HUGO ID Detailed Result 8978

PMID	Match String	Actual String	Score	Flanking text	Edited by	Edit
12654515	PI3K	PI3-K	2.6	VEGF activated both PI3-K and MAPK activities in mouse NSC34 motor neuron-like cells
12654515	PI3K	PI3-K	2.6	active as well as dominant negative mutants of MAPK and PI3-K revealed that the protective effects of VEGF were mediated via
12654515	PI3K	PI3-K	2.6	that the protective effects of VEGF were mediated via the PI3-K activity and that MAPK activation was not associated with NSC34
12654515	PI3K	PI3-K	2.6	motor neuron-like cell death from mutant G93A-SOD1 effects via PI3-K/Akt PI3-K Akt activation
12654515	PI3K	PI3-K	2.6	initiate several intracellular signal transduction systems including phosphatidylinositol 3-kinase (PI3-K) PI3-K and mitogen-activated protein kinase (MAPK) MAPK 42
12654515	PI3K	PI3-K	2.6	VEGF activates both PI3-K and MAPK activities in NSC34 motor neuron-like cells
12654515	PI3K	PI3-K	2.6	and constitutively active and dominant negative mutants of MAPK and PI3-K we further demonstrate that PI3-K activity but not MAPK activity
12654515	PI3K	PI3-K	2.6	negative mutants of MAPK and PI3-K we further demonstrate that PI3-K activity but not MAPK activity protects mouse NSC34 cells from
12654515	PI3K	PI3-K	2.6	neuron-like cell survival is mediated by activation of the PI3-K/Akt PI3-K Akt pathway 2
12654515	PI3K	PI3-K	2.6	Wild-type and constitutively active PI3-K catalytic subunit p110 (myristoylated) myristoylated and dominant negative PI3-K regulatory
12654515	PI3K	PI3-K	2.6	active PI3-K catalytic subunit p110 (myristoylated) myristoylated and dominant negative PI3-K regulatory subunit p85 were purchased from Upstate Biochemical (Lake Lake
12654515	PI3K	PI3-K	2.6	were immunoprecipitated with p85 antibody and were subsequently used for PI3-K activity assay
12654515	PI3K	PI3-K	2.6	VEGF transiently activates PI3-K and MAPK activities
12654515	PI3K	PI3-K	2.6	PI3-K and/or and or MAPK signaling pathways underlie critical components of
12654515	PI3K	PI3-K	2.6	Thus we tested whether VEGF regulates PI3-K and/or and or MAPK activation in NSC34 cells
12654515	PI3K	PI3-K	2.6	VEGF induced concentration- and time-dependent increases in PI3-K and MAPK activities ( Fig 3 and Fig 4 suggesting
12654515	PI3K	PI3-K	2.6	VEGF-mediated PI3-K activity not MAPK activity promotes mouse NSC34 motor neuron-like cell
12654515	PI3K	PI3-K	2.6	To further examine the respective contributions of the PI3-K and MAPK signaling pathways to VEGF-induced cell survival the PI3-K
12654515	PI3K	PI3-K	2.6	PI3-K and MAPK signaling pathways to VEGF-induced cell survival the PI3-K inhibitors LY294002 at 50 _amp_#x3bc M or Wortmannin at 20
12654515	PI3K	PI3-K	2.6	PI3-K blockers reduced NSC34 cell viability even in the presence of
12654515	PI3K	PI3-K	2.6	In addition transfection with the constitutively active catalytic subunit of PI3-K P110 but not with the constitutively active MEK1 the upstream
12654515	PI3K	PI3-K	2.6	Conversely transfections with the dominant negative regulatory subunit of PI3-K P85 promoted cell death even in the presence of VEGF
12654515	PI3K	PI3-K	2.6	One of the downstream effectors of PI3-K is Akt activation
12654515	PI3K	PI3-K	2.6	It is well established that VEGF can activate both PI3-K and MAPK (MEK/ERK) MEK ERK pathways yet the protective effect
12654515	PI3K	PI3-K	2.6	of Matsuzaki et al 34 who showed that both the PI3-K and MAPK pathways participate in neuronal cell protection by VEGF
12654515	PI3K	PI3-K	2.6	It has become apparent that activation of kinases such as PI3-K or MAPK does not constitute an isolated event but rather
12654515	PI3K	PI3-K	2.6	Thus it is possible that the PI3-K/Akt PI3-K Akt signaling module recruited by VEGF in our experiments is
12654515	PI3K	PI3-K	2.6	activation is essential for implementation of the protective effect by PI3-K on mutant G93A-SOD1-mediated motor neuron-like cell survival
12654515	PI3K	PI3-K	2.6	is now well established as a critical protein activated by PI3-K governing the balance between survival and apoptosis 7 and 13
12654515	PI3K	PI3-K	2.6	We now demonstrate that the activation of PI3-K/Akt PI3-K Akt signaling pathways by VEGF can promote motor neuron-like cell
12654515	PI3K	PI3-K	2.6	However since the activation of PI3-K/Akt PI3-K Akt is a transient event ( Fig 4 the long-lasting
12654515	PI3K	PI3-K	2.6	pharmacological and molecular genetic approaches we have demonstrated that PI3-K/Akt PI3-K Akt activation is the primary contributor to the neuroprotective function
12654515	PI3K	PI3-K	2.6	VEGF activated PI3-K activity in mouse NSC34 motor neuron-like cells
12654515	PI3K	PI3-K	2.6	(25_amp_#x2013;200 25_amp_#x2013 200 ng/ml) ng ml and then assayed for PI3-K activity as described in Materials and methods
12654515	PI3K	PI3-K	2.6	(B) B The increase of PI3-K activity in three independent experiments compared to that of vector
12654515	PI3K	PI3-K	2.6	of time (30_amp_#x2013;180 30_amp_#x2013 180 min and then assayed for PI3-K activity as described in Materials and methods
12654515	PI3K	PI3-K	2.6	(D) D The increase of PI3-K activity in three independent experiments compared to that of vector
12654515	PI3K	PI3-K	2.6	Activation of PI3-K/Akt PI3-K Akt pathways by VEGF contributed to the protection from mutant
12654515	PI3K	PI3-K	2.6	(A) A PI3-K activity inhibitor LY294002 not MAPK activity inhibitor PD98059 contributed to
12654515	PI3K	PI3-K	2.6	(B) B Constitutively active PI3-K catalytic subunit (p110), p110 not constitutively active MEK1 contributed to
12654515	PI3K	PI3-K	2.6	(C) C Dominant negative p85 of PI3-K regulatory subunit not dominant negative MEK1 contributed to the loss
12654515	pi3-kinase	pi3 kinase	1.0	pi3 kinase activity assay