Learned by Reading
In the ICWSM 2009 Weblog Corpus:
Whole genome – microarray analyses suggest that these mutants cause constitutive activation of osmoregulatory signaling pathways.
(Parse)
(S1 (NP (NP (JJ Whole) (NN genome)) (: -)
(S (NP (JJ microarray) (NNS analyses))
(VP (VBP suggest)
(SBAR (IN that)
(S (NP (DT these) (NNS mutants))
(VP (VBP cause)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (JJ osmoregulatory) (VBG signaling) (NNS pathways)))
(. .)))
In Wikipedia:
Recently on other components of the Wnt signaling pathway have also demonstrated a likely role for constitutive activation of this pathway in the etiology of hepatoblastoma.
(Parse)
(S1 (S (NP (NP (RB Recently))
(PP (IN on)
(NP (NP (JJ other) (NNS components))
(PP (IN of)
(NP (DT the) (JJ Wnt) (VBG signaling) (NN pathway)))
(VP (AUX have) (ADVP (RB also))
(VP (VBN demonstrated)
(NP (DT a) (JJ likely) (NN role))
(PP (IN for)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (DT this) (NN pathway)))))
(PP (IN in)
(NP (NP (DT the) (NN etiology))
(PP (IN of)
(NP (NN hepatoblastoma))))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Constitutive activation of the RTK / RAS / MAPK causes all six VPCs to be activated resulting in a multivulva (Muv) phenotype.
(Parse)
(S1 (S (NP (NP (JJ Constitutive) (NN activation))
(PP (IN of)
(NP (DT the) (NNP RTK) (NNP /) (NNP RAS) (NNP /))))
(ADVP (RB MAPK))
(VP (VBZ causes)
(S (NP (DT all) (CD six) (NNS VPCs))
(VP (TO to)
(VP (AUX be)
(VP (VBN activated)
(S (VP (VBG resulting)
(PP (IN in)
(NP (DT a) (CD multivulva) (-LRB- -LRB-) (NNP Muv) (-RRB- -RRB-) (NN phenotype))))
(. .)))
In the ICWSM 2009 Weblog Corpus:
RESULTS: It was found that constitutive activation of PSA expression was the result of sustained occupancy by the AR at the regulatory region of this gene.
(Parse)
(S1 (NP (NP (NNS RESULTS)) (: :)
(S (NP (PRP It))
(VP (AUX was)
(VP (VBN found)
(SBAR (IN that)
(S (NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (NNP PSA) (NN expression))))
(VP (AUX was)
(NP (NP (DT the) (NN result))
(PP (IN of)
(NP (NP (JJ sustained) (NN occupancy))
(PP (IN by)
(NP (DT the) (NNP AR)))
(PP (IN at)
(NP (NP (DT the) (JJ regulatory) (NN region))
(PP (IN of)
(NP (DT this) (NN gene)))))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Mutation of pry – 1 leads to constitutive activation of BAR – 1 / beta – catenin – dependent Wnt signaling and results in a range of developmental defects.
(Parse)
(S1 (S (NP (NP (NN Mutation))
(PP (IN of)
(NP (VB pry) (: -)
(NP (NP (CD 1) (NNS leads))
(PP (TO to)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (NN BAR)))
(: -)
(NP (CD 1) (NNP /) (NN beta)) (: -)
(NP (NN catenin)) (: -)
(NP (JJ dependent) (NNP Wnt)))))
(VP (VBG signaling) (CC and) (VBZ results)
(PP (IN in)
(NP (NP (DT a) (NN range))
(PP (IN of)
(NP (JJ developmental) (NNS defects)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Constitutive activation of S6K in the MBH mimicked the effect of the HFD in normal chow? fed animals, while suppression of S6K by overexpression of dominant – negative S6K or dominant – negative raptor in the MBH restored the ability of MBH insulin to suppress HGP after HFD feeding.
(Parse)
(S1 (S (NP (NP (JJ Constitutive) (NN activation))
(PP (IN of)
(NP (NNP S6K)))
(PP (IN in)
(NP (DT the) (NNP MBH))))
(VP (VBD mimicked)
(NP (NP (DT the) (NN effect))
(PP (IN of)
(NP (DT the) (NNP HFD))))
(PP (IN in)
(NP (JJ normal) (NN chow)))
(. ?)
(VP (VBN fed)
(NP (NNS animals)) (, ,)
(SBAR (IN while)
(S (NP (NP (NN suppression))
(PP (IN of)
(NP (NNP S6K)))
(PP (IN by)
(NP (NP (NN overexpression))
(PP (IN of)
(NP (NP (JJ dominant) (PRN (: -) (UCP (NP (JJ negative) (NNS S6K)) (CC or)
(ADJP (JJ dominant)))
(: -)) (JJ negative) (NN raptor))
(PP (IN in)
(NP (DT the) (NNP MBH)))))
(VP (VBD restored)
(NP (NP (DT the) (NN ability))
(PP (IN of)
(NP (JJ MBH) (NN insulin)))
(S (VP (TO to)
(VP (VB suppress)
(NP (NNS HGP))
(PP (IN after)
(NP (NNP HFD) (NN feeding)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Induction of cell adhesion correlated with cation – induced binding to ICAM – 1, clustering of LFA – 1 into lipid rafts and constitutive activation of the Rap1 and Rac1 GTPases.
(Parse)
(S1 (S (NP (NP (NN Induction))
(PP (IN of)
(NP (NN cell) (NN adhesion))))
(VP (VBD correlated)
(PP (IN with)
(NP (NP (NN cation)) (PRN (: -)
(VP (VBN induced)
(PP (VBG binding)
(PP (TO to)
(NP (NNP ICAM)))))
(: -)) (CD 1)))
(, ,)
(S (VP (VBG clustering)
(PP (IN of)
(NP (CD LFA) (: -) (CD 1)))
(PP (IN into)
(NP (NP (NN lipid) (NNS rafts)) (CC and)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (DT the) (NNP Rap1) (CC and) (NNP Rac1) (NNS GTPases)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
We here describe that constitutive activation of the Stat5 – PI3K – Akt – cascade controls neoplastic MC development.
(Parse)
(S1 (S (S (NP (PRP We)) (ADVP (RB here))
(VP (VBP describe)
(NP (NP (DT that) (JJ constitutive) (NN activation))
(PP (IN of)
(NP (DT the) (NNP Stat5) (PRN (: -)
(NP (CD PI3K)) (: -)) (NNP Akt)))
(: -)
(S (NP (NN cascade))
(VP (VBZ controls)
(NP (JJ neoplastic) (NNP MC) (NN development))))
(. .)))
In Wikipedia:
Phosphoinositide – 3 – kinase (PI – 3 – K) activates an important cell survival signaling pathway, and constitutive activation is seen in ovarian, head and neck, urinary tract, cervical and small cell lung cancer.
(Parse)
(S1 (S (S (NP (NP (NNP Phosphoinositide) (PRN (: -)
(NP (CD 3)) (: -)) (NN kinase)) (PRN (-LRB- -LRB-)
(NP (NN PI)) (: -)
(NP (NP (CD 3)) (: -)
(NP (NNP K)))
(-RRB- -RRB-)))
(VP (VBZ activates)
(NP (NP (DT an) (JJ important) (NN cell) (NN survival))
(VP (VBG signaling)
(NP (NN pathway)))
(, ,) (CC and)
(S (NP (JJ constitutive) (NN activation))
(VP (AUX is)
(VP (VBN seen)
(PP (IN in)
(NP (NP (NN ovarian) (, ,) (NN head) (CC and) (NN neck)) (, ,)
(NP (JJ urinary) (NN tract)) (, ,)
(NP (JJ cervical) (CC and) (JJ small) (NN cell) (NN lung) (NN cancer))))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Glucose stimulates a 3 – fold increase in the rate of ChREBP nuclear entry, but trapping ChREBP in the nucleus by mutagenesis or with a nuclear export inhibitor does not lead to constitutive activation.
(Parse)
(S1 (S (S (NP (NN Glucose))
(VP (VBZ stimulates)
(NP (DT a) (CD 3))))
(: -)
(S (VP (VB fold)
(NP (NN increase))
(PP (IN in)
(NP (NP (DT the) (NN rate))
(PP (IN of)
(NP (NNP ChREBP) (JJ nuclear) (NN entry))))
(, ,) (CC but)
(S (S (VP (VBG trapping)
(NP (NNP ChREBP))
(PP (IN in)
(NP (DT the) (NN nucleus)))
(PP (PP (IN by)
(NP (NN mutagenesis)))
(CC or)
(PP (IN with)
(NP (DT a) (JJ nuclear) (NN export) (NN inhibitor)))
(VP (AUX does) (RB not)
(VP (VB lead)
(PP (TO to)
(NP (JJ constitutive) (NN activation)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Constitutive activation of mitogen – activated protein kinase (MAPK) is a property common to many oncoproteins, including Mos, Ras, and Raf, and is essential for their transforming activities.
(Parse)
(S1 (S (NP (NP (JJ Constitutive) (NN activation))
(PP (IN of)
(NP (NP (NNS mitogen)) (PRN (: -)
(NP (VBN activated) (NN protein) (NN kinase)) (-LRB- -LRB-)
(NP (NNP MAPK)) (-RRB- -RRB-)))))
(VP (VP (AUX is)
(ADJP (NP (DT a) (NN property)) (JJ common)
(PP (TO to)
(NP (NP (JJ many) (NNS oncoproteins)) (, ,)
(PP (VBG including)
(NP (NNP Mos) (, ,) (NNP Ras) (, ,) (CC and) (NN Raf)))
(, ,)))))
(CC and)
(VP (AUX is)
(ADJP (JJ essential)
(PP (IN for)
(NP (PRP$ their) (VBG transforming) (NNS activities)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
In small cell lung cancer (SCLC), non – small cell lung cancer (NSCLC), and malignant pleural mesothelioma (MPM), MET is dysregulated via overexpression, constitutive activation, gene amplification, ligand – dependent activation, mutation or epigenetic mechanisms.
(Parse)
(S1 (FRAG (PP (IN In)
(NP (NP (JJ small) (NN cell) (NN lung) (NN cancer)) (PRN (-LRB- -LRB-)
(NP (NNP SCLC)) (-RRB- -RRB-)) (, ,)
(NP (NN non)) (: -)
(NP (NP (JJ small) (NN cell) (NN lung) (NN cancer)) (PRN (-LRB- -LRB-)
(NP (NNP NSCLC)) (-RRB- -RRB-)))
(, ,) (CC and)
(NP (JJ malignant) (JJ pleural) (NN mesothelioma))))
(PRN (-LRB- -LRB-) (JJ MPM) (-RRB- -RRB-)) (, ,)
(VP (VBD MET)
(SBAR (S (VP (AUX is)
(VP (VBN dysregulated)
(PP (IN via)
(NP (NP (NN overexpression)) (, ,)
(NP (JJ constitutive) (NN activation)) (, ,)
(NP (NN gene) (NN amplification)) (, ,)
(NP (NNP ligand)))
(: -)
(NP (NP (JJ dependent) (NN activation)) (, ,)
(NP (NN mutation)) (CC or)
(NP (JJ epigenetic) (NNS mechanisms)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Previous studies have demonstrated that mutations in cuticle collagens required for annular furrow formation (e. g., dpy – 2, 7, 8, and 10) and mutations in a group of non – collagen proteins that are thought to be secreted from the hypodermis to the cuticle (e. g., osm – 7, osm – 11, and osr – 1) cause constitutive activation of the glycerol accumulation pathway.
(Parse)
(S1 (S (NP (JJ Previous) (NNS studies))
(VP (AUX have)
(VP (VBN demonstrated)
(PP (IN that)
(NP (NP (NNS mutations))
(PP (IN in)
(NP (NP (NP (NP (JJ cuticle) (NNS collagens))
(VP (VBN required)
(PP (IN for)
(NP (NP (JJ annular) (NN furrow) (NN formation)) (PRN (-LRB- -LRB-)
(NP (NNP e) (. .) (NNP g) (. .)) (, ,)
(NP (NP (NN dpy)) (: -)
(NP (CD 2) (, ,) (CD 7) (, ,) (CD 8) (, ,) (CC and) (CD 10)))
(-RRB- -RRB-)) (CC and)
(NP (NP (NNS mutations))
(PP (IN in)
(NP (NP (DT a) (NN group))
(PP (IN of)
(NP (NN non))))
(: -)
(NP (NP (NN collagen) (NNS proteins))
(SBAR (WHNP (WDT that))
(S (VP (AUX are)
(VP (VBN thought)
(S (VP (TO to)
(VP (AUX be)
(VP (VBN secreted)
(PP (IN from)
(NP (NP (DT the) (NN hypodermis))
(PP (TO to)
(NP (NP (DT the) (JJ cuticle) (-LRB- -LRB-) (LST (LS e) (. .)) (NNP g) (. .)) (, ,)
(NP (NN osm)))
(: -)
(NP (CD 7)) (, ,)
(NP (NN osm)) (: -)
(NP (CD 11)) (, ,) (CC and)
(NP (NN osr)))
(: -)
(S (LST (LS 1) (-RRB- -RRB-))
(VP (VB cause)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (DT the) (NN glycerol) (NN accumulation) (NN pathway)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
One, ga199, can affect wild – type vulval induction byitself and another, ga136, can suppress the Muv phenotype caused by constitutive activation of let – 60 ras.
(Parse)
(S1 (S (S (NP (NP (NN One)) (, ,)
(NP (CD ga199)) (, ,))
(VP (MD can)
(VP (VB affect)
(ADJP (JJ wild)))))
(: -)
(S (NP (NP (NN type) (JJ vulval) (NN induction) (NN byitself)) (CC and)
(NP (NP (DT another)) (, ,)
(NP (CD ga136)) (, ,)))
(VP (MD can)
(VP (VB suppress)
(NP (NP (DT the) (NNP Muv) (NN phenotype))
(VP (VBN caused)
(PP (IN by)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (VB let) (: -) (CD 60) (FW ras))))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Approximately 90 % of normal moles and 60 % of early invasive cutaneous melanomas contain a T1799A B – Raf mutation (V600EB – Raf), leading to 10 times higher enzyme activity and constitutive activation of the mitogen – activated protein kinase pathway.
(Parse)
(S1 (S (NP (NP (NP (QP (RB Approximately) (CD 90)) (NN %))
(PP (IN of)
(NP (JJ normal) (NNS moles))))
(CC and)
(NP (NP (CD 60) (NN %))
(PP (IN of)
(NP (JJ early) (JJ invasive) (JJ cutaneous) (NNS melanomas)))))
(VP (VBP contain)
(NP (DT a) (NNP T1799A) (NNP B) (PRN (: -)
(NP (NP (NN Raf) (NN mutation)) (PRN (-LRB- -LRB-)
(NP (NNP V600EB)) (: -)
(NP (NN Raf)) (-RRB- -RRB-)) (, ,)
(VP (VBG leading)
(PP (TO to)
(NP (NP (ADJP (NP (CD 10) (NNS times)) (JJR higher)) (JJ enzyme) (NN activity)) (CC and)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (DT the) (NN mitogen)))))
(: -)) (VBN activated) (NN protein) (NN kinase) (NN pathway)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
The intrinsic GTPase activity of the alpha subunit is reduced by this mutation, presumably resulting in constitutive activation of its signal transduction pathway.
(Parse)
(S1 (S (NP (NP (DT The) (JJ intrinsic) (JJ GTPase) (NN activity))
(PP (IN of)
(NP (DT the) (NN alpha) (NN subunit))))
(VP (AUX is)
(VP (VBN reduced)
(PP (IN by)
(NP (DT this) (NN mutation)))
(, ,)
(S (ADVP (RB presumably))
(VP (VBG resulting)
(PP (IN in)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (PRP$ its) (NN signal) (NN transduction) (JJ pathway)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Stat3 – regulated factors produced by both tumor cells and tumor – derived myeloid cells also induced constitutive activation of Stat3 in tumor endothelium, and inhibiting Stat3 in ECs substantially reduced in vitro tumor factorinduced endothelial migration and tube formation.
(Parse)
(S1 (FRAG (NP (NNP Stat3)) (: -)
(S (S (NP (JJ regulated) (NNS factors))
(VP (VBN produced)
(PP (IN by)
(NP (PDT both)
(NP (NN tumor) (NNS cells)) (CC and)
(NP (NN tumor)))
(: -)
(S (NP (VBN derived) (JJ myeloid) (NNS cells)) (ADVP (RB also))
(VP (VBN induced)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (NNP Stat3))))
(PP (IN in)
(NP (NN tumor) (NN endothelium)))))
(, ,) (CC and)
(S (VP (VBG inhibiting)
(NP (NNP Stat3))
(PP (IN in)
(NP (NP (NNS ECs))
(VP (ADVP (RB substantially)) (VBN reduced)
(PP (IN in)
(NP (NN vitro) (NN tumor) (JJ factorinduced) (JJ endothelial) (NN migration) (CC and) (NN tube) (NN formation)))
(. .)))
In the ICWSM 2009 Weblog Corpus:
Similarly, the constitutive activation of signaling cascades that stimulate cell growth has a profound impact on anabolic metabolism.
(Parse)
(S1 (S (ADVP (RB Similarly)) (, ,)
(NP (NP (DT the) (JJ constitutive) (NN activation))
(PP (IN of)
(NP (NP (VBG signaling) (NNS cascades))
(SBAR (WHNP (WDT that))
(S (VP (VB stimulate)
(NP (NN cell) (NN growth)))))
(VP (AUX has)
(NP (NP (DT a) (JJ profound) (NN impact))
(PP (IN on)
(NP (JJ anabolic) (NN metabolism)))))
(. .)))
In the ICWSM 2009 Weblog Corpus:
To identify genes encoding negative regulators of the glp – 1 signalling pathway, we screened for enhancer mutations that confer a tumorous phenotype in a sensitized glp – 1 genetic background, glp – 1 (oz112oz120). glp – 1 (oz112oz120) was identified as a cis intragenic revertant of glp – 1 (oz112gf), a novel glp – 1 (gf) mutation which results in constitutive activation of the glp – 1 (oz112gf) receptor.
(Parse)
(S1 (FRAG (S (VP (TO To)
(VP (VB identify)
(NP (NNS genes))
(PP (VBG encoding)
(NP (NP (JJ negative) (NNS regulators))
(PP (IN of)
(NP (DT the) (NN glp)))))
(: -)
(S (NP (CD 1) (VBG signalling) (NN pathway)) (, ,)
(NP (PRP we))
(VP (VBN screened)
(PP (IN for)
(NP (NP (NN enhancer) (NNS mutations))
(SBAR (WHNP (WDT that))
(S (VP (VBP confer)
(NP (DT a) (JJ tumorous) (NN phenotype))
(PP (IN in)
(NP (DT a) (JJ sensitized) (NN glp))))
(: -)
(NP (CD 1) (JJ genetic) (NN background)) (, ,)
(NP (NP (NN glp)) (: -)
(NP (NP (CD 1)) (PRN (-LRB- -LRB-)
(NP (CD oz112oz120)) (-RRB- -RRB-)) (. .) (JJ glp)) (: -)
(S (NP (NP (CD 1)) (PRN (-LRB- -LRB-)
(NP (CD oz112oz120)) (-RRB- -RRB-)))
(VP (AUX was)
(VP (VBN identified)
(PP (IN as)
(NP (NP (NP (DT a) (NN cis)) (JJ intragenic) (NN revertant))
(PP (IN of)
(NP (NP (NN glp)) (: -)
(NP (NP (CD 1)) (PRN (-LRB- -LRB-)
(NP (CD oz112gf)) (-RRB- -RRB-)) (, ,)
(NP (DT a) (NN novel) (NN glp)))
(: -)
(NP (NP (CD 1) (PRN (-LRB- -LRB-)
(NP (NNP gf)) (-RRB- -RRB-)) (NN mutation))
(SBAR (WHNP (WDT which))
(S (VP (VBZ results)
(PP (IN in)
(NP (NP (JJ constitutive) (NN activation))
(PP (IN of)
(NP (DT the) (NN glp)))
(: -)
(NP (CD 1) (PRN (-LRB- -LRB-)
(NP (CD oz112gf)) (-RRB- -RRB-)) (NN receptor))))
(. .)))
And 31 more sentences.