increased phosphorylation of focal adhesion kinase (FAK) at Tyr(397)/Tyr(861) and enhanced adhesion to fibronectin.	Tyrosine	139-142	PTK2 protein tyrosine kinase 2	Mus musculus	108-129
23637231-3	2013	We show that cells stably depleted of LKB1 or its co-activator STRADalpha have increased phosphorylation of focal adhesion kinase (FAK) at Tyr(397)/Tyr(861) and enhanced adhesion to fibronectin.	Tyrosine	139-142	PTK2 protein tyrosine kinase 2	Mus musculus	131-134
23637231-3	2013	We show that cells stably depleted of LKB1 or its co-activator STRADalpha have increased phosphorylation of focal adhesion kinase (FAK) at Tyr(397)/Tyr(861) and enhanced adhesion to fibronectin.	Tyrosine	148-151	PTK2 protein tyrosine kinase 2	Mus musculus	131-134
23255596-5	2013	This mutation disrupted the function of FAK scaffolding to mediate endophilin A2 phosphorylation at Tyr-315 by Src, leading to the decreased surface expression of MT1-MMP, as observed previously in transformed fibroblasts in vitro.	Tyrosine	100-103	PTK2 protein tyrosine kinase 2	Mus musculus	40-43
23208732-9	2013	Finally, small molecule FAK inhibition in a nude mouse model resulted in a significant decrease in metastatic tumor burden in SK-N-BE(2) injected animals.	sk-n-be	126-133	PTK2 protein tyrosine kinase 2	Mus musculus	24-27
22614008-5	2013	In addition, we demonstrated that nicotine-mediated MUC4 upregulation promotes the PC cell migration through the activation of the downstream effectors, such as HER2, c-Src and FAK; this effect was attenuated by shRNA-mediated MUC4 abrogation, further implying that these nicotine-mediated pathological effects on PC cells are MUC4 dependent.	Nicotine	34-42	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Dasatinib	41-50	PTK2 protein tyrosine kinase 2	Mus musculus	111-114
23114714-2	2013	Treatment of both cell lines with either dasatinib or sunitinib reduced phosphorylation of PDGFR, VEGFR2, Akt, FAK, Src (dasatinib only) and Cav-1, and reduced cellular and secreted levels of Cav-1.	Sunitinib	54-63	PTK2 protein tyrosine kinase 2	Mus musculus	111-114
23231952-10	2013	FAK knockdown partially prevents this inhibitory effect, indicating that FAK is a relevant target of sorafenib.	Sorafenib	101-110	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
23231952-10	2013	FAK knockdown partially prevents this inhibitory effect, indicating that FAK is a relevant target of sorafenib.	Sorafenib	101-110	PTK2 protein tyrosine kinase 2	Mus musculus	73-76
22989773-6	2013	Subsequently, C(16)-Cer increased focal adhesion kinase (FAK) and Paxillin phosphorylation, which were inhibited by PKC inhibitor Bisindolylmaleimide I (1muM).	bisindolylmaleimide I	130-151	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
23710450-7	2013	Competitively blocking VN-integrin receptors with echistatin (1 mug/mL) results in a decrease of viability/proliferation, cell cycle progression, cellular uptake, and FAK/ERK activation showing the involvement of Vitronectin receptors in signal transduction.	echistatin	50-60	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
23573143-4	2013	The expression level of phosphorylated FAK, Akt, ERK1/2, and Rb was decreased p21 expression while level was increased in WEHI-3 treated with GLY.	Glycine	142-145	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
23573143-8	2013	Accordingly, GLY demonstrated an inhibitory effect on tumor growth with a regulatory mechanism partially through inhibiting FAK, Akt, and ERK expression in WEHI-3 cells.	Glycine	13-16	PTK2 protein tyrosine kinase 2	Mus musculus	124-127
23349702-7	2013	In addition, FSP induced the tyrosine phosphorylation of FAK and paxillin in attached epithelial cells.	Tyrosine	29-37	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
22264674-10	2012	FAK protein was localized along cellular extensions on SA-treated c.p.Ti and the expression of FAK mRNA was significantly higher on these disks than on c.p.Ti and AO c.p.Ti after 72h (P<0.05).	2-chloro-10-(4'(N-beta-hydroxyethyl)piperazinyl-1')acetylphenothiazine	55-57	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
22971575-2	2012	Previously, we have shown that skin-specific loss of fak prevents chemically induced skin carcinogenesis in mice following phorbol ester treatment.	Phorbol Esters	123-136	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
22971575-3	2012	In this study, we show that skin-specific deletion of fak prevents mobilization of stem cells within the bulge region of the hair follicle, which are the precursors of papillomas following phorbol ester treatment.	Phorbol Esters	189-202	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
22971575-6	2012	We show that FAK is required for the nuclear localization of beta-catenin in the skin following phorbol ester treatment and the transcriptional activation of the beta-catenin target gene c-Myc.	Phorbol Esters	96-109	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
22974528-9	2012	Phosphorylation of Tyr-925 of FAK in response to EGF was significantly reduced in KO cell compared to WT cells.	Tyrosine	19-22	PTK2 protein tyrosine kinase 2	Mus musculus	30-33
22974528-11	2012	Collectively, these studies indicate that EBP50, by scaffolding EGF receptor and FAK, facilitates activation of FAK, focal adhesion turnover, and migration of VSMC.	vsmc	159-163	PTK2 protein tyrosine kinase 2	Mus musculus	81-84
22015944-0	2012	The novel indole compound SK228 induces apoptosis and FAK/Paxillin disruption in tumor cell lines and inhibits growth of tumor graft in the nude mouse.	indole	10-16	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
22015944-0	2012	The novel indole compound SK228 induces apoptosis and FAK/Paxillin disruption in tumor cell lines and inhibits growth of tumor graft in the nude mouse.	1,4-bis(di(5-hydroxy-1H-indol-3-yl)methyl)benzene	26-31	PTK2 protein tyrosine kinase 2	Mus musculus	54-57
22015944-13	2012	In addition, SK228 inhibits cancer cell invasion via FAK/Paxillin disruption at noncytotoxic doses.	1,4-bis(di(5-hydroxy-1H-indol-3-yl)methyl)benzene	13-18	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
22498697-5	2012	These RIPcre(+)fak(fl/fl) mice exhibited glucose intolerance without changes in insulin sensitivity.	Glucose	41-48	PTK2 protein tyrosine kinase 2	Mus musculus	15-18
22498697-7	2012	FAK-deficient beta-cells exhibited impaired insulin secretion with normal glucose sensing and preserved Ca(2+) influx in response to glucose, but a reduced number of docked insulin granules and insulin exocytosis were found, which was associated with a decrease in focal proteins, paxillin and talin, and an impairment in actin depolymerization.	Glucose	74-81	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
22498697-7	2012	FAK-deficient beta-cells exhibited impaired insulin secretion with normal glucose sensing and preserved Ca(2+) influx in response to glucose, but a reduced number of docked insulin granules and insulin exocytosis were found, which was associated with a decrease in focal proteins, paxillin and talin, and an impairment in actin depolymerization.	Glucose	133-140	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
22705303-0	2012	Oral administration of FAK inhibitor TAE226 inhibits the progression of peritoneal dissemination of colorectal cancer.	TAE226	37-43	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
22705303-3	2012	Since we and other groups have reported that the inhibition of FAK activity exhibited a potent anticancer effect in several cancer models, we hypothesized that TAE226, a novel ATP-competitive tyrosine kinase inhibitor designed to target FAK, can prevent the occurrence and progression of peritoneal dissemination.	TAE226	160-166	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
22705303-3	2012	Since we and other groups have reported that the inhibition of FAK activity exhibited a potent anticancer effect in several cancer models, we hypothesized that TAE226, a novel ATP-competitive tyrosine kinase inhibitor designed to target FAK, can prevent the occurrence and progression of peritoneal dissemination.	TAE226	160-166	PTK2 protein tyrosine kinase 2	Mus musculus	237-240
22705303-8	2012	Taken together, a possible strategy for inhibiting peritoneal dissemination by targeting FAK with TAE226 appears to be applicable through anti-proliferative and anti-invasion/anti-migration mechanisms.	TAE226	98-104	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
22366060-4	2012	An aberrant increase in FAK tyrosine phosphorylation was observed in insulin resistant Neuro-2a (N2A) cells.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	24-27
22366060-5	2012	Downregulation of FAK expression utilizing RNAi mediated gene silencing in insulin resistant N2A cells completely ameliorated the impaired insulin/PI3K signaling and glucose uptake.	Glucose	166-173	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
22366060-6	2012	FAK silencing in primary cortical neurons also showed marked enhancement in glucose uptake.	Glucose	76-83	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
22320676-6	2012	Herein, using a mouse model, PV-IgG administration showed an increased level of FAK phosphorylated on 397 and 925 tyrosine residues in the basal layer of epidermis.	Tyrosine	114-122	PTK2 protein tyrosine kinase 2	Mus musculus	80-83
22492165-8	2012	Pharmacologic or siRNA-mediated targeting of FAK resulted in marked abrogation of bleomycin-induced lung fibrosis in mice.	Bleomycin	82-91	PTK2 protein tyrosine kinase 2	Mus musculus	45-48
22155722-6	2012	The total number as well as the fraction of cycling Lin(-)Sca-1(+)c-kit(+) (LSK) cells is increased in Fak(-/-) mice compared to controls, while hematopoietic progenitors and mature blood cells are unaffected.	lsk	76-79	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
22139838-5	2012	Total internal reflection fluorescence microscopy revealed the glucose-responsive co-localization of focal adhesion kinase (FAK) and paxillin with integrin beta1 at the basal cell surface after short term stimulation.	Glucose	63-70	PTK2 protein tyrosine kinase 2	Mus musculus	101-122
22056317-9	2012	Moreover, inhibition of the mTOR complex by rapamycin extinguished the cardiac hypertrophy of the transgenic FAK mice.	Sirolimus	44-53	PTK2 protein tyrosine kinase 2	Mus musculus	109-112
22139838-5	2012	Total internal reflection fluorescence microscopy revealed the glucose-responsive co-localization of focal adhesion kinase (FAK) and paxillin with integrin beta1 at the basal cell surface after short term stimulation.	Glucose	63-70	PTK2 protein tyrosine kinase 2	Mus musculus	124-127
22139838-6	2012	In addition, blockade of the interaction between beta1 integrins and the extracellular matrix with an anti-beta1 integrin antibody (Ha2/5) inhibited short term glucose-induced phosphorylation of FAK (Tyr-397), paxillin (Tyr-118), and ERK1/2 (Thr-202/Tyr-204).	Glucose	160-167	PTK2 protein tyrosine kinase 2	Mus musculus	195-198
22139838-6	2012	In addition, blockade of the interaction between beta1 integrins and the extracellular matrix with an anti-beta1 integrin antibody (Ha2/5) inhibited short term glucose-induced phosphorylation of FAK (Tyr-397), paxillin (Tyr-118), and ERK1/2 (Thr-202/Tyr-204).	Tyrosine	200-203	PTK2 protein tyrosine kinase 2	Mus musculus	195-198
22139838-6	2012	In addition, blockade of the interaction between beta1 integrins and the extracellular matrix with an anti-beta1 integrin antibody (Ha2/5) inhibited short term glucose-induced phosphorylation of FAK (Tyr-397), paxillin (Tyr-118), and ERK1/2 (Thr-202/Tyr-204).	Tyrosine	220-223	PTK2 protein tyrosine kinase 2	Mus musculus	195-198
22139838-7	2012	Pharmacological inhibition of FAK activity blocked glucose-induced actin cytoskeleton remodeling and glucose-induced disruption of the F-actin/SNAP-25 association at the plasma membrane as well as the distribution of insulin granules to regions in close proximity to the plasma membrane.	Glucose	51-58	PTK2 protein tyrosine kinase 2	Mus musculus	30-33
22139838-7	2012	Pharmacological inhibition of FAK activity blocked glucose-induced actin cytoskeleton remodeling and glucose-induced disruption of the F-actin/SNAP-25 association at the plasma membrane as well as the distribution of insulin granules to regions in close proximity to the plasma membrane.	Glucose	101-108	PTK2 protein tyrosine kinase 2	Mus musculus	30-33
22139838-8	2012	Furthermore, FAK inhibition also completely blocked short term glucose-induced activation of the Akt/AS160 signaling pathway.	Glucose	63-70	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
22139838-8	2012	Furthermore, FAK inhibition also completely blocked short term glucose-induced activation of the Akt/AS160 signaling pathway.	as160	101-106	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	46-53	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	46-53	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	46-53	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	193-200	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	193-200	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	193-200	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	as160	364-369	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	as160	364-369	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	as160	364-369	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	193-200	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	193-200	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22139838-9	2012	In conclusion, these results indicate 1) that glucose-induced activation of FAK, paxillin, and ERK1/2 is mediated by beta1 integrin intracellular signaling, 2) a mechanism whereby FAK mediates glucose-induced actin cytoskeleton remodeling, hence allowing docking and fusion of insulin granules to the plasma membrane, and 3) a possible functional role for the Akt/AS160 signaling pathway in the FAK-mediated regulation of glucose-stimulated insulin secretion.	Glucose	193-200	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
22279574-0	2012	Mitochondrial apoptosis and FAK signaling disruption by a novel histone deacetylase inhibitor, HTPB, in antitumor and antimetastatic mouse models.	htpb	95-99	PTK2 protein tyrosine kinase 2	Mus musculus	28-31
22407353-8	2012	This was accompanied by a decrease of focal adhesion number, a diminution of fak and pyk2 phosphorylation at Tyr-576, Tyr-861 and Tyr-579, respectively leading to their dissociations from beta1 integrin and inhibition of PI 3-kinase activity.	Tyrosine	109-112	PTK2 protein tyrosine kinase 2	Mus musculus	77-80
22407353-9	2012	Etxfag also induced a cell retraction accompanied by a redistribution of phosphorylated fak and pyk2 in the perinuclear region and lipid raft relocalization.	etxfag	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	88-91
23028449-7	2012	FAK-/- osteoblasts showed an ablated prostaglandin E(2) (PGE(2)) response to fluid flow shear.	Dinoprostone	37-55	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
23028449-7	2012	FAK-/- osteoblasts showed an ablated prostaglandin E(2) (PGE(2)) response to fluid flow shear.	Dinoprostone	57-63	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
23028449-9	2012	Re-expression of FAK containing site-specific mutations at Tyr-397 and Tyr-925 phosphorylation sites did not rescue the phenotype, suggesting that these sites are important in osteoblast mechanotransduction.	Tyrosine	59-62	PTK2 protein tyrosine kinase 2	Mus musculus	17-20
22761690-8	2012	Further experiments demonstrated that carbon monoxide and bilirubin, the byproducts derived from heme degradation by HO-1, enhanced macrophage migration by increasing phosphorylation of p38 and FAK, respectively.	Heme	97-101	PTK2 protein tyrosine kinase 2	Mus musculus	194-197
22761690-8	2012	Further experiments demonstrated that carbon monoxide and bilirubin, the byproducts derived from heme degradation by HO-1, enhanced macrophage migration by increasing phosphorylation of p38 and FAK, respectively.	Carbon Monoxide	38-53	PTK2 protein tyrosine kinase 2	Mus musculus	194-197
22761690-8	2012	Further experiments demonstrated that carbon monoxide and bilirubin, the byproducts derived from heme degradation by HO-1, enhanced macrophage migration by increasing phosphorylation of p38 and FAK, respectively.	Bilirubin	58-67	PTK2 protein tyrosine kinase 2	Mus musculus	194-197
22204307-7	2011	We further demonstrated that infection of wild-type cells induces increasing amounts of phosphorylated FAK and growth factor receptors (EGFR and PDGFR) during the course of infection, correlating with accumulating Cdc42-GTP levels and C. jejuni invasion over time.	cdc42-gtp	214-223	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
21982831-4	2011	Tamoxifen treatment of FAK(loxP/loxP)//gammaGT-Cre-ER(T2) mice caused renal-specific fak recombination (FAK(DeltaloxP/DeltaloxP)) and reduction of FAK expression in proximal tubules.	Tamoxifen	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
22919583-5	2011	We also demonstrate that C. jejuni activates FAK autophosphorylation activity at Y-397 and phosphorylation of Y-925, which is required for stimulating two downstream guanine exchange factors, DOCK180 and Tiam-1, which are upstream of Rac1.	Guanine	166-173	PTK2 protein tyrosine kinase 2	Mus musculus	45-48
21982831-4	2011	Tamoxifen treatment of FAK(loxP/loxP)//gammaGT-Cre-ER(T2) mice caused renal-specific fak recombination (FAK(DeltaloxP/DeltaloxP)) and reduction of FAK expression in proximal tubules.	Tamoxifen	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	85-88
21982831-9	2011	This was associated with reduced c-Jun N-terminal kinase-dependent phosphorylation of paxillin at serine 178 in FAK-deficient cells, which is required for focal adhesion turnover.	Serine	98-104	PTK2 protein tyrosine kinase 2	Mus musculus	112-115
21982831-4	2011	Tamoxifen treatment of FAK(loxP/loxP)//gammaGT-Cre-ER(T2) mice caused renal-specific fak recombination (FAK(DeltaloxP/DeltaloxP)) and reduction of FAK expression in proximal tubules.	Tamoxifen	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
21982831-4	2011	Tamoxifen treatment of FAK(loxP/loxP)//gammaGT-Cre-ER(T2) mice caused renal-specific fak recombination (FAK(DeltaloxP/DeltaloxP)) and reduction of FAK expression in proximal tubules.	Tamoxifen	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
21982831-8	2011	The conditional fak deletion did not affect cell survival after hydrogen peroxide-induced cellular stress, whereas it impaired the recovery of focal adhesions that were disrupted by hydrogen peroxide.	Hydrogen Peroxide	182-199	PTK2 protein tyrosine kinase 2	Mus musculus	16-19
22067150-6	2011	In agreement with this interpretation is that cell stiffness and cytoskeletal stability in FAK-/- cells is partially restored to wild-type level after rho-kinase inhibition with Y27632.	Y 27632	178-184	PTK2 protein tyrosine kinase 2	Mus musculus	91-94
21115886-6	2010	RESULTS: Saracatinib inhibited major pathways in the metastatic cascade in vitro, including Src and FAK activation.	saracatinib	9-20	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
21734098-9	2011	In addition, AGE-BSA or suppression of NRP1 both reduced the phosphorylation of focal adhesion kinase (FAK) and Erk1/2 in PMA-stimulated differentiated podocytes.	Tetradecanoylphorbol Acetate	122-125	PTK2 protein tyrosine kinase 2	Mus musculus	80-101
21734098-9	2011	In addition, AGE-BSA or suppression of NRP1 both reduced the phosphorylation of focal adhesion kinase (FAK) and Erk1/2 in PMA-stimulated differentiated podocytes.	Tetradecanoylphorbol Acetate	122-125	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
21876123-3	2011	We found that hydrophobic phenylalanine substitutions of both tyrosines diminished the binding of tail-interacting proteins, including talins and kindlins, resulting in reduced beta1-mediated adhesion, focal adhesion kinase (FAK) signaling, and epidermal progenitor cell-derived skin tumors.	Phenylalanine	26-39	PTK2 protein tyrosine kinase 2	Mus musculus	202-223
21876123-3	2011	We found that hydrophobic phenylalanine substitutions of both tyrosines diminished the binding of tail-interacting proteins, including talins and kindlins, resulting in reduced beta1-mediated adhesion, focal adhesion kinase (FAK) signaling, and epidermal progenitor cell-derived skin tumors.	Phenylalanine	26-39	PTK2 protein tyrosine kinase 2	Mus musculus	225-228
21876123-3	2011	We found that hydrophobic phenylalanine substitutions of both tyrosines diminished the binding of tail-interacting proteins, including talins and kindlins, resulting in reduced beta1-mediated adhesion, focal adhesion kinase (FAK) signaling, and epidermal progenitor cell-derived skin tumors.	Tyrosine	62-71	PTK2 protein tyrosine kinase 2	Mus musculus	202-223
21876123-3	2011	We found that hydrophobic phenylalanine substitutions of both tyrosines diminished the binding of tail-interacting proteins, including talins and kindlins, resulting in reduced beta1-mediated adhesion, focal adhesion kinase (FAK) signaling, and epidermal progenitor cell-derived skin tumors.	Tyrosine	62-71	PTK2 protein tyrosine kinase 2	Mus musculus	225-228
21506116-0	2011	Caveolin-1 and integrin beta1 regulate embryonic stem cell proliferation via p38 MAPK and FAK in high glucose.	Glucose	102-109	PTK2 protein tyrosine kinase 2	Mus musculus	90-93
21506116-7	2011	Moreover, phosphorylation of both Src and focal adhesion kinase (FAK) were increased by high glucose, which were inhibited by IN beta1 antibody.	Glucose	93-100	PTK2 protein tyrosine kinase 2	Mus musculus	42-63
21506116-7	2011	Moreover, phosphorylation of both Src and focal adhesion kinase (FAK) were increased by high glucose, which were inhibited by IN beta1 antibody.	Glucose	93-100	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
21506116-8	2011	In addition, high glucose increased the expression levels of PINCH1/2, integrin-linked kinase (ILK), and alpha-parvin [PIP] complex proteins, which were all inhibited by the FAK siRNA and Src specific inhibitor (PP2, 10(-7)  M).	Glucose	18-25	PTK2 protein tyrosine kinase 2	Mus musculus	174-177
21289086-0	2011	FAK phosphorylation at Tyr-925 regulates cross-talk between focal adhesion turnover and cell protrusion.	Tyrosine	23-26	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
21289086-2	2011	Focal adhesion kinase (FAK), a major signaling component of FAs, is involved in the disassembly process of FAs through phosphorylation and dephosphorylation of its tyrosine residues, but the role of such phosphorylations in nascent FA formation and turnover near the cell front and in cell protrusion is less well understood.	Tyrosine	164-172	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
21289086-2	2011	Focal adhesion kinase (FAK), a major signaling component of FAs, is involved in the disassembly process of FAs through phosphorylation and dephosphorylation of its tyrosine residues, but the role of such phosphorylations in nascent FA formation and turnover near the cell front and in cell protrusion is less well understood.	Tyrosine	164-172	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
21289086-3	2011	In the present study, we demonstrate that, depending on the phosphorylation status of Tyr-925 residue, FAK modulates cell migration via two specific mechanisms.	Tyrosine	86-89	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
21289086-7	2011	Together, our results demonstrate that phosphorylation of FAK at Tyr-925 is required for FAK-mediated cell migration and cell protrusion.	Tyrosine	65-68	PTK2 protein tyrosine kinase 2	Mus musculus	58-61
21289086-7	2011	Together, our results demonstrate that phosphorylation of FAK at Tyr-925 is required for FAK-mediated cell migration and cell protrusion.	Tyrosine	65-68	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
21347260-8	2011	We found that pUC treatment reduced FAK phosphorylation at Y925 more efficiently compared to pU2 treatment.	puc	14-17	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
21347357-11	2011	A FAK selective inhibitor TAE-226, blocked TXA(2) generation.	TAE226	26-33	PTK2 protein tyrosine kinase 2	Mus musculus	2-5
21347357-11	2011	A FAK selective inhibitor TAE-226, blocked TXA(2) generation.	txa	43-46	PTK2 protein tyrosine kinase 2	Mus musculus	2-5
21686284-1	2011	We recently reported that a complex between focal adhesion kianse (FAK) and the molecular scaffold RACK1 controlled nascent integrin adhesion formation and cell polarization, via peripheral recruitment of the cAMP - degrading PDE4D5 isoform.	Cyclic AMP	209-213	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
20872237-8	2010	We found that a clinically approved camptothecin analog, irinotecan suppressed the migration, Cdc42 activity, and autophosphorylation of FAK, and attenuated integrin beta1 distribution selectively in LM8 cells.	Camptothecin	36-48	PTK2 protein tyrosine kinase 2	Mus musculus	137-140
20872237-8	2010	We found that a clinically approved camptothecin analog, irinotecan suppressed the migration, Cdc42 activity, and autophosphorylation of FAK, and attenuated integrin beta1 distribution selectively in LM8 cells.	Irinotecan	57-67	PTK2 protein tyrosine kinase 2	Mus musculus	137-140
21154724-3	2010	We have generated endothelial-specific tamoxifen-inducible FAK knockout mice by crossing FAK-floxed (FAKfl/fl) mice with the platelet derived growth factor b (Pdgfb)-iCreER mice.	Tamoxifen	39-48	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
21154724-3	2010	We have generated endothelial-specific tamoxifen-inducible FAK knockout mice by crossing FAK-floxed (FAKfl/fl) mice with the platelet derived growth factor b (Pdgfb)-iCreER mice.	Tamoxifen	39-48	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
21154724-4	2010	Tamoxifen-treatment of Pdgfb-iCreER;FAKfl/fl mice results in FAK deletion in adult endothelial cells (ECs) without any adverse effects.	Tamoxifen	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
20682312-0	2010	Oxazolone-induced over-expression of focal adhesion kinase in colonic epithelial cells of colitis mouse model.	Oxazolone	0-9	PTK2 protein tyrosine kinase 2	Mus musculus	37-58
20589831-8	2010	In addition, LTD(4)-stimulated migration through increased activation of focal adhesion kinase (FAK) and paxillin which were blocked by Akt inhibitor and cyclosporine A.	Cyclosporine	154-168	PTK2 protein tyrosine kinase 2	Mus musculus	73-94
20589831-8	2010	In addition, LTD(4)-stimulated migration through increased activation of focal adhesion kinase (FAK) and paxillin which were blocked by Akt inhibitor and cyclosporine A.	Cyclosporine	154-168	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
20873854-6	2010	Caspase-3-dependent cleavage of the glutamate cysteine ligase (GCL) catalytic subunit and focal adhesion kinase (FAK) were greater in cells treated with (S)-HNE at 48 h. (S)-HNE also caused a greater number of subG1 nuclei, a hallmark of apoptosis, at 30 h after treatment.	4-hydroxy-2-nonenal	153-160	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
20873854-6	2010	Caspase-3-dependent cleavage of the glutamate cysteine ligase (GCL) catalytic subunit and focal adhesion kinase (FAK) were greater in cells treated with (S)-HNE at 48 h. (S)-HNE also caused a greater number of subG1 nuclei, a hallmark of apoptosis, at 30 h after treatment.	4-hydroxy-2-nonenal	170-177	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
20927316-6	2010	Western blot analysis showed that ATN-658 treatment decreased the phosphorylation of serine/threonine protein kinase B (AKT), mitogen-activated protein kinase (MAPK), and focal adhesion kinase (FAK) without affecting AKT, MAPK, and FAK total protein expression.	ATN-658	34-41	PTK2 protein tyrosine kinase 2	Mus musculus	171-192
20927316-6	2010	Western blot analysis showed that ATN-658 treatment decreased the phosphorylation of serine/threonine protein kinase B (AKT), mitogen-activated protein kinase (MAPK), and focal adhesion kinase (FAK) without affecting AKT, MAPK, and FAK total protein expression.	ATN-658	34-41	PTK2 protein tyrosine kinase 2	Mus musculus	194-197
20927316-6	2010	Western blot analysis showed that ATN-658 treatment decreased the phosphorylation of serine/threonine protein kinase B (AKT), mitogen-activated protein kinase (MAPK), and focal adhesion kinase (FAK) without affecting AKT, MAPK, and FAK total protein expression.	ATN-658	34-41	PTK2 protein tyrosine kinase 2	Mus musculus	232-235
20886051-5	2010	Furthermore, we noticed a ~2-fold increase in tyrosine phosphorylation of FAK in irradiated cells.	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
20472666-6	2010	In understanding the underlying mechanisms, we found that celastrol activated p38 mitogen-activated protein kinase (MAPK) by phosphorylation before the decrement of phosphorylated FAK and that this action was independent of the presence of fibronectin.	celastrol	58-67	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
20472666-7	2010	Using 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580), a specific inhibitor of p38 MAPK, the effects of celastrol on beta1 integrin function, cell-ECM adhesion, and phosphorylation of FAK were partially attenuated.	SB 203580	79-87	PTK2 protein tyrosine kinase 2	Mus musculus	219-222
20442405-8	2010	In E8.5 embryos and primary MEFs, FAK R454 mutation resulted in decreased c-Src Tyr-416 phosphorylation.	Tyrosine	80-83	PTK2 protein tyrosine kinase 2	Mus musculus	34-37
20442405-10	2010	Within immortalized MEFs, FAK activity was required for fibronectin-stimulated FAK-p190RhoGAP association and p190RhoGAP tyrosine phosphorylation linked to decreased RhoA GTPase activity, focal adhesion turnover, and directional motility.	Tyrosine	121-129	PTK2 protein tyrosine kinase 2	Mus musculus	26-29
20232318-9	2010	In a further study, phosphorylations of integrin beta1, focal adhesion kinase (FAK), and paxillin by NECA were restrained by caffeine as well as the Src blocker, PP2.	Adenosine-5'-(N-ethylcarboxamide)	101-105	PTK2 protein tyrosine kinase 2	Mus musculus	56-77
20232318-9	2010	In a further study, phosphorylations of integrin beta1, focal adhesion kinase (FAK), and paxillin by NECA were restrained by caffeine as well as the Src blocker, PP2.	Adenosine-5'-(N-ethylcarboxamide)	101-105	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
20232318-9	2010	In a further study, phosphorylations of integrin beta1, focal adhesion kinase (FAK), and paxillin by NECA were restrained by caffeine as well as the Src blocker, PP2.	Caffeine	125-133	PTK2 protein tyrosine kinase 2	Mus musculus	56-77
20232318-9	2010	In a further study, phosphorylations of integrin beta1, focal adhesion kinase (FAK), and paxillin by NECA were restrained by caffeine as well as the Src blocker, PP2.	Caffeine	125-133	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
20232318-11	2010	We conclude that NECA-stimulated Cx43 phosphorylation mediated by PI3K/Akt, PKC, MAPKs, and NF-kappaB, which subsequently stimulated cell migration and proliferation through Src, integrin beta1, FAK, and paxillin signal pathways.	Adenosine-5'-(N-ethylcarboxamide)	17-21	PTK2 protein tyrosine kinase 2	Mus musculus	195-198
20146670-7	2010	Acceleration of differentiation is mediated by earlier activation of the signalling pathways from heparan sulfate in the extracellular matrix to both FAK (focal adhesion kinase) and MAPK (mitogen-activated protein kinase).	Heparitin Sulfate	98-113	PTK2 protein tyrosine kinase 2	Mus musculus	150-153
20213651-0	2010	High intracellular iron oxide nanoparticle concentrations affect cellular cytoskeleton and focal adhesion kinase-mediated signaling.	ferric oxide	19-29	PTK2 protein tyrosine kinase 2	Mus musculus	91-112
20234191-4	2010	As increased FAK expression and tyrosine phosphorylation are associated with tumor progression, inhibitors of FAK are being tested for anti-tumor effects.	Tyrosine	32-40	PTK2 protein tyrosine kinase 2	Mus musculus	110-113
20234191-5	2010	Here, we analyze PND-1186, a substituted pyridine reversible inhibitor of FAK activity with a 50% inhibitory concentration (IC50) of 1.5 nM in vitro.	PND 1186	17-25	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
20234191-5	2010	Here, we analyze PND-1186, a substituted pyridine reversible inhibitor of FAK activity with a 50% inhibitory concentration (IC50) of 1.5 nM in vitro.	pyridine	41-49	PTK2 protein tyrosine kinase 2	Mus musculus	74-77
20234191-6	2010	PND-1186 has an IC50 of ~100 nM in breast carcinoma cells as determined by anti-phospho-specific immunoblotting to FAK Tyr-397.	Tyrosine	119-122	PTK2 protein tyrosine kinase 2	Mus musculus	115-118
20234193-4	2010	Here, we show that the FAK inhibitor PND-1186 blocks FAK Tyr-397 phosphorylation in vivo and exhibits anti-tumor efficacy in orthotopic breast carcinoma mouse tumor models.	Tyrosine	57-60	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
20234193-4	2010	Here, we show that the FAK inhibitor PND-1186 blocks FAK Tyr-397 phosphorylation in vivo and exhibits anti-tumor efficacy in orthotopic breast carcinoma mouse tumor models.	Tyrosine	57-60	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
20234193-6	2010	showed promising pharmacokinetics (PK) and inhibited tumor FAK Tyr-397 phosphorylation for 12 hours.	Tyrosine	63-66	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
20146670-7	2010	Acceleration of differentiation is mediated by earlier activation of the signalling pathways from heparan sulfate in the extracellular matrix to both FAK (focal adhesion kinase) and MAPK (mitogen-activated protein kinase).	Heparitin Sulfate	98-113	PTK2 protein tyrosine kinase 2	Mus musculus	155-176
19839056-4	2009	Adhesion of BMPCs to purified extracellular matrix proteins induced focal adhesion kinase (Fak) phosphorylation and formation of branching point structures in a alpha(4) and alpha(5) integrin-dependent manner.	bmpcs	12-17	PTK2 protein tyrosine kinase 2	Mus musculus	68-89
19776009-2	2009	Although autophosphorylation on Tyr-397 appears required for FAK functions in vitro, its role in vivo has not been established.	Tyrosine	32-35	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
19839056-4	2009	Adhesion of BMPCs to purified extracellular matrix proteins induced focal adhesion kinase (Fak) phosphorylation and formation of branching point structures in a alpha(4) and alpha(5) integrin-dependent manner.	bmpcs	12-17	PTK2 protein tyrosine kinase 2	Mus musculus	91-94
19500106-3	2009	In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells.	Fluorouracil	81-95	PTK2 protein tyrosine kinase 2	Mus musculus	50-71
19628583-10	2009	In parallel, caveolin-1, FAK, vinculin, and paxillin are phosphorylated on Tyr residues apparently by GnRH-activated c-Src.	Tyrosine	75-78	PTK2 protein tyrosine kinase 2	Mus musculus	25-28
19501627-2	2009	In vitro studies reported tyrosine dephosphorylation of FAK under insulin resistance in C2C12 skeletal muscle cells.	Tyrosine	26-34	PTK2 protein tyrosine kinase 2	Mus musculus	56-59
19500106-3	2009	In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells.	Fluorouracil	81-95	PTK2 protein tyrosine kinase 2	Mus musculus	73-76
19500106-3	2009	In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells.	Fluorouracil	97-101	PTK2 protein tyrosine kinase 2	Mus musculus	50-71
19500106-3	2009	In the current study, we investigated the role of focal adhesion kinase (FAK) in 5-fluorouracil (5-FU) chemoresistance in colon carcinoma MCS culture cells.	Fluorouracil	97-101	PTK2 protein tyrosine kinase 2	Mus musculus	73-76
19500106-6	2009	However, silencing of FAK combined with 5-FU treatment significantly decreased the 50% inhibitory concentration (IC(50)) of 5-FU and markedly increased the population of apoptosis cells, which was associated with the reduction of the levels of Akt and nuclear factor-kappa B (NF-kappaB).	Fluorouracil	124-128	PTK2 protein tyrosine kinase 2	Mus musculus	22-25
19500106-7	2009	Moreover, knockdown of FAK could inhibit tumor growth and increase the sensitivity of the tumor to 5-FU in the nude mouse xenograft.	Fluorouracil	99-103	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
19500106-8	2009	These results indicate that while not affecting cellular proliferation in the absence of 5-FU, RNA interference targeting FAK potentiated 5-FU-induced cytotoxicity in vitro and in vivo, and partially reversed multicellular resistance, which may contribute to its chemosensitizing effect through efficiently suppressing Akt/NF-kappaB activity.	Fluorouracil	138-142	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
19596799-5	2009	After stimulation by mechanical force, FAK and gelsolin were recruited to magnetite beads and there was increased phosphorylation of Tyr397FAK.	tyr397fak	133-142	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
19596799-9	2009	Type-I phosphatidylinositol 4-phosphate 5 kinase-gamma (PIP5KIgamma), which generates PtdIns(4,5)P(2), associated with FAK and was required for force-mediated SMA-promoter activity and actin assembly.	Phosphatidylinositols	7-27	PTK2 protein tyrosine kinase 2	Mus musculus	119-122
19596799-9	2009	Type-I phosphatidylinositol 4-phosphate 5 kinase-gamma (PIP5KIgamma), which generates PtdIns(4,5)P(2), associated with FAK and was required for force-mediated SMA-promoter activity and actin assembly.	1,2-dihexadecanoyl-sn-glycero-3-phospho-(1D-myo-inositol-4,5-bisphosphate)	86-98	PTK2 protein tyrosine kinase 2	Mus musculus	119-122
19561112-6	2009	In addition, we observed significant reduction in NADPH oxidase-mediated superoxide production and complement-mediated phagocytosis in FAK null neutrophils.	Superoxides	73-83	PTK2 protein tyrosine kinase 2	Mus musculus	135-138
19561112-9	2009	Disruption of FAK also reduced chemoattractant-elicited superoxide production in suspended neutrophils in the absence of cell adhesion.	Superoxides	56-66	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
19561112-11	2009	Consistent with decreased PtdIns(3,4,5)P3/Akt signaling in FAK null neutrophils, we also observed accelerated spontaneous death in these cells.	phosphatidylinositol 3,4,5-triphosphate	26-41	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
19371329-11	2009	Moreover, DiOHF inhibited smooth muscle cell spreading (a FAK-mediated response) and proliferation.	3',4'-dihydroxyflavonol	10-15	PTK2 protein tyrosine kinase 2	Mus musculus	58-61
19371329-12	2009	CONCLUSIONS AND IMPLICATIONS: This is the first report on a flavonoid compound (DiOHF) that is a potent FAK inhibitor.	Flavonoids	60-69	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
19371329-0	2009	3",4"-Dihydroxyflavonol down-regulates monocyte chemoattractant protein-1 in smooth muscle: role of focal adhesion kinase and PDGF receptor signalling.	3',4'-dihydroxyflavonol	0-23	PTK2 protein tyrosine kinase 2	Mus musculus	100-121
19371329-4	2009	The effect of DiOHF was associated with a suppression of focal adhesion kinase (FAK)-mediated signalling.	3',4'-dihydroxyflavonol	14-19	PTK2 protein tyrosine kinase 2	Mus musculus	57-78
19371329-4	2009	The effect of DiOHF was associated with a suppression of focal adhesion kinase (FAK)-mediated signalling.	3',4'-dihydroxyflavonol	14-19	PTK2 protein tyrosine kinase 2	Mus musculus	80-83
19371329-12	2009	CONCLUSIONS AND IMPLICATIONS: This is the first report on a flavonoid compound (DiOHF) that is a potent FAK inhibitor.	3',4'-dihydroxyflavonol	80-85	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
19371329-15	2009	Our results suggest that DiOHF might be a useful tool for dissection of the (patho)physiological roles of FAK signalling.	3',4'-dihydroxyflavonol	25-30	PTK2 protein tyrosine kinase 2	Mus musculus	106-109
19371329-5	2009	In vitro kinase assays demonstrated that DiOHF is a potent inhibitor of FAK kinase activity (EC(50)= 2.4 micromol x L(-1)).	3',4'-dihydroxyflavonol	41-46	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
19056463-5	2009	Furthermore, it was also found that the phosphorylation of FAK Tyr-861 and GSK-3beta Ser-9 was reduced in N2a/Swe.Delta9 cells, which can be possibly taken as a reasonable explanation for the underlying mechanism.	Tyrosine	63-66	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
19358301-1	2009	Focal adhesion kinase (FAK) is constitutively activated and tyrosine phosphorylated in BCR/ABL-transformed hematopoietic cells, but the role it plays during leukemogenesis remains unclear.	Tyrosine	60-68	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
19358301-6	2009	In addition, FAK silencing enhanced in vitro and in vivo efficacy of ABL tyrosine kinase inhibitor imatinib in BCR/ABL-BaF3 cells.	Imatinib Mesylate	99-107	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
19358301-1	2009	Focal adhesion kinase (FAK) is constitutively activated and tyrosine phosphorylated in BCR/ABL-transformed hematopoietic cells, but the role it plays during leukemogenesis remains unclear.	Tyrosine	60-68	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
19098120-2	2009	This revealed that bis-phosphorylated pTyr(576)/Tyr(577)-FAK was a biomarker of Src activity and inactivation in vitro and in cell culture.	Phosphotyrosine	38-42	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
19098120-2	2009	This revealed that bis-phosphorylated pTyr(576)/Tyr(577)-FAK was a biomarker of Src activity and inactivation in vitro and in cell culture.	Tyrosine	39-42	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
19098120-6	2009	Phosphorylation of FAK at Tyr(576)/Tyr(577) was inhibited by AZD0530 in a dose-dependent manner both in cell culture and in vitro.	Tyrosine	26-29	PTK2 protein tyrosine kinase 2	Mus musculus	19-22
19098120-6	2009	Phosphorylation of FAK at Tyr(576)/Tyr(577) was inhibited by AZD0530 in a dose-dependent manner both in cell culture and in vitro.	Tyrosine	35-38	PTK2 protein tyrosine kinase 2	Mus musculus	19-22
19098120-6	2009	Phosphorylation of FAK at Tyr(576)/Tyr(577) was inhibited by AZD0530 in a dose-dependent manner both in cell culture and in vitro.	saracatinib	61-68	PTK2 protein tyrosine kinase 2	Mus musculus	19-22
19098120-8	2009	When normal MEFs and Y(529)FSrc-expressing MEFs were treated with pervanadate (a global phosphatase inhibitor), pTyr(576)/pTyr(577)-FAK accounted for almost 60% of the total FAK present in the cells.	pervanadate	66-77	PTK2 protein tyrosine kinase 2	Mus musculus	132-135
19098120-8	2009	When normal MEFs and Y(529)FSrc-expressing MEFs were treated with pervanadate (a global phosphatase inhibitor), pTyr(576)/pTyr(577)-FAK accounted for almost 60% of the total FAK present in the cells.	pervanadate	66-77	PTK2 protein tyrosine kinase 2	Mus musculus	174-177
19098120-8	2009	When normal MEFs and Y(529)FSrc-expressing MEFs were treated with pervanadate (a global phosphatase inhibitor), pTyr(576)/pTyr(577)-FAK accounted for almost 60% of the total FAK present in the cells.	Phosphotyrosine	112-116	PTK2 protein tyrosine kinase 2	Mus musculus	132-135
19098120-8	2009	When normal MEFs and Y(529)FSrc-expressing MEFs were treated with pervanadate (a global phosphatase inhibitor), pTyr(576)/pTyr(577)-FAK accounted for almost 60% of the total FAK present in the cells.	Phosphotyrosine	122-126	PTK2 protein tyrosine kinase 2	Mus musculus	132-135
18793427-7	2008	FIT-mediated tyrosine phosphorylation of NTK substrates p130Cas, paxillin and FAK and cortactin was observed at focal adhesions, while FIT-mediated phosphorylation of cortactin was also seen at the cell periphery.	Tyrosine	13-21	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
18805968-8	2009	Furthermore, silencing of Rap1a and Rap1b prevented phosphorylation of tyrosine 397 in focal adhesion kinase (FAK) and vascular endothelial growth factor-induced Akt1-activation.	Tyrosine	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	87-108
18805968-8	2009	Furthermore, silencing of Rap1a and Rap1b prevented phosphorylation of tyrosine 397 in focal adhesion kinase (FAK) and vascular endothelial growth factor-induced Akt1-activation.	Tyrosine	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	110-113
19139121-0	2009	Inhibition of focal adhesion kinase as a potential therapeutic strategy for imatinib-resistant gastrointestinal stromal tumor.	Imatinib Mesylate	76-84	PTK2 protein tyrosine kinase 2	Mus musculus	14-35
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	Imatinib Mesylate	77-85	PTK2 protein tyrosine kinase 2	Mus musculus	55-58
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	Imatinib Mesylate	77-85	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
19139121-5	2009	KIT820Tyr cells appeared to maintain the activities of FAK and AKT under the imatinib treatment, suggesting that FAK might play a role in cell survival in imatinib-resistant cells.	Imatinib Mesylate	155-163	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
19139121-6	2009	When FAK activity in those cells was inhibited by TAE226, cell growth was equally suppressed and the cells underwent apoptosis regardless of the c-KIT mutation types.	TAE226	50-56	PTK2 protein tyrosine kinase 2	Mus musculus	5-8
19139121-9	2009	Targeting FAK could be a potential therapeutic strategy for imatinib-resistant GISTs.	Imatinib Mesylate	60-68	PTK2 protein tyrosine kinase 2	Mus musculus	10-13
18930785-7	2009	Mechanistically, the inhibition by morelloflavone of VSMC migration was through its negative regulatory effects on several migration-related kinases, including FAK, Src, ERK, and RhoA.	morelloflavone	35-49	PTK2 protein tyrosine kinase 2	Mus musculus	160-163
18930785-7	2009	Mechanistically, the inhibition by morelloflavone of VSMC migration was through its negative regulatory effects on several migration-related kinases, including FAK, Src, ERK, and RhoA.	vsmc	53-57	PTK2 protein tyrosine kinase 2	Mus musculus	160-163
18771597-8	2008	FAK-mediated actin remodeling resulted into subsequent glucose uptake via PI3K-dependent pathway.	Glucose	55-62	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
18771597-10	2008	CONCLUSION: The data confirms that FAK regulates glucose uptake through actin reorganization in skeletal muscle.	Glucose	49-56	PTK2 protein tyrosine kinase 2	Mus musculus	35-38
18771597-1	2008	BACKGROUND: Focal Adhesion Kinase (FAK) is recently reported to regulate insulin resistance by regulating glucose uptake in C2C12 skeletal muscle cells.	Glucose	106-113	PTK2 protein tyrosine kinase 2	Mus musculus	12-33
18771597-11	2008	FAK overexpression supports actin remodeling and subsequent glucose uptake in a PI3K dependent manner.	Glucose	60-67	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
18771597-1	2008	BACKGROUND: Focal Adhesion Kinase (FAK) is recently reported to regulate insulin resistance by regulating glucose uptake in C2C12 skeletal muscle cells.	Glucose	106-113	PTK2 protein tyrosine kinase 2	Mus musculus	35-38
18771597-12	2008	Inhibition of FAK prevents insulin-stimulated remodeling of actin filaments resulting into decreased Glut-4 translocation and glucose uptake generating insulin resistance.	Glucose	126-133	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
18771597-2	2008	However, the underlying mechanism for FAK-mediated glucose transporter-4 translocation (Glut-4), responsible for glucose uptake, remains unknown.	Glucose	51-58	PTK2 protein tyrosine kinase 2	Mus musculus	38-41
18704196-5	2008	Ex vivo treatment of Co26 and Co51 colon cancer cells with colchicine inhibited pressure-stimulated cell adhesion to murine surgical wounds and blocked pressure-induced FAK and Akt phosphorylation.	Colchicine	59-69	PTK2 protein tyrosine kinase 2	Mus musculus	169-172
18505823-6	2008	Biochemical analysis of the HPKO fibroblasts revealed a sustained hyperphosphorylation of focal adhesion kinase (FAK) at tyrosine 397 as well as a twofold increase in RhoA activation.	Tyrosine	121-129	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
18523140-6	2008	Basal tyrosine phosphorylation of focal adhesion kinase (FAK) is increased in cells expressing active PLD2, as is phosphorylation of Akt; inactive PLD2 has no effect.	Tyrosine	6-14	PTK2 protein tyrosine kinase 2	Mus musculus	34-55
18523140-6	2008	Basal tyrosine phosphorylation of focal adhesion kinase (FAK) is increased in cells expressing active PLD2, as is phosphorylation of Akt; inactive PLD2 has no effect.	Tyrosine	6-14	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
18587052-5	2008	FAK-silenced animals are less glucose tolerant and have physiological and biochemical parameters similar to that of high fat diet (HFD)-fed insulin-resistant animals.	Glucose	30-37	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
18391070-2	2008	Surprisingly, tamoxifen-inducible conditional knockout of FAK in adult blood vessels (inducible EC-specific FAK knockout [i-EC-FAK-KO]) produces no vascular phenotype, and these animals are capable of developing a robust growth factor-induced angiogenic response.	Tamoxifen	14-23	PTK2 protein tyrosine kinase 2	Mus musculus	58-61
18356303-4	2008	Molecular analysis of integrin-mediated signaling revealed a higher phosphorylation of FAK at tyrosine 925 in FHL2-knockout cells compared to their wild-type counterpart.	Tyrosine	94-102	PTK2 protein tyrosine kinase 2	Mus musculus	87-90
18391070-2	2008	Surprisingly, tamoxifen-inducible conditional knockout of FAK in adult blood vessels (inducible EC-specific FAK knockout [i-EC-FAK-KO]) produces no vascular phenotype, and these animals are capable of developing a robust growth factor-induced angiogenic response.	Tamoxifen	14-23	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
18391070-2	2008	Surprisingly, tamoxifen-inducible conditional knockout of FAK in adult blood vessels (inducible EC-specific FAK knockout [i-EC-FAK-KO]) produces no vascular phenotype, and these animals are capable of developing a robust growth factor-induced angiogenic response.	Tamoxifen	14-23	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
17914455-6	2008	Simultaneously, Shb knockdown causes reduced focal adhesion kinase (FAK) activation, monitored as phosphorylation of the regulatory residues tyrosines 576/577.	Tyrosine	141-150	PTK2 protein tyrosine kinase 2	Mus musculus	68-71
17914455-8	2008	The altered FAK activity coincided with an elongated cell phenotype that was particularly noticeable in the presence of staurosporine.	Staurosporine	120-133	PTK2 protein tyrosine kinase 2	Mus musculus	12-15
17922492-4	2008	This FAK/Src chimera is subject to adhesion-dependent activation and promotes tyrosine phosphorylation of p130Cas and paxillin to higher steady-state levels than is achieved by wild-type FAK.	Tyrosine	78-86	PTK2 protein tyrosine kinase 2	Mus musculus	5-8
18233957-7	2008	These results indicate that the SH3-encoding exon of Cas participates in cell motility, tyrosine-phosphorylation of FAK and Cas, FAK/Cas/Src/CrkII complex formation, recruitment of Cas to focal adhesions and regulation of cell motility-associated gene expression in primary fibroblasts.	Tyrosine	88-96	PTK2 protein tyrosine kinase 2	Mus musculus	116-119
18195107-7	2008	p190RhoGEF overexpression enhances RhoA activation and FA formation in MEFs dependent on FAK binding and associated with p190RhoGEF FA recruitment and tyrosine phosphorylation.	Tyrosine	151-159	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
17922492-4	2008	This FAK/Src chimera is subject to adhesion-dependent activation and promotes tyrosine phosphorylation of p130Cas and paxillin to higher steady-state levels than is achieved by wild-type FAK.	Tyrosine	78-86	PTK2 protein tyrosine kinase 2	Mus musculus	187-190
19030106-3	2008	Recently, a novel bis-anilino pyrimidine inhibitor, TAE226, was reported to efficiently inhibit FAK signaling, arrest tumor growth and invasion and prolong the life of mice with glioma or ovarian tumor implants.	bis-anilino pyrimidine	18-40	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
19030106-3	2008	Recently, a novel bis-anilino pyrimidine inhibitor, TAE226, was reported to efficiently inhibit FAK signaling, arrest tumor growth and invasion and prolong the life of mice with glioma or ovarian tumor implants.	TAE226	52-58	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
17878380-7	2007	TLR4 signaling also led to increased serine phosphorylation of intestinal focal adhesion kinase (FAK).	Serine	37-43	PTK2 protein tyrosine kinase 2	Mus musculus	74-95
17976369-0	2007	Phosphorylation of focal adhesion kinase at Tyrosine 407 negatively regulates Ras transformation of fibroblasts.	Tyrosine	44-52	PTK2 protein tyrosine kinase 2	Mus musculus	19-40
17976369-1	2007	Focal adhesion kinase (FAK) mediates signal transduction in response to multiple extracellular inputs, via tyrosine phosphorylation at specific residues.	Tyrosine	107-115	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
17976369-1	2007	Focal adhesion kinase (FAK) mediates signal transduction in response to multiple extracellular inputs, via tyrosine phosphorylation at specific residues.	Tyrosine	107-115	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
17976369-2	2007	We recently reported that FAK Tyr-407 phosphorylation negatively regulates the enzymatic and biological activities of FAK, unlike phosphorylation of other tyrosine residues.	Tyrosine	30-33	PTK2 protein tyrosine kinase 2	Mus musculus	26-29
17976369-2	2007	We recently reported that FAK Tyr-407 phosphorylation negatively regulates the enzymatic and biological activities of FAK, unlike phosphorylation of other tyrosine residues.	Tyrosine	30-33	PTK2 protein tyrosine kinase 2	Mus musculus	118-121
17976369-3	2007	In this study, we further investigated the effect of FAK Tyr-407 phosphorylation on cell transformation.	Tyrosine	57-60	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
17976369-5	2007	Consistently, FAK Tyr-407 phosphorylation was decreased in parallel with cell transformation in H-Ras-inducible NIH3T3 cells and increased during trichostatin A-induced detransformation of both K-Ras transformed rat-2 fibroblasts and H-Ras transformed NIH3T3 cells.	Tyrosine	18-21	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
17976369-5	2007	Consistently, FAK Tyr-407 phosphorylation was decreased in parallel with cell transformation in H-Ras-inducible NIH3T3 cells and increased during trichostatin A-induced detransformation of both K-Ras transformed rat-2 fibroblasts and H-Ras transformed NIH3T3 cells.	trichostatin A	146-160	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
17976369-6	2007	In addition, overexpression of a phosphorylation-mimicking FAK Tyr-407 mutant inhibited morphological transformation of H-Ras-inducible NIH3T3 cells and inhibited invasion activity and anchorage-independent growth of H-Ras-transformed NIH3T3 cells.	Tyrosine	63-66	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
17976369-7	2007	Taken together, these data strongly suggest that FAK Tyr-407 phosphorylation negatively regulates transformation of fibroblasts.	Tyrosine	53-56	PTK2 protein tyrosine kinase 2	Mus musculus	49-52
17878380-7	2007	TLR4 signaling also led to increased serine phosphorylation of intestinal focal adhesion kinase (FAK).	Serine	37-43	PTK2 protein tyrosine kinase 2	Mus musculus	97-100
17289681-0	2007	Preferential phosphorylation of focal adhesion kinase tyrosine 861 is critical for mediating an anti-apoptotic response to hyperosmotic stress.	Tyrosine	54-62	PTK2 protein tyrosine kinase 2	Mus musculus	32-53
17333113-1	2007	AIMS/HYPOTHESIS: On the basis of our previous studies, we investigated the possible role of focal adhesion kinase (FAK) in the development of insulin resistance in skeletal muscle, a major organ responsible for insulin-stimulated glucose uptake.	Glucose	230-237	PTK2 protein tyrosine kinase 2	Mus musculus	92-113
17333113-1	2007	AIMS/HYPOTHESIS: On the basis of our previous studies, we investigated the possible role of focal adhesion kinase (FAK) in the development of insulin resistance in skeletal muscle, a major organ responsible for insulin-stimulated glucose uptake.	Glucose	230-237	PTK2 protein tyrosine kinase 2	Mus musculus	115-118
17333113-3	2007	RESULTS: A significant decrease in tyrosine phosphorylation of FAK in insulin-resistant C2C12 cells was observed.	Tyrosine	35-43	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
17333113-5	2007	Increased levels of FAK in insulin-resistant C2C12 skeletal muscle cells increased insulin sensitivity and glucose uptake.	Glucose	107-114	PTK2 protein tyrosine kinase 2	Mus musculus	20-23
17333113-7	2007	FAK was also found to interact downstream with insulin receptor substrate-1, phosphatidylinositol 3-kinase and protein kinase C and glycogen synthase kinase 3beta, leading to translocation of glucose transporter 4 and resulting in the regulation of glucose uptake.	Glucose	192-199	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
17526730-7	2007	Interestingly, chemotaxis was significantly attenuated in isolated FAK-null cardiomyocytes in comparison to genetic controls, and these effects were concomitant with reduced tyrosine phosphorylation of Crk-associated substrate (CAS).	Tyrosine	174-182	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
17289681-1	2007	The results presented here demonstrate that focal adhesion kinase (FAK) Tyr-861 is the predominant tyrosine phosphorylation site stimulated by hyperosmotic stress in a variety of cell types, including epithelial cell lines (ileum-derived IEC-18, colon-derived Caco2, and stomach-derived NCI-N87), FAK null fibroblasts re-expressing FAK, and Src family kinase triple null fibroblasts (SYF cells) in which c-Src has been restored (YF cells).	Tyrosine	72-75	PTK2 protein tyrosine kinase 2	Mus musculus	44-65
17303567-0	2007	Focal adhesion kinase is negatively regulated by phosphorylation at tyrosine 407.	Tyrosine	68-76	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
17289681-2	2007	We show that hyperosmotic stress-stimulated FAK phosphorylation in epithelial cells is inhibited by Src family kinase inhibitors PP2 and SU6656 and that it does not occur in SYF cells.	SU 6656	137-143	PTK2 protein tyrosine kinase 2	Mus musculus	44-47
17289681-1	2007	The results presented here demonstrate that focal adhesion kinase (FAK) Tyr-861 is the predominant tyrosine phosphorylation site stimulated by hyperosmotic stress in a variety of cell types, including epithelial cell lines (ileum-derived IEC-18, colon-derived Caco2, and stomach-derived NCI-N87), FAK null fibroblasts re-expressing FAK, and Src family kinase triple null fibroblasts (SYF cells) in which c-Src has been restored (YF cells).	Tyrosine	72-75	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
17289681-6	2007	We propose that FAK/c-Src bipartite enzyme is a sensor of cytoplasmic shrinkage, and that the phosphorylation on FAK Tyr-861 by Src and subsequent reorganization of F-actin can initiate an anti-apoptotic signaling pathway that protects cells from hyperosmotic stress.	Tyrosine	117-120	PTK2 protein tyrosine kinase 2	Mus musculus	16-19
17289681-6	2007	We propose that FAK/c-Src bipartite enzyme is a sensor of cytoplasmic shrinkage, and that the phosphorylation on FAK Tyr-861 by Src and subsequent reorganization of F-actin can initiate an anti-apoptotic signaling pathway that protects cells from hyperosmotic stress.	Tyrosine	117-120	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
17303567-1	2007	Focal adhesion kinase (FAK) mediates signal transduction in response to multiple extracellular inputs via tyrosine phosphorylation at specific residues.	Tyrosine	106-114	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
17303567-1	2007	Focal adhesion kinase (FAK) mediates signal transduction in response to multiple extracellular inputs via tyrosine phosphorylation at specific residues.	Tyrosine	106-114	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
17289681-1	2007	The results presented here demonstrate that focal adhesion kinase (FAK) Tyr-861 is the predominant tyrosine phosphorylation site stimulated by hyperosmotic stress in a variety of cell types, including epithelial cell lines (ileum-derived IEC-18, colon-derived Caco2, and stomach-derived NCI-N87), FAK null fibroblasts re-expressing FAK, and Src family kinase triple null fibroblasts (SYF cells) in which c-Src has been restored (YF cells).	Tyrosine	72-75	PTK2 protein tyrosine kinase 2	Mus musculus	297-300
17303567-2	2007	Although several tyrosine phosphorylation events have been linked to FAK activation and downstream signal transduction, the function of FAK phosphorylation at Tyr(407) was previously unknown.	Tyrosine	17-25	PTK2 protein tyrosine kinase 2	Mus musculus	69-72
17289681-1	2007	The results presented here demonstrate that focal adhesion kinase (FAK) Tyr-861 is the predominant tyrosine phosphorylation site stimulated by hyperosmotic stress in a variety of cell types, including epithelial cell lines (ileum-derived IEC-18, colon-derived Caco2, and stomach-derived NCI-N87), FAK null fibroblasts re-expressing FAK, and Src family kinase triple null fibroblasts (SYF cells) in which c-Src has been restored (YF cells).	Tyrosine	72-75	PTK2 protein tyrosine kinase 2	Mus musculus	297-300
17303567-2	2007	Although several tyrosine phosphorylation events have been linked to FAK activation and downstream signal transduction, the function of FAK phosphorylation at Tyr(407) was previously unknown.	Tyrosine	159-162	PTK2 protein tyrosine kinase 2	Mus musculus	136-139
17303567-3	2007	Here, we show for the first time that phosphorylation of FAK Tyr(407) increases during serum starvation, contact inhibition, and cell cycle arrest, all conditions under which activating FAK Tyr(397) phosphorylation decreases.	Tyrosine	61-64	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
17303567-3	2007	Here, we show for the first time that phosphorylation of FAK Tyr(407) increases during serum starvation, contact inhibition, and cell cycle arrest, all conditions under which activating FAK Tyr(397) phosphorylation decreases.	Tyrosine	61-64	PTK2 protein tyrosine kinase 2	Mus musculus	186-189
17303567-3	2007	Here, we show for the first time that phosphorylation of FAK Tyr(407) increases during serum starvation, contact inhibition, and cell cycle arrest, all conditions under which activating FAK Tyr(397) phosphorylation decreases.	Tyrosine	190-193	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
17303567-3	2007	Here, we show for the first time that phosphorylation of FAK Tyr(407) increases during serum starvation, contact inhibition, and cell cycle arrest, all conditions under which activating FAK Tyr(397) phosphorylation decreases.	Tyrosine	190-193	PTK2 protein tyrosine kinase 2	Mus musculus	186-189
17303567-4	2007	Transfection of NIH3T3 cells with a phosphorylation-mimicking FAK 407E mutant decreased autophosphorylation at Tyr(397) and inhibited both FAK kinase activity in vitro and FAK-mediated functions such as cell adhesion, spreading, proliferation, and migration.	Tyrosine	111-114	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
17303567-4	2007	Transfection of NIH3T3 cells with a phosphorylation-mimicking FAK 407E mutant decreased autophosphorylation at Tyr(397) and inhibited both FAK kinase activity in vitro and FAK-mediated functions such as cell adhesion, spreading, proliferation, and migration.	Tyrosine	111-114	PTK2 protein tyrosine kinase 2	Mus musculus	139-142
17303567-4	2007	Transfection of NIH3T3 cells with a phosphorylation-mimicking FAK 407E mutant decreased autophosphorylation at Tyr(397) and inhibited both FAK kinase activity in vitro and FAK-mediated functions such as cell adhesion, spreading, proliferation, and migration.	Tyrosine	111-114	PTK2 protein tyrosine kinase 2	Mus musculus	139-142
17303567-6	2007	Taken together, these data suggest the novel concept that FAK Tyr(407) phosphorylation negatively regulates the enzymatic and biological activities of FAK.	Tyrosine	62-65	PTK2 protein tyrosine kinase 2	Mus musculus	58-61
17303567-6	2007	Taken together, these data suggest the novel concept that FAK Tyr(407) phosphorylation negatively regulates the enzymatic and biological activities of FAK.	Tyrosine	62-65	PTK2 protein tyrosine kinase 2	Mus musculus	151-154
17289681-1	2007	The results presented here demonstrate that focal adhesion kinase (FAK) Tyr-861 is the predominant tyrosine phosphorylation site stimulated by hyperosmotic stress in a variety of cell types, including epithelial cell lines (ileum-derived IEC-18, colon-derived Caco2, and stomach-derived NCI-N87), FAK null fibroblasts re-expressing FAK, and Src family kinase triple null fibroblasts (SYF cells) in which c-Src has been restored (YF cells).	Tyrosine	99-107	PTK2 protein tyrosine kinase 2	Mus musculus	44-65
17289681-1	2007	The results presented here demonstrate that focal adhesion kinase (FAK) Tyr-861 is the predominant tyrosine phosphorylation site stimulated by hyperosmotic stress in a variety of cell types, including epithelial cell lines (ileum-derived IEC-18, colon-derived Caco2, and stomach-derived NCI-N87), FAK null fibroblasts re-expressing FAK, and Src family kinase triple null fibroblasts (SYF cells) in which c-Src has been restored (YF cells).	Tyrosine	99-107	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
17285141-0	2007	Polyethylenimine-complexed plasmid particles targeting focal adhesion kinase function as melanoma tumor therapeutics.	Polyethyleneimine	0-16	PTK2 protein tyrosine kinase 2	Mus musculus	55-76
16769050-5	2006	HRGP/HRGP330 treatment of endothelial cells induced disruption of actin stress fibers, a process reversed by treatment of cells with the FAK inhibitor geldanamycin.	geldanamycin	151-163	PTK2 protein tyrosine kinase 2	Mus musculus	137-140
16972260-7	2006	We demonstrated that Hcy induces autophosphorylation of focal adhesion kinase (FAK) (a member of the protein tyrosine kinase (PTK) family) at Tyr-397.	Homocysteine	21-24	PTK2 protein tyrosine kinase 2	Mus musculus	56-77
16972260-7	2006	We demonstrated that Hcy induces autophosphorylation of focal adhesion kinase (FAK) (a member of the protein tyrosine kinase (PTK) family) at Tyr-397.	Homocysteine	21-24	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
16972260-7	2006	We demonstrated that Hcy induces autophosphorylation of focal adhesion kinase (FAK) (a member of the protein tyrosine kinase (PTK) family) at Tyr-397.	Tyrosine	142-145	PTK2 protein tyrosine kinase 2	Mus musculus	56-77
16972260-7	2006	We demonstrated that Hcy induces autophosphorylation of focal adhesion kinase (FAK) (a member of the protein tyrosine kinase (PTK) family) at Tyr-397.	Tyrosine	142-145	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
16972260-9	2006	In addition to that, Hcy-mediated TGF-beta1 induction was inhibited by TGF-beta R1 kinase inhibitor II (ALK5 inhibitor II) and attenuated FAK phosphorylation and alpha-SMA expression.	Homocysteine	21-24	PTK2 protein tyrosine kinase 2	Mus musculus	138-141
16972260-12	2006	Taken together our results demonstrate that Hcy-mediated TGF-beta1 upregulation triggers endothelial-myofibroblast differentiation secondary to FAK phosphorylation and that Hcy-induced ERK activation is involved in ECM remodeling by altering collagen type-1 homeostasis.	Homocysteine	44-47	PTK2 protein tyrosine kinase 2	Mus musculus	144-147
16890932-4	2006	Treatment with a synthetic MMP inhibitor, GM6001, in utero enhanced the branching pattern in both wild type and null lungs accompanied by a restoration of fibronectin localization, signaling through FAK and epithelial cell proliferation in null lungs.	N-(2(R)-2-(hydroxamidocarbonylmethyl)-4-methylpentanoyl)-L-tryptophan methylamide	42-48	PTK2 protein tyrosine kinase 2	Mus musculus	199-202
16971554-9	2006	TCDD enhanced the steady state Src-mediated phosphorylation of FAK but not of paxillin.	Polychlorinated Dibenzodioxins	0-4	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
16407416-7	2006	In parallel, focal adhesion kinase (FAK) activity (assessed by detecting pY397-FAK) was influenced by compliance, with maximal activity occurring in cells cultured on polystyrene.	Polystyrenes	167-178	PTK2 protein tyrosine kinase 2	Mus musculus	13-34
16407416-7	2006	In parallel, focal adhesion kinase (FAK) activity (assessed by detecting pY397-FAK) was influenced by compliance, with maximal activity occurring in cells cultured on polystyrene.	Polystyrenes	167-178	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
16508962-4	2006	Changes in cytoskeletal organization and phospho FAK (tyr 397) localization were evident after 60 min on cells adhering to ROUGH surfaces.	Tyrosine	54-57	PTK2 protein tyrosine kinase 2	Mus musculus	49-52
16738308-0	2006	Src SH2 arginine 175 is required for cell motility: specific focal adhesion kinase targeting and focal adhesion assembly function.	Arginine	8-16	PTK2 protein tyrosine kinase 2	Mus musculus	61-82
16508962-0	2006	Adhesion and proliferation of fibroblasts on RF plasma-deposited nanostructured fluorocarbon coatings: evidence of FAK activation.	Fluorocarbons	80-92	PTK2 protein tyrosine kinase 2	Mus musculus	115-118
16508962-3	2006	We have found that the statistically significant increase of cell proliferation rate and FAK (a nonreceptor tyrosine kinase) activation detected on ROUGH fluorocarbon surfaces is due to the presence of nanostructures.	Fluorocarbons	154-166	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
15893751-2	2005	Recently, we have shown that LPA stimulates p21-activated kinase (PAK) that is critical for focal adhesion kinase (FAK) phosphorylation and cell motility.	lysophosphatidic acid	29-32	PTK2 protein tyrosine kinase 2	Mus musculus	92-113
16374517-9	2006	Last, decreased tyrosine phosphorylation of FAK substrates p130Cas and paxillin were observed in CFKO mice compared with the control littermates.	Tyrosine	16-24	PTK2 protein tyrosine kinase 2	Mus musculus	44-47
16293639-0	2006	Activation of the lutropin/choriogonadotropin receptor in MA-10 cells leads to the tyrosine phosphorylation of the focal adhesion kinase by a pathway that involves Src family kinases.	Tyrosine	83-91	PTK2 protein tyrosine kinase 2	Mus musculus	115-136
16293639-1	2006	We show that activation of the endogenous or recombinant lutropin/choriogonadotropin receptor (LHR) in mouse Leydig tumor cells (MA-10 cells) leads to the tyrosine phosphorylation of the focal adhesion kinase (FAK) and one of its substrates (paxillin).	Tyrosine	155-163	PTK2 protein tyrosine kinase 2	Mus musculus	187-208
16293639-1	2006	We show that activation of the endogenous or recombinant lutropin/choriogonadotropin receptor (LHR) in mouse Leydig tumor cells (MA-10 cells) leads to the tyrosine phosphorylation of the focal adhesion kinase (FAK) and one of its substrates (paxillin).	Tyrosine	155-163	PTK2 protein tyrosine kinase 2	Mus musculus	210-213
16293639-2	2006	Using specific antibodies to the five tyrosine residues of FAK that become phosphorylated, we show that activation of the LHR increases the phosphorylation of Tyr576 and Tyr577, but it does not affect the phosphorylation of Tyr397, Tyr861, or Tyr925.	Tyrosine	38-46	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
16293639-7	2006	Studies involving activation of other G protein-coupled receptors, overexpression of the different Galpha-subunits, and the use of second messenger analogs suggest that the LHR-induced phosphorylation of FAK-Tyr576 in MA-10 cells is mediated by SFKs, and that this family of kinases is, in turn, independently or cooperatively activated by the LHR-induced stimulation of Gs and Gq/11-mediated pathways.	gq/11	378-383	PTK2 protein tyrosine kinase 2	Mus musculus	204-207
16489009-4	2006	The mechanism of action of HRGP330 involves subversion of focal adhesion function by disruption of integrin-linked kinase (ILK) and focal adhesion kinase (FAK) functions, inhibition of vascular endothelial growth factor (VEGF)-induced tyrosine phosphorylation of the FAK substrate alpha-actinin, and, as a consequence, an arrest in endothelial cell motility.	hrgp330	27-34	PTK2 protein tyrosine kinase 2	Mus musculus	132-153
16489009-4	2006	The mechanism of action of HRGP330 involves subversion of focal adhesion function by disruption of integrin-linked kinase (ILK) and focal adhesion kinase (FAK) functions, inhibition of vascular endothelial growth factor (VEGF)-induced tyrosine phosphorylation of the FAK substrate alpha-actinin, and, as a consequence, an arrest in endothelial cell motility.	hrgp330	27-34	PTK2 protein tyrosine kinase 2	Mus musculus	155-158
16489009-4	2006	The mechanism of action of HRGP330 involves subversion of focal adhesion function by disruption of integrin-linked kinase (ILK) and focal adhesion kinase (FAK) functions, inhibition of vascular endothelial growth factor (VEGF)-induced tyrosine phosphorylation of the FAK substrate alpha-actinin, and, as a consequence, an arrest in endothelial cell motility.	hrgp330	27-34	PTK2 protein tyrosine kinase 2	Mus musculus	267-270
15893751-2	2005	Recently, we have shown that LPA stimulates p21-activated kinase (PAK) that is critical for focal adhesion kinase (FAK) phosphorylation and cell motility.	lysophosphatidic acid	29-32	PTK2 protein tyrosine kinase 2	Mus musculus	115-118
15893751-4	2005	LPA induced p85 beta-PIX binding to FAK in NIH-3T3 cells that was inhibited by pretreatment of the cells with phosphoinositide 3-kinase inhibitor, LY294002.	lysophosphatidic acid	0-3	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
15893751-4	2005	LPA induced p85 beta-PIX binding to FAK in NIH-3T3 cells that was inhibited by pretreatment of the cells with phosphoinositide 3-kinase inhibitor, LY294002.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	147-155	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
15893751-6	2005	Transfection of the cells with specific p85 beta-PIX siRNA led to drastic inhibition of LPA-induced FAK phosphorylation, peripheral redistribution of p85 beta-PIX with FAK and GIT1, and cell motility.	lysophosphatidic acid	88-91	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
15761030-7	2005	IGF-I increased tyrosine phosphorylation of the focal adhesion kinase (FAK) Pyk2 (calcium-dependent proline-rich tyrosine kinase-2) to a much greater extent than FAK, and increased association of Src with Pyk2 but not FAK.	Tyrosine	16-24	PTK2 protein tyrosine kinase 2	Mus musculus	48-69
15761030-7	2005	IGF-I increased tyrosine phosphorylation of the focal adhesion kinase (FAK) Pyk2 (calcium-dependent proline-rich tyrosine kinase-2) to a much greater extent than FAK, and increased association of Src with Pyk2 but not FAK.	Tyrosine	16-24	PTK2 protein tyrosine kinase 2	Mus musculus	71-74
15761030-7	2005	IGF-I increased tyrosine phosphorylation of the focal adhesion kinase (FAK) Pyk2 (calcium-dependent proline-rich tyrosine kinase-2) to a much greater extent than FAK, and increased association of Src with Pyk2 but not FAK.	Calcium	82-89	PTK2 protein tyrosine kinase 2	Mus musculus	48-69
15761030-7	2005	IGF-I increased tyrosine phosphorylation of the focal adhesion kinase (FAK) Pyk2 (calcium-dependent proline-rich tyrosine kinase-2) to a much greater extent than FAK, and increased association of Src with Pyk2 but not FAK.	Calcium	82-89	PTK2 protein tyrosine kinase 2	Mus musculus	71-74
15665032-6	2005	When MMI270 (a broad-spectrum MMP inhibitor) was added together with HGF, decreases in FN-CCB domain expression and FAK phosphorylation by HGF were restored, and these events were associated with an inhibition of HGF-induced apoptosis, suggesting that increased activities of MMPs underlie the major mechanism of HGF-mediated apoptosis in myofibroblasts.	CGS 27023A	5-11	PTK2 protein tyrosine kinase 2	Mus musculus	116-119
15845548-2	2005	A rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but little is known about the regulation of FAK phosphorylation at serine residues.	Tyrosine	24-32	PTK2 protein tyrosine kinase 2	Mus musculus	75-78
15845548-2	2005	A rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but little is known about the regulation of FAK phosphorylation at serine residues.	Serine	232-238	PTK2 protein tyrosine kinase 2	Mus musculus	75-78
15845548-2	2005	A rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but little is known about the regulation of FAK phosphorylation at serine residues.	Serine	232-238	PTK2 protein tyrosine kinase 2	Mus musculus	209-212
15845548-3	2005	Stimulation of Swiss 3T3 cells with the G protein-coupled receptor agonists bombesin, vasopressin, or bradykinin induced an extremely rapid (within 5 s) increase in FAK phosphorylation at Ser-843.	Serine	188-191	PTK2 protein tyrosine kinase 2	Mus musculus	165-168
15845548-4	2005	The phosphorylation of this residue preceded FAK phosphorylation at Tyr-397, the major autophosphorylation site, and FAK phosphorylation at Ser-910.	Tyrosine	68-71	PTK2 protein tyrosine kinase 2	Mus musculus	45-48
15845548-4	2005	The phosphorylation of this residue preceded FAK phosphorylation at Tyr-397, the major autophosphorylation site, and FAK phosphorylation at Ser-910.	Serine	140-143	PTK2 protein tyrosine kinase 2	Mus musculus	117-120
15845548-5	2005	Treatment of intact cells with ionomycin stimulated a rapid increase in FAK phosphorylation at Ser-843, indicating that an increase in intracellular Ca2+ concentration ([Ca2+]i) is a potential pathway leading to FAK-Ser-843 phosphorylation.	Ionomycin	31-40	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
15845548-5	2005	Treatment of intact cells with ionomycin stimulated a rapid increase in FAK phosphorylation at Ser-843, indicating that an increase in intracellular Ca2+ concentration ([Ca2+]i) is a potential pathway leading to FAK-Ser-843 phosphorylation.	Ionomycin	31-40	PTK2 protein tyrosine kinase 2	Mus musculus	212-215
15845548-5	2005	Treatment of intact cells with ionomycin stimulated a rapid increase in FAK phosphorylation at Ser-843, indicating that an increase in intracellular Ca2+ concentration ([Ca2+]i) is a potential pathway leading to FAK-Ser-843 phosphorylation.	Serine	95-98	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
15845548-5	2005	Treatment of intact cells with ionomycin stimulated a rapid increase in FAK phosphorylation at Ser-843, indicating that an increase in intracellular Ca2+ concentration ([Ca2+]i) is a potential pathway leading to FAK-Ser-843 phosphorylation.	Serine	95-98	PTK2 protein tyrosine kinase 2	Mus musculus	212-215
15845548-5	2005	Treatment of intact cells with ionomycin stimulated a rapid increase in FAK phosphorylation at Ser-843, indicating that an increase in intracellular Ca2+ concentration ([Ca2+]i) is a potential pathway leading to FAK-Ser-843 phosphorylation.	Serine	216-219	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
15845548-5	2005	Treatment of intact cells with ionomycin stimulated a rapid increase in FAK phosphorylation at Ser-843, indicating that an increase in intracellular Ca2+ concentration ([Ca2+]i) is a potential pathway leading to FAK-Ser-843 phosphorylation.	Serine	216-219	PTK2 protein tyrosine kinase 2	Mus musculus	212-215
15845548-7	2005	Furthermore, activated CaMKII directly phosphorylated the recombinant COOH-terminal region of FAK at a residue equivalent to Ser-843.	Serine	125-128	PTK2 protein tyrosine kinase 2	Mus musculus	94-97
15845548-8	2005	Thus, our results demonstrate that G protein-coupled receptor activation induces rapid FAK phosphorylation at Ser-843 through Ca2+, calmodulin, and CaMKII.	Serine	110-113	PTK2 protein tyrosine kinase 2	Mus musculus	87-90
15601818-2	2004	4-Hydroxy-tamoxifen treatment induced fak deletion in the epidermis, and suppressed chemically induced skin tumor formation.	4'-hydroxytamoxifen	0-19	PTK2 protein tyrosine kinase 2	Mus musculus	38-41
15557280-1	2005	We have reported previously that the expression of focal adhesion kinase (FAK) is elevated in glioblastomas and that expression of FAK promotes the proliferation of glioblastoma cells propagated in either soft agar or in the C.B.17 severe combined immunodeficiency (scid) mouse brain.	Agar	210-214	PTK2 protein tyrosine kinase 2	Mus musculus	51-72
15557280-1	2005	We have reported previously that the expression of focal adhesion kinase (FAK) is elevated in glioblastomas and that expression of FAK promotes the proliferation of glioblastoma cells propagated in either soft agar or in the C.B.17 severe combined immunodeficiency (scid) mouse brain.	Agar	210-214	PTK2 protein tyrosine kinase 2	Mus musculus	131-134
15681821-4	2005	In a murine model of intratracheal bleomycin-induced lung fibrosis, regions of active fibrogenesis demonstrate elevated expression of PKB/Akt and FAK phosphorylation in vivo, effects that are attenuated in mice receiving daily intraperitoneal injections of AG1879 (bleomycin-AG1879) versus a chemically inactive analog (bleomycin-control).	Bleomycin	35-44	PTK2 protein tyrosine kinase 2	Mus musculus	146-149
15681821-5	2005	PKB/Akt and FAK phosphorylation are elevated in fibroblasts isolated from lungs of bleomycin-injured mice, effects that are inhibited in bleomycin-AG1879 mice.	Bleomycin	83-92	PTK2 protein tyrosine kinase 2	Mus musculus	12-15
15681821-5	2005	PKB/Akt and FAK phosphorylation are elevated in fibroblasts isolated from lungs of bleomycin-injured mice, effects that are inhibited in bleomycin-AG1879 mice.	Bleomycin	137-146	PTK2 protein tyrosine kinase 2	Mus musculus	12-15
16132110-1	2005	Upon cell adhesion to extracellular matrix proteins, focal adhesion kinase (FAK) rapidly undergoes autophosphorylation on its Tyr-397 which consequently serves as a binding site for the Src homology 2 domains of the Src family protein kinases and several other intracellular signaling molecules.	Tyrosine	126-129	PTK2 protein tyrosine kinase 2	Mus musculus	53-74
16132110-1	2005	Upon cell adhesion to extracellular matrix proteins, focal adhesion kinase (FAK) rapidly undergoes autophosphorylation on its Tyr-397 which consequently serves as a binding site for the Src homology 2 domains of the Src family protein kinases and several other intracellular signaling molecules.	Tyrosine	126-129	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
15842360-9	2005	Further examination revealed that SHPS-1 inhibited the tyrosine phosphorylation of alpha-actinin, a downstream effector of FAK, but not of cortactin.	Tyrosine	55-63	PTK2 protein tyrosine kinase 2	Mus musculus	123-126
15842360-10	2005	Thus, it is likely that the SHPS-1/CD47 interaction inhibits alpha(IIb)beta(3)-mediated outside-in signaling by interfering with the downstream pathway of FAK.	beta(3)	71-78	PTK2 protein tyrosine kinase 2	Mus musculus	155-158
16388318-5	2005	We have previously reported that in B16a cells FAK is constitutively active and tyrosine-phosphorylated.	Tyrosine	80-88	PTK2 protein tyrosine kinase 2	Mus musculus	47-50
15283702-6	2004	Collagen plus U46619 also induced significant phosphorylation of FAK (focal adhesion kinase).	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	14-20	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
15283702-6	2004	Collagen plus U46619 also induced significant phosphorylation of FAK (focal adhesion kinase).	15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid	14-20	PTK2 protein tyrosine kinase 2	Mus musculus	70-91
15302877-7	2004	In contrast, overexpression of the N17 mutant of Cdc42 disrupted hyperosmotic stress-stimulated FAK Tyr-397 localization to focal contacts.	Tyrosine	100-103	PTK2 protein tyrosine kinase 2	Mus musculus	96-99
15302877-0	2004	Hyperosmotic stress induces rapid focal adhesion kinase phosphorylation at tyrosines 397 and 577.	Tyrosine	75-84	PTK2 protein tyrosine kinase 2	Mus musculus	34-55
15302877-8	2004	Additionally, treatment of cells with Clostridium difficile toxin B potently inhibited hyperosmotic stress-induced FAK tyrosine phosphorylation.	Tyrosine	119-127	PTK2 protein tyrosine kinase 2	Mus musculus	115-118
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Sucrose	90-97	PTK2 protein tyrosine kinase 2	Mus musculus	154-175
15302877-10	2004	Our results indicate that FAK plays a fundamental role in protecting cells from hyperosmotic stress, and that the pathway(s) that mediates FAK autophosphorylation at Tyr-397 in response to osmotic stress can be distinguished from the pathways utilized by many other stimuli, including neuropeptides and bioactive lipids (Rho- and Rho-associated kinase-dependent), tyrosine kinase receptor agonists (phosphatidylinositol 3-kinase-dependent), and integrins (Src-dependent).	Tyrosine	166-169	PTK2 protein tyrosine kinase 2	Mus musculus	26-29
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Sucrose	90-97	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
15302877-10	2004	Our results indicate that FAK plays a fundamental role in protecting cells from hyperosmotic stress, and that the pathway(s) that mediates FAK autophosphorylation at Tyr-397 in response to osmotic stress can be distinguished from the pathways utilized by many other stimuli, including neuropeptides and bioactive lipids (Rho- and Rho-associated kinase-dependent), tyrosine kinase receptor agonists (phosphatidylinositol 3-kinase-dependent), and integrins (Src-dependent).	Tyrosine	166-169	PTK2 protein tyrosine kinase 2	Mus musculus	139-142
15174091-0	2004	PDGF and FGF induce focal adhesion kinase (FAK) phosphorylation at Ser-910: dissociation from Tyr-397 phosphorylation and requirement for ERK activation.	Serine	67-70	PTK2 protein tyrosine kinase 2	Mus musculus	43-46
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Sorbitol	101-109	PTK2 protein tyrosine kinase 2	Mus musculus	154-175
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Sorbitol	101-109	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Tyrosine	201-204	PTK2 protein tyrosine kinase 2	Mus musculus	154-175
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Tyrosine	201-204	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Tyrosine	253-256	PTK2 protein tyrosine kinase 2	Mus musculus	154-175
15302877-2	2004	Hyperosmotic stress induced by treatment of Swiss 3T3 cells with the non-permeant solutes sucrose or sorbitol, rapidly and robustly stimulated endogenous focal adhesion kinase (FAK) phosphorylation at Tyr-397, the major autophosphorylation site, and at Tyr-577, within the kinase activation loop.	Tyrosine	253-256	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
15302877-3	2004	Hyperosmotic stress-stimulated FAK phosphorylation at Tyr-397 occurred via a Src-independent pathway, whereas Tyr-577 phosphorylation was completely blocked by exposure to the Src family kinase inhibitor PP-2.	Tyrosine	54-57	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
15273716-5	2004	CAS expression led to a substantial increase in the phosphotyrosine content of FAK and paxillin, supporting a role for CAS as a positive regulator of Src activity at integrin adhesion sites.	Phosphotyrosine	52-67	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
15174091-0	2004	PDGF and FGF induce focal adhesion kinase (FAK) phosphorylation at Ser-910: dissociation from Tyr-397 phosphorylation and requirement for ERK activation.	Serine	67-70	PTK2 protein tyrosine kinase 2	Mus musculus	20-41
15219947-5	2004	Downregulation of FAK (which would impair integrin mediated signal transduction cascade) and reduction of MMP-2 activity could be important reasons for anti-metastatic property of curcumin.	Curcumin	180-188	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
15174091-0	2004	PDGF and FGF induce focal adhesion kinase (FAK) phosphorylation at Ser-910: dissociation from Tyr-397 phosphorylation and requirement for ERK activation.	Tyrosine	94-97	PTK2 protein tyrosine kinase 2	Mus musculus	20-41
15174091-0	2004	PDGF and FGF induce focal adhesion kinase (FAK) phosphorylation at Ser-910: dissociation from Tyr-397 phosphorylation and requirement for ERK activation.	Tyrosine	94-97	PTK2 protein tyrosine kinase 2	Mus musculus	43-46
15174091-1	2004	A rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but very little is known about the regulation of FAK phosphorylation at serine residues.	Tyrosine	24-32	PTK2 protein tyrosine kinase 2	Mus musculus	52-73
15174091-1	2004	A rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but very little is known about the regulation of FAK phosphorylation at serine residues.	Tyrosine	24-32	PTK2 protein tyrosine kinase 2	Mus musculus	75-78
15174091-1	2004	A rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but very little is known about the regulation of FAK phosphorylation at serine residues.	Serine	237-243	PTK2 protein tyrosine kinase 2	Mus musculus	214-217
15174091-2	2004	Stimulation of Swiss 3T3 cells with platelet-derived growth factor (PDGF) promoted a striking increase in the phosphorylation of FAK at Ser-910, as revealed by site-specific antibodies that recognized the phosphorylated state of this residue.	Serine	136-139	PTK2 protein tyrosine kinase 2	Mus musculus	129-132
15174091-3	2004	FAK phosphorylation at Ser-910 could be distinguished from that at Tyr-397 in terms of dose-response relationships and kinetics.	Serine	23-26	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
15174091-4	2004	Furthermore, the selective phosphoinositide 3-kinase (PI 3-kinase) inhibitors wortmannin and LY 294002 abrogated FAK phosphorylation at Tyr-397 but did not interfere with PDGF-induced FAK phosphorylation at Ser-910.	Wortmannin	78-88	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
15174091-4	2004	Furthermore, the selective phosphoinositide 3-kinase (PI 3-kinase) inhibitors wortmannin and LY 294002 abrogated FAK phosphorylation at Tyr-397 but did not interfere with PDGF-induced FAK phosphorylation at Ser-910.	Wortmannin	78-88	PTK2 protein tyrosine kinase 2	Mus musculus	184-187
15174091-4	2004	Furthermore, the selective phosphoinositide 3-kinase (PI 3-kinase) inhibitors wortmannin and LY 294002 abrogated FAK phosphorylation at Tyr-397 but did not interfere with PDGF-induced FAK phosphorylation at Ser-910.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	93-102	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
15174091-4	2004	Furthermore, the selective phosphoinositide 3-kinase (PI 3-kinase) inhibitors wortmannin and LY 294002 abrogated FAK phosphorylation at Tyr-397 but did not interfere with PDGF-induced FAK phosphorylation at Ser-910.	Tyrosine	136-139	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
15174091-4	2004	Furthermore, the selective phosphoinositide 3-kinase (PI 3-kinase) inhibitors wortmannin and LY 294002 abrogated FAK phosphorylation at Tyr-397 but did not interfere with PDGF-induced FAK phosphorylation at Ser-910.	Serine	207-210	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
15174091-5	2004	Conversely, treatment with U0126, a potent inhibitor of MEK-mediated ERK activation, prevented FAK phosphorylation at Ser-910 induced by PDGF but did not interfere with PDGF-induced FAK phosphorylation at Tyr-397.	U 0126	27-32	PTK2 protein tyrosine kinase 2	Mus musculus	95-98
15174091-5	2004	Conversely, treatment with U0126, a potent inhibitor of MEK-mediated ERK activation, prevented FAK phosphorylation at Ser-910 induced by PDGF but did not interfere with PDGF-induced FAK phosphorylation at Tyr-397.	Serine	118-121	PTK2 protein tyrosine kinase 2	Mus musculus	95-98
15174091-7	2004	FGF but not insulin promoted a striking ERK-dependent phosphorylation of FAK at Ser-910.	Serine	80-83	PTK2 protein tyrosine kinase 2	Mus musculus	73-76
15174091-8	2004	Our results indicate that FAK phosphorylation at Tyr-397 and FAK phosphorylation at Ser-910 are induced in response to PDGF stimulation through different signaling pathways, namely PI 3-kinase and ERK, respectively.	Tyrosine	49-52	PTK2 protein tyrosine kinase 2	Mus musculus	26-29
15174091-8	2004	Our results indicate that FAK phosphorylation at Tyr-397 and FAK phosphorylation at Ser-910 are induced in response to PDGF stimulation through different signaling pathways, namely PI 3-kinase and ERK, respectively.	Serine	84-87	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
15034138-5	2004	Phosphorylation of tyrosines in focal adhesion kinase (FAK) and the Y416 in c-Src in response to beta1A(K756L)-mediated adhesion was similar to that induced by wild-type beta1.	Tyrosine	19-28	PTK2 protein tyrosine kinase 2	Mus musculus	32-53
15123632-0	2004	Phosphorylation of focal adhesion kinase at tyrosine 861 is crucial for Ras transformation of fibroblasts.	Tyrosine	44-52	PTK2 protein tyrosine kinase 2	Mus musculus	19-40
15123632-1	2004	Although elevated expression and increased tyrosine phosphorylation of focal adhesion kinase (FAK) are crucial for tumor progression, the mechanism by which FAK promotes oncogenic transformation is unclear.	Tyrosine	43-51	PTK2 protein tyrosine kinase 2	Mus musculus	71-92
15123632-1	2004	Although elevated expression and increased tyrosine phosphorylation of focal adhesion kinase (FAK) are crucial for tumor progression, the mechanism by which FAK promotes oncogenic transformation is unclear.	Tyrosine	43-51	PTK2 protein tyrosine kinase 2	Mus musculus	94-97
15123632-2	2004	We have therefore determined the role of FAK phosphorylation at tyrosine 861 in the oncogenic transformation of NIH3T3 fibroblasts.	Tyrosine	64-72	PTK2 protein tyrosine kinase 2	Mus musculus	41-44
15123632-3	2004	FAK phosphorylation at tyrosine 861 was increased in both constitutively H-Ras-transformed and H-Ras-inducible NIH3T3 cells, in parallel with cell transformation.	Tyrosine	23-31	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
15123632-5	2004	In contrast to unaltered FAK/Src activity, the association of FAK and p130(CAS) was decreased in FAK Y861F-transfected cells, and FAK phosphorylation at tyrosine 861 enhanced this association in vitro.	Tyrosine	153-161	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
15123632-5	2004	In contrast to unaltered FAK/Src activity, the association of FAK and p130(CAS) was decreased in FAK Y861F-transfected cells, and FAK phosphorylation at tyrosine 861 enhanced this association in vitro.	Tyrosine	153-161	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
15123632-5	2004	In contrast to unaltered FAK/Src activity, the association of FAK and p130(CAS) was decreased in FAK Y861F-transfected cells, and FAK phosphorylation at tyrosine 861 enhanced this association in vitro.	Tyrosine	153-161	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
15123632-7	2004	Taken together, these results strongly suggest that FAK phosphorylation at tyrosine 861 is crucial for H-Ras-induced transformation through regulation of the association of FAK with p130(CAS).	Tyrosine	75-83	PTK2 protein tyrosine kinase 2	Mus musculus	52-55
15123632-7	2004	Taken together, these results strongly suggest that FAK phosphorylation at tyrosine 861 is crucial for H-Ras-induced transformation through regulation of the association of FAK with p130(CAS).	Tyrosine	75-83	PTK2 protein tyrosine kinase 2	Mus musculus	173-176
15034138-5	2004	Phosphorylation of tyrosines in focal adhesion kinase (FAK) and the Y416 in c-Src in response to beta1A(K756L)-mediated adhesion was similar to that induced by wild-type beta1.	Tyrosine	19-28	PTK2 protein tyrosine kinase 2	Mus musculus	55-58
15132756-2	2004	Integrin binding to extracellular matrix increases tyrosine phosphorylation of focal adhesion kinase (FAK).	Tyrosine	51-59	PTK2 protein tyrosine kinase 2	Mus musculus	79-100
15132756-2	2004	Integrin binding to extracellular matrix increases tyrosine phosphorylation of focal adhesion kinase (FAK).	Tyrosine	51-59	PTK2 protein tyrosine kinase 2	Mus musculus	102-105
14966364-7	2004	The effects of mannitol in various doses on cell contraction and activation of PKC and FAK were also assayed.	Mannitol	15-23	PTK2 protein tyrosine kinase 2	Mus musculus	87-90
14966364-10	2004	Results of tyrosine phosphorylation and immunoprecipitation showed that FAK may be involved in this contraction process.	Tyrosine	11-19	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
14966364-13	2004	Activation of PKC alpha, delta, and FAK with the resultant inhibition of mesangial cell contraction by mannitol was found to be dose-dependent.	Mannitol	103-111	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
14966364-15	2004	Furthermore, the mannitol-induced hypocontractility involving PKC and FAK occurred in a dose-dependent manner.	Mannitol	17-25	PTK2 protein tyrosine kinase 2	Mus musculus	70-73
14989777-9	2004	The Ligustrazine promotes the recovery of bone marrow microenvironment probably by increasing the expression of phosphorylated FAK and MAPK in BMSCs.	tetramethylpyrazine	4-16	PTK2 protein tyrosine kinase 2	Mus musculus	127-130
14634134-1	2003	Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine kinase that plays an important role in many cellular processes and is tyrosine phosphorylated after FcepsilonRI aggregation in mast cells.	Tyrosine	53-61	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
15554394-4	2004	In non-malignant keratinocytes, phosphotyrosine staining co-localized with paxillin and FAK.	Phosphotyrosine	32-47	PTK2 protein tyrosine kinase 2	Mus musculus	88-91
15554394-6	2004	In contrast, the co-localization of phosphotyrosine with either paxillin or FAK along the cell periphery was almost absent in the SCC cells or in keratinocytes that were treated with okadaic acid to inhibit PP-2A activity.	Phosphotyrosine	36-51	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
15554394-6	2004	In contrast, the co-localization of phosphotyrosine with either paxillin or FAK along the cell periphery was almost absent in the SCC cells or in keratinocytes that were treated with okadaic acid to inhibit PP-2A activity.	Okadaic Acid	183-195	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
15554394-8	2004	These studies indicate PP-2A maintains the organization and tyrosine-phosphorylated state of the focal adhesion proteins FAK and paxillin, and that the loss of PP-2A activity results in a loss of cytoskeletal organization, as is seen in SCC.	Tyrosine	60-68	PTK2 protein tyrosine kinase 2	Mus musculus	121-124
14634134-1	2003	Focal adhesion kinase (FAK) is a nonreceptor protein tyrosine kinase that plays an important role in many cellular processes and is tyrosine phosphorylated after FcepsilonRI aggregation in mast cells.	Tyrosine	53-61	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
14634134-6	2003	The FAK-deficient mast cells had a reduction in the content of chondroitin/dermatan sulfate, the major glycosaminoglycan component of the granular matrix.	Chondroitin	63-74	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
14634134-6	2003	The FAK-deficient mast cells had a reduction in the content of chondroitin/dermatan sulfate, the major glycosaminoglycan component of the granular matrix.	Dermatan Sulfate	75-91	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
14634134-6	2003	The FAK-deficient mast cells had a reduction in the content of chondroitin/dermatan sulfate, the major glycosaminoglycan component of the granular matrix.	Glycosaminoglycans	103-120	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
14634134-11	2003	These results indicate that FAK plays a role in regulating the glycosaminoglycan content of the secretory granules and influences the cell surface morphology of mast cells.	Glycosaminoglycans	63-80	PTK2 protein tyrosine kinase 2	Mus musculus	28-31
12692126-3	2003	Lysophosphatidic acid and epidermal growth factor (EGF) also stimulated FAK phosphorylation at Ser-910.	lysophosphatidic acid	0-21	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
12702722-6	2003	Neuro-2a cell binding to laminin increased endogenous FAK and p190RhoGEF tyrosine phosphorylation, and co-transfection of a dominant-negative inhibitor of FAK activity, termed FRNK, inhibited lamininstimulated p190RhoGEF tyrosine phosphorylation and p21 RhoA GTP binding.	Tyrosine	221-229	PTK2 protein tyrosine kinase 2	Mus musculus	155-158
12702722-6	2003	Neuro-2a cell binding to laminin increased endogenous FAK and p190RhoGEF tyrosine phosphorylation, and co-transfection of a dominant-negative inhibitor of FAK activity, termed FRNK, inhibited lamininstimulated p190RhoGEF tyrosine phosphorylation and p21 RhoA GTP binding.	Tyrosine	221-229	PTK2 protein tyrosine kinase 2	Mus musculus	176-180
12702722-6	2003	Neuro-2a cell binding to laminin increased endogenous FAK and p190RhoGEF tyrosine phosphorylation, and co-transfection of a dominant-negative inhibitor of FAK activity, termed FRNK, inhibited lamininstimulated p190RhoGEF tyrosine phosphorylation and p21 RhoA GTP binding.	Guanosine Triphosphate	259-262	PTK2 protein tyrosine kinase 2	Mus musculus	155-158
12702722-6	2003	Neuro-2a cell binding to laminin increased endogenous FAK and p190RhoGEF tyrosine phosphorylation, and co-transfection of a dominant-negative inhibitor of FAK activity, termed FRNK, inhibited lamininstimulated p190RhoGEF tyrosine phosphorylation and p21 RhoA GTP binding.	Guanosine Triphosphate	259-262	PTK2 protein tyrosine kinase 2	Mus musculus	176-180
12702722-7	2003	Overexpression of FAK in Neuro-2a cells increased both endogenous p190RhoGEF tyrosine phosphorylation and RhoA activity, whereas these events were inhibited by FRNK co-expression.	Tyrosine	77-85	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
12702722-8	2003	Because insulin-like growth factor 1 treatment of Neuro-2a cells increased FAK tyrosine phosphorylation and enhanced p190RhoGEF-mediated activation of RhoA, our results support the conclusion that FAK association with p190RhoGEF functions as a signaling pathway downstream of integrins and growth factor receptors to stimulate Rho activity.	Tyrosine	79-87	PTK2 protein tyrosine kinase 2	Mus musculus	75-78
12702722-8	2003	Because insulin-like growth factor 1 treatment of Neuro-2a cells increased FAK tyrosine phosphorylation and enhanced p190RhoGEF-mediated activation of RhoA, our results support the conclusion that FAK association with p190RhoGEF functions as a signaling pathway downstream of integrins and growth factor receptors to stimulate Rho activity.	Tyrosine	79-87	PTK2 protein tyrosine kinase 2	Mus musculus	197-200
14623342-0	2003	RNA interference targeting focal adhesion kinase enhances pancreatic adenocarcinoma gemcitabine chemosensitivity.	gemcitabine	84-95	PTK2 protein tyrosine kinase 2	Mus musculus	27-48
14623342-2	2003	We tested the hypothesis that FAK is a determinant of gemcitabine chemoresistance in pancreatic adenocarcinoma cells and examined the effect of inhibiting FAK expression on gemcitabine-induced cytotoxicity in vitro and in vivo.	gemcitabine	54-65	PTK2 protein tyrosine kinase 2	Mus musculus	30-33
14623342-8	2003	While not affecting cellular proliferation or apoptosis in the absence of gemcitabine, FAK siRNA potentiated gemcitabine-induced cytotoxicity in vitro and in vivo.	gemcitabine	109-120	PTK2 protein tyrosine kinase 2	Mus musculus	87-90
12941275-0	2003	Serine 732 phosphorylation of FAK by Cdk5 is important for microtubule organization, nuclear movement, and neuronal migration.	Serine	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	30-33
12702722-3	2003	Here, we report that FAK interacts with p190RhoGEF, a RhoA-specific GDP/GTP exchange factor, in neuronal cells and in brain tissue extracts by co-immunoprecipitation and co-localization analyses.	Guanosine Triphosphate	72-75	PTK2 protein tyrosine kinase 2	Mus musculus	21-24
12692126-1	2003	A rapid increase in the tyrosine phosphorylation of focal adhesion kinase (FAK) has been extensively documented in cells stimulated by multiple signaling molecules, but virtually nothing is known about the regulation of FAK phosphorylation at serine residues.	Tyrosine	24-32	PTK2 protein tyrosine kinase 2	Mus musculus	75-78
12692126-2	2003	Stimulation of Swiss 3T3 cells with bombesin promoted a striking increase ( approximately 13-fold) in the phosphorylation of FAK at Ser-910, as revealed by site-specific antibodies that recognized the phosphorylated state of this residue.	Serine	132-135	PTK2 protein tyrosine kinase 2	Mus musculus	125-128
12692126-3	2003	Lysophosphatidic acid and epidermal growth factor (EGF) also stimulated FAK phosphorylation at Ser-910.	Serine	95-98	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
12692126-4	2003	Direct activation of protein kinase C isoforms with phorbol-12,13-dibutyrate (PDB) also promoted striking phosphorylation of FAK at Ser-910.	Phorbol 12,13-Dibutyrate	52-76	PTK2 protein tyrosine kinase 2	Mus musculus	125-128
12692126-4	2003	Direct activation of protein kinase C isoforms with phorbol-12,13-dibutyrate (PDB) also promoted striking phosphorylation of FAK at Ser-910.	Serine	132-135	PTK2 protein tyrosine kinase 2	Mus musculus	125-128
12692126-5	2003	Treatment with the protein kinase C inhibitor GF I or Ro 31-8220 or chronic exposure to PDB prevented the increase in FAK phosphorylation at Ser-910 induced by bombesin or PDB but not by EGF.	ser-910	141-148	PTK2 protein tyrosine kinase 2	Mus musculus	118-121
12692126-6	2003	Treatment with the ERK inhibitors U0126 and PD98059 prevented FAK phosphorylation at Ser-910 in response to all of the stimuli tested.	U 0126	34-39	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
12692126-6	2003	Treatment with the ERK inhibitors U0126 and PD98059 prevented FAK phosphorylation at Ser-910 in response to all of the stimuli tested.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	44-51	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
12692126-6	2003	Treatment with the ERK inhibitors U0126 and PD98059 prevented FAK phosphorylation at Ser-910 in response to all of the stimuli tested.	Serine	85-88	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
12692126-7	2003	Furthermore, incubation of activated ERK2 with FAK immunocomplexes leads to FAK phosphorylation at Ser-910 in vitro.	Serine	99-102	PTK2 protein tyrosine kinase 2	Mus musculus	47-50
12692126-7	2003	Furthermore, incubation of activated ERK2 with FAK immunocomplexes leads to FAK phosphorylation at Ser-910 in vitro.	Serine	99-102	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
12692126-8	2003	Our results demonstrate, for the first time, that stimulation with bombesin, lysophosphatidic acid, PDB, or EGF induces phosphorylation of endogenous FAK at Ser-910 via an ERK-dependent pathway in Swiss 3T3 cells.	lysophosphatidic acid	77-98	PTK2 protein tyrosine kinase 2	Mus musculus	150-153
12692126-8	2003	Our results demonstrate, for the first time, that stimulation with bombesin, lysophosphatidic acid, PDB, or EGF induces phosphorylation of endogenous FAK at Ser-910 via an ERK-dependent pathway in Swiss 3T3 cells.	Serine	157-160	PTK2 protein tyrosine kinase 2	Mus musculus	150-153
12464388-3	2003	Fibroblast growth factor 2 (FGF-2) stimulation lead to a direct association between Shb and FAK, which was mediated by the phosphotyrosine binding (PTB) domain of Shb.	Phosphotyrosine	123-138	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
12551902-3	2003	The Lar-interacting domain of Trio is constitutively tyrosine-phosphorylated when expressed in COS-7 cells and was highly phosphorylated when it was co-transfected with FAK.	Tyrosine	53-61	PTK2 protein tyrosine kinase 2	Mus musculus	169-172
12551902-5	2003	Tyrosine-phosphorylated FAK and Trio were present mainly in the detergent-insoluble fraction of cell lysates, and co-expression of Trio and FAK resulted in increased amounts of Trio present in the detergent-insoluble fraction.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	24-27
12551902-5	2003	Tyrosine-phosphorylated FAK and Trio were present mainly in the detergent-insoluble fraction of cell lysates, and co-expression of Trio and FAK resulted in increased amounts of Trio present in the detergent-insoluble fraction.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	140-143
12551902-7	2003	A FAK phosphorylation site, tyrosine residue 2737, was identified in subdomain I of the Trio kinase domain.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	2-5
12466150-6	2003	Furthermore, inhibiting Src tyrosine kinase decreases TNF-induced focal adhesion kinase (FAK) tyrosine phosphorylation and cellular migration.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	66-87
12466150-6	2003	Furthermore, inhibiting Src tyrosine kinase decreases TNF-induced focal adhesion kinase (FAK) tyrosine phosphorylation and cellular migration.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
12466150-7	2003	We therefore conclude that TNFR2 activates a novel Src-regulated pathway involving FAK tyrosine phosphorylation that enhances migration of intestinal epithelial cells.	Tyrosine	87-95	PTK2 protein tyrosine kinase 2	Mus musculus	83-86
12548551-0	2003	Dissociation of focal adhesion kinase and paxillin tyrosine phosphorylation induced by bombesin and lysophosphatidic acid from epidermal growth factor receptor transactivation in Swiss 3T3 cells.	lysophosphatidic acid	100-121	PTK2 protein tyrosine kinase 2	Mus musculus	16-37
12548551-1	2003	Tyrosine phosphorylation of the nonreceptor tyrosine kinase p125 focal adhesion kinase (FAK) and the adapter protein paxillin is rapidly increased by multiple agonists, including bombesin (BOM) and lysophosphatidic acid (LPA), through heptahelical G protein-coupled receptors (GPCRs).	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	65-86
12548551-1	2003	Tyrosine phosphorylation of the nonreceptor tyrosine kinase p125 focal adhesion kinase (FAK) and the adapter protein paxillin is rapidly increased by multiple agonists, including bombesin (BOM) and lysophosphatidic acid (LPA), through heptahelical G protein-coupled receptors (GPCRs).	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	88-91
12548551-1	2003	Tyrosine phosphorylation of the nonreceptor tyrosine kinase p125 focal adhesion kinase (FAK) and the adapter protein paxillin is rapidly increased by multiple agonists, including bombesin (BOM) and lysophosphatidic acid (LPA), through heptahelical G protein-coupled receptors (GPCRs).	lysophosphatidic acid	198-219	PTK2 protein tyrosine kinase 2	Mus musculus	65-86
12548551-1	2003	Tyrosine phosphorylation of the nonreceptor tyrosine kinase p125 focal adhesion kinase (FAK) and the adapter protein paxillin is rapidly increased by multiple agonists, including bombesin (BOM) and lysophosphatidic acid (LPA), through heptahelical G protein-coupled receptors (GPCRs).	lysophosphatidic acid	198-219	PTK2 protein tyrosine kinase 2	Mus musculus	88-91
12548551-1	2003	Tyrosine phosphorylation of the nonreceptor tyrosine kinase p125 focal adhesion kinase (FAK) and the adapter protein paxillin is rapidly increased by multiple agonists, including bombesin (BOM) and lysophosphatidic acid (LPA), through heptahelical G protein-coupled receptors (GPCRs).	lysophosphatidic acid	221-224	PTK2 protein tyrosine kinase 2	Mus musculus	65-86
12548551-1	2003	Tyrosine phosphorylation of the nonreceptor tyrosine kinase p125 focal adhesion kinase (FAK) and the adapter protein paxillin is rapidly increased by multiple agonists, including bombesin (BOM) and lysophosphatidic acid (LPA), through heptahelical G protein-coupled receptors (GPCRs).	lysophosphatidic acid	221-224	PTK2 protein tyrosine kinase 2	Mus musculus	88-91
12548551-3	2003	The experiments presented here were designed to test the role of epidermal growth factor receptor (EGFR) transactivation in the rapid increase of tyrosine phosphorylation of FAK and paxillin induced by GPCR agonists.	Tyrosine	146-154	PTK2 protein tyrosine kinase 2	Mus musculus	174-177
12548551-6	2003	Collectively, our results clearly dissociate EGFR transactivation from the tyrosine phosphorylation of FAK and paxillin induced by multiple GPCR agonists.	Tyrosine	75-83	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
12515828-5	2003	Reintroduction of active (but not inactive) PTP alpha restored FAK Tyr-397 phosphorylation.	Tyrosine	67-70	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
12588524-2	2003	Here, we demonstrate the application of sapphire-attached tissue culture cells (PtK2 epithelial cells and mouse myoblasts) to metal-mirror impact freezing.	Metals	126-131	PTK2 protein tyrosine kinase 2	Mus musculus	80-84
12455030-6	2003	Phosphorylation of the FAK located at downstream of integrin molecules was markedly reduced in GM(2)(+) transfectants, suggesting that GM(2) suppressed cell adhesion signals via fibronectin-integrin interaction.	gm(2)(+)	95-103	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
12455030-6	2003	Phosphorylation of the FAK located at downstream of integrin molecules was markedly reduced in GM(2)(+) transfectants, suggesting that GM(2) suppressed cell adhesion signals via fibronectin-integrin interaction.	gm(2)	95-100	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
12515828-9	2003	Our paper establishes that PTP alpha is required for early integrin-proximal events, acting upstream of FAK to affect the timely and efficient phosphorylation of FAK Tyr-397.	Tyrosine	166-169	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
12515828-9	2003	Our paper establishes that PTP alpha is required for early integrin-proximal events, acting upstream of FAK to affect the timely and efficient phosphorylation of FAK Tyr-397.	Tyrosine	166-169	PTK2 protein tyrosine kinase 2	Mus musculus	162-165
12091389-14	2002	During integrin ligation, phosphocaveolin-2 (Tyr(P)(19)) co-localizes with activated FAK at focal adhesions.	Tyrosine	45-48	PTK2 protein tyrosine kinase 2	Mus musculus	85-88
12678405-7	2003	In addition, curcumin treatment inhibited pp125 focal adhesion kinase (FAK), tyrosine phosphorylation of a 120 kD protein, and collagenase activity.	Curcumin	13-21	PTK2 protein tyrosine kinase 2	Mus musculus	71-74
12456636-4	2002	FRNK expression disrupted the formation of a v-Src-FAK signaling complex, inhibited p130Cas tyrosine phosphorylation, and attenuated v-Src-stimulated ERK and JNK kinase activation.	Tyrosine	92-100	PTK2 protein tyrosine kinase 2	Mus musculus	0-4
14529092-9	2003	The immunoblot confirmed the tyrosine phosphorylation of FAK in B16F10 cells grown in presence of alpha5 monoclonal antibody, indicating the transduction of signal via FAK.	Tyrosine	29-37	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
14529092-9	2003	The immunoblot confirmed the tyrosine phosphorylation of FAK in B16F10 cells grown in presence of alpha5 monoclonal antibody, indicating the transduction of signal via FAK.	Tyrosine	29-37	PTK2 protein tyrosine kinase 2	Mus musculus	168-171
12385003-6	2002	AS-ODN and LT also inhibited the tyrosine phosphorylation of FAK when cells were plated on vitronectin, fibronectin, or type-1 collagen.	Tyrosine	33-41	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
12385003-7	2002	This inhibition of cell spreading and of tyrosine phosphorylation of FAK could be negated by Mg(2+).	Tyrosine	41-49	PTK2 protein tyrosine kinase 2	Mus musculus	69-72
12385003-7	2002	This inhibition of cell spreading and of tyrosine phosphorylation of FAK could be negated by Mg(2+).	magnesium ion	93-99	PTK2 protein tyrosine kinase 2	Mus musculus	69-72
12105199-2	2002	In this study, we have found that Y27632, a specific inhibitor for Rho-associated kinase (Rho-kinase), dramatically reversed the round cell morphology of FAK(-/-) cells to a spread fibroblast-like shape in 30 min and significantly enhanced their motility.	Y 27632	34-40	PTK2 protein tyrosine kinase 2	Mus musculus	154-157
12110680-5	2002	Levels of ERK activation in B16-F10 cells transfected with wild-type or mutant FAK are closely associated with rates of proliferation and bromodeoxyuridine (BrdUrd) incorporation of tumor cells grown in mCLCA1-coated dishes, the ability to form tumor cell colonies on CLCA-expressing endothelial cell monolayers, and the extent of pulmonary metastatic growth.	Bromodeoxyuridine	138-155	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
12190987-9	2002	Based on the above data, we propose that PKC downregulation results in enhanced tyrosine phosphorylation of FAK, Cas, and paxillin, thus promoting the establishment of Cas-CrkII complex, leading to activation of JNK and that these interactions are dependent upon the integrity of actin cytoskeleton during muscle cell differentiation.	Tyrosine	80-88	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
12105199-3	2002	The effects of Y27632 on the FAK(-/-) cell morphology and motility were concomitant with reorganization of the actin cytoskeleton and redistribution of focal adhesions.	Y 27632	15-21	PTK2 protein tyrosine kinase 2	Mus musculus	29-32
12105199-5	2002	Furthermore, coincident with the formation of cortical actin filaments, myosin light chain (MLC), Ser-19-phosphorylated MLC, and MLC kinase mainly accumulated at the FAK(-/-) cell periphery.	Serine	98-101	PTK2 protein tyrosine kinase 2	Mus musculus	166-169
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.	diacetylmonoxime	174-198	PTK2 protein tyrosine kinase 2	Mus musculus	207-210
12087088-5	2002	FN-null fibroblasts (which express syndecan-4) exhibit reduced phosphorylation of focal adhesion kinase (FAK) tyrosine 397 (Tyr(397)) when adherent to CBD compared with FN-adherent cells.	Tyrosine	110-118	PTK2 protein tyrosine kinase 2	Mus musculus	105-108
12087088-5	2002	FN-null fibroblasts (which express syndecan-4) exhibit reduced phosphorylation of focal adhesion kinase (FAK) tyrosine 397 (Tyr(397)) when adherent to CBD compared with FN-adherent cells.	Tyrosine	124-127	PTK2 protein tyrosine kinase 2	Mus musculus	105-108
12087088-9	2002	The phosphorylation levels of FAK Tyr(397) were lower in FN-adherent syndecan-4-null fibroblasts compared with syndecan-4-wild type and these levels were rescued by the addition of LPA or re-expression of syndecan-4.	Tyrosine	34-37	PTK2 protein tyrosine kinase 2	Mus musculus	30-33
12087088-10	2002	These data indicate that syndecan-4 ligation regulates the phosphorylation of FAK Tyr(397) and that this mechanism is dependent on Rho but not protein kinase C activation.	Tyrosine	82-85	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
12163181-0	2002	CB1 cannabinoid receptor-mediated tyrosine phosphorylation of focal adhesion kinase-related non-kinase.	Tyrosine	34-42	PTK2 protein tyrosine kinase 2	Mus musculus	62-102
12163181-1	2002	The effect of cannabinoid on the tyrosine phosphorylation of focal adhesion kinase (FAK) and focal adhesion kinase-related non-kinase (FRNK) was investigated in differentiated mouse neuroblastoma N1E-115 cells.	Cannabinoids	14-25	PTK2 protein tyrosine kinase 2	Mus musculus	61-82
12163181-1	2002	The effect of cannabinoid on the tyrosine phosphorylation of focal adhesion kinase (FAK) and focal adhesion kinase-related non-kinase (FRNK) was investigated in differentiated mouse neuroblastoma N1E-115 cells.	Cannabinoids	14-25	PTK2 protein tyrosine kinase 2	Mus musculus	84-87
12163181-1	2002	The effect of cannabinoid on the tyrosine phosphorylation of focal adhesion kinase (FAK) and focal adhesion kinase-related non-kinase (FRNK) was investigated in differentiated mouse neuroblastoma N1E-115 cells.	Cannabinoids	14-25	PTK2 protein tyrosine kinase 2	Mus musculus	93-133
12163181-1	2002	The effect of cannabinoid on the tyrosine phosphorylation of focal adhesion kinase (FAK) and focal adhesion kinase-related non-kinase (FRNK) was investigated in differentiated mouse neuroblastoma N1E-115 cells.	Tyrosine	33-41	PTK2 protein tyrosine kinase 2	Mus musculus	61-82
12163181-1	2002	The effect of cannabinoid on the tyrosine phosphorylation of focal adhesion kinase (FAK) and focal adhesion kinase-related non-kinase (FRNK) was investigated in differentiated mouse neuroblastoma N1E-115 cells.	Tyrosine	33-41	PTK2 protein tyrosine kinase 2	Mus musculus	84-87
12163181-2	2002	HU-210, a potent cannabinoid agonist, elicited a time-dependent enhancement of tyrosine phosphorylation of FRNK, but not FAK.	HU 211	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	107-111
12163181-2	2002	HU-210, a potent cannabinoid agonist, elicited a time-dependent enhancement of tyrosine phosphorylation of FRNK, but not FAK.	Cannabinoids	17-28	PTK2 protein tyrosine kinase 2	Mus musculus	107-111
12163181-2	2002	HU-210, a potent cannabinoid agonist, elicited a time-dependent enhancement of tyrosine phosphorylation of FRNK, but not FAK.	Tyrosine	79-87	PTK2 protein tyrosine kinase 2	Mus musculus	107-111
12163181-3	2002	Pretreatment of cells with antisense oligodeoxynucleotide targeting CB1 cannabinoid receptor abolished HU-210-induced FRNK tyrosine phosphorylation.	Oligodeoxyribonucleotides	37-57	PTK2 protein tyrosine kinase 2	Mus musculus	118-122
12163181-3	2002	Pretreatment of cells with antisense oligodeoxynucleotide targeting CB1 cannabinoid receptor abolished HU-210-induced FRNK tyrosine phosphorylation.	HU 211	103-109	PTK2 protein tyrosine kinase 2	Mus musculus	118-122
12163181-3	2002	Pretreatment of cells with antisense oligodeoxynucleotide targeting CB1 cannabinoid receptor abolished HU-210-induced FRNK tyrosine phosphorylation.	Tyrosine	123-131	PTK2 protein tyrosine kinase 2	Mus musculus	118-122
12163181-4	2002	In addition, pretreatment of cells with 8-Br-cAMP also blocked HU-210-induced FRNK tyrosine phosphorylation.	8-Bromo Cyclic Adenosine Monophosphate	40-49	PTK2 protein tyrosine kinase 2	Mus musculus	78-82
12163181-4	2002	In addition, pretreatment of cells with 8-Br-cAMP also blocked HU-210-induced FRNK tyrosine phosphorylation.	Tyrosine	83-91	PTK2 protein tyrosine kinase 2	Mus musculus	78-82
12163181-5	2002	These data demonstrated that HU-210 induces FRNK tyrosine phosphorylation by activating G(i)-coupled CB1 cannabinoid receptor in N1E-115 cells.	HU 211	29-35	PTK2 protein tyrosine kinase 2	Mus musculus	44-48
12163181-5	2002	These data demonstrated that HU-210 induces FRNK tyrosine phosphorylation by activating G(i)-coupled CB1 cannabinoid receptor in N1E-115 cells.	Tyrosine	49-57	PTK2 protein tyrosine kinase 2	Mus musculus	44-48
12163181-6	2002	This newly discovered, cannabinoid-induced FRNK tyrosine phosphorylation might be a novel mechanism for cannabinoid-induced functional changes.	Cannabinoids	23-34	PTK2 protein tyrosine kinase 2	Mus musculus	43-47
12163181-6	2002	This newly discovered, cannabinoid-induced FRNK tyrosine phosphorylation might be a novel mechanism for cannabinoid-induced functional changes.	Tyrosine	48-56	PTK2 protein tyrosine kinase 2	Mus musculus	43-47
12163181-6	2002	This newly discovered, cannabinoid-induced FRNK tyrosine phosphorylation might be a novel mechanism for cannabinoid-induced functional changes.	Cannabinoids	104-115	PTK2 protein tyrosine kinase 2	Mus musculus	43-47
12190987-0	2002	PKC-regulated myogenesis is associated with increased tyrosine phosphorylation of FAK, Cas, and paxillin, formation of Cas-CRK complex, and JNK activation.	Tyrosine	54-62	PTK2 protein tyrosine kinase 2	Mus musculus	82-85
12190987-5	2002	We showed that, during differentiation, downregulation of PKC expression results in increased tyrosine phosphorylation of FAK, Cas, and paxillin, concomitant with enhanced Cas-CrkII complex formation, which leads to activation of JNK2.	Tyrosine	94-102	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
11784715-8	2002	The prevention of the FAK-paxillin association with U0126 correlated with an inhibition of the HGF-mediated FAK tyrosine phosphorylation and inhibition of HGF-dependent cell spreading and adhesion.	U 0126	52-57	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
12083796-0	2002	Mitogen-induced, FAK-dependent tyrosine phosphorylation of the SSeCKS scaffolding protein.	Tyrosine	31-39	PTK2 protein tyrosine kinase 2	Mus musculus	17-20
12083796-4	2002	Tyrosine phosphorylation of SSeCKS was apparent in cells deficient in Src, Fyn, Yes, or Abl tyrosine kinases or in NIH3T3 cells expressing a temperature-sensitive v-Src allele, but not in FAK-deficient embryo fibroblasts.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	188-191
12083796-11	2002	This correlated with increased coprecipitation of SSeCKS with biotin-phalloidin-bound F-actin from FAK-/- compared to FAK+/+ cell lysates.	Biotin	62-68	PTK2 protein tyrosine kinase 2	Mus musculus	99-102
12083796-11	2002	This correlated with increased coprecipitation of SSeCKS with biotin-phalloidin-bound F-actin from FAK-/- compared to FAK+/+ cell lysates.	Phalloidine	69-79	PTK2 protein tyrosine kinase 2	Mus musculus	99-102
12114453-9	2002	In addition, FNIII14 abrogated the VN-stimulated tyrosine phosphorylation of intracellular signaling proteins, including focal adhesion kinase (p125(FAK)) and paxillin, suggesting that such a diversity of FNIII14 effects might be because of the negative regulation of p125(FAK) and paxillin tyrosine phosphorylation, which has been involved in adhesion signals transduced by different integrins.	Tyrosine	49-57	PTK2 protein tyrosine kinase 2	Mus musculus	144-154
12114453-9	2002	In addition, FNIII14 abrogated the VN-stimulated tyrosine phosphorylation of intracellular signaling proteins, including focal adhesion kinase (p125(FAK)) and paxillin, suggesting that such a diversity of FNIII14 effects might be because of the negative regulation of p125(FAK) and paxillin tyrosine phosphorylation, which has been involved in adhesion signals transduced by different integrins.	Tyrosine	49-57	PTK2 protein tyrosine kinase 2	Mus musculus	144-153
12083484-6	2002	In migrating mouse SMC expressing CD9, focal adhesion kinase (FAK) tyrosine phosphorylation was doubled.	Tyrosine	67-75	PTK2 protein tyrosine kinase 2	Mus musculus	39-60
12083484-6	2002	In migrating mouse SMC expressing CD9, focal adhesion kinase (FAK) tyrosine phosphorylation was doubled.	Tyrosine	67-75	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
11980671-5	2002	Compared with nonneoplastic adult brain biopsies, the levels of FAK protein are elevated as are its levels of activation as assessed by autophosphorylation and overall tyrosine phosphorylation.	Tyrosine	168-176	PTK2 protein tyrosine kinase 2	Mus musculus	64-67
11821402-4	2002	Of the six tyrosine phosphorylation sites in pp125FAK, phosphorylation at position 861 (Tyr-861) was clearly decreased during detransformation by TSA.	Tyrosine	11-19	PTK2 protein tyrosine kinase 2	Mus musculus	45-53
11821402-4	2002	Of the six tyrosine phosphorylation sites in pp125FAK, phosphorylation at position 861 (Tyr-861) was clearly decreased during detransformation by TSA.	Tyrosine	88-91	PTK2 protein tyrosine kinase 2	Mus musculus	45-53
11821402-6	2002	Furthermore, phosphorylation of Tyr-861 was reduced substantially by the Src family kinase inhibitor, PP1, while overexpression of Src kinase increased its phosphorylation, implying that Src kinase regulates phosphorylation of pp125FAK at Tyr-861.	Tyrosine	32-35	PTK2 protein tyrosine kinase 2	Mus musculus	227-235
11821402-6	2002	Furthermore, phosphorylation of Tyr-861 was reduced substantially by the Src family kinase inhibitor, PP1, while overexpression of Src kinase increased its phosphorylation, implying that Src kinase regulates phosphorylation of pp125FAK at Tyr-861.	Tyrosine	239-242	PTK2 protein tyrosine kinase 2	Mus musculus	227-235
11821402-7	2002	All of these findings suggest that increased phosphorylation of pp125FAK at Tyr-861 correlates with Ras-induced transformation of fibroblasts, and TSA is able to detransform them through regulation of pp125FAK phosphorylation at Tyr-861 by an Src family kinase.	Tyrosine	76-79	PTK2 protein tyrosine kinase 2	Mus musculus	64-72
11821402-7	2002	All of these findings suggest that increased phosphorylation of pp125FAK at Tyr-861 correlates with Ras-induced transformation of fibroblasts, and TSA is able to detransform them through regulation of pp125FAK phosphorylation at Tyr-861 by an Src family kinase.	trichostatin A	147-150	PTK2 protein tyrosine kinase 2	Mus musculus	201-209
11821402-7	2002	All of these findings suggest that increased phosphorylation of pp125FAK at Tyr-861 correlates with Ras-induced transformation of fibroblasts, and TSA is able to detransform them through regulation of pp125FAK phosphorylation at Tyr-861 by an Src family kinase.	Tyrosine	229-232	PTK2 protein tyrosine kinase 2	Mus musculus	64-72
11821402-7	2002	All of these findings suggest that increased phosphorylation of pp125FAK at Tyr-861 correlates with Ras-induced transformation of fibroblasts, and TSA is able to detransform them through regulation of pp125FAK phosphorylation at Tyr-861 by an Src family kinase.	Tyrosine	229-232	PTK2 protein tyrosine kinase 2	Mus musculus	201-209
11927607-4	2002	In cultured endothelial cells, VEGF, but not basic fibroblast growth factor, promotes the Src-mediated phosphorylation of FAK on tyrosine 861, which contributes to the formation of a FAK/alpha(v)beta5 signaling complex.	Tyrosine	129-137	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
11927607-4	2002	In cultured endothelial cells, VEGF, but not basic fibroblast growth factor, promotes the Src-mediated phosphorylation of FAK on tyrosine 861, which contributes to the formation of a FAK/alpha(v)beta5 signaling complex.	Tyrosine	129-137	PTK2 protein tyrosine kinase 2	Mus musculus	183-186
11784715-8	2002	The prevention of the FAK-paxillin association with U0126 correlated with an inhibition of the HGF-mediated FAK tyrosine phosphorylation and inhibition of HGF-dependent cell spreading and adhesion.	U 0126	52-57	PTK2 protein tyrosine kinase 2	Mus musculus	22-25
12083796-13	2002	These data suggest that mitogen-induced, FAK-dependent tyrosine phosphorylation of SSeCKS modulates its binding to the actin-based cytoskeleton, suggesting a role for SSeCKS in mitogen-induced cytoskeletal reorganization.	Tyrosine	55-63	PTK2 protein tyrosine kinase 2	Mus musculus	41-44
12027949-0	2002	Focal adhesion kinase tyrosine phosphorylation is associated with myogenesis and modulated by insulin.	Tyrosine	22-30	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
12027949-5	2002	The data strongly indicate that FAK tyrosine phosphorylation, necessary for skeletal muscle differentiation, is modulated by insulin.	Tyrosine	36-44	PTK2 protein tyrosine kinase 2	Mus musculus	32-35
12027949-6	2002	Thus, for the first time, we report the differential regulation of FAK tyrosine phosphorylation by insulin during skeletal muscle differentiation.	Tyrosine	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
11784715-7	2002	HGF induced an increase in paxillin-FAK association that was inhibited by pretreatment with U0126 and reproduced by in vitro phosphorylation of paxillin with ERK.	U 0126	92-97	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
11784715-8	2002	The prevention of the FAK-paxillin association with U0126 correlated with an inhibition of the HGF-mediated FAK tyrosine phosphorylation and inhibition of HGF-dependent cell spreading and adhesion.	Tyrosine	112-120	PTK2 protein tyrosine kinase 2	Mus musculus	22-25
11784715-8	2002	The prevention of the FAK-paxillin association with U0126 correlated with an inhibition of the HGF-mediated FAK tyrosine phosphorylation and inhibition of HGF-dependent cell spreading and adhesion.	Tyrosine	112-120	PTK2 protein tyrosine kinase 2	Mus musculus	108-111
11784715-10	2002	Thus, these data suggest that HGF can induce serine/threonine phosphorylation of paxillin most probably mediated directly by ERK, resulting in the recruitment and activation of FAK and subsequent enhancement of cell spreading and adhesion.	Serine	45-51	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
11784715-10	2002	Thus, these data suggest that HGF can induce serine/threonine phosphorylation of paxillin most probably mediated directly by ERK, resulting in the recruitment and activation of FAK and subsequent enhancement of cell spreading and adhesion.	Threonine	52-61	PTK2 protein tyrosine kinase 2	Mus musculus	177-180
11791180-5	2002	Paxillin null ES cells exhibit delayed spreading on integrin binding substrates fibronectin and laminin, and there is reduced tyrosine phosphorylation of Focal Adhesion Kinase (FAK).	Tyrosine	126-134	PTK2 protein tyrosine kinase 2	Mus musculus	154-175
11791180-8	2002	These results demonstrate that paxillin contributes to attachment-dependent tyrosine phosphorylation of FAK and early cell spreading in ES cells.	Tyrosine	76-84	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
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
11792571-0	2002	Fluoroaluminate stimulates phosphorylation of p130 Cas and Fak and increases attachment and spreading of preosteoblastic MC3T3-E1 cells.	fluoroaluminum	0-15	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
11792571-8	2002	The addition of fluoroaluminate during cell attachment to type I collagen further stimulated phosphorylation of p130 Cas and of Fak.	fluoroaluminum	16-31	PTK2 protein tyrosine kinase 2	Mus musculus	128-131
11444850-1	2001	An early signaling event during the adhesion and spreading of cells is integrin-mediated tyrosine phosphorylation of the cytoskeletal adaptor protein paxillin and the non-receptor tyrosine kinase pp125(FAK) at focal contacts.	Tyrosine	89-97	PTK2 protein tyrosine kinase 2	Mus musculus	202-205
11731413-2	2001	We found that fak +/- heterozygous mice display reduced 7,12-dimethylbenz[a]anthracene-induced papilloma formation that correlates with reduced FAK protein expression in the skin.	7,12-dimethylbenz[a	56-75	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
11731413-2	2001	We found that fak +/- heterozygous mice display reduced 7,12-dimethylbenz[a]anthracene-induced papilloma formation that correlates with reduced FAK protein expression in the skin.	anthracene	76-86	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
11731413-2	2001	We found that fak +/- heterozygous mice display reduced 7,12-dimethylbenz[a]anthracene-induced papilloma formation that correlates with reduced FAK protein expression in the skin.	anthracene	76-86	PTK2 protein tyrosine kinase 2	Mus musculus	144-147
11731413-5	2001	Because 7,12-dimethylbenz[a]anthracene induces an activating mutation of H-ras, this provides one possible explanation for suppression of papilloma formation when FAK protein is limiting.	7,12-dimethylbenz[a]	8-28	PTK2 protein tyrosine kinase 2	Mus musculus	163-166
11731413-5	2001	Because 7,12-dimethylbenz[a]anthracene induces an activating mutation of H-ras, this provides one possible explanation for suppression of papilloma formation when FAK protein is limiting.	anthracene	28-38	PTK2 protein tyrosine kinase 2	Mus musculus	163-166
11468287-1	2001	In hippocampus endocannabinoids modulate synaptic function and plasticity and increase tyrosine phosphorylation of several proteins, including focal adhesion kinase (FAK).	Tyrosine	87-95	PTK2 protein tyrosine kinase 2	Mus musculus	143-164
11468287-1	2001	In hippocampus endocannabinoids modulate synaptic function and plasticity and increase tyrosine phosphorylation of several proteins, including focal adhesion kinase (FAK).	Tyrosine	87-95	PTK2 protein tyrosine kinase 2	Mus musculus	166-169
11468287-2	2001	Autophosphorylation of FAK on Tyr-397 is generally a critical step for its activation, allowing the recruitment of Src family kinases, and phosphorylation of FAK and associated proteins.	Tyrosine	30-33	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
11468287-2	2001	Autophosphorylation of FAK on Tyr-397 is generally a critical step for its activation, allowing the recruitment of Src family kinases, and phosphorylation of FAK and associated proteins.	Tyrosine	30-33	PTK2 protein tyrosine kinase 2	Mus musculus	158-161
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	anandamide	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	133-136
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	anandamide	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	171-174
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	glyceryl 2-arachidonate	15-37	PTK2 protein tyrosine kinase 2	Mus musculus	133-136
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	glyceryl 2-arachidonate	15-37	PTK2 protein tyrosine kinase 2	Mus musculus	171-174
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	Endocannabinoids	43-59	PTK2 protein tyrosine kinase 2	Mus musculus	133-136
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	Dronabinol	65-92	PTK2 protein tyrosine kinase 2	Mus musculus	133-136
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	Dronabinol	65-92	PTK2 protein tyrosine kinase 2	Mus musculus	171-174
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	Tyrosine	105-113	PTK2 protein tyrosine kinase 2	Mus musculus	133-136
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	Tyrosine	105-113	PTK2 protein tyrosine kinase 2	Mus musculus	171-174
11468287-4	2001	Anandamide and 2-arachidonoylglycerol, two endocannabinoids, and Delta9-tetrahydrocannabinol, stimulated tyrosine phosphorylation of FAK+6,7, a neuronal splice isoform of FAK, on several residues including Tyr-397.	Tyrosine	206-209	PTK2 protein tyrosine kinase 2	Mus musculus	133-136
11468287-5	2001	Cannabinoids increased phosphorylation of p130-Cas, a protein associated with FAK, but had no effect on PYK2, a tyrosine kinase related to FAK and enriched in hippocampus.	Cannabinoids	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
11468287-8	2001	PP2, an Src family kinase inhibitor, prevented the effects of cannabinoids on p130-Cas and on FAK+6,7 tyrosines 577 and 925, but not 397, indicating that FAK autophosphorylation was upstream of Src family kinases in response to CB1-R stimulation.	Tyrosine	102-111	PTK2 protein tyrosine kinase 2	Mus musculus	154-157
11513976-3	2001	Here we show that tubulogenesis by BCR-FLTm1 depends on FAK and that FAK tyrosine phosphorylation and association with an activated Flt-1 receptor complex is increased after vascular endothelial growth factor stimulation of NIH3T3 cells overexpressing Flt-1.	Tyrosine	73-81	PTK2 protein tyrosine kinase 2	Mus musculus	69-72
11578694-4	2001	Using the murine macrophage cell line J774, we demonstrate that FcgammaRII-RIII cross-linking induces a time- and dose-dependent increase in tyrosine phosphorylation of the focal adhesion kinase pp125FAK that correlates with an increase in its catalytic activity.	Tyrosine	141-149	PTK2 protein tyrosine kinase 2	Mus musculus	195-203
11359909-8	2001	Consistent with this, FAK tyrosine phosphorylation was reduced in cells from tumors growing in transplanted, athymic, nude mice, which have an intact autocrine regulation of the EGFR.	Tyrosine	26-34	PTK2 protein tyrosine kinase 2	Mus musculus	22-25
11382927-0	2001	Calyculin-A induces focal adhesion assembly and tyrosine phosphorylation of p125(Fak), p130(Cas), and paxillin in Swiss 3T3 cells.	calyculin A	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	81-84
11382927-1	2001	Treatment of intact Swiss 3T3 cells with calyculin-A, an inhibitor of myosin light chain (MLC) phosphatase, induces tyrosine phosphorylation of p125(Fak) in a sharply concentration- and time-dependent manner.	calyculin A	41-52	PTK2 protein tyrosine kinase 2	Mus musculus	149-152
11382927-1	2001	Treatment of intact Swiss 3T3 cells with calyculin-A, an inhibitor of myosin light chain (MLC) phosphatase, induces tyrosine phosphorylation of p125(Fak) in a sharply concentration- and time-dependent manner.	Tyrosine	116-124	PTK2 protein tyrosine kinase 2	Mus musculus	149-152
11382927-3	2001	The stimulatory effect of calyculin-A was observed at low nanomolar concentrations (<10 nM); at higher concentrations (>10 nM) tyrosine phosphorylation of p125(Fak) was strikingly decreased.	calyculin A	26-37	PTK2 protein tyrosine kinase 2	Mus musculus	166-169
11382927-4	2001	Calyculin-A induced tyrosine phosphorylation of p125(Fak) through a protein kinase C- and Ca(2+)-independent pathway.	calyculin A	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
11382927-4	2001	Calyculin-A induced tyrosine phosphorylation of p125(Fak) through a protein kinase C- and Ca(2+)-independent pathway.	Tyrosine	20-28	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
11382927-10	2001	Thus, calyculin-A induces transient focal adhesion assembly and tyrosine phosphorylation of p125(Fak), p130(Cas), and paxillin, acting downstream of ROK.	calyculin A	6-17	PTK2 protein tyrosine kinase 2	Mus musculus	97-100
11399057-0	2001	Y-27632, an inhibitor of Rho-associated kinases, prevents tyrosine phosphorylation of focal adhesion kinase and paxillin induced by bombesin: dissociation from tyrosine phosphorylation of p130(CAS).	Y 27632	0-7	PTK2 protein tyrosine kinase 2	Mus musculus	86-107
11399057-0	2001	Y-27632, an inhibitor of Rho-associated kinases, prevents tyrosine phosphorylation of focal adhesion kinase and paxillin induced by bombesin: dissociation from tyrosine phosphorylation of p130(CAS).	Tyrosine	58-66	PTK2 protein tyrosine kinase 2	Mus musculus	86-107
11399057-1	2001	A rapid increase in tyrosine phosphorylation of focal adhesion kinase (FAK), paxillin, and Crk-associated substrate (CAS) are prominent early events triggered by many G protein-coupled receptors (GPCRs), but the mechanisms involved remain unclear.	Tyrosine	20-28	PTK2 protein tyrosine kinase 2	Mus musculus	48-69
11399057-1	2001	A rapid increase in tyrosine phosphorylation of focal adhesion kinase (FAK), paxillin, and Crk-associated substrate (CAS) are prominent early events triggered by many G protein-coupled receptors (GPCRs), but the mechanisms involved remain unclear.	Tyrosine	20-28	PTK2 protein tyrosine kinase 2	Mus musculus	71-74
11399057-2	2001	Here, we examined whether the Rho-associated protein serine/threonine kinase family (ROCK) is a critical Rho effector in the pathway that links GPCR activation to the tyrosine phosphorylation of FAK, CAS, and paxillin.	Tyrosine	167-175	PTK2 protein tyrosine kinase 2	Mus musculus	195-198
11399057-3	2001	Treatment of Swiss 3T3 cells with Y-27632, a preferential inhibitor of ROCK, dramatically inhibited the formation of actin stress fibers, the assembly of focal contacts, and the increase in tyrosine phosphorylation of FAK and paxillin induced by bombesin in these cells.	Y 27632	34-41	PTK2 protein tyrosine kinase 2	Mus musculus	218-221
11399057-3	2001	Treatment of Swiss 3T3 cells with Y-27632, a preferential inhibitor of ROCK, dramatically inhibited the formation of actin stress fibers, the assembly of focal contacts, and the increase in tyrosine phosphorylation of FAK and paxillin induced by bombesin in these cells.	Tyrosine	190-198	PTK2 protein tyrosine kinase 2	Mus musculus	218-221
11399057-5	2001	HA-1077, a preferential inhibitor of ROCK activity structurally unrelated to Y-27632, also attenuated the increase in the tyrosine phosphorylation of FAK and paxillin but did not affect the tyrosine phosphorylation of CAS induced by bombesin in Swiss 3T3 cells.	fasudil	0-7	PTK2 protein tyrosine kinase 2	Mus musculus	150-153
11399057-5	2001	HA-1077, a preferential inhibitor of ROCK activity structurally unrelated to Y-27632, also attenuated the increase in the tyrosine phosphorylation of FAK and paxillin but did not affect the tyrosine phosphorylation of CAS induced by bombesin in Swiss 3T3 cells.	Tyrosine	122-130	PTK2 protein tyrosine kinase 2	Mus musculus	150-153
11399057-6	2001	The results demonstrate that ROCK-dependent tyrosine phosphorylation of FAK and paxillin can be dissociated from a ROCK-independent pathway leading to tyrosine phosphorylation of CAS.	Tyrosine	44-52	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
10891511-0	2000	The cytoplasmic tyrosines of integrin subunit beta1 are involved in focal adhesion kinase activation.	Tyrosine	16-25	PTK2 protein tyrosine kinase 2	Mus musculus	68-89
11314030-6	2001	Such mutants, Crk Delta255 or Crk Delta242 Extended Linker (Crk Delta242([EL])), characterized by a disruption in the SH3 linker/C-terminal SH3 boundary, induced robust hyperphosphorylation of focal adhesion kinase (FAK) on Tyr(397), hyperphosphorylation of focal adhesion proteins p130(cas) and paxillin and increased focal adhesion formation in NIH3T3 cells.	Tyrosine	224-227	PTK2 protein tyrosine kinase 2	Mus musculus	193-214
11746506-6	2001	In addition, EGCG significantly inhibited the tyrosine phosphorylation of focal adhesion kinase (FAK) and the activity of matrix metalloproteinase-9 (MMP-9).	epigallocatechin gallate	13-17	PTK2 protein tyrosine kinase 2	Mus musculus	74-95
11746506-6	2001	In addition, EGCG significantly inhibited the tyrosine phosphorylation of focal adhesion kinase (FAK) and the activity of matrix metalloproteinase-9 (MMP-9).	epigallocatechin gallate	13-17	PTK2 protein tyrosine kinase 2	Mus musculus	97-100
11746506-6	2001	In addition, EGCG significantly inhibited the tyrosine phosphorylation of focal adhesion kinase (FAK) and the activity of matrix metalloproteinase-9 (MMP-9).	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	74-95
11746506-6	2001	In addition, EGCG significantly inhibited the tyrosine phosphorylation of focal adhesion kinase (FAK) and the activity of matrix metalloproteinase-9 (MMP-9).	Tyrosine	46-54	PTK2 protein tyrosine kinase 2	Mus musculus	97-100
11746506-9	2001	These results demonstrate that combination treatment with EGCG and dacarbazine strongly inhibits melanoma growth and metastasis, and the action mechanisms of EGCG are associated with the inhibition of cell spreading, cell-extracellular matrix and cell-cell interactions, MMP-9 and FAK activities.	epigallocatechin gallate	158-162	PTK2 protein tyrosine kinase 2	Mus musculus	281-284
11279163-1	2001	Plating suspended Swiss 3T3 cells onto fibronectin-coated dishes promoted phosphorylation of endogenous focal adhesion kinase (FAK) at Tyr-397, the major autophosphorylation site, and at Tyr-577, located in the activation loop, as revealed by site-specific antibodies that recognize the phosphorylated form of these residues.	Tyrosine	135-138	PTK2 protein tyrosine kinase 2	Mus musculus	127-130
11279163-1	2001	Plating suspended Swiss 3T3 cells onto fibronectin-coated dishes promoted phosphorylation of endogenous focal adhesion kinase (FAK) at Tyr-397, the major autophosphorylation site, and at Tyr-577, located in the activation loop, as revealed by site-specific antibodies that recognize the phosphorylated form of these residues.	Tyrosine	187-190	PTK2 protein tyrosine kinase 2	Mus musculus	127-130
11279163-3	2001	Furthermore, fibronectin-mediated FAK phosphorylation at Tyr-397 was dramatically reduced in SYF cells (deficient in Src, Yes, and Fyn expression).	Tyrosine	57-60	PTK2 protein tyrosine kinase 2	Mus musculus	34-37
11279163-4	2001	Stimulation of Swiss 3T3 cells with bombesin also induced a rapid increase in the phosphorylation of endogenous FAK at Tyr-397.	Tyrosine	119-122	PTK2 protein tyrosine kinase 2	Mus musculus	112-115
11279163-7	2001	Lysophosphatidic acid also induced FAK phosphorylation at Tyr-397 in SYF cells.	lysophosphatidic acid	0-21	PTK2 protein tyrosine kinase 2	Mus musculus	35-38
11279163-7	2001	Lysophosphatidic acid also induced FAK phosphorylation at Tyr-397 in SYF cells.	Tyrosine	58-61	PTK2 protein tyrosine kinase 2	Mus musculus	35-38
11279163-8	2001	Our results identify, for first time, the existence of Src-dependent and Src-independent pathways leading to FAK autophosphorylation at Tyr-397 stimulated by adhesion-dependent signals and G protein-coupled receptor agonists in the same cell.	Tyrosine	136-139	PTK2 protein tyrosine kinase 2	Mus musculus	109-112
11196148-0	2001	(+)-Catechin inhibits intestinal tumor formation and suppresses focal adhesion kinase activation in the min/+ mouse.	Catechin	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	64-85
11196148-7	2001	Mechanistic studies linked this effect to (+)-catechin-induced changes in integrin-mediated intestinal cell-survival signaling, including structural alteration of the actin cytoskeleton and decreased focal adhesion kinase (FAK) tyrosine phosphorylation.	Catechin	42-54	PTK2 protein tyrosine kinase 2	Mus musculus	200-221
11196148-7	2001	Mechanistic studies linked this effect to (+)-catechin-induced changes in integrin-mediated intestinal cell-survival signaling, including structural alteration of the actin cytoskeleton and decreased focal adhesion kinase (FAK) tyrosine phosphorylation.	Catechin	42-54	PTK2 protein tyrosine kinase 2	Mus musculus	223-226
11196148-7	2001	Mechanistic studies linked this effect to (+)-catechin-induced changes in integrin-mediated intestinal cell-survival signaling, including structural alteration of the actin cytoskeleton and decreased focal adhesion kinase (FAK) tyrosine phosphorylation.	Tyrosine	228-236	PTK2 protein tyrosine kinase 2	Mus musculus	223-226
11196148-9	2001	Confirming the relevance of this signaling pathway, treatment of Min/+ mice with (+)-catechin reduced the expression of phosphorylated FAK to a level similar to the wild-type littermate controls.	Catechin	81-93	PTK2 protein tyrosine kinase 2	Mus musculus	135-138
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
10880515-6	2000	These include bombesin-induced assembly of focal adhesions, formation of parallel arrays of actin stress fibers, increase in the tyrosine phosphorylation of focal adhesion kinase (FAK), p130(Cas), and paxillin, and formation of a complex between FAK and Src.	Tyrosine	129-137	PTK2 protein tyrosine kinase 2	Mus musculus	157-178
10880515-6	2000	These include bombesin-induced assembly of focal adhesions, formation of parallel arrays of actin stress fibers, increase in the tyrosine phosphorylation of focal adhesion kinase (FAK), p130(Cas), and paxillin, and formation of a complex between FAK and Src.	Tyrosine	129-137	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
10931187-0	2000	Echistatin inhibits pp125FAK autophosphorylation, paxillin phosphorylation and pp125FAK-paxillin interaction in fibronectin-adherent melanoma cells.	echistatin	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	20-28
10931187-0	2000	Echistatin inhibits pp125FAK autophosphorylation, paxillin phosphorylation and pp125FAK-paxillin interaction in fibronectin-adherent melanoma cells.	echistatin	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	79-87
10931187-1	2000	Echistatin, a snake-venom RGD-containing protein, was previously shown to disrupt cell-matrix adhesion by a mechanism that involves the reduction of pp125FAK tyrosine phosphorylation levels.	Tyrosine	158-166	PTK2 protein tyrosine kinase 2	Mus musculus	149-157
10931187-2	2000	The aim of this study was to establish the sequence of events downstream pp125FAK dephosphorylation that could be responsible for echistatin-induced disassembly of actin cytoskeleton and focal adhesions in fibronectin-adherent B16-BL6 melanoma cells.	echistatin	130-140	PTK2 protein tyrosine kinase 2	Mus musculus	73-81
10931187-3	2000	The results obtained show that echistatin induces a decrease of both autophosphorylation and kinase activity of pp125FAK.	echistatin	31-41	PTK2 protein tyrosine kinase 2	Mus musculus	112-120
10931187-4	2000	One hour of cell exposure to echistatin caused a 39% decrease of pp125FAK Tyr397 phosphorylation and a 31% reduction of pp125FAK autophosphorylation activity as measured by immune-complex kinase assay.	echistatin	29-39	PTK2 protein tyrosine kinase 2	Mus musculus	65-73
10931187-4	2000	One hour of cell exposure to echistatin caused a 39% decrease of pp125FAK Tyr397 phosphorylation and a 31% reduction of pp125FAK autophosphorylation activity as measured by immune-complex kinase assay.	echistatin	29-39	PTK2 protein tyrosine kinase 2	Mus musculus	120-128
10931187-5	2000	Furthermore, 1 h of cell treatment by echistatin produced a 63% decrease of paxillin phosphorylation, as well as a reduction in the amount of paxillin bound to pp125FAK.	echistatin	38-48	PTK2 protein tyrosine kinase 2	Mus musculus	160-168
10931187-6	2000	Immunofluorescence analysis of echistatin treated cells showed the concomitant disappearance of both paxillin and pp125FAK from focal adhesions.	echistatin	31-41	PTK2 protein tyrosine kinase 2	Mus musculus	114-122
10891511-3	2000	Focal adhesion kinase (FAK) tyrosine phosphorylation and activation were severely impaired in response to beta1-dependent adhesion in GD25-beta1A(Y783/795F) cells compared to that in wild-type GD25-beta1A or mutants in which only a single tyrosine was altered (beta1A(Y783F) or beta1A(Y795F)).	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
10891511-3	2000	Focal adhesion kinase (FAK) tyrosine phosphorylation and activation were severely impaired in response to beta1-dependent adhesion in GD25-beta1A(Y783/795F) cells compared to that in wild-type GD25-beta1A or mutants in which only a single tyrosine was altered (beta1A(Y783F) or beta1A(Y795F)).	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
10891511-3	2000	Focal adhesion kinase (FAK) tyrosine phosphorylation and activation were severely impaired in response to beta1-dependent adhesion in GD25-beta1A(Y783/795F) cells compared to that in wild-type GD25-beta1A or mutants in which only a single tyrosine was altered (beta1A(Y783F) or beta1A(Y795F)).	Tyrosine	239-247	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
10891511-3	2000	Focal adhesion kinase (FAK) tyrosine phosphorylation and activation were severely impaired in response to beta1-dependent adhesion in GD25-beta1A(Y783/795F) cells compared to that in wild-type GD25-beta1A or mutants in which only a single tyrosine was altered (beta1A(Y783F) or beta1A(Y795F)).	Tyrosine	239-247	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
10891511-5	2000	Indeed, beta1A-dependent tyrosine phosphorylation of tensin and paxillin was lost in the beta1A(Y783/795F) cells, consistent with the impairment in FAK activation.	Tyrosine	25-33	PTK2 protein tyrosine kinase 2	Mus musculus	148-151
10891511-9	2000	These observations argue that tyrosines 783 and 795 within the cytoplasmic tail of integrin subunit beta1A are critical mediators of FAK activation and cell spreading in GD25 cells.	Tyrosine	30-39	PTK2 protein tyrosine kinase 2	Mus musculus	133-136
10737896-0	2000	Tyrosine phosphorylation of p125(Fak), p130(Cas), and paxillin does not require extracellular signal-regulated kinase activation in Swiss 3T3 cells stimulated by bombesin or platelet-derived growth factor.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	33-36
10809752-1	2000	GM3 ganglioside at the surface of mouse melanoma B16 cells is clustered and organized with signal transducer molecules c-Src, Rho A, and focal adhesion kinase (FAK) to form a membrane unit separable from caveolae, which are enriched in cholesterol and caveolin but do not contain GM3 or the above three signal transducers.	Cholesterol	236-247	PTK2 protein tyrosine kinase 2	Mus musculus	160-163
10809752-2	2000	The GM3-enriched membrane units are involved in GM3-dependent cell adhesion coupled with activation of c-Src, Rho A, and FAK and are termed the "glycosphingolipid signaling domain" or the "glycosignaling domain" (GSD).	Glycosphingolipids	145-162	PTK2 protein tyrosine kinase 2	Mus musculus	121-124
10737896-1	2000	The experiments presented here were designed to examine the contribution of the extracellular signal-regulated mitogen-activated protein kinases (ERKs) to the tyrosine phosphorylation of the focal adhesion proteins p125(Fak), p130(Cas), and paxillin induced by G protein-coupled receptors (GPCRs) and tyrosine kinase receptors in Swiss 3T3 cells.	Tyrosine	159-167	PTK2 protein tyrosine kinase 2	Mus musculus	220-223
10737896-3	2000	Exposure of the cells to two structurally unrelated mitogen-activated protein kinase or ERK kinase (MEK) inhibitors, PD98059 and U0126, completely abrogated ERK activation but did not prevent tyrosine phosphorylation of p125(Fak), p130(Cas), and paxillin.	U 0126	129-134	PTK2 protein tyrosine kinase 2	Mus musculus	225-228
10559474-3	1999	Cytostatin inhibited tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin upon B16 cell adhesion to fibronectin.	cytostatin	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	49-70
11019781-3	2000	In addition, FGF-1-transduced fibroblasts demonstrated a > 10-fold increase in migration, an observation correlated with increased tyrosine phosphorylation of p125FAK and p130CAS.	Tyrosine	134-142	PTK2 protein tyrosine kinase 2	Mus musculus	162-169
10818470-2	2000	We found that EDG-5-induced Rho activation followed by enhanced tyrosine phosphorylation of FAK and paxillin, and beta 1-integrin activation leading to overexpression of focal adhesion sites, as well as increment of stress fiber formation, must be the molecular basis of inhibition of haptotactic cell motility by Sph-1-P.	Tyrosine	64-72	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
10623465-9	2000	Stimulation of tyrosine phosphorylation on FAK, p130(Cas), and paxillin by adhesion via integrin alphaVbeta3 to fibronectin or vitronectin was not disturbed in GD25-beta1B cells compared to the untransfected GD25 cells, nor were any negative effects of beta1B observed on alphaVbeta3-mediated cell attachment, spreading, and actin organization, or on the cell proliferation rate.	Tyrosine	15-23	PTK2 protein tyrosine kinase 2	Mus musculus	43-46
10559474-3	1999	Cytostatin inhibited tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin upon B16 cell adhesion to fibronectin.	cytostatin	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
10559474-3	1999	Cytostatin inhibited tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin upon B16 cell adhesion to fibronectin.	Tyrosine	21-29	PTK2 protein tyrosine kinase 2	Mus musculus	49-70
10559474-3	1999	Cytostatin inhibited tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin upon B16 cell adhesion to fibronectin.	Tyrosine	21-29	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
10430888-2	1999	Integrin-ligand interactions stimulate FAK tyrosine phosphorylation and activation of FAK signaling functions.	Tyrosine	43-51	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
10497197-1	1999	Stimulation of quiescent Swiss 3T3 cells with bombesin induces a rapid increase in the formation of complexes between focal adhesion kinase (FAK) and Src family members, which can be extracted with a buffer containing Triton, deoxycholate, and SDS but not with a buffer containing Triton alone.	Deoxycholic Acid	226-238	PTK2 protein tyrosine kinase 2	Mus musculus	118-139
10497197-1	1999	Stimulation of quiescent Swiss 3T3 cells with bombesin induces a rapid increase in the formation of complexes between focal adhesion kinase (FAK) and Src family members, which can be extracted with a buffer containing Triton, deoxycholate, and SDS but not with a buffer containing Triton alone.	Deoxycholic Acid	226-238	PTK2 protein tyrosine kinase 2	Mus musculus	141-144
10497197-1	1999	Stimulation of quiescent Swiss 3T3 cells with bombesin induces a rapid increase in the formation of complexes between focal adhesion kinase (FAK) and Src family members, which can be extracted with a buffer containing Triton, deoxycholate, and SDS but not with a buffer containing Triton alone.	Sodium Dodecyl Sulfate	244-247	PTK2 protein tyrosine kinase 2	Mus musculus	118-139
10497197-1	1999	Stimulation of quiescent Swiss 3T3 cells with bombesin induces a rapid increase in the formation of complexes between focal adhesion kinase (FAK) and Src family members, which can be extracted with a buffer containing Triton, deoxycholate, and SDS but not with a buffer containing Triton alone.	Sodium Dodecyl Sulfate	244-247	PTK2 protein tyrosine kinase 2	Mus musculus	141-144
10497197-3	1999	Bradykinin, endothelin, and lysophosphatidic acid also stimulated FAK-Src complex formation.	lysophosphatidic acid	28-49	PTK2 protein tyrosine kinase 2	Mus musculus	66-69
10497197-4	1999	Bombesin stimulated FAK/Src association through a Ca(2+) and phosphatidylinositol 3"-kinase-independent pathway that requires the integrity of the actin filament network and is partly dependent on functional protein kinase C. Treatment with the selective Src kinase inhibitor PP-2 inhibited both FAK activation and phosphorylation of FAK at Tyr(577) induced by bombesin in intact cells.	Phosphatidylinositols	61-81	PTK2 protein tyrosine kinase 2	Mus musculus	20-23
10497197-4	1999	Bombesin stimulated FAK/Src association through a Ca(2+) and phosphatidylinositol 3"-kinase-independent pathway that requires the integrity of the actin filament network and is partly dependent on functional protein kinase C. Treatment with the selective Src kinase inhibitor PP-2 inhibited both FAK activation and phosphorylation of FAK at Tyr(577) induced by bombesin in intact cells.	Tyrosine	341-344	PTK2 protein tyrosine kinase 2	Mus musculus	20-23
10446223-3	1999	Here, we report that the SH2 domain of Grb7 can directly interact with FAK through Tyr-397, a major autophosphorylation site in vitro and in vivo.	Tyrosine	83-86	PTK2 protein tyrosine kinase 2	Mus musculus	71-74
10583594-2	1999	In this report we demonstrate that the activation of murine mast cells through alphav-integrin, as well as through the high affinity immunoglobulin E (IgE) receptor (FcepsilonRI), results in enhanced tyrosine phosphorylation of focal adhesion kinase (FAK), a cytoplasmic protein tyrosine kinase involved in mitogenic and oncogenic signal transduction.	Tyrosine	200-208	PTK2 protein tyrosine kinase 2	Mus musculus	228-249
10583594-2	1999	In this report we demonstrate that the activation of murine mast cells through alphav-integrin, as well as through the high affinity immunoglobulin E (IgE) receptor (FcepsilonRI), results in enhanced tyrosine phosphorylation of focal adhesion kinase (FAK), a cytoplasmic protein tyrosine kinase involved in mitogenic and oncogenic signal transduction.	Tyrosine	200-208	PTK2 protein tyrosine kinase 2	Mus musculus	251-254
10583594-7	1999	Protein kinase C depletion in mast cells and calcium depletion in the medium caused decreased tyrosine phosphorylation of FAK, indicating that optimal tyrosine phosphorylation of FAK is regulated by both pathways.	Calcium	45-52	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
10583594-7	1999	Protein kinase C depletion in mast cells and calcium depletion in the medium caused decreased tyrosine phosphorylation of FAK, indicating that optimal tyrosine phosphorylation of FAK is regulated by both pathways.	Calcium	45-52	PTK2 protein tyrosine kinase 2	Mus musculus	179-182
10583594-7	1999	Protein kinase C depletion in mast cells and calcium depletion in the medium caused decreased tyrosine phosphorylation of FAK, indicating that optimal tyrosine phosphorylation of FAK is regulated by both pathways.	Tyrosine	94-102	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
10583594-7	1999	Protein kinase C depletion in mast cells and calcium depletion in the medium caused decreased tyrosine phosphorylation of FAK, indicating that optimal tyrosine phosphorylation of FAK is regulated by both pathways.	Tyrosine	94-102	PTK2 protein tyrosine kinase 2	Mus musculus	179-182
10583594-7	1999	Protein kinase C depletion in mast cells and calcium depletion in the medium caused decreased tyrosine phosphorylation of FAK, indicating that optimal tyrosine phosphorylation of FAK is regulated by both pathways.	Tyrosine	151-159	PTK2 protein tyrosine kinase 2	Mus musculus	122-125
10583594-7	1999	Protein kinase C depletion in mast cells and calcium depletion in the medium caused decreased tyrosine phosphorylation of FAK, indicating that optimal tyrosine phosphorylation of FAK is regulated by both pathways.	Tyrosine	151-159	PTK2 protein tyrosine kinase 2	Mus musculus	179-182
10583594-8	1999	These data are consistent with the conclusion that the tyrosine phosphorylation of FAK represents at least one example of a point of convergence in the intracellular tyrosine phosphorylation cascades induced by alphav integrin-and FcepsilonRI-mediated signal transduction pathways in mast cells.	Tyrosine	55-63	PTK2 protein tyrosine kinase 2	Mus musculus	83-86
10583594-8	1999	These data are consistent with the conclusion that the tyrosine phosphorylation of FAK represents at least one example of a point of convergence in the intracellular tyrosine phosphorylation cascades induced by alphav integrin-and FcepsilonRI-mediated signal transduction pathways in mast cells.	Tyrosine	166-174	PTK2 protein tyrosine kinase 2	Mus musculus	83-86
10430888-3	1999	Here evidence is presented that the FAK autophosphorylation site Tyr-397 mediates a direct interaction with the C-terminal Src homology 2 domain of phospholipase C (PLC)-gamma1 and that this is required for both adhesion-dependent association of the two molecules and increased inositol phosphate production in mouse embryo fibroblasts.	Tyrosine	65-68	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
10430888-3	1999	Here evidence is presented that the FAK autophosphorylation site Tyr-397 mediates a direct interaction with the C-terminal Src homology 2 domain of phospholipase C (PLC)-gamma1 and that this is required for both adhesion-dependent association of the two molecules and increased inositol phosphate production in mouse embryo fibroblasts.	Inositol Phosphates	278-296	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
10430888-4	1999	Overexpression of FAK and PLC-gamma1 in COS-7 cells increases PLC-gamma1 enzymatic activity and tyrosine phosphorylation, also dependent on FAK Tyr-397.	carbonyl sulfide	40-43	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
10430888-4	1999	Overexpression of FAK and PLC-gamma1 in COS-7 cells increases PLC-gamma1 enzymatic activity and tyrosine phosphorylation, also dependent on FAK Tyr-397.	Tyrosine	96-104	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
10430888-4	1999	Overexpression of FAK and PLC-gamma1 in COS-7 cells increases PLC-gamma1 enzymatic activity and tyrosine phosphorylation, also dependent on FAK Tyr-397.	Tyrosine	144-147	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
10430888-4	1999	Overexpression of FAK and PLC-gamma1 in COS-7 cells increases PLC-gamma1 enzymatic activity and tyrosine phosphorylation, also dependent on FAK Tyr-397.	Tyrosine	144-147	PTK2 protein tyrosine kinase 2	Mus musculus	140-143
10228160-7	1999	Fibronectin-induced tyrosine phosphorylation of focal adhesion proteins, including the focal adhesion kinase FAK, was nearly eliminated in the absence of Src, Yes and Fyn.	Tyrosine	20-28	PTK2 protein tyrosine kinase 2	Mus musculus	109-112
10417825-4	1999	Focal adhesion kinase (FAK)(p125) and paxillin(p68) were highly expressed and tyrosine phosphorylated during development but declined to low levels following renal maturation (postnatal day 20) in normal mice.	Tyrosine	78-86	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
10417825-4	1999	Focal adhesion kinase (FAK)(p125) and paxillin(p68) were highly expressed and tyrosine phosphorylated during development but declined to low levels following renal maturation (postnatal day 20) in normal mice.	Tyrosine	78-86	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
10417825-7	1999	In kidneys from postnatal day 20 bcl-2 -/- mice, tyrosine phosphorylation of p125 FAK and p68 paxillin was not down-regulated.	Tyrosine	49-57	PTK2 protein tyrosine kinase 2	Mus musculus	77-85
10457217-0	1999	Glomerular overexpression and increased tyrosine phosphorylation of focal adhesion kinase p125FAK in lupus-prone MRL/MP-lpr/lpr mice.	Tyrosine	40-48	PTK2 protein tyrosine kinase 2	Mus musculus	90-97
10457217-8	1999	FAK in MRL-lpr glomeruli is highly tyrosine phosphorylated and is associated with adapter protein Grb2.	Tyrosine	35-43	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
10427099-8	1999	On the other hand, clustering of tetraspanins in cells attached to collagen enhanced tyrosine phosphorylation of FAK.	Tyrosine	85-93	PTK2 protein tyrosine kinase 2	Mus musculus	113-116
10427099-9	1999	Furthermore, ectopic expression of CD9 in fibrosarcoma cells affected adhesion-induced tyrosine phosphorylation of FAK, that correlated with the reorganization of the cortical actin cytoskeleton.	Tyrosine	87-95	PTK2 protein tyrosine kinase 2	Mus musculus	115-118
10373530-0	1999	Induced focal adhesion kinase (FAK) expression in FAK-null cells enhances cell spreading and migration requiring both auto- and activation loop phosphorylation sites and inhibits adhesion-dependent tyrosine phosphorylation of Pyk2.	Tyrosine	198-206	PTK2 protein tyrosine kinase 2	Mus musculus	8-29
10373530-0	1999	Induced focal adhesion kinase (FAK) expression in FAK-null cells enhances cell spreading and migration requiring both auto- and activation loop phosphorylation sites and inhibits adhesion-dependent tyrosine phosphorylation of Pyk2.	Tyrosine	198-206	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
10373530-0	1999	Induced focal adhesion kinase (FAK) expression in FAK-null cells enhances cell spreading and migration requiring both auto- and activation loop phosphorylation sites and inhibits adhesion-dependent tyrosine phosphorylation of Pyk2.	Tyrosine	198-206	PTK2 protein tyrosine kinase 2	Mus musculus	50-53
10373530-2	1999	Following cell adhesion to components of the extracellular matrix, FAK becomes phosphorylated at multiple sites, including tyrosines 397, 576, and 577.	Tyrosine	123-132	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
10373530-7	1999	Using these Tet-FAK cells, we demonstrated that both the FAK autophosphorylation and activation loop sites are critical for maximum adhesion-induced FAK activation and FAK-enhanced cell spreading and migration responses.	tetramethylenedisulfotetramine	12-15	PTK2 protein tyrosine kinase 2	Mus musculus	16-19
10373530-7	1999	Using these Tet-FAK cells, we demonstrated that both the FAK autophosphorylation and activation loop sites are critical for maximum adhesion-induced FAK activation and FAK-enhanced cell spreading and migration responses.	tetramethylenedisulfotetramine	12-15	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
10373530-7	1999	Using these Tet-FAK cells, we demonstrated that both the FAK autophosphorylation and activation loop sites are critical for maximum adhesion-induced FAK activation and FAK-enhanced cell spreading and migration responses.	tetramethylenedisulfotetramine	12-15	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
10373530-7	1999	Using these Tet-FAK cells, we demonstrated that both the FAK autophosphorylation and activation loop sites are critical for maximum adhesion-induced FAK activation and FAK-enhanced cell spreading and migration responses.	tetramethylenedisulfotetramine	12-15	PTK2 protein tyrosine kinase 2	Mus musculus	57-60
9973229-0	1999	Focal adhesion kinase-dependent apoptosis of melanoma induced by tyrosine and phenylalanine deficiency.	Tyrosine	65-73	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
10331747-5	1999	Immune complex kinase assays and metabolic labeling with [32P]orthophosphate also revealed the specific loss of pp125FAK-associated proteins in the metastatic keratinocytes.	Phosphate-32P	57-76	PTK2 protein tyrosine kinase 2	Mus musculus	112-120
9973229-5	1999	Expression and Tyr phosphorylation of focal adhesion kinase (FAK) were inhibited in both melanoma cell lines by deprivation of Tyr and Phe but not by deprivation of glutamine or serum.	Tyrosine	15-18	PTK2 protein tyrosine kinase 2	Mus musculus	38-59
9973229-5	1999	Expression and Tyr phosphorylation of focal adhesion kinase (FAK) were inhibited in both melanoma cell lines by deprivation of Tyr and Phe but not by deprivation of glutamine or serum.	Tyrosine	15-18	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
9973229-5	1999	Expression and Tyr phosphorylation of focal adhesion kinase (FAK) were inhibited in both melanoma cell lines by deprivation of Tyr and Phe but not by deprivation of glutamine or serum.	Tyrosine	127-130	PTK2 protein tyrosine kinase 2	Mus musculus	38-59
9973229-5	1999	Expression and Tyr phosphorylation of focal adhesion kinase (FAK) were inhibited in both melanoma cell lines by deprivation of Tyr and Phe but not by deprivation of glutamine or serum.	Tyrosine	127-130	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
9973229-5	1999	Expression and Tyr phosphorylation of focal adhesion kinase (FAK) were inhibited in both melanoma cell lines by deprivation of Tyr and Phe but not by deprivation of glutamine or serum.	Phenylalanine	135-138	PTK2 protein tyrosine kinase 2	Mus musculus	38-59
9973229-5	1999	Expression and Tyr phosphorylation of focal adhesion kinase (FAK) were inhibited in both melanoma cell lines by deprivation of Tyr and Phe but not by deprivation of glutamine or serum.	Phenylalanine	135-138	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
9973229-5	1999	Expression and Tyr phosphorylation of focal adhesion kinase (FAK) were inhibited in both melanoma cell lines by deprivation of Tyr and Phe but not by deprivation of glutamine or serum.	Glutamine	165-174	PTK2 protein tyrosine kinase 2	Mus musculus	38-59
9973229-6	1999	Tyr phosphorylation of FAK in Tyr- and Phe-deprived melanoma cells was enhanced within 30 min of refeeding with complete DMEM.	Tyrosine	0-3	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
9973229-6	1999	Tyr phosphorylation of FAK in Tyr- and Phe-deprived melanoma cells was enhanced within 30 min of refeeding with complete DMEM.	Tyrosine	30-33	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
9973229-6	1999	Tyr phosphorylation of FAK in Tyr- and Phe-deprived melanoma cells was enhanced within 30 min of refeeding with complete DMEM.	Phenylalanine	39-42	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
9973229-6	1999	Tyr phosphorylation of FAK in Tyr- and Phe-deprived melanoma cells was enhanced within 30 min of refeeding with complete DMEM.	dmem	121-125	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
9973229-7	1999	FAK protein expression recovered within 60 min, and cell viability recovered within 24 h. Genistein, a tyrosine kinase inhibitor that specifically inhibits Tyr phosphorylation of FAK, did not induce apoptosis in A375 melanoma cells at a concentration of 50 microM.	Genistein	90-99	PTK2 protein tyrosine kinase 2	Mus musculus	179-182
9973229-7	1999	FAK protein expression recovered within 60 min, and cell viability recovered within 24 h. Genistein, a tyrosine kinase inhibitor that specifically inhibits Tyr phosphorylation of FAK, did not induce apoptosis in A375 melanoma cells at a concentration of 50 microM.	Tyrosine	156-159	PTK2 protein tyrosine kinase 2	Mus musculus	179-182
9973229-9	1999	These data collectively indicate that apoptosis induced by Tyr and Phe deprivation is FAK-dependent.	Tyrosine	59-62	PTK2 protein tyrosine kinase 2	Mus musculus	86-89
9973229-9	1999	These data collectively indicate that apoptosis induced by Tyr and Phe deprivation is FAK-dependent.	Phenylalanine	67-70	PTK2 protein tyrosine kinase 2	Mus musculus	86-89
9837978-2	1998	We have demonstrated previously that growth hormone (GH) activates focal adhesion kinase (FAK), and this activation results in the tyrosine phosphorylation of two FAK substrates, namely paxillin and tensin.	Tyrosine	131-139	PTK2 protein tyrosine kinase 2	Mus musculus	67-88
9837978-2	1998	We have demonstrated previously that growth hormone (GH) activates focal adhesion kinase (FAK), and this activation results in the tyrosine phosphorylation of two FAK substrates, namely paxillin and tensin.	Tyrosine	131-139	PTK2 protein tyrosine kinase 2	Mus musculus	90-93
9837978-2	1998	We have demonstrated previously that growth hormone (GH) activates focal adhesion kinase (FAK), and this activation results in the tyrosine phosphorylation of two FAK substrates, namely paxillin and tensin.	Tyrosine	131-139	PTK2 protein tyrosine kinase 2	Mus musculus	163-166
9748296-5	1998	IGF-I also promoted the formation of a complex between p130(Cas) and c-Crk and elicited a parallel increase in the tyrosine phosphorylation of p125(Fak) and paxillin.	Tyrosine	115-123	PTK2 protein tyrosine kinase 2	Mus musculus	148-151
9813103-5	1998	Attachment to fibronectin induces tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin in parental cells and cells transfected with the wild-type PTP1B, while in cells transfected with the mutant PTP1B, such induction is not observed.	Tyrosine	34-42	PTK2 protein tyrosine kinase 2	Mus musculus	62-83
9813103-5	1998	Attachment to fibronectin induces tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin in parental cells and cells transfected with the wild-type PTP1B, while in cells transfected with the mutant PTP1B, such induction is not observed.	Tyrosine	34-42	PTK2 protein tyrosine kinase 2	Mus musculus	85-88
9790958-0	1998	Vanadate-dependent FAK activation is accomplished by the sustained FAK Tyr-576/577 phosphorylation.	Vanadates	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	19-22
9790958-0	1998	Vanadate-dependent FAK activation is accomplished by the sustained FAK Tyr-576/577 phosphorylation.	Vanadates	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
9790958-0	1998	Vanadate-dependent FAK activation is accomplished by the sustained FAK Tyr-576/577 phosphorylation.	Tyrosine	71-74	PTK2 protein tyrosine kinase 2	Mus musculus	19-22
9790958-0	1998	Vanadate-dependent FAK activation is accomplished by the sustained FAK Tyr-576/577 phosphorylation.	Tyrosine	71-74	PTK2 protein tyrosine kinase 2	Mus musculus	67-70
9790958-2	1998	It is well established that Tyr-397 is the FAK autophosphorylation site and Tyr-407, -576/577, -861, and -925 are the sites on murine FAK that are mediated by Src family kinases.	Tyrosine	28-31	PTK2 protein tyrosine kinase 2	Mus musculus	43-46
9790958-2	1998	It is well established that Tyr-397 is the FAK autophosphorylation site and Tyr-407, -576/577, -861, and -925 are the sites on murine FAK that are mediated by Src family kinases.	Tyrosine	28-31	PTK2 protein tyrosine kinase 2	Mus musculus	134-137
9790958-2	1998	It is well established that Tyr-397 is the FAK autophosphorylation site and Tyr-407, -576/577, -861, and -925 are the sites on murine FAK that are mediated by Src family kinases.	Tyrosine	76-79	PTK2 protein tyrosine kinase 2	Mus musculus	134-137
9774338-4	1998	Pyk2 tyrosine phosphorylation was enhanced by fibronectin (FN) stimulation of FAK- but not FAK+ cells.	Tyrosine	5-13	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
9774338-5	1998	Increased Pyk2 tyrosine phosphorylation paralleled the time-course of Grb2 binding to Shc and activation of ERK2 in FAK- cells.	Tyrosine	15-23	PTK2 protein tyrosine kinase 2	Mus musculus	116-119
9790958-4	1998	Both the phosphotyrosine content and the enzymatic activity of FAK are increased in response to vanadate.	Phosphotyrosine	9-24	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
9790958-4	1998	Both the phosphotyrosine content and the enzymatic activity of FAK are increased in response to vanadate.	Vanadates	96-104	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
9790958-5	1998	Interestingly, sustained FAK Tyr-576/577 and -863 phosphorylations are detected in vanadate-treated FAK overexpressors and are dependent on FAK autophosphorylation.	Tyrosine	29-32	PTK2 protein tyrosine kinase 2	Mus musculus	25-28
9790958-5	1998	Interestingly, sustained FAK Tyr-576/577 and -863 phosphorylations are detected in vanadate-treated FAK overexpressors and are dependent on FAK autophosphorylation.	Tyrosine	29-32	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
9790958-5	1998	Interestingly, sustained FAK Tyr-576/577 and -863 phosphorylations are detected in vanadate-treated FAK overexpressors and are dependent on FAK autophosphorylation.	Tyrosine	29-32	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
9790958-5	1998	Interestingly, sustained FAK Tyr-576/577 and -863 phosphorylations are detected in vanadate-treated FAK overexpressors and are dependent on FAK autophosphorylation.	Vanadates	83-91	PTK2 protein tyrosine kinase 2	Mus musculus	25-28
9790958-5	1998	Interestingly, sustained FAK Tyr-576/577 and -863 phosphorylations are detected in vanadate-treated FAK overexpressors and are dependent on FAK autophosphorylation.	Vanadates	83-91	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
9790958-5	1998	Interestingly, sustained FAK Tyr-576/577 and -863 phosphorylations are detected in vanadate-treated FAK overexpressors and are dependent on FAK autophosphorylation.	Vanadates	83-91	PTK2 protein tyrosine kinase 2	Mus musculus	100-103
9790958-6	1998	Further analysis of sodium vanadate-treated FAK overexpressors reveals that the enhanced FAK kinase activity parallels its elevated Tyr-576/577 phosphorylation.	Vanadates	20-35	PTK2 protein tyrosine kinase 2	Mus musculus	44-47
9790958-6	1998	Further analysis of sodium vanadate-treated FAK overexpressors reveals that the enhanced FAK kinase activity parallels its elevated Tyr-576/577 phosphorylation.	Vanadates	20-35	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
9790958-6	1998	Further analysis of sodium vanadate-treated FAK overexpressors reveals that the enhanced FAK kinase activity parallels its elevated Tyr-576/577 phosphorylation.	Tyrosine	132-135	PTK2 protein tyrosine kinase 2	Mus musculus	44-47
9790958-6	1998	Further analysis of sodium vanadate-treated FAK overexpressors reveals that the enhanced FAK kinase activity parallels its elevated Tyr-576/577 phosphorylation.	Tyrosine	132-135	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
9699518-4	1998	In the surviving p6 cells in suspension cultures, the focal adhesion kinase (FAK) is tyrosyl phosphorylated by IGF-I, although this phosphorylation occurs only after several hours.	cyclo(tyrosyl-tyrosyl)	85-92	PTK2 protein tyrosine kinase 2	Mus musculus	54-75
9729519-0	1998	Urea and NaCl differentially regulate FAK and RAFTK/PYK2 in mIMCD3 renal medullary cells.	Urea	0-4	PTK2 protein tyrosine kinase 2	Mus musculus	38-41
9729519-0	1998	Urea and NaCl differentially regulate FAK and RAFTK/PYK2 in mIMCD3 renal medullary cells.	Sodium Chloride	9-13	PTK2 protein tyrosine kinase 2	Mus musculus	38-41
9729519-5	1998	NaCl activated FAK at 1, 5, and 15 min (25-40%), whereas urea-inducible FAK activation (30%) was not evident until fully 15 min of treatment.	Sodium Chloride	0-4	PTK2 protein tyrosine kinase 2	Mus musculus	15-18
9729519-5	1998	NaCl activated FAK at 1, 5, and 15 min (25-40%), whereas urea-inducible FAK activation (30%) was not evident until fully 15 min of treatment.	Urea	57-61	PTK2 protein tyrosine kinase 2	Mus musculus	72-75
9699518-4	1998	In the surviving p6 cells in suspension cultures, the focal adhesion kinase (FAK) is tyrosyl phosphorylated by IGF-I, although this phosphorylation occurs only after several hours.	cyclo(tyrosyl-tyrosyl)	85-92	PTK2 protein tyrosine kinase 2	Mus musculus	77-80
9662335-0	1998	Lysophosphatidic acid-induced association of SHP-2 with SHPS-1: roles of RHO, FAK, and a SRC family kinase.	lysophosphatidic acid	0-21	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
9720924-2	1998	By analyzing FAK-deficient (FAK-/-) cells transiently expressing Cas mutant proteins, we demonstrate here that the Src homology 3 (SH3) domain of Cas is indispensable for adhesion-mediated Cas phosphorylation in this mutant cell line.	Calcium	146-149	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
9720924-2	1998	By analyzing FAK-deficient (FAK-/-) cells transiently expressing Cas mutant proteins, we demonstrate here that the Src homology 3 (SH3) domain of Cas is indispensable for adhesion-mediated Cas phosphorylation in this mutant cell line.	Calcium	146-149	PTK2 protein tyrosine kinase 2	Mus musculus	28-31
9720924-2	1998	By analyzing FAK-deficient (FAK-/-) cells transiently expressing Cas mutant proteins, we demonstrate here that the Src homology 3 (SH3) domain of Cas is indispensable for adhesion-mediated Cas phosphorylation in this mutant cell line.	Calcium	146-149	PTK2 protein tyrosine kinase 2	Mus musculus	13-16
9720924-2	1998	By analyzing FAK-deficient (FAK-/-) cells transiently expressing Cas mutant proteins, we demonstrate here that the Src homology 3 (SH3) domain of Cas is indispensable for adhesion-mediated Cas phosphorylation in this mutant cell line.	Calcium	146-149	PTK2 protein tyrosine kinase 2	Mus musculus	28-31
9720924-3	1998	While the FAK directly binds to Cas-SH3, our findings imply that SH3-binding molecule(s) other than FAK might regulate Cas phosphorylation, at least in FAK-/- cells.	Calcium	32-35	PTK2 protein tyrosine kinase 2	Mus musculus	10-13
9720924-5	1998	CAKbeta expressed by FAK-/- cells was associated in vivo with Cas in a Cas-SH3-dependent manner.	Calcium	62-65	PTK2 protein tyrosine kinase 2	Mus musculus	21-24
9720924-6	1998	Moreover, integrin stimulation induces tyrosine phosphorylation of CAKbeta in FAK-/- cells.	Tyrosine	39-47	PTK2 protein tyrosine kinase 2	Mus musculus	78-81
9668122-0	1998	Bombesin, vasopressin, lysophosphatidic acid, and sphingosylphosphorylcholine induce focal adhesion kinase activation in intact Swiss 3T3 cells.	lysophosphatidic acid	23-44	PTK2 protein tyrosine kinase 2	Mus musculus	85-106
9668122-0	1998	Bombesin, vasopressin, lysophosphatidic acid, and sphingosylphosphorylcholine induce focal adhesion kinase activation in intact Swiss 3T3 cells.	sphingosine phosphorylcholine	50-77	PTK2 protein tyrosine kinase 2	Mus musculus	85-106
9668122-3	1998	Addition of vasopressin, lysophosphatidic acid, and sphingosylphosphorylcholine also elicited a rapid increase in FAK-associated tyrosine kinase activity.	lysophosphatidic acid	25-46	PTK2 protein tyrosine kinase 2	Mus musculus	114-117
9668122-3	1998	Addition of vasopressin, lysophosphatidic acid, and sphingosylphosphorylcholine also elicited a rapid increase in FAK-associated tyrosine kinase activity.	sphingosine phosphorylcholine	52-79	PTK2 protein tyrosine kinase 2	Mus musculus	114-117
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
9662335-5	1998	LPA-induced tyrosine phosphorylation of SHPS-1 was markedly reduced in either focal adhesion kinase (FAK)-deficient mouse cells or CHO cells overexpressing the tyrosine kinase CSK.	lysophosphatidic acid	0-3	PTK2 protein tyrosine kinase 2	Mus musculus	78-99
9662335-5	1998	LPA-induced tyrosine phosphorylation of SHPS-1 was markedly reduced in either focal adhesion kinase (FAK)-deficient mouse cells or CHO cells overexpressing the tyrosine kinase CSK.	lysophosphatidic acid	0-3	PTK2 protein tyrosine kinase 2	Mus musculus	101-104
9461600-7	1998	The increased formation of stress fibers and focal adhesions in CAP-expressing cells was correlated with decreased tyrosine phosphorylation of p125FAK in growing cells or upon integrin-mediated cell adhesion.	Tyrosine	115-123	PTK2 protein tyrosine kinase 2	Mus musculus	143-150
9662335-5	1998	LPA-induced tyrosine phosphorylation of SHPS-1 was markedly reduced in either focal adhesion kinase (FAK)-deficient mouse cells or CHO cells overexpressing the tyrosine kinase CSK.	Tyrosine	12-20	PTK2 protein tyrosine kinase 2	Mus musculus	78-99
9662335-5	1998	LPA-induced tyrosine phosphorylation of SHPS-1 was markedly reduced in either focal adhesion kinase (FAK)-deficient mouse cells or CHO cells overexpressing the tyrosine kinase CSK.	Tyrosine	12-20	PTK2 protein tyrosine kinase 2	Mus musculus	101-104
9662335-8	1998	These results indicate that LPA-induced tyrosine phosphorylation of SHPS-1 and its association with SHP-2 may be mediated by a RHO-dependent pathway that includes FAK and a SRC family kinase.	lysophosphatidic acid	28-31	PTK2 protein tyrosine kinase 2	Mus musculus	163-166
9662335-8	1998	These results indicate that LPA-induced tyrosine phosphorylation of SHPS-1 and its association with SHP-2 may be mediated by a RHO-dependent pathway that includes FAK and a SRC family kinase.	Tyrosine	40-48	PTK2 protein tyrosine kinase 2	Mus musculus	163-166
9556630-8	1998	In this study, we show that in MC3T3-E1 cells, fluoroaluminate induces a 110-kDa tyrosine-phosphorylated protein that we identify as Pyk2, a cytoplasmic tyrosine kinase related to Fak (focal adhesion kinase).	fluoroaluminum	47-62	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
9556630-8	1998	In this study, we show that in MC3T3-E1 cells, fluoroaluminate induces a 110-kDa tyrosine-phosphorylated protein that we identify as Pyk2, a cytoplasmic tyrosine kinase related to Fak (focal adhesion kinase).	fluoroaluminum	47-62	PTK2 protein tyrosine kinase 2	Mus musculus	185-206
9556630-8	1998	In this study, we show that in MC3T3-E1 cells, fluoroaluminate induces a 110-kDa tyrosine-phosphorylated protein that we identify as Pyk2, a cytoplasmic tyrosine kinase related to Fak (focal adhesion kinase).	Tyrosine	81-89	PTK2 protein tyrosine kinase 2	Mus musculus	180-183
9556630-8	1998	In this study, we show that in MC3T3-E1 cells, fluoroaluminate induces a 110-kDa tyrosine-phosphorylated protein that we identify as Pyk2, a cytoplasmic tyrosine kinase related to Fak (focal adhesion kinase).	Tyrosine	81-89	PTK2 protein tyrosine kinase 2	Mus musculus	185-206
9535903-6	1998	A close association of GM3 with c-Src, Rho, and FAK was indicated by co-immunoprecipitation of GM3 present in GEM by anti-GM3 monoclonal antibody DH2, followed by Western blotting with antibodies directed to these transducer molecules.	(-)-taxifolin	146-149	PTK2 protein tyrosine kinase 2	Mus musculus	48-51
9535903-8	1998	1) Tyrosine phosphorylation in FAK was greatly enhanced in B16 cells adhered to Gg3-coated plates but was minimal in cells adhered to GM3-coated, GlcCer-coated, or noncoated plates.	Tyrosine	3-11	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
9535903-8	1998	1) Tyrosine phosphorylation in FAK was greatly enhanced in B16 cells adhered to Gg3-coated plates but was minimal in cells adhered to GM3-coated, GlcCer-coated, or noncoated plates.	{1-hydroxy-3-[methyl(4-phenylbutyl)amino]propane-1,1-diyl}bis(phosphonic acid)	80-83	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
9535903-8	1998	1) Tyrosine phosphorylation in FAK was greatly enhanced in B16 cells adhered to Gg3-coated plates but was minimal in cells adhered to GM3-coated, GlcCer-coated, or noncoated plates.	Glucosylceramides	146-152	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
9502075-7	1998	EDb mono-repeat was also more potent for inducing both limited cell spreading and FAK tyrosine phosphorylation than its neighboring repeats III7 or III8.	Tyrosine	86-94	PTK2 protein tyrosine kinase 2	Mus musculus	82-85
9421230-4	1997	The results indicated that AlFx dose-dependently enhanced the tyr phos of the cell adhesion proteins FAK and paxillin, as well as of the adaptor molecules p46shc, p52shc, and p66shc and their association with GRB2.	alfx	27-31	PTK2 protein tyrosine kinase 2	Mus musculus	101-104
9421230-4	1997	The results indicated that AlFx dose-dependently enhanced the tyr phos of the cell adhesion proteins FAK and paxillin, as well as of the adaptor molecules p46shc, p52shc, and p66shc and their association with GRB2.	Tyrosine	62-65	PTK2 protein tyrosine kinase 2	Mus musculus	101-104
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
9361011-6	1997	Attachment of cells to COL(I) stimulated tyrosine phosphorylation of focal adhesion kinase (FAK) and extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinase (MAPK), and enhanced MAPK activity.	Tyrosine	41-49	PTK2 protein tyrosine kinase 2	Mus musculus	69-90
9361011-6	1997	Attachment of cells to COL(I) stimulated tyrosine phosphorylation of focal adhesion kinase (FAK) and extracellular signal-regulated kinase (ERK), a mitogen-activated protein kinase (MAPK), and enhanced MAPK activity.	Tyrosine	41-49	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
9270872-0	1997	Echistatin induces decrease of pp125FAK phosphorylation, disassembly of actin cytoskeleton and focal adhesions, and detachment of fibronectin-adherent melanoma cells.	echistatin	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	31-39
9223455-3	1997	Associated with DIGEM, many signal transducer molecules such as c-Src, FAK, and the low-molecular-weight G-proteins Rho A and H-Ras were also found.	digem	16-21	PTK2 protein tyrosine kinase 2	Mus musculus	71-74
9270872-6	1997	Echistatin treatment down-regulated the phosphorylation of pp125FAK in fibronectin-adherent cells in a dose- and time-dependent fashion.	echistatin	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	59-67
9270872-7	1997	The reduction of pp125FAK phosphorylation preceded cell detachment and occurred even in the presence of orthovanadate, an inhibitor of protein tyrosine phosphatases.	Vanadates	104-117	PTK2 protein tyrosine kinase 2	Mus musculus	17-25
9375372-2	1997	Though originally identified as a putative substrate for the oncogenic tyrosine kinase pp60v-src, it is now well-established that FAK tyrosine phosphorylation is induced by adhesion of cell surface integrins to extracellular matrix and by a variety of other extracellular factors including the ligands for receptor tyrosine kinases and for seven transmembrane domain G-protein-coupled receptors.	Tyrosine	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	130-133
9184086-2	1997	To prove that this activity is also shown by IFs in quasi-intact cells, digitonin-permeabilized epithelial PtK2 and mouse fibroblast cells were treated with FITC-labeled, single-stranded oligodeoxyribonucleotides and analyzed, after indirect decoration of their IF systems with TRITC-conjugated antibodies, by fluorescence microscopy.	Digitonin	72-81	PTK2 protein tyrosine kinase 2	Mus musculus	107-111
9184086-11	1997	In accord with these fluorescence microscopic data, transmission electron microscopy of permeabilized cells treated with gold-conjugated oligonucleotides revealed decoration of IFs and membrane systems with gold particles, whereby in PtK2 cells these structures showed a distinctly heavier labeling than in fibroblasts.	Oligonucleotides	137-153	PTK2 protein tyrosine kinase 2	Mus musculus	234-238
9032297-5	1997	FN-stimulated FAK phosphotyrosine (P.Tyr) and Grb2 binding to FAK were reduced, whereas the tyrosine phosphorylation of another signaling protein, p130cas, was not detected in the Src- cells.	Tyrosine	25-33	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
9129051-4	1997	Although FAK was upregulated in the cells stimulated by GM-CSF (GM-treated cells), the kinase was barely detectable in the cells cultured with IL-3 (IL-3-treated cells).	gm	56-58	PTK2 protein tyrosine kinase 2	Mus musculus	9-12
9145910-2	1997	To explore this issue, we investigated the effect of the number of receptors for gastrin-releasing peptide (GRP) on ligand affinity and on the ability to activate intracellular messengers [PLC, tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK)] and cause receptor modulation (internalization, desensitization, down-regulation) and ligand degradation.	Tyrosine	194-202	PTK2 protein tyrosine kinase 2	Mus musculus	222-248
9032297-2	1997	FAK autophosphorylation at Tyr-397 promotes Src homology 2 (SH2) domain binding of Src family PTKs, and c-Src phosphorylation of FAK at Tyr-925 creates an SH2 binding site for the Grb2 SH2-SH3 adaptor protein.	Tyrosine	27-30	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
8986614-5	1996	Phenylarsine oxide treatment of serum-starved cells induced increased tyrosine phosphorylation of p125FAK and paxillin in a dose-dependent manner and induced assembly of focal adhesions and actin stress fibers, showing that inhibition of one or more phenylarsine oxide-sensitive tyrosine phosphatases is a sufficient stimulus for triggering focal adhesion and actin stress fiber formation in adherent cells.	oxophenylarsine	0-18	PTK2 protein tyrosine kinase 2	Mus musculus	98-105
9032297-2	1997	FAK autophosphorylation at Tyr-397 promotes Src homology 2 (SH2) domain binding of Src family PTKs, and c-Src phosphorylation of FAK at Tyr-925 creates an SH2 binding site for the Grb2 SH2-SH3 adaptor protein.	Tyrosine	136-139	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
9032297-2	1997	FAK autophosphorylation at Tyr-397 promotes Src homology 2 (SH2) domain binding of Src family PTKs, and c-Src phosphorylation of FAK at Tyr-925 creates an SH2 binding site for the Grb2 SH2-SH3 adaptor protein.	Tyrosine	136-139	PTK2 protein tyrosine kinase 2	Mus musculus	129-132
9032297-5	1997	FN-stimulated FAK phosphotyrosine (P.Tyr) and Grb2 binding to FAK were reduced, whereas the tyrosine phosphorylation of another signaling protein, p130cas, was not detected in the Src- cells.	Phosphotyrosine	18-33	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
9032297-5	1997	FN-stimulated FAK phosphotyrosine (P.Tyr) and Grb2 binding to FAK were reduced, whereas the tyrosine phosphorylation of another signaling protein, p130cas, was not detected in the Src- cells.	Tyrosine	37-40	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
8986614-5	1996	Phenylarsine oxide treatment of serum-starved cells induced increased tyrosine phosphorylation of p125FAK and paxillin in a dose-dependent manner and induced assembly of focal adhesions and actin stress fibers, showing that inhibition of one or more phenylarsine oxide-sensitive tyrosine phosphatases is a sufficient stimulus for triggering focal adhesion and actin stress fiber formation in adherent cells.	Tyrosine	70-78	PTK2 protein tyrosine kinase 2	Mus musculus	98-105
8970151-5	1996	Furthermore, LPA-induced p42mapk activation involved a pertussis toxin-sensitive guanylate nucleotide-binding protein, whereas tyrosine phosphorylation of p125FAK in response to LPA was not prevented by pretreatment with pertussis toxin.	Tyrosine	127-135	PTK2 protein tyrosine kinase 2	Mus musculus	155-162
8940124-8	1996	These results suggest that RAFTK, as well as p125(FAK), may be important in phosphotyrosine-signaling events within the focal adhesion.	Phosphotyrosine	76-91	PTK2 protein tyrosine kinase 2	Mus musculus	50-53
8970151-0	1996	Dissociation of mitogen-activated protein kinase activation from p125 focal adhesion kinase tyrosine phosphorylation in Swiss 3T3 cells stimulated by bombesin, lysophosphatidic acid, and platelet-derived growth factor.	Tyrosine	92-100	PTK2 protein tyrosine kinase 2	Mus musculus	65-91
8970151-5	1996	Furthermore, LPA-induced p42mapk activation involved a pertussis toxin-sensitive guanylate nucleotide-binding protein, whereas tyrosine phosphorylation of p125FAK in response to LPA was not prevented by pretreatment with pertussis toxin.	lysophosphatidic acid	178-181	PTK2 protein tyrosine kinase 2	Mus musculus	155-162
8970151-0	1996	Dissociation of mitogen-activated protein kinase activation from p125 focal adhesion kinase tyrosine phosphorylation in Swiss 3T3 cells stimulated by bombesin, lysophosphatidic acid, and platelet-derived growth factor.	lysophosphatidic acid	160-181	PTK2 protein tyrosine kinase 2	Mus musculus	65-91
8970151-7	1996	Thus, our results demonstrate that p42mapk activation in response to bombesin, LPA, and PDGF can be dissociated from p125FAK tyrosine phosphorylation in Swiss 3T3 cells.	Tyrosine	125-133	PTK2 protein tyrosine kinase 2	Mus musculus	117-124
8970151-1	1996	The experiments presented here were designed to examine the contribution of p125 focal adhesion kinase (p125FAK) tyrosine phosphorylation to the activation of the mitogen-activated protein kinase cascade induced by bombesin, lysophosphatidic acid (LPA), and platelet-derived growth factor (PDGF) in Swiss 3T3 cells.	Tyrosine	113-121	PTK2 protein tyrosine kinase 2	Mus musculus	76-102
8930401-8	1996	Met and substrates such as phosphatidylinositol 3-kinase, Src homology and collagen-like, pp60c-src, focal adhesion kinase p125FAK, and paxillin were associated with tyrosine-phosphorylated complexes in a hepatocyte cell line established from the transgenic liver.	Tyrosine	166-174	PTK2 protein tyrosine kinase 2	Mus musculus	123-130
8970151-1	1996	The experiments presented here were designed to examine the contribution of p125 focal adhesion kinase (p125FAK) tyrosine phosphorylation to the activation of the mitogen-activated protein kinase cascade induced by bombesin, lysophosphatidic acid (LPA), and platelet-derived growth factor (PDGF) in Swiss 3T3 cells.	Tyrosine	113-121	PTK2 protein tyrosine kinase 2	Mus musculus	104-111
8970151-1	1996	The experiments presented here were designed to examine the contribution of p125 focal adhesion kinase (p125FAK) tyrosine phosphorylation to the activation of the mitogen-activated protein kinase cascade induced by bombesin, lysophosphatidic acid (LPA), and platelet-derived growth factor (PDGF) in Swiss 3T3 cells.	lysophosphatidic acid	225-246	PTK2 protein tyrosine kinase 2	Mus musculus	76-102
8970151-1	1996	The experiments presented here were designed to examine the contribution of p125 focal adhesion kinase (p125FAK) tyrosine phosphorylation to the activation of the mitogen-activated protein kinase cascade induced by bombesin, lysophosphatidic acid (LPA), and platelet-derived growth factor (PDGF) in Swiss 3T3 cells.	lysophosphatidic acid	225-246	PTK2 protein tyrosine kinase 2	Mus musculus	104-111
8970151-1	1996	The experiments presented here were designed to examine the contribution of p125 focal adhesion kinase (p125FAK) tyrosine phosphorylation to the activation of the mitogen-activated protein kinase cascade induced by bombesin, lysophosphatidic acid (LPA), and platelet-derived growth factor (PDGF) in Swiss 3T3 cells.	lysophosphatidic acid	248-251	PTK2 protein tyrosine kinase 2	Mus musculus	76-102
8970151-1	1996	The experiments presented here were designed to examine the contribution of p125 focal adhesion kinase (p125FAK) tyrosine phosphorylation to the activation of the mitogen-activated protein kinase cascade induced by bombesin, lysophosphatidic acid (LPA), and platelet-derived growth factor (PDGF) in Swiss 3T3 cells.	lysophosphatidic acid	248-251	PTK2 protein tyrosine kinase 2	Mus musculus	104-111
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.	Tyrosine	14-22	PTK2 protein tyrosine kinase 2	Mus musculus	42-49
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
8970151-4	1996	The protein kinase C inhibitor GF 109203X and down-regulation of protein kinase C by prolonged pretreatment of cells with phorbol esters blocked bombesin-stimulated activation of p42mapk, p90rsk, and MAPK kinase-1 but did not prevent bombesin-induced tyrosine phosphorylation of p125FAK.	bisindolylmaleimide I	31-41	PTK2 protein tyrosine kinase 2	Mus musculus	279-286
8970151-4	1996	The protein kinase C inhibitor GF 109203X and down-regulation of protein kinase C by prolonged pretreatment of cells with phorbol esters blocked bombesin-stimulated activation of p42mapk, p90rsk, and MAPK kinase-1 but did not prevent bombesin-induced tyrosine phosphorylation of p125FAK.	Phorbol Esters	122-136	PTK2 protein tyrosine kinase 2	Mus musculus	279-286
8970151-5	1996	Furthermore, LPA-induced p42mapk activation involved a pertussis toxin-sensitive guanylate nucleotide-binding protein, whereas tyrosine phosphorylation of p125FAK in response to LPA was not prevented by pretreatment with pertussis toxin.	lysophosphatidic acid	13-16	PTK2 protein tyrosine kinase 2	Mus musculus	155-162
8589330-4	1995	Because p125FAK was found to play a role in the signal transduction of not only integrins but also various neurotransmitters, including bombesin, endothelin, and vasopressin in Swiss 3T3 cells and Rat-1 fibroblasts, whether ET-1 could stimulate the tyrosine phosphorylation of p125FAK in glomerular mesangial cells was examined.	Tyrosine	249-257	PTK2 protein tyrosine kinase 2	Mus musculus	8-15
9172776-2	1996	A recombinant baculovirus was generated which contains the mouse FAK cDNA cloned into a histidine tag transfer vector.	Histidine	88-97	PTK2 protein tyrosine kinase 2	Mus musculus	65-68
8939572-2	1996	These signals are triggered by interactions between integrin and the ECM and involve tyrosine phosphorylation of specific proteins, including focal adhesion kinase (FAK) and paxillin, and the assembly of focal adhesions and actin bundles.	Tyrosine	85-93	PTK2 protein tyrosine kinase 2	Mus musculus	142-163
8939572-2	1996	These signals are triggered by interactions between integrin and the ECM and involve tyrosine phosphorylation of specific proteins, including focal adhesion kinase (FAK) and paxillin, and the assembly of focal adhesions and actin bundles.	Tyrosine	85-93	PTK2 protein tyrosine kinase 2	Mus musculus	165-168
8939572-3	1996	In matrix-adherent, serum-starved Swiss 3T3 cells, the system of focal adhesions and actin bundles is poorly developed, and the level of tyrosine phosphorylation of FAK and paxillin is low.	Tyrosine	137-145	PTK2 protein tyrosine kinase 2	Mus musculus	165-168
8939572-6	1996	RESULTS: In serum-starved Swiss 3T3 cells, the disruption of microtubules by nocodazole or vinblastine, without the addition of external growth factors, induces the rapid assembly of focal adhesions and microfilament bundles, tyrosine phosphorylation of FAK and paxillin, and subsequent enhancement of DNA synthesis.	Nocodazole	77-87	PTK2 protein tyrosine kinase 2	Mus musculus	254-257
8939572-6	1996	RESULTS: In serum-starved Swiss 3T3 cells, the disruption of microtubules by nocodazole or vinblastine, without the addition of external growth factors, induces the rapid assembly of focal adhesions and microfilament bundles, tyrosine phosphorylation of FAK and paxillin, and subsequent enhancement of DNA synthesis.	Vinblastine	91-102	PTK2 protein tyrosine kinase 2	Mus musculus	254-257
8816475-5	1996	Using a tryptic phosphopeptide mapping approach, the in vivo phosphorylation of the Grb2 binding site on FAK (Tyr-925) was detected after fibronectin stimulation of NIH 3T3 cells and was constitutively phosphorylated in v-Src-transformed NIH 3T3 cells.	Tyrosine	110-113	PTK2 protein tyrosine kinase 2	Mus musculus	105-108
8856665-4	1996	This displacement of endogenous FAK in both BALB/c 3T3 cells and human umbilical vein endothelial cells loaded with GST-Cterm decreased focal adhesion phosphotyrosine content.	Phosphotyrosine	151-166	PTK2 protein tyrosine kinase 2	Mus musculus	32-35
8645141-0	1996	Focal adhesion kinase (p125FAK) and paxillin are substrates for sphingomyelinase-induced tyrosine phosphorylation in Swiss 3T3 fibroblasts.	Tyrosine	89-97	PTK2 protein tyrosine kinase 2	Mus musculus	23-30
8645141-3	1996	The 120 and 70 kDa tyrosine-phosphorylated peptides were identified as p125 focal adhesion kinase (p125FAK) and paxillin respectively by the use of specific antibodies against the proteins.	Tyrosine	19-27	PTK2 protein tyrosine kinase 2	Mus musculus	71-97
8645141-3	1996	The 120 and 70 kDa tyrosine-phosphorylated peptides were identified as p125 focal adhesion kinase (p125FAK) and paxillin respectively by the use of specific antibodies against the proteins.	Tyrosine	19-27	PTK2 protein tyrosine kinase 2	Mus musculus	99-106
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
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.	Tyrosine	110-118	PTK2 protein tyrosine kinase 2	Mus musculus	138-145
8645141-7	1996	This was in sharp contrast with a wortmannin-sensitive phosphorylation of p125FAK observed in platelet-derived growth factor (PGDF)-stimulated cells.	Wortmannin	34-44	PTK2 protein tyrosine kinase 2	Mus musculus	74-81
8645141-7	1996	This was in sharp contrast with a wortmannin-sensitive phosphorylation of p125FAK observed in platelet-derived growth factor (PGDF)-stimulated cells.	pgdf	126-130	PTK2 protein tyrosine kinase 2	Mus musculus	74-81
8645141-8	1996	Thus hydrolysis of sphingomyelin is considered to regulate the tyrosine kinase cascade including p125FAK and paxillin by a mechanism distinct from PDGF.	Sphingomyelins	19-32	PTK2 protein tyrosine kinase 2	Mus musculus	97-104
8743960-5	1996	Activated Rho stimulates the tyrosine phosphorylation of a number of proteins, including three proteins known to localise to focal adhesions, pp125FAK, p130 and paxillin.	Tyrosine	29-37	PTK2 protein tyrosine kinase 2	Mus musculus	142-150
8654393-0	1996	The association of focal adhesion kinase with a 200-kDa protein that is tyrosine phosphorylated in response to platelet-derived growth factor.	Tyrosine	72-80	PTK2 protein tyrosine kinase 2	Mus musculus	19-40
8654393-4	1996	In this report, we describe the association of FAK with a 200-kDa protein (pp200) that is tyrosine phosphorylated in response to PDGF stimulation in NIH 3T3 cells.	Tyrosine	90-98	PTK2 protein tyrosine kinase 2	Mus musculus	47-50
8654393-6	1996	Furthermore, we found that the tyrosine phosphorylation of FAK-associated pp200 upon PDGF stimulation is largely independent of cell adhesion or the integrity of the cytoskeleton.	Tyrosine	31-39	PTK2 protein tyrosine kinase 2	Mus musculus	59-62
8550600-2	1996	Tyrosine phosphorylation induced by rPMT occurred after a pronounced lag period (1 h) and was blocked by either lysosomotrophic agents or incubation at 22 degrees C. Focal adhesion kinase (p125FAK) and paxillin are prominent substrates for rPMT-stimulated tyrosine phosphorylation.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	189-196
8550600-2	1996	Tyrosine phosphorylation induced by rPMT occurred after a pronounced lag period (1 h) and was blocked by either lysosomotrophic agents or incubation at 22 degrees C. Focal adhesion kinase (p125FAK) and paxillin are prominent substrates for rPMT-stimulated tyrosine phosphorylation.	rpmt	36-40	PTK2 protein tyrosine kinase 2	Mus musculus	189-196
8550600-6	1996	In addition, tyrosine phosphorylation of p125FAK and paxillin in response to rPMT was completely abolished when cells were subsequently treated with platelet-derived growth factor at a concentration (30 ng/ml) that disrupted the actin cytoskeleton.	Tyrosine	13-21	PTK2 protein tyrosine kinase 2	Mus musculus	41-48
8550600-6	1996	In addition, tyrosine phosphorylation of p125FAK and paxillin in response to rPMT was completely abolished when cells were subsequently treated with platelet-derived growth factor at a concentration (30 ng/ml) that disrupted the actin cytoskeleton.	rpmt	77-81	PTK2 protein tyrosine kinase 2	Mus musculus	41-48
8550600-7	1996	Our results demonstrate for the first time that rPMT, a bacterial toxin, induces tyrosine phosphorylation of p125FAK and paxillin and promotes actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells.	rpmt	48-52	PTK2 protein tyrosine kinase 2	Mus musculus	109-116
8550600-7	1996	Our results demonstrate for the first time that rPMT, a bacterial toxin, induces tyrosine phosphorylation of p125FAK and paxillin and promotes actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells.	Tyrosine	81-89	PTK2 protein tyrosine kinase 2	Mus musculus	109-116
7479864-4	1995	These SH3 domains bind to the same proline-rich region of FAK (APPKPSR) encompassing residues 711-717.	Proline	35-42	PTK2 protein tyrosine kinase 2	Mus musculus	58-61
7479864-8	1995	The Src family kinase Fyn, whose Src homology 2 (SH2) domain binds to the major FAK autophosphorylation site (tyrosine 397), was also identified in the two-hybrid screen.	Tyrosine	110-118	PTK2 protein tyrosine kinase 2	Mus musculus	80-83
7593207-10	1995	Immunoprecipitation with anti-phosphotyrosine antibody PY20 revealed increased tyrosine phosphorylation, post 12(S)-HETE stimulation, of proteins migrating at 120, 76, and 42/44 kd, of which the 120 kd protein co-migrated with pp125FAK.	Tyrosine	37-45	PTK2 protein tyrosine kinase 2	Mus musculus	227-235
7593207-12	1995	The present study suggests that 12(S)-HETE promoted melanoma cell spreading on fibronectin involves tyrosine phosphorylation of pp125FAK and protein kinase C- and tyrosine kinase-dependent focal adhesion formation.	Hydroxyeicosatetraenoic Acids	34-42	PTK2 protein tyrosine kinase 2	Mus musculus	128-136
7593207-12	1995	The present study suggests that 12(S)-HETE promoted melanoma cell spreading on fibronectin involves tyrosine phosphorylation of pp125FAK and protein kinase C- and tyrosine kinase-dependent focal adhesion formation.	Tyrosine	100-108	PTK2 protein tyrosine kinase 2	Mus musculus	128-136
7544314-10	1995	Tyrosine phosphorylation is a critical regulator of FAK, and impairments in FAK signal transduction in fyn mutants may contribute to the mutant neural phenotype.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	52-55
7592646-0	1995	Sphingosylphosphorylcholine rapidly induces tyrosine phosphorylation of p125FAK and paxillin, rearrangement of the actin cytoskeleton and focal contact assembly.	sphingosine phosphorylcholine	0-27	PTK2 protein tyrosine kinase 2	Mus musculus	72-79
7592646-0	1995	Sphingosylphosphorylcholine rapidly induces tyrosine phosphorylation of p125FAK and paxillin, rearrangement of the actin cytoskeleton and focal contact assembly.	Tyrosine	44-52	PTK2 protein tyrosine kinase 2	Mus musculus	72-79
7592646-3	1995	Focal adhesion kinase (p125FAK) and paxillin were identified as prominent substrates for SPC-stimulated tyrosine phosphorylation.	Tyrosine	104-112	PTK2 protein tyrosine kinase 2	Mus musculus	23-30
7592646-4	1995	An increase in tyrosine phosphorylation of p125FAK was detected as soon as 30 s after SPC stimulation, reaching a maximum after 2.5 min.	Tyrosine	15-23	PTK2 protein tyrosine kinase 2	Mus musculus	43-50
7592646-5	1995	SPC induced tyrosine phosphorylation of p125FAK in a concentration-dependent fashion; a half-maximum effect occurred at 250 nM.	Tyrosine	12-20	PTK2 protein tyrosine kinase 2	Mus musculus	40-47
7592646-6	1995	Tyrosine phosphorylation of p125FAK induced by SPC could be dissociated from both protein kinase C activation and Ca2+ mobilization from intracellular stores.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	28-35
7592646-10	1995	Cytochalasin D, which disrupts the network of actin microfilaments, completely prevented SPC-induced tyrosine phosphorylation of p125FAK.	Tyrosine	101-109	PTK2 protein tyrosine kinase 2	Mus musculus	129-136
7592646-11	1995	In addition, tyrosine phosphorylation of p125FAK was markedly inhibited in the presence of platelet-derived growth factor at a concentration (30 ng/ml) that disrupts actin stress fibers.	Tyrosine	13-21	PTK2 protein tyrosine kinase 2	Mus musculus	41-48
7556524-2	1995	To elucidate a possible functional relationship between FAK and BCR-ABL oncoprotein detected in Philadelphia chromosome-positive (Ph+) leukemias, we investigated the tyrosine phosphorylation state of FAK in a murine growth factor-dependent cell line and in its stable human bcr-abl cDNA transfectant.	Tyrosine	166-174	PTK2 protein tyrosine kinase 2	Mus musculus	200-203
7566154-1	1995	The intracellular protein tyrosine kinase FAK (focal adhesion kinase) was originally identified gy its high level of tyrosine phosphorylation in v-src-transformed cells.	Tyrosine	26-34	PTK2 protein tyrosine kinase 2	Mus musculus	42-45
7566154-1	1995	The intracellular protein tyrosine kinase FAK (focal adhesion kinase) was originally identified gy its high level of tyrosine phosphorylation in v-src-transformed cells.	Tyrosine	26-34	PTK2 protein tyrosine kinase 2	Mus musculus	47-68
7589452-2	1995	Inhibitors of protein tyrosine kinases, methyl 2,5-dihydroxycinnamate and herbimycin A, inhibited tyrosine-phosphorylation of FAK and the adhesion of 3T3 cells to fibronectin.	methyl 2,5-dihydroxycinnamate	40-69	PTK2 protein tyrosine kinase 2	Mus musculus	126-129
7589452-2	1995	Inhibitors of protein tyrosine kinases, methyl 2,5-dihydroxycinnamate and herbimycin A, inhibited tyrosine-phosphorylation of FAK and the adhesion of 3T3 cells to fibronectin.	herbimycin	74-86	PTK2 protein tyrosine kinase 2	Mus musculus	126-129
7589452-2	1995	Inhibitors of protein tyrosine kinases, methyl 2,5-dihydroxycinnamate and herbimycin A, inhibited tyrosine-phosphorylation of FAK and the adhesion of 3T3 cells to fibronectin.	Tyrosine	22-30	PTK2 protein tyrosine kinase 2	Mus musculus	126-129
7589452-5	1995	When calphostin C (20 microM) was added to sub-confluent monolayer cultures, serine-phosphorylation of FAK was inhibited by 67% within 2 h, and decrease in the amount of FAK and rounding up of the cells began after 4 h. Label-chase experiments indicated that about 60% of 35S-labeled FAK degraded within 1-2 h after addition of calphostin C to monolayer cultures.	calphostin C	5-17	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
7589452-5	1995	When calphostin C (20 microM) was added to sub-confluent monolayer cultures, serine-phosphorylation of FAK was inhibited by 67% within 2 h, and decrease in the amount of FAK and rounding up of the cells began after 4 h. Label-chase experiments indicated that about 60% of 35S-labeled FAK degraded within 1-2 h after addition of calphostin C to monolayer cultures.	calphostin C	5-17	PTK2 protein tyrosine kinase 2	Mus musculus	170-173
7589452-5	1995	When calphostin C (20 microM) was added to sub-confluent monolayer cultures, serine-phosphorylation of FAK was inhibited by 67% within 2 h, and decrease in the amount of FAK and rounding up of the cells began after 4 h. Label-chase experiments indicated that about 60% of 35S-labeled FAK degraded within 1-2 h after addition of calphostin C to monolayer cultures.	calphostin C	5-17	PTK2 protein tyrosine kinase 2	Mus musculus	170-173
7589452-5	1995	When calphostin C (20 microM) was added to sub-confluent monolayer cultures, serine-phosphorylation of FAK was inhibited by 67% within 2 h, and decrease in the amount of FAK and rounding up of the cells began after 4 h. Label-chase experiments indicated that about 60% of 35S-labeled FAK degraded within 1-2 h after addition of calphostin C to monolayer cultures.	Serine	77-83	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
7589452-5	1995	When calphostin C (20 microM) was added to sub-confluent monolayer cultures, serine-phosphorylation of FAK was inhibited by 67% within 2 h, and decrease in the amount of FAK and rounding up of the cells began after 4 h. Label-chase experiments indicated that about 60% of 35S-labeled FAK degraded within 1-2 h after addition of calphostin C to monolayer cultures.	Sulfur-35	272-275	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
7589452-5	1995	When calphostin C (20 microM) was added to sub-confluent monolayer cultures, serine-phosphorylation of FAK was inhibited by 67% within 2 h, and decrease in the amount of FAK and rounding up of the cells began after 4 h. Label-chase experiments indicated that about 60% of 35S-labeled FAK degraded within 1-2 h after addition of calphostin C to monolayer cultures.	calphostin C	328-340	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
7589452-6	1995	These results indicated that serine-phosphorylation of FAK induced by protein kinase C was important in the regulation of metabolic stability of FAK.	Serine	29-35	PTK2 protein tyrosine kinase 2	Mus musculus	55-58
7589452-6	1995	These results indicated that serine-phosphorylation of FAK induced by protein kinase C was important in the regulation of metabolic stability of FAK.	Serine	29-35	PTK2 protein tyrosine kinase 2	Mus musculus	145-148
7539261-0	1995	An inward rectifier K+ current modulates in neuroblastoma cells the tyrosine phosphorylation of the pp125FAK and associated proteins: role in neuritogenesis.	Tyrosine	68-76	PTK2 protein tyrosine kinase 2	Mus musculus	100-108
7593264-6	1995	Herbimycin A, a tyrosine kinase inhibitor, not only suppressed tyrosine phosphorylation of p125FAK but also changed the intracellular localization of p125FAK and disrupted a ringed structure of F-actin-containing podosomes in osteoclast-like cells.	herbimycin	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	91-98
7593264-6	1995	Herbimycin A, a tyrosine kinase inhibitor, not only suppressed tyrosine phosphorylation of p125FAK but also changed the intracellular localization of p125FAK and disrupted a ringed structure of F-actin-containing podosomes in osteoclast-like cells.	herbimycin	0-12	PTK2 protein tyrosine kinase 2	Mus musculus	150-157
7593264-6	1995	Herbimycin A, a tyrosine kinase inhibitor, not only suppressed tyrosine phosphorylation of p125FAK but also changed the intracellular localization of p125FAK and disrupted a ringed structure of F-actin-containing podosomes in osteoclast-like cells.	Tyrosine	16-24	PTK2 protein tyrosine kinase 2	Mus musculus	91-98
7593264-6	1995	Herbimycin A, a tyrosine kinase inhibitor, not only suppressed tyrosine phosphorylation of p125FAK but also changed the intracellular localization of p125FAK and disrupted a ringed structure of F-actin-containing podosomes in osteoclast-like cells.	Tyrosine	16-24	PTK2 protein tyrosine kinase 2	Mus musculus	150-157
7593264-7	1995	Antisense oligodeoxynucleotides to p125FAK inhibited dentine resorption by osteoclast-like cells, whereas sense oligodeoxynucleotides did not.	Oligodeoxyribonucleotides	10-31	PTK2 protein tyrosine kinase 2	Mus musculus	35-42
7593264-8	1995	These results suggest that p125FAK is involved in osteoclastic bone resorption and that tyrosine phosphorylation of p125FAK is critical for regulating osteoclast function.	Tyrosine	88-96	PTK2 protein tyrosine kinase 2	Mus musculus	116-123
7615549-0	1995	Characterization of tyrosine phosphorylation of paxillin in vitro by focal adhesion kinase.	Tyrosine	20-28	PTK2 protein tyrosine kinase 2	Mus musculus	69-90
7615549-1	1995	The concomitant tyrosine phosphorylation of the focal adhesion protein, paxillin, and the tyrosine kinase, focal adhesion kinase (FAK), in response to multiple stimuli including integrin-mediated cell adhesion suggests that paxillin phosphorylation is closely coupled to FAK activity.	Tyrosine	16-24	PTK2 protein tyrosine kinase 2	Mus musculus	271-274
7615549-2	1995	In the present study, we have identified a specific tyrosine residue within paxillin, tyrosine 118 (Tyr-118), that represents the principle site of phosphorylation by FAK in vitro.	Tyrosine	52-60	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
7615549-2	1995	In the present study, we have identified a specific tyrosine residue within paxillin, tyrosine 118 (Tyr-118), that represents the principle site of phosphorylation by FAK in vitro.	Tyrosine	86-94	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
7615549-2	1995	In the present study, we have identified a specific tyrosine residue within paxillin, tyrosine 118 (Tyr-118), that represents the principle site of phosphorylation by FAK in vitro.	Tyrosine	100-103	PTK2 protein tyrosine kinase 2	Mus musculus	167-170
7615549-3	1995	The identification of this site as a target for FAK phosphorylation was accomplished by immunoprecipitating FAK and performing in vitro kinase assays, using as substrate either glutathione S-transferase (GST)-paxillin fusion proteins containing truncations in paxillin sequence or fusion proteins with phenylalanine substitutions for tyrosine residues.	Phenylalanine	302-315	PTK2 protein tyrosine kinase 2	Mus musculus	48-51
7615549-3	1995	The identification of this site as a target for FAK phosphorylation was accomplished by immunoprecipitating FAK and performing in vitro kinase assays, using as substrate either glutathione S-transferase (GST)-paxillin fusion proteins containing truncations in paxillin sequence or fusion proteins with phenylalanine substitutions for tyrosine residues.	Tyrosine	334-342	PTK2 protein tyrosine kinase 2	Mus musculus	48-51
7673357-11	1995	Anti-phosphotyrosine immunoblotting and in vitro kinase assays of MASMC lysates have revealed that, under conditions which promote focal adhesion formation, pp125FAK remains inactive.	Phosphotyrosine	5-20	PTK2 protein tyrosine kinase 2	Mus musculus	157-165
7539261-6	1995	Immunoprecipitation of pp125FAK revealed that the phosphorylation of this kinase and several associated proteins was significantly and reversibly inhibited by Cs+, indicating that integrin-mediated activation of KIR channels is a limiting step upstream to the phosphorylation of pp125FAK in the commitment to neuritogenesis.	Cesium	159-162	PTK2 protein tyrosine kinase 2	Mus musculus	23-31
7539261-6	1995	Immunoprecipitation of pp125FAK revealed that the phosphorylation of this kinase and several associated proteins was significantly and reversibly inhibited by Cs+, indicating that integrin-mediated activation of KIR channels is a limiting step upstream to the phosphorylation of pp125FAK in the commitment to neuritogenesis.	Cesium	159-162	PTK2 protein tyrosine kinase 2	Mus musculus	279-287
7525558-0	1994	Sphingosine induces p125FAK and paxillin tyrosine phosphorylation, actin stress fiber formation, and focal contact assembly in Swiss 3T3 cells.	Sphingosine	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	20-27
7896849-3	1995	Specifically, GTP gamma S stimulated tyrosine phosphorylation of both focal adhesion kinase (p125FAK) and paxillin.	Guanosine Triphosphate	14-17	PTK2 protein tyrosine kinase 2	Mus musculus	93-100
7896849-3	1995	Specifically, GTP gamma S stimulated tyrosine phosphorylation of both focal adhesion kinase (p125FAK) and paxillin.	Tyrosine	37-45	PTK2 protein tyrosine kinase 2	Mus musculus	93-100
7896849-10	1995	Pretreatment with the Clostridium botulinum C3 exoenzyme which inactivates p21rho, markedly reduced the ability of GTP gamma S to stimulate tyrosine phosphorylation of M(r) 110,000-130,000 and 70,000-80,000 bands including p125FAK and paxillin in permeabilized Swiss 3T3 cells.	Guanosine Triphosphate	115-118	PTK2 protein tyrosine kinase 2	Mus musculus	223-230
7896849-10	1995	Pretreatment with the Clostridium botulinum C3 exoenzyme which inactivates p21rho, markedly reduced the ability of GTP gamma S to stimulate tyrosine phosphorylation of M(r) 110,000-130,000 and 70,000-80,000 bands including p125FAK and paxillin in permeabilized Swiss 3T3 cells.	Tyrosine	140-148	PTK2 protein tyrosine kinase 2	Mus musculus	223-230
7896849-12	1995	This peptide also inhibited tyrosine phosphorylation of p125FAK and paxillin.	Tyrosine	28-36	PTK2 protein tyrosine kinase 2	Mus musculus	56-63
7896849-14	1995	Using permeabilized cells, our findings demonstrate that GTP gamma S stimulates tyrosine phosphorylation of p125FAK and paxillin and that a functional p21rho is implicated in this process.	Guanosine Triphosphate	57-60	PTK2 protein tyrosine kinase 2	Mus musculus	108-115
7896849-14	1995	Using permeabilized cells, our findings demonstrate that GTP gamma S stimulates tyrosine phosphorylation of p125FAK and paxillin and that a functional p21rho is implicated in this process.	Tyrosine	80-88	PTK2 protein tyrosine kinase 2	Mus musculus	108-115
7766995-3	1995	We have identified sequence variants in the 3" untranslated regions of the focal adhesion kinase gene in mice and used a PCR-based oligonucleotide hybridization assay to map the mouse gene (Fadk) to Chromosome (Chr) 15 distal to the myelocytomatosis protooncogene (Myc).	Oligonucleotides	131-146	PTK2 protein tyrosine kinase 2	Mus musculus	190-194
7997267-2	1994	Increased FAK tyrosine phosphorylation occurs upon integrin engagement with fibronectin.	Tyrosine	14-22	PTK2 protein tyrosine kinase 2	Mus musculus	10-13
7997267-5	1994	The GRB2 SH2 domain binds directly to tyrosine-phosphorylated FAK.	Tyrosine	38-46	PTK2 protein tyrosine kinase 2	Mus musculus	62-65
7997267-6	1994	Mutation of tyrosine residue 925 of FAK (YENV motif) to phenylalanine blocks GRB2 SH2-domain binding to FAK in vitro.	Tyrosine	12-20	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
7997267-6	1994	Mutation of tyrosine residue 925 of FAK (YENV motif) to phenylalanine blocks GRB2 SH2-domain binding to FAK in vitro.	Tyrosine	12-20	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
7997267-6	1994	Mutation of tyrosine residue 925 of FAK (YENV motif) to phenylalanine blocks GRB2 SH2-domain binding to FAK in vitro.	Phenylalanine	56-69	PTK2 protein tyrosine kinase 2	Mus musculus	36-39
7997267-6	1994	Mutation of tyrosine residue 925 of FAK (YENV motif) to phenylalanine blocks GRB2 SH2-domain binding to FAK in vitro.	Phenylalanine	56-69	PTK2 protein tyrosine kinase 2	Mus musculus	104-107
7997267-8	1994	Phosphorylation of FAK at Tyr 925 upon fibronectin stimulation creates an SH2-binding site for GRB2 which may link integrin engagement to the activation of the Ras/MAPK signal transduction pathway.	Tyrosine	26-29	PTK2 protein tyrosine kinase 2	Mus musculus	19-22
7896849-0	1995	Guanosine 5"-3-O-(thio)triphosphate stimulates tyrosine phosphorylation of p125FAK and paxillin in permeabilized Swiss 3T3 cells.	Guanosine 5'-O-(3-Thiotriphosphate)	0-35	PTK2 protein tyrosine kinase 2	Mus musculus	75-82
7896849-0	1995	Guanosine 5"-3-O-(thio)triphosphate stimulates tyrosine phosphorylation of p125FAK and paxillin in permeabilized Swiss 3T3 cells.	Tyrosine	47-55	PTK2 protein tyrosine kinase 2	Mus musculus	75-82
7525357-0	1994	Botulinum C3 exoenzyme blocks the tyrosine phosphorylation of p125FAK and paxillin induced by bombesin and endothelin.	Tyrosine	34-42	PTK2 protein tyrosine kinase 2	Mus musculus	62-69
7525558-4	1994	Focal adhesion kinase (p125FAK) and paxillin were identified as prominent substrates for sphingosine-stimulated tyrosine phosphorylation.	Sphingosine	89-100	PTK2 protein tyrosine kinase 2	Mus musculus	23-30
7525558-4	1994	Focal adhesion kinase (p125FAK) and paxillin were identified as prominent substrates for sphingosine-stimulated tyrosine phosphorylation.	Tyrosine	112-120	PTK2 protein tyrosine kinase 2	Mus musculus	23-30
7525558-5	1994	Cell permeable ceramides also stimulated tyrosine phosphorylation of the M(r) 110,000-130,000 band as well as p125FAK, but the effect was less pronounced than that of sphingosine.	Ceramides	15-24	PTK2 protein tyrosine kinase 2	Mus musculus	110-117
7525558-10	1994	In addition, tyrosine phosphorylation of p125FAK and paxillin in response to sphingosine was completely prevented when cells were stimulated in the presence of platelet-derived growth factor at a concentration (30 ng/ml) that caused disruption of the actin cytoskeleton.	Tyrosine	13-21	PTK2 protein tyrosine kinase 2	Mus musculus	41-48
7525558-10	1994	In addition, tyrosine phosphorylation of p125FAK and paxillin in response to sphingosine was completely prevented when cells were stimulated in the presence of platelet-derived growth factor at a concentration (30 ng/ml) that caused disruption of the actin cytoskeleton.	Sphingosine	77-88	PTK2 protein tyrosine kinase 2	Mus musculus	41-48
7525558-11	1994	Our results demonstrate, for the first time, that sphingosine induces p125FAK and paxillin tyrosine phosphorylation, actin stress fiber formation and focal adhesion assembly in Swiss 3T3 cells.	Sphingosine	50-61	PTK2 protein tyrosine kinase 2	Mus musculus	70-77
8062907-2	1994	Acidic and basic fibroblast growth factors also stimulated the phosphorylation of serine and tyrosine of FAK in cells adhered to poly-L-lysine, but epidermal growth factor and platelet-derived growth factor did not.	Tyrosine	93-101	PTK2 protein tyrosine kinase 2	Mus musculus	105-108
7929090-0	1994	Focal adhesion-associated proteins p125FAK and paxillin are substrates for bradykinin-stimulated tyrosine phosphorylation in Swiss 3T3 cells.	Tyrosine	97-105	PTK2 protein tyrosine kinase 2	Mus musculus	35-42
7929090-2	1994	BK (1 microM) stimulated tyrosine phosphorylation of p125FAK and paxillin.	Tyrosine	25-33	PTK2 protein tyrosine kinase 2	Mus musculus	53-60
7929090-6	1994	The phosphotyrosine content of p125FAK, paxillin, and p130 was also increased following stimulation with phorbol 12-myristate 13-acetate (PMA) (0.1 microM).	Phosphotyrosine	4-19	PTK2 protein tyrosine kinase 2	Mus musculus	31-38
7929090-6	1994	The phosphotyrosine content of p125FAK, paxillin, and p130 was also increased following stimulation with phorbol 12-myristate 13-acetate (PMA) (0.1 microM).	Tetradecanoylphorbol Acetate	105-136	PTK2 protein tyrosine kinase 2	Mus musculus	31-38
7929090-6	1994	The phosphotyrosine content of p125FAK, paxillin, and p130 was also increased following stimulation with phorbol 12-myristate 13-acetate (PMA) (0.1 microM).	Tetradecanoylphorbol Acetate	138-141	PTK2 protein tyrosine kinase 2	Mus musculus	31-38
7929090-9	1994	Furthermore, only a small inhibition of BK- and PMA-stimulated phosphorylation of p125FAK was observed following pretreatment with 25 microM BAPTA/AM.	1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid	141-146	PTK2 protein tyrosine kinase 2	Mus musculus	82-89
7929090-10	1994	In all, these results show that multiple mechanisms are involved in BK-stimulated tyrosine phosphorylation of p125FAK, paxillin, Ras-GAP-associated p125, and src transformation-associated p130.	Tyrosine	82-90	PTK2 protein tyrosine kinase 2	Mus musculus	110-117
8062907-0	1994	Stimulation of tyrosine- and serine-phosphorylation of focal adhesion kinase in mouse 3T3 cells by fibronectin and fibroblast growth factor.	Tyrosine	15-23	PTK2 protein tyrosine kinase 2	Mus musculus	55-76
8062907-0	1994	Stimulation of tyrosine- and serine-phosphorylation of focal adhesion kinase in mouse 3T3 cells by fibronectin and fibroblast growth factor.	Serine	29-35	PTK2 protein tyrosine kinase 2	Mus musculus	55-76
8062907-1	1994	Phosphorylation of both tyrosine and serine residues of focal adhesion kinase (FAK) was stimulated by the adhesion of BALB/c mouse 3T3 cells to fibronectin, but phosphorylation of threonine was not detectable.	Tyrosine	24-32	PTK2 protein tyrosine kinase 2	Mus musculus	56-77
8062907-1	1994	Phosphorylation of both tyrosine and serine residues of focal adhesion kinase (FAK) was stimulated by the adhesion of BALB/c mouse 3T3 cells to fibronectin, but phosphorylation of threonine was not detectable.	Tyrosine	24-32	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
8062907-1	1994	Phosphorylation of both tyrosine and serine residues of focal adhesion kinase (FAK) was stimulated by the adhesion of BALB/c mouse 3T3 cells to fibronectin, but phosphorylation of threonine was not detectable.	Serine	37-43	PTK2 protein tyrosine kinase 2	Mus musculus	56-77
8062907-1	1994	Phosphorylation of both tyrosine and serine residues of focal adhesion kinase (FAK) was stimulated by the adhesion of BALB/c mouse 3T3 cells to fibronectin, but phosphorylation of threonine was not detectable.	Serine	37-43	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
8062907-1	1994	Phosphorylation of both tyrosine and serine residues of focal adhesion kinase (FAK) was stimulated by the adhesion of BALB/c mouse 3T3 cells to fibronectin, but phosphorylation of threonine was not detectable.	Threonine	180-189	PTK2 protein tyrosine kinase 2	Mus musculus	56-77
8062907-1	1994	Phosphorylation of both tyrosine and serine residues of focal adhesion kinase (FAK) was stimulated by the adhesion of BALB/c mouse 3T3 cells to fibronectin, but phosphorylation of threonine was not detectable.	Threonine	180-189	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
8062907-2	1994	Acidic and basic fibroblast growth factors also stimulated the phosphorylation of serine and tyrosine of FAK in cells adhered to poly-L-lysine, but epidermal growth factor and platelet-derived growth factor did not.	Lysine	129-142	PTK2 protein tyrosine kinase 2	Mus musculus	105-108
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
7527052-10	1994	Within 10 minutes, the addition of serum or LPA induced a marked increase in the levels of pp125FAK and paxillin immune-precipitated by an anti-phosphotyrosine antibody.	lysophosphatidic acid	44-47	PTK2 protein tyrosine kinase 2	Mus musculus	91-99
7527052-11	1994	The results suggest that both pp125FAK and paxillin undergo changes in tyrosine phosphorylation upon activation of rhoA, and that these changes are associated with the assembly of focal adhesions and actin stress fibres.	Tyrosine	71-79	PTK2 protein tyrosine kinase 2	Mus musculus	30-38
7514714-2	1994	In NIH/3T3 cells transfected with the c-src/F527 gene, an increase in the level of tyrosine phosphorylation of several proteins, including pp125FAK, within a group of proteins of 120 kDa, of p85 (cortactin), and of p62 is observed, which is due to the elevated kinase activity of the resulting encoded pp60F527 protein.	Tyrosine	83-91	PTK2 protein tyrosine kinase 2	Mus musculus	139-147
7510708-5	1994	Immunoprecipitation of lysates of LPA-treated cells with monoclonal antibodies that specifically recognize focal adhesion kinase (p125FAK), paxillin, and p130 revealed that these proteins are prominent substrates for LPA-stimulated tyrosine phosphorylation.	lysophosphatidic acid	34-37	PTK2 protein tyrosine kinase 2	Mus musculus	130-137
7510708-5	1994	Immunoprecipitation of lysates of LPA-treated cells with monoclonal antibodies that specifically recognize focal adhesion kinase (p125FAK), paxillin, and p130 revealed that these proteins are prominent substrates for LPA-stimulated tyrosine phosphorylation.	lysophosphatidic acid	217-220	PTK2 protein tyrosine kinase 2	Mus musculus	130-137
7510708-5	1994	Immunoprecipitation of lysates of LPA-treated cells with monoclonal antibodies that specifically recognize focal adhesion kinase (p125FAK), paxillin, and p130 revealed that these proteins are prominent substrates for LPA-stimulated tyrosine phosphorylation.	Tyrosine	232-240	PTK2 protein tyrosine kinase 2	Mus musculus	130-137
7510708-9	1994	Furthermore, tyrosine phosphorylation of p125FAK induced by LPA was completely prevented when cells were stimulated in the presence of platelet-derived growth factor at a concentration (30 ng/ml) that causes disruption of actin stress fibers.	Tyrosine	13-21	PTK2 protein tyrosine kinase 2	Mus musculus	41-48
7510708-9	1994	Furthermore, tyrosine phosphorylation of p125FAK induced by LPA was completely prevented when cells were stimulated in the presence of platelet-derived growth factor at a concentration (30 ng/ml) that causes disruption of actin stress fibers.	lysophosphatidic acid	60-63	PTK2 protein tyrosine kinase 2	Mus musculus	41-48
7510708-10	1994	This suggests that the integrity of the actin cytoskeleton is essential for LPA-induced tyrosine phosphorylation and reveals a novel cross-talk between LPA and platelet-derived growth factor on p125FAK tyrosine phosphorylation.	lysophosphatidic acid	76-79	PTK2 protein tyrosine kinase 2	Mus musculus	194-201
7510708-10	1994	This suggests that the integrity of the actin cytoskeleton is essential for LPA-induced tyrosine phosphorylation and reveals a novel cross-talk between LPA and platelet-derived growth factor on p125FAK tyrosine phosphorylation.	lysophosphatidic acid	152-155	PTK2 protein tyrosine kinase 2	Mus musculus	194-201
7510708-10	1994	This suggests that the integrity of the actin cytoskeleton is essential for LPA-induced tyrosine phosphorylation and reveals a novel cross-talk between LPA and platelet-derived growth factor on p125FAK tyrosine phosphorylation.	Tyrosine	202-210	PTK2 protein tyrosine kinase 2	Mus musculus	194-201
8276872-7	1994	Cytochalasin D, which disrupts the actin cytoskeleton, completely inhibited the tyrosine phosphorylation of p125FAK and paxillin by PDGF.	Tyrosine	80-88	PTK2 protein tyrosine kinase 2	Mus musculus	108-115
8276872-11	1994	Further, the tyrosine phosphorylation of both p125FAK and paxillin induced by bombesin (10 nM) was completely prevented when cells were stimulated with bombesin in the presence of 30 ng/ml PDGF.	Tyrosine	13-21	PTK2 protein tyrosine kinase 2	Mus musculus	46-53
1801924-1	1991	The cell-permeant heavy metal chelator N,N,N",N"-tetrakis(2-pyridylmethyl)ethylenediamine(TPEN) was found to counteract phorbol ester-induced actin reorganization in PTK2 and Swiss 3T3 cells.	Metals	24-29	PTK2 protein tyrosine kinase 2	Mus musculus	166-170
7883787-10	1994	However, LPA stimulates tyrosine phosphorylation of a number of proteins, including the focal adhesion kinase, pp125FAK, and genistein, a tyrosine kinase inhibitor, prevents this increase in tyrosine phosphorylation.	lysophosphatidic acid	9-12	PTK2 protein tyrosine kinase 2	Mus musculus	111-119
7883787-10	1994	However, LPA stimulates tyrosine phosphorylation of a number of proteins, including the focal adhesion kinase, pp125FAK, and genistein, a tyrosine kinase inhibitor, prevents this increase in tyrosine phosphorylation.	Tyrosine	24-32	PTK2 protein tyrosine kinase 2	Mus musculus	111-119
8365468-0	1993	Lysophosphatidic acid induces tyrosine phosphorylation and activation of MAP-kinase and focal adhesion kinase in cultured Swiss 3T3 cells.	lysophosphatidic acid	0-21	PTK2 protein tyrosine kinase 2	Mus musculus	88-109
8365468-3	1993	Tyrosine phosphorylation of p64 peaked at 1 min and declined rapidly, whereas that of MAP-kinase and FAK peaked at 5 and 10 min after the addition of LPA, respectively.	lysophosphatidic acid	150-153	PTK2 protein tyrosine kinase 2	Mus musculus	101-104
1382065-3	1992	Treatment of Swiss 3T3 cells with the mitogenic peptides bombesin, vasopressin, and endothelin caused a striking increase in the tyrosine phosphorylation of p125FAK, as judged either by anti-phosphotyrosine (anti-Tyr(P)) Western blots of anti-p125FAK immunoprecipitates, or by anti-p125FAK immunoblots of anti-Tyr(P) immunoprecipitates.	Tyrosine	213-216	PTK2 protein tyrosine kinase 2	Mus musculus	157-164
1382065-3	1992	Treatment of Swiss 3T3 cells with the mitogenic peptides bombesin, vasopressin, and endothelin caused a striking increase in the tyrosine phosphorylation of p125FAK, as judged either by anti-phosphotyrosine (anti-Tyr(P)) Western blots of anti-p125FAK immunoprecipitates, or by anti-p125FAK immunoblots of anti-Tyr(P) immunoprecipitates.	Tyrosine	310-313	PTK2 protein tyrosine kinase 2	Mus musculus	157-164
1382065-4	1992	Bombesin-stimulated tyrosine phosphorylation of p125FAK was detectable within seconds and concentration-dependent (half-maximum effect of 0.3 nM).	Tyrosine	20-28	PTK2 protein tyrosine kinase 2	Mus musculus	48-55
1528852-4	1992	FadK is phosphorylated on tyrosine in growing cultures of BALB/c 3T3 cells but contains little or no phosphotyrosine in cells detached by trypsinization.	Tyrosine	26-34	PTK2 protein tyrosine kinase 2	Mus musculus	0-4
8314789-0	1993	Bombesin stimulation of p125 focal adhesion kinase tyrosine phosphorylation.	Tyrosine	51-59	PTK2 protein tyrosine kinase 2	Mus musculus	24-50
8314789-2	1993	Activation of protein kinase C (PKC) in quiescent Swiss 3T3 cells using either the tumor promoter phorbol 12,13-dibutyrate (PDB) or diacylglycerols increased the tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK) by 3.8-fold.	12,13-dibutyrate	106-122	PTK2 protein tyrosine kinase 2	Mus musculus	190-216
8314789-2	1993	Activation of protein kinase C (PKC) in quiescent Swiss 3T3 cells using either the tumor promoter phorbol 12,13-dibutyrate (PDB) or diacylglycerols increased the tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK) by 3.8-fold.	12,13-dibutyrate	106-122	PTK2 protein tyrosine kinase 2	Mus musculus	218-225
8314789-2	1993	Activation of protein kinase C (PKC) in quiescent Swiss 3T3 cells using either the tumor promoter phorbol 12,13-dibutyrate (PDB) or diacylglycerols increased the tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK) by 3.8-fold.	Diglycerides	132-147	PTK2 protein tyrosine kinase 2	Mus musculus	190-216
8314789-2	1993	Activation of protein kinase C (PKC) in quiescent Swiss 3T3 cells using either the tumor promoter phorbol 12,13-dibutyrate (PDB) or diacylglycerols increased the tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK) by 3.8-fold.	Diglycerides	132-147	PTK2 protein tyrosine kinase 2	Mus musculus	218-225
8314789-2	1993	Activation of protein kinase C (PKC) in quiescent Swiss 3T3 cells using either the tumor promoter phorbol 12,13-dibutyrate (PDB) or diacylglycerols increased the tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK) by 3.8-fold.	Tyrosine	162-170	PTK2 protein tyrosine kinase 2	Mus musculus	190-216
8314789-2	1993	Activation of protein kinase C (PKC) in quiescent Swiss 3T3 cells using either the tumor promoter phorbol 12,13-dibutyrate (PDB) or diacylglycerols increased the tyrosine phosphorylation of p125 focal adhesion kinase (p125FAK) by 3.8-fold.	Tyrosine	162-170	PTK2 protein tyrosine kinase 2	Mus musculus	218-225
8314789-3	1993	PDB stimulation of p125FAK tyrosine phosphorylation was detected within 1 min and reached a maximum within 5 min, considerably slower than PDB stimulation of 80K/MARCKS phosphorylation which was maximal within 1 min.	Tyrosine	27-35	PTK2 protein tyrosine kinase 2	Mus musculus	19-26
8314789-4	1993	In sharp contrast, bombesin-induced tyrosine phosphorylation of p125FAK reached a maximum (8-fold stimulation) within 1 min after addition of the peptide and occurred with a half-maximal effect of 0.08 nM, 6-fold lower than the half-maximal effect of bombesin on 80K/MARCKS phosphorylation.	Tyrosine	36-44	PTK2 protein tyrosine kinase 2	Mus musculus	64-71
8314789-5	1993	Down-regulation of PKC by prolonged treatment with PDB blocked the effect of PDB on p125FAK tyrosine phosphorylation but had no effect on the response to bombesin.	Tyrosine	92-100	PTK2 protein tyrosine kinase 2	Mus musculus	84-91
8314789-6	1993	A selective inhibitor of PKC, GF 109203X, markedly inhibited the stimulation of p125FAK tyrosine phosphorylation by PDB but had little effect on the response to bombesin, vasopressin, and endothelin.	bisindolylmaleimide I	30-40	PTK2 protein tyrosine kinase 2	Mus musculus	80-87
8314789-6	1993	A selective inhibitor of PKC, GF 109203X, markedly inhibited the stimulation of p125FAK tyrosine phosphorylation by PDB but had little effect on the response to bombesin, vasopressin, and endothelin.	Tyrosine	88-96	PTK2 protein tyrosine kinase 2	Mus musculus	80-87
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
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.	Tyrosine	157-165	PTK2 protein tyrosine kinase 2	Mus musculus	149-156
1385444-0	1992	Tyrosine phosphorylation of paxillin and pp125FAK accompanies cell adhesion to extracellular matrix: a role in cytoskeletal assembly.	Tyrosine	0-8	PTK2 protein tyrosine kinase 2	Mus musculus	41-49
1382065-3	1992	Treatment of Swiss 3T3 cells with the mitogenic peptides bombesin, vasopressin, and endothelin caused a striking increase in the tyrosine phosphorylation of p125FAK, as judged either by anti-phosphotyrosine (anti-Tyr(P)) Western blots of anti-p125FAK immunoprecipitates, or by anti-p125FAK immunoblots of anti-Tyr(P) immunoprecipitates.	Tyrosine	129-137	PTK2 protein tyrosine kinase 2	Mus musculus	157-164
1382065-3	1992	Treatment of Swiss 3T3 cells with the mitogenic peptides bombesin, vasopressin, and endothelin caused a striking increase in the tyrosine phosphorylation of p125FAK, as judged either by anti-phosphotyrosine (anti-Tyr(P)) Western blots of anti-p125FAK immunoprecipitates, or by anti-p125FAK immunoblots of anti-Tyr(P) immunoprecipitates.	Phosphotyrosine	191-206	PTK2 protein tyrosine kinase 2	Mus musculus	157-164
1801924-1	1991	The cell-permeant heavy metal chelator N,N,N",N"-tetrakis(2-pyridylmethyl)ethylenediamine(TPEN) was found to counteract phorbol ester-induced actin reorganization in PTK2 and Swiss 3T3 cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	90-94	PTK2 protein tyrosine kinase 2	Mus musculus	166-170
1801924-1	1991	The cell-permeant heavy metal chelator N,N,N",N"-tetrakis(2-pyridylmethyl)ethylenediamine(TPEN) was found to counteract phorbol ester-induced actin reorganization in PTK2 and Swiss 3T3 cells.	Phorbol Esters	120-133	PTK2 protein tyrosine kinase 2	Mus musculus	166-170
1801924-2	1991	By using fluorescence and the higher resolution technique of photoelectron microscopy to monitor actin patterns, 15-min pretreatment with 25-50 microM TPEN was found to dramatically reduce actin alterations resulting from subsequent phorbol ester treatment in PTK2 cells.	N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine	151-155	PTK2 protein tyrosine kinase 2	Mus musculus	260-264
1801924-2	1991	By using fluorescence and the higher resolution technique of photoelectron microscopy to monitor actin patterns, 15-min pretreatment with 25-50 microM TPEN was found to dramatically reduce actin alterations resulting from subsequent phorbol ester treatment in PTK2 cells.	Phorbol Esters	233-246	PTK2 protein tyrosine kinase 2	Mus musculus	260-264
30001432-0	2018	FAK auto-phosphorylation site tyrosine 397 is required for development but dispensable for normal skin homeostasis.	Tyrosine	30-38	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
2185942-2	1990	For example, PTK2 cells exposed to 20 nM staurosporine exhibited a progressive thinning and loss of cytoplasmic actin microfilament bundles over a 60-min period.	Staurosporine	41-54	PTK2 protein tyrosine kinase 2	Mus musculus	13-17
33811437-0	2021	miR-365 secreted from M2 Macrophage-derived extracellular vesicles promotes pancreatic ductal adenocarcinoma progression through the BTG2/FAK/AKT axis.	mir-365	0-7	PTK2 protein tyrosine kinase 2	Mus musculus	138-141
30001432-2	2018	Despite the large interest in FAK, the in vivo contribution of FAK auto-phosphorylation site tyrosine (Y) 397 to FAK function is incompletely understood.	Tyrosine	93-101	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
30001432-2	2018	Despite the large interest in FAK, the in vivo contribution of FAK auto-phosphorylation site tyrosine (Y) 397 to FAK function is incompletely understood.	Tyrosine	93-101	PTK2 protein tyrosine kinase 2	Mus musculus	63-66
30001432-5	2018	When Y397 is mutated to a glutamate mice survive beyond mid-gestation like mice where Y397 is lost by deletion of FAK exon 15.	Glutamic Acid	26-35	PTK2 protein tyrosine kinase 2	Mus musculus	114-117
34270980-8	2022	Notably, FAK knockout increased cellular sensitivity to the Stat3 inhibitor CPA7, while FAK reintroduction restored resistance to this drug.	cpa7	76-80	PTK2 protein tyrosine kinase 2	Mus musculus	9-12
34784956-0	2021	Focal adhesion kinase inhibitor TAE226 combined with Sorafenib slows down hepatocellular carcinoma by multiple epigenetic effects.	TAE226	32-38	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
34856074-7	2022	Cell lines treated with trametinib or AZD6244 in combination with AZD0424 had reduced EGFR, FAK and SRC compensatory activation, and, cell viability was synergistically inhibited.	trametinib	24-34	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
34856074-7	2022	Cell lines treated with trametinib or AZD6244 in combination with AZD0424 had reduced EGFR, FAK and SRC compensatory activation, and, cell viability was synergistically inhibited.	AZD 6244	38-45	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
34420157-3	2021	In continuation with our previous findings, we have further evaluated the mechanistic role of ATN-161 in vitro and found that oxygen and glucose deprivation and reperfusion (OGD/R)-induced inflammation, oxidative stress, apoptosis, mitochondrial depolarization, and fibrosis attenuate tight junction integrity via induction of alpha5, NLRP3, p-FAK, and p-AKT signaling in mouse brain endothelial cells.	Oxygen	126-132	PTK2 protein tyrosine kinase 2	Mus musculus	344-347
34420157-4	2021	ATN-161 treatment (10 microM) effectively inhibited OGD/R-induced extracellular matrix (ECM) deposition by reducing integrin alpha5, MMP-9, and fibronectin expression, as well as reducing oxidative stress by reducing mitochondrial superoxide radicals, intracellular ROS, inflammation by reducing NLRP3 inflammasome, tight junction loss by reducing claudin-5 and ZO-1 expression levels, mitochondrial damage by inhibiting mitochondrial depolarization, and apoptosis via regulation of p-FAK and p-AKT levels.	acetyl-prolyl-histidyl-seryl-cysteinyl-asparaginamide	0-7	PTK2 protein tyrosine kinase 2	Mus musculus	485-488
34795411-0	2021	ADT-OH inhibits malignant melanoma metastasis in mice via suppressing CSE/CBS and FAK/Paxillin signaling pathway.	5-(4-hydroxyphenyl)-3H-1,2-dithiole-3-thione	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	82-85
34795411-7	2021	LC-MS/MS and bioinformatics analyses revealed that ADT-OH treatment inhibited the EMT process in B16F10 and A375 cells by reducing the expression of FAK and the downstream response protein Paxillin.	5-(4-hydroxyphenyl)-3H-1,2-dithiole-3-thione	51-57	PTK2 protein tyrosine kinase 2	Mus musculus	149-152
34795411-8	2021	Overexpression of FAK reversed the inhibitory effects of ADT-OH on melanoma cell migration.	5-(4-hydroxyphenyl)-3H-1,2-dithiole-3-thione	57-63	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
34795411-11	2021	Collectively, these results demonstrate that ADT-OH inhibits the EMT process in melanoma cells by suppressing the CSE/CBS and FAK signaling pathways, thereby exerting its antimetastatic activity.	5-(4-hydroxyphenyl)-3H-1,2-dithiole-3-thione	45-51	PTK2 protein tyrosine kinase 2	Mus musculus	126-129
34743335-3	2022	Our current study addresses the kinase activity dependency of endothelial-cell FAK sensitisation to the DNA damaging chemotherapeutic drug doxorubicin.	Doxorubicin	139-150	PTK2 protein tyrosine kinase 2	Mus musculus	79-82
34743335-4	2022	FAK is recognised as a therapeutic target in tumour cells, leading to the development of a range of inhibitors, the majority being ATP competitive kinase inhibitors.	Adenosine Triphosphate	131-134	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
34743335-5	2022	We demonstrate that inactivation of endothelial-cell FAK kinase domain (kinase dead) (EC-FAK kinase-dead) in established subcutaneous B16F0 tumours, improves melanoma cells sensitisation to doxorubicin.	Doxorubicin	190-201	PTK2 protein tyrosine kinase 2	Mus musculus	53-56
34743335-5	2022	We demonstrate that inactivation of endothelial-cell FAK kinase domain (kinase dead) (EC-FAK kinase-dead) in established subcutaneous B16F0 tumours, improves melanoma cells sensitisation to doxorubicin.	Doxorubicin	190-201	PTK2 protein tyrosine kinase 2	Mus musculus	89-92
34743335-6	2022	Doxorubicin treatment in EC-FAK kinase-dead mice reduced the percentage change in exponential B16F0 tumour growth further than in wild-type mice.	Doxorubicin	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	28-31
34743335-8	2022	Doxorubicin reduced perivascular malignant cell proliferation, whilst enhancing perivascular tumour cell apoptosis and DNA-damage in tumours grown in EC-FAK kinase dead mice 48 hrs after doxorubicin injection.	Doxorubicin	0-11	PTK2 protein tyrosine kinase 2	Mus musculus	153-156
34743335-9	2022	Human pulmonary microvascular endothelial-cells treated with the pharmacological FAK kinase inhibitors defactinib, PF-562,271 or PF-573,228 in combination with doxorubicin, also reduced cytokine expression levels.	defactinib	103-113	PTK2 protein tyrosine kinase 2	Mus musculus	81-84
34743335-9	2022	Human pulmonary microvascular endothelial-cells treated with the pharmacological FAK kinase inhibitors defactinib, PF-562,271 or PF-573,228 in combination with doxorubicin, also reduced cytokine expression levels.	Doxorubicin	160-171	PTK2 protein tyrosine kinase 2	Mus musculus	81-84
34784956-9	2021	Combined TAE226 and SOR treatment reduced HCC growth both in vitro and in vivo by affecting tumour-promoting gene expression and inducing epigenetic changes via dysregulation of FAK nuclear interactome.	TAE226	9-15	PTK2 protein tyrosine kinase 2	Mus musculus	178-181
34784956-11	2021	TAE226-mediated FAK depletion and SOR-promoted MAPK down-modulation caused a decrease in the nuclear amount of HDAC1/2 and a consequent increase of the histone H3 lysine 27 acetylation, thus counteracting histone H3 lysine 27 trimethylation.	TAE226	0-6	PTK2 protein tyrosine kinase 2	Mus musculus	16-19
34384759-0	2021	FAK inhibitor PF-431396 suppresses IgE-mediated mast cell activation and allergic inflammation in mice.	PF-431396	14-23	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
34416073-5	2021	In mice, a single dose of GSK215 induced rapid and prolonged FAK degradation, giving a long-lasting effect on FAK levels (~96 h) and a marked PK/PD disconnect.	GSK215	26-32	PTK2 protein tyrosine kinase 2	Mus musculus	61-64
34416073-5	2021	In mice, a single dose of GSK215 induced rapid and prolonged FAK degradation, giving a long-lasting effect on FAK levels (~96 h) and a marked PK/PD disconnect.	GSK215	26-32	PTK2 protein tyrosine kinase 2	Mus musculus	110-113
34648846-2	2021	However, phase II clinical trials of a FAK inhibitor (Defactinib) have only shown modest antitumor activity.	defactinib	54-64	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
34214842-6	2021	Furthermore, phosphoantibody array analyses of a sample of the tumor suggested that 16c inhibited the malignant proliferation of hepatocellular carcinoma (HCC) cells through decreasing the phosphorylation in the FAK cascade.	16c	84-87	PTK2 protein tyrosine kinase 2	Mus musculus	212-215
34384759-4	2021	FAK activity was manipulated with short hairpin RNA (shRNA) knockdown, FAK overexpression, and the FAK inhibitor PF-431396 (PF).	PF-431396	113-122	PTK2 protein tyrosine kinase 2	Mus musculus	0-3
34384759-4	2021	FAK activity was manipulated with short hairpin RNA (shRNA) knockdown, FAK overexpression, and the FAK inhibitor PF-431396 (PF).	PF-431396	113-122	PTK2 protein tyrosine kinase 2	Mus musculus	99-102
34384759-7	2021	Our results showed that FAK overexpression increased IgE-mediated degranulation and reduced the dexamethasone inhibitory effect on MCs activation.	Dexamethasone	96-109	PTK2 protein tyrosine kinase 2	Mus musculus	24-27
34384759-8	2021	The FAK inhibitor PF diminished MC release of beta-hexosaminidase (beta-hex), histamine, and inflammatory cytokines, via a mechanism that involves MAPK and NF-kappaB signaling pathways.	Histamine	78-87	PTK2 protein tyrosine kinase 2	Mus musculus	4-7
34384759-10	2021	Inhibition of CaMKII activation by KN-93 suppressed FAK activity and its downstream pathway.	KN 93	35-40	PTK2 protein tyrosine kinase 2	Mus musculus	52-55
34153254-12	2021	CONCLUSION: These data illustrate that FAK/pFAK is implicated in the signaled dysfunction of excessive mechanical loading during TMJ OA and that iFAK treatment can moderately attenuate the progression of cartilage degeneration in the mandibular condyle.	ifak	145-149	PTK2 protein tyrosine kinase 2	Mus musculus	39-42
34465607-9	2021	Mechanically, FSK stimulated FAK activation in tubular epithelial cells, which was blocked by a protein kinase A (PKA) inhibitor.	Colforsin	14-17	PTK2 protein tyrosine kinase 2	Mus musculus	29-32
34576160-7	2021	Using focal adhesion kinase (FAK) inhibitor PF573228, we found that PF-573228 inhibited the phosphorylation of FAK and reversed the upward trend of Col XV-induced protein expression levels of IRE1alpha, C/EBP-homologous protein (CHOP), and 78 kDa glucose-regulated protein (GRP78).	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	44-52	PTK2 protein tyrosine kinase 2	Mus musculus	6-27
34576160-7	2021	Using focal adhesion kinase (FAK) inhibitor PF573228, we found that PF-573228 inhibited the phosphorylation of FAK and reversed the upward trend of Col XV-induced protein expression levels of IRE1alpha, C/EBP-homologous protein (CHOP), and 78 kDa glucose-regulated protein (GRP78).	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	44-52	PTK2 protein tyrosine kinase 2	Mus musculus	29-32
34576160-7	2021	Using focal adhesion kinase (FAK) inhibitor PF573228, we found that PF-573228 inhibited the phosphorylation of FAK and reversed the upward trend of Col XV-induced protein expression levels of IRE1alpha, C/EBP-homologous protein (CHOP), and 78 kDa glucose-regulated protein (GRP78).	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	68-77	PTK2 protein tyrosine kinase 2	Mus musculus	6-27
34576160-7	2021	Using focal adhesion kinase (FAK) inhibitor PF573228, we found that PF-573228 inhibited the phosphorylation of FAK and reversed the upward trend of Col XV-induced protein expression levels of IRE1alpha, C/EBP-homologous protein (CHOP), and 78 kDa glucose-regulated protein (GRP78).	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	68-77	PTK2 protein tyrosine kinase 2	Mus musculus	29-32
34576160-7	2021	Using focal adhesion kinase (FAK) inhibitor PF573228, we found that PF-573228 inhibited the phosphorylation of FAK and reversed the upward trend of Col XV-induced protein expression levels of IRE1alpha, C/EBP-homologous protein (CHOP), and 78 kDa glucose-regulated protein (GRP78).	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	68-77	PTK2 protein tyrosine kinase 2	Mus musculus	111-114
34465607-10	2021	Inhibition of FAK activation by inhibitors or transfected cells with mutant FAK constructs interrupted FSK-mediated Src activation and upregulation of ERK and mTOR pathways.	Colforsin	103-106	PTK2 protein tyrosine kinase 2	Mus musculus	14-17
34465607-10	2021	Inhibition of FAK activation by inhibitors or transfected cells with mutant FAK constructs interrupted FSK-mediated Src activation and upregulation of ERK and mTOR pathways.	Colforsin	103-106	PTK2 protein tyrosine kinase 2	Mus musculus	76-79
34264955-6	2021	Instead, we demonstrate that brigatinib inhibited multiple tyrosine kinases, including EphA2, Fer and focal adhesion kinase 1 (FAK1).	brigatinib	29-39	PTK2 protein tyrosine kinase 2	Mus musculus	102-125
34324343-0	2021	Identification of Thieno(3,2-d)pyrimidine Derivatives as Dual Inhibitors of Focal Adhesion Kinase and FMS-like Tyrosine Kinase 3.	thienopyrimidine	18-41	PTK2 protein tyrosine kinase 2	Mus musculus	76-97
34324343-2	2021	To identify novel FAK inhibitors, we designed and synthesized various thieno(3,2-d)pyrimidine derivatives.	thienopyrimidine	70-93	PTK2 protein tyrosine kinase 2	Mus musculus	18-21
34405025-0	2021	A Luminacin D Analog HL142 Inhibits Ovarian Tumor Growth and Metastasis by Reversing EMT and Attenuating the TGFbeta and FAK Pathways.	luminacin D	2-13	PTK2 protein tyrosine kinase 2	Mus musculus	121-124
34264955-6	2021	Instead, we demonstrate that brigatinib inhibited multiple tyrosine kinases, including EphA2, Fer and focal adhesion kinase 1 (FAK1).	brigatinib	29-39	PTK2 protein tyrosine kinase 2	Mus musculus	127-131
34262662-9	2021	In conclusion, DSG3, as an oncogene, contributed to the tumorigenicity of PDAC through activating Src-FAK signaling.	pdac	74-78	PTK2 protein tyrosine kinase 2	Mus musculus	102-105
35325397-3	2022	Focal adhesion kinase (FAK), one tyrosine kinase localizing to focal adhesions, has been shown to be phosphorylated at tyrosine 925 (Y925) by Src, an important downstream molecule of Reelin signaling.	Tyrosine	119-127	PTK2 protein tyrosine kinase 2	Mus musculus	0-21
35079920-0	2022	MiR-15p-5p Mediates the Coordination of ICAM-1 and FAK to Promote Endothelial Cell Proliferation and Migration.	mir-15p-5p	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	51-54
34071408-0	2021	Atovaquone Suppresses the Growth of Metastatic Triple-Negative Breast Tumors in Lungs and Brain by Inhibiting Integrin/FAK Signaling Axis.	Atovaquone	0-10	PTK2 protein tyrosine kinase 2	Mus musculus	119-122
35325397-3	2022	Focal adhesion kinase (FAK), one tyrosine kinase localizing to focal adhesions, has been shown to be phosphorylated at tyrosine 925 (Y925) by Src, an important downstream molecule of Reelin signaling.	Tyrosine	119-127	PTK2 protein tyrosine kinase 2	Mus musculus	23-26
35628403-8	2022	Interestingly, the FAK activator, cytotoxic necrotizing factor-1 (CNF1), significantly suppresses all of the SMG-induced alterations in MC3T3-E1 cells and the HU model.	N-SUCCINYL METHIONINE	109-112	PTK2 protein tyrosine kinase 2	Mus musculus	19-22
35379785-9	2022	Moreover, miR-4731-5p exerted an inhibitory effect on glycolysis, EMT, migration, and invasion in breast cancer cells via regulation of PAICS-dependent phosphorylation of FAK.	mir-4731-5p	10-21	PTK2 protein tyrosine kinase 2	Mus musculus	171-174
35350066-7	2022	Phosphoproteomics analysis showed a downregulation of the MAPK, RAF, and PAK signaling pathways in gemcitabine-treated FAK-depleted ECs compared to gemcitabine-treated wild-type ECs.	gemcitabine	99-110	PTK2 protein tyrosine kinase 2	Mus musculus	119-122
35364069-0	2022	Chenodeoxycholic acid inhibits lung adenocarcinoma progression via the integrin alpha5beta1/FAK/p53 signaling pathway.	Chenodeoxycholic Acid	0-21	PTK2 protein tyrosine kinase 2	Mus musculus	92-95
35364069-12	2022	Mechanistically, CDCA inhibited the integrin alpha5beta1 signaling pathway in LUAD cells by inhibiting the expression of the alpha5 and beta1 subunits of integrin and phosphorylated FAK.	Chenodeoxycholic Acid	17-21	PTK2 protein tyrosine kinase 2	Mus musculus	182-185
35364069-13	2022	Moreover, CDCA induced an increase in the levels of p53, a downstream gene of the integrin alpha5beta1/FAK pathway.	Chenodeoxycholic Acid	10-14	PTK2 protein tyrosine kinase 2	Mus musculus	103-106
35364069-15	2022	CONCLUSIONS: Our findings indicate that CDCA attenuates LUAD pathogenesis in vitro and in vivo via the integrin alpha5beta1/FAK/p53 axis.	Chenodeoxycholic Acid	40-44	PTK2 protein tyrosine kinase 2	Mus musculus	124-127
35379785-11	2022	Collectively, our findings indicated that miR-4731-5p inhibited breast cancer cell glycolysis and EMT through the reduction of PAICS-induced phosphorylation of FAK.	mir-4731-5p	42-53	PTK2 protein tyrosine kinase 2	Mus musculus	160-163
35178052-12	2022	Treatment with PF271 inhibited FAK-Pyk2 activation, thus blunting the inflammatory abnormalities orchestrated by sepsis.	pf271	15-20	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
35164001-8	2022	The results of the present study provide novel evidence that alpha-cubebenoate can stimulate apoptosis and inhibit metastasis by regulating the MAPK, PI3K/AKT, and FAK/MLC signaling pathways.	alpha-cubebenoate	61-78	PTK2 protein tyrosine kinase 2	Mus musculus	164-167
35115949-3	2021	This study aimed to investigate the effect of the combination of the FAK inhibitor VS4718 and anti-PD1 for the treatment of HCC in a mouse model and its possible mechanism of action.	PND 1186	83-89	PTK2 protein tyrosine kinase 2	Mus musculus	69-72
35115949-12	2021	This study suggested that combination of the FAK inhibitor VS4718 and anti-PD1 could be a potential therapy for HCC by improving the immune environment, reducing liver fibrosis and simultaneously preventing PD1 from binding to the increased PD-L1 induced by FAK inhibitor VS4718.	PND 1186	59-65	PTK2 protein tyrosine kinase 2	Mus musculus	45-48
35115949-12	2021	This study suggested that combination of the FAK inhibitor VS4718 and anti-PD1 could be a potential therapy for HCC by improving the immune environment, reducing liver fibrosis and simultaneously preventing PD1 from binding to the increased PD-L1 induced by FAK inhibitor VS4718.	PND 1186	59-65	PTK2 protein tyrosine kinase 2	Mus musculus	258-261
35115949-12	2021	This study suggested that combination of the FAK inhibitor VS4718 and anti-PD1 could be a potential therapy for HCC by improving the immune environment, reducing liver fibrosis and simultaneously preventing PD1 from binding to the increased PD-L1 induced by FAK inhibitor VS4718.	PND 1186	272-278	PTK2 protein tyrosine kinase 2	Mus musculus	258-261
35191227-15	2022	Further analyses suggested that phosphoserine induced a M2-like phenotype in macrophages, which was related to the activation of phosphoserine receptors including T-cell immunoglobin mucin 4 (TIM4) and the FAK-SRC-STAT3 signaling pathway as well as elevated the expression of the histone demethylase Jumonji domain-containing protein 3 (JMJD3).	Phosphoserine	32-45	PTK2 protein tyrosine kinase 2	Mus musculus	206-209