HUGO ID Detailed Result 6871

PMID	Match String	Actual String	Score	Flanking text	Edited by	Edit
12614931	p38	p38	1.7	manner as an anti-apoptotic messenger possibly through activation of the p38 mitogen-activated protein kinase (MAPK) MAPK signal transduction pathway 46
12614931	MAPK	MAPK	1.7	possibly through activation of the p38 mitogen-activated protein kinase (MAPK) MAPK signal transduction pathway 46
12654515	MAPK	MAPK	2.2	VEGF activated both PI3-K and MAPK activities in mouse NSC34 motor neuron-like cells
12654515	MAPK	MAPK	2.2	and constitutively active as well as dominant negative mutants of MAPK and PI3-K revealed that the protective effects of VEGF were
12654515	MAPK	MAPK	2.2	of VEGF were mediated via the PI3-K activity and that MAPK activation was not associated with NSC34 cell survival
12654515	MAPK	MAPK	2.2	including phosphatidylinositol 3-kinase (PI3-K) PI3-K and mitogen-activated protein kinase (MAPK) MAPK 42
12654515	MAPK	MAPK	2.2	VEGF activates both PI3-K and MAPK activities in NSC34 motor neuron-like cells
12654515	MAPK	MAPK	2.2	pharmacological inhibitors and constitutively active and dominant negative mutants of MAPK and PI3-K we further demonstrate that PI3-K activity but not
12654515	MAPK	MAPK	2.2	and PI3-K we further demonstrate that PI3-K activity but not MAPK activity protects mouse NSC34 cells from mutant G93A-SOD1 effects
12654515	MAP	MAP	2.2	MAP kinase activation assay
12654515	MAP	MAP	2.2	MAP kinase activation was measured by the phosphorylation of ERK1/2 ERK1
12654515	ERK	ERK	2.2	membrane and probed with anti-phospho-ERK1/2 anti-phospho-ERK1 2 antibody that recognizes ERK only when it is phosphorylated at Thr202 and Tyr204 (Cell
12654515	MAPK	MAPK	2.2	VEGF transiently activates PI3-K and MAPK activities
12654515	MAPK	MAPK	2.2	PI3-K and/or and or MAPK signaling pathways underlie critical components of the survival-related activity of
12654515	MAPK	MAPK	2.2	Thus we tested whether VEGF regulates PI3-K and/or and or MAPK activation in NSC34 cells
12654515	MAPK	MAPK	2.2	VEGF induced concentration- and time-dependent increases in PI3-K and MAPK activities ( Fig 3 and Fig 4 suggesting that these
12654515	MAPK	MAPK	2.2	VEGF-mediated PI3-K activity not MAPK activity promotes mouse NSC34 motor neuron-like cell survival in the
12654515	MAPK	MAPK	2.2	To further examine the respective contributions of the PI3-K and MAPK signaling pathways to VEGF-induced cell survival the PI3-K inhibitors LY294002
12654515	MAPK	MAPK	2.2	at 20 _amp_#x3bc M (data data not shown and the MAPK inhibitor PD98059 at 20 _amp_#x3bc M were administered to the
12654515	ERK	ERK	2.2	with the constitutively active MEK1 the upstream activating kinase of ERK prevented mutant G93A-SOD1-mediated NSC34 cell death ( Fig 5B
12654515	MAPK	MAPK	2.2	on the activation of the PI3-K-Akt pathway and independent of MAPK activation
12654515	MAPK	MAPK	2.2	is well established that VEGF can activate both PI3-K and MAPK (MEK/ERK) MEK ERK pathways yet the protective effect of VEGF
12654515	ERK	ERK	2.2	that VEGF can activate both PI3-K and MAPK (MEK/ERK) MEK ERK pathways yet the protective effect of VEGF on motor neuron-like
12654515	MAPK	MAPK	2.2	While the specific functional roles played by the MAPK pathway are unclear it is likely that this pathway may
12654515	MAPK	MAPK	2.2	et al 34 who showed that both the PI3-K and MAPK pathways participate in neuronal cell protection by VEGF against glutamate
12654515	MAPK	MAPK	2.2	become apparent that activation of kinases such as PI3-K or MAPK does not constitute an isolated event but rather represents a
12654515	MAPK	MAPK-related	2.2	our experiments is associated with survival and the activation of MAPK-related signaling pathways is primarily related to proliferation in mouse NSC34
12654515	MAPK	MAPK	2.2	VEGF activated MAPK activity in mouse NSC34 motor neuron-like cells
12654515	MAPK	MAPK	2.2	(B) B The increase of MAPK activity in three independent experiments compared to that of vector
12654515	MAPK	MAPK	2.2	(D) D The increase of MAPK activity in three independent experiments compared to that of vector
12654515	MAPK	MAPK	2.2	(A) A PI3-K activity inhibitor LY294002 not MAPK activity inhibitor PD98059 contributed to the loss of the protection
12893007	MAP	MAP	0.3	of an abnormal form of normally occurring microtubule-associated protein (MAP), MAP termed tau
14739060	MAP	MAP	0.3	for neurons astrocytes and microglia such as mitogene-activated protein (MAP) MAP kinase cascade activation ion transport calcium mobilization and apoptosis program
16194581	ERK	ERK	2.3	The levels of extracellular signal regulated kinase (ERK) ERK and protein kinase C (PKC) PKC were elevated in the
16194581	ERK	ERK	2.3	Both ERK and PKC kinases are important in mediating cognitive function especially
16194581	ERK2	ERK2	2.3	After these tests the hippocampal expression of signaling markers including ERK1 and ERK2 as well as PKC-_amp_#x3b1 and PKC-_amp_#x3b3 were analyzed
16194581	ERK2	ERK2	2.3	tests the hippocampal expression of signaling markers including ERK1 and ERK2 as well as PKC-_amp_#x3b1 and PKC-_amp_#x3b3 were analyzed by immunoblotting
16194581	ERK2	ERK2	2.3	The expression of ERK1 and ERK2 positively correlated with inclined screen latency (measurement measurement
16194581	ERK2	ERK2	2.3	The expression of ERK1 and ERK2 positively correlated with inclined screen latency (measurement measurement of muscle
16194581	ERK	ERK	2.3	The localized expression of ERK and insulin-like growth factor 1 (IGF-1) IGF-1 and its receptor
16194581	ERK	ERK	2.3	significant increases in the protein levels of IGF-1 IGF-1R and ERK and these increases were also inversely correlated with the number
16194581	MAP	MAP	2.3	mechanisms involving neurogenesis neurotrophic factor IGF-1 and its receptor and MAP kinase signal transduction cascades
17191135	ERK	ERKs	0.0	The activated forms of ERKs (extracellular extracellular signal-regulated kinases were also decreased in cells overexpressing	Junguk Hur
17191135	ERK	ERKs	0.0	overexpressing HO-1 although no changes in the expression of total ERKs were observed 93	Junguk Hur
17496232	p38	p38	2.2	of proliferating and proapoptotic cascades like ERK1/2 ERK1 2 or p38 MAPK
17496232	MAPK	MAPK	2.2	proliferating and proapoptotic cascades like ERK1/2 ERK1 2 or p38 MAPK
17496232	p38	p38	2.2	higher NO ONOO and H 2 O 2 levels activate p38 MAPK which regulates cyclin D 1 expression negatively resulting in
17496232	MAPK	MAPK	2.2	NO ONOO and H 2 O 2 levels activate p38 MAPK which regulates cyclin D 1 expression negatively resulting in cell
17496232	MAPK	MAPKs	2.2	Representative Western blot of cyclin D 1 and MAPKs in tumoral cells (P07) P07 and in lysates of postnatal
17496232	MAPK	MAPKs	2.2	and H 2 O 2 are confluent on modulation of MAPKs and cyclin D 1
17496232	MAPK	MAPKs	2.2	MAPKs including SAPK/JNK, SAPK JNK p38 MAPK and ERK are believed
17496232	p38	p38	2.2	MAPKs including SAPK/JNK, SAPK JNK p38 MAPK and ERK are believed to be redox-dependent biomolecules that
17496232	MAPK	MAPK	2.2	MAPKs including SAPK/JNK, SAPK JNK p38 MAPK and ERK are believed to be redox-dependent biomolecules that modulate
17496232	ERK	ERK	2.2	MAPKs including SAPK/JNK, SAPK JNK p38 MAPK and ERK are believed to be redox-dependent biomolecules that modulate cell proliferation
17496232	ERK	ERKs	2.2	ERKs stimulate cell proliferation and induction of active cyclin D 1
17496232	ERK	ERKs	2.2	moderate elevation of intracellular Ca and leads to activation of ERKs and potentiates cell division functionally blocking Ca or inhibiting calmodulin
17496232	MAPK	MAPK	2.2	potentiates cell division functionally blocking Ca or inhibiting calmodulin or MAPK activities prevents ERK activation and antagonizes the mitogenic effect of
17496232	ERK	ERK	2.2	functionally blocking Ca or inhibiting calmodulin or MAPK activities prevents ERK activation and antagonizes the mitogenic effect of NO ( 90
17496232	p38	p38	2.2	On the other hand p38 SAPK transcriptionally downregulates cyclin D 1
17496232	p38	p38	2.2	cyclin D 1 activity and expression the former by activating p38 pathway ( 37
17496232	p38	p38	2.2	8 who reported a temporal inverse correlation between activation of p38 MAPK and cyclin D 1 content during liver development or
17496232	MAPK	MAPK	2.2	who reported a temporal inverse correlation between activation of p38 MAPK and cyclin D 1 content during liver development or liver
17496232	p38	p38	2.2	Similarly NO activates p38 MAPK and suppresses proliferation through the activation of JAK2-STAT5 and
17496232	MAPK	MAPK	2.2	Similarly NO activates p38 MAPK and suppresses proliferation through the activation of JAK2-STAT5 and cyclin
17496232	p38	p38	2.2	signal pathways involving both production of NO and activation of p38 MAPK pathway ( 93
17496232	MAPK	MAPK	2.2	pathways involving both production of NO and activation of p38 MAPK pathway ( 93
17496232	MAPK	MAPKs	2.2	57 attempted to connect oxidative stress and NO levels to MAPKs D cyclins and cell proliferation
17496232	MAPK	MAPK	2.2	redox effect on the protein or actions on ERK-MEK (MAPK MAPK kinase interactions
17496232	MAPK	MAPK	2.2	In this way it was proposed that duration of MAPK activation determines whether a stimulus produces proliferation or differentiation (
17496232	p38	p38	2.2	For instance activation of p38 MAPK and cell cycle arrest may finally progress to apoptosis
17496232	MAPK	MAPK	2.2	For instance activation of p38 MAPK and cell cycle arrest may finally progress to apoptosis in
17496232	p38	p38	2.2	apoptosis in the presence of NO which may activate the p38 MAPK pathway
17496232	MAPK	MAPK	2.2	in the presence of NO which may activate the p38 MAPK pathway
17496232	p38	p38	2.2	In accord the p38 inhibitor SB-203580 blocks proapoptotic effects of NO in SH-SY5Y neurons
17496232	p38	p38	2.2	The activating NO effects and p38 MAPK signaling probably result in Bax translocation to mitochondria a
17496232	MAPK	MAPK	2.2	The activating NO effects and p38 MAPK signaling probably result in Bax translocation to mitochondria a well-known
17496232	p38	p38	2.2	microM H 2 O 2 causes a rapid activation of p38 MAPK cascade with phosphorylation of MKK3/6 MKK3 6 and p38
17496232	MAPK	MAPK	2.2	H 2 O 2 causes a rapid activation of p38 MAPK cascade with phosphorylation of MKK3/6 MKK3 6 and p38 MAPK
17496232	p38	p38	2.2	p38 MAPK cascade with phosphorylation of MKK3/6 MKK3 6 and p38 MAPK and activating transcription factors (ATF)-1 ATF -1 (cAMP cAMP
17496232	MAPK	MAPK	2.2	MAPK cascade with phosphorylation of MKK3/6 MKK3 6 and p38 MAPK and activating transcription factors (ATF)-1 ATF -1 (cAMP cAMP response
17496232	p38	p38	2.2	and were cancelled by N -acetylcysteine or SB-203580 a specific p38 MAPK inhibitor
17496232	MAPK	MAPK	2.2	were cancelled by N -acetylcysteine or SB-203580 a specific p38 MAPK inhibitor
17496232	p38	p38	2.2	In this case also p38 and ERK were activated by H 2 O 2 however
17496232	ERK	ERK	2.2	In this case also p38 and ERK were activated by H 2 O 2 however only JNK-related
17496232	p38	p38	2.2	Early activation of p38 MAPK and ERK does not seem to be dependent on
17496232	MAPK	MAPK	2.2	Early activation of p38 MAPK and ERK does not seem to be dependent on cytotoxic
17496232	ERK	ERK	2.2	Early activation of p38 MAPK and ERK does not seem to be dependent on cytotoxic factors like
17496232	p38	p38	2.2	suggest that physiological H 2 O 2 -dependent activation of p38 MAPK may proceed many steps before a significant Ca release
17496232	MAPK	MAPK	2.2	that physiological H 2 O 2 -dependent activation of p38 MAPK may proceed many steps before a significant Ca release from
17496232	MAPK	MAPK	2.2	Mitochondrial redox contribution to the activation of MAPK cascades was also confirmed in the hypothyroid model
17496232	p38	p38	2.2	2 O 2 and peroxynitrite with the concomitant activation of p38 MAPK and the inactivation of ERK1/2 ERK1 2
17496232	MAPK	MAPK	2.2	O 2 and peroxynitrite with the concomitant activation of p38 MAPK and the inactivation of ERK1/2 ERK1 2
17496232	MAPK	MAPK	2.2	As shown before this MAPK pattern is consistent with cell cycle arrest and inhibition of
17496232	MAPK	MAPK	2.2	hypothyroid cell signaling back to control status indicates that differential MAPK activation and cyclin D 1 expression should not depend on
17496232	ERK	ERK	2.2	cell types and its expression is positively regulated by the ERK pathway and antagonized by stress-activated p38 MAPK cascade ( 84
17496232	p38	p38	2.2	positively regulated by the ERK pathway and antagonized by stress-activated p38 MAPK cascade ( 84
17496232	MAPK	MAPK	2.2	regulated by the ERK pathway and antagonized by stress-activated p38 MAPK cascade ( 84
17496232	p38	p38	2.2	liver development cyclin D 1 content is inversely related to p38 MAPK activity which in turn may be regulated by ROS
17496232	MAPK	MAPK	2.2	development cyclin D 1 content is inversely related to p38 MAPK activity which in turn may be regulated by ROS (
17496232	MAPK	MAPK	2.2	observed that modulation of mtNOS and subsequent redox changes regulate MAPK cascades and cell cycle regulatory proteins in the sequence of
17496232	p38	p38	2.2	1 expression associated with high ERK1/2 ERK1 2 and low p38 MAPK activities
17496232	MAPK	MAPK	2.2	expression associated with high ERK1/2 ERK1 2 and low p38 MAPK activities
17496232	MAPK	MAPK	2.2	Moreover isolated hepatocyte proliferation rate may be modulated by MAPK inhibitors or stimulators like U-0126 (MEK MEK inhibitor SB-202190 (p38
17496232	p38	p38	2.2	inhibitors or stimulators like U-0126 (MEK MEK inhibitor SB-202190 (p38 p38 inhibitor or anisomycin (p38 p38 activator suggesting that hepatocyte proliferation
17496232	p38	p38	2.2	(MEK MEK inhibitor SB-202190 (p38 p38 inhibitor or anisomycin (p38 p38 activator suggesting that hepatocyte proliferation signaling is related to a
17496232	p38	p38	2.2	cell death with the activation of JNK/SAPK JNK SAPK and p38 MAPK and caspase 3 or inactivation of NF-kappaB.
17496232	MAPK	MAPK	2.2	death with the activation of JNK/SAPK JNK SAPK and p38 MAPK and caspase 3 or inactivation of NF-kappaB.
17496232	p38	p38	2.2	Because proapoptotic p38 or JNK1/2 JNK1 2 did not become phosphorylated we surmise
17496232	MAPK	MAPKs	2.2	setting H 2 O 2 ss with differential activation of MAPKs Akt and cyclin D In this sense very low NO
17956327	ERK	ERK	0.9	(tropomyosin tropomyosin receptor kinase B resulting in the phosphorylation of ERK (extracellular-signal-regulated extracellular-signal-regulated kinase MAPKs (mitogen-activated mitogen-activated protein kinases and Akt
17956327	MAPK	MAPKs	0.9	B resulting in the phosphorylation of ERK (extracellular-signal-regulated extracellular-signal-regulated kinase MAPKs (mitogen-activated mitogen-activated protein kinases and Akt also called PKB (protein
17956327	ERK	ERK	0.9	phosphatases that may play a role in neural plasticity including ERK and the serine/threonine serine threonine protein phosphatases 1 2A and
17956327	ERK	ERK	0.9	is necessary for pLTF 42 and activated forms of both ERK and PKB (Akt) Akt are increased in the ventral cervical
17956327	ERK	ERK	0.9	Abbreviations used AIH acute intermittent hypoxia BDNF brain-derived neurotrophic factor ERK extracellular-signal-regulated kinase 5-HT 5-hydroxytryptamine LTF long-term facilitation pLTF phrenic LTF
15031734	mitogen-activated protein kinase 1	mitogen activated protein kinase 1	1.0	hne activates c jun aminoterminal kinases and mitogen activated protein kinase 1 also known as p38 thereby stimulating an apoptotic cascade 15 .
15031734	mitogen-activated protein kinase 1	mitogen activated protein kinase 1	1.0	beta actin catalase creatine kinase frataxin glucose transporter type 3 glutathione peroxidase glutathione reductase mitogen activated protein kinase 1 sod alpha synuclein xanthine dehydrogenase