PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33741347-9	2021	All cases of PCh and CCh showed diffuse immunopositivities for cytokeratin 8, pan-cytokeratin and brachyury.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	13-16	keratin 8	Homo sapiens	63-76
10319753-9	1999	CONCLUSION: TcPT thyroid scintigraphy in the neonate with PCH provides a more specific diagnosis, is useful for selecting patients for re-evaluation to uncover transient PCH and discontinue TRT and defines dyshormonogenesis, which is familial and requires genetic counseling.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	58-61	TCPT	Homo sapiens	12-16
10319753-9	1999	CONCLUSION: TcPT thyroid scintigraphy in the neonate with PCH provides a more specific diagnosis, is useful for selecting patients for re-evaluation to uncover transient PCH and discontinue TRT and defines dyshormonogenesis, which is familial and requires genetic counseling.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	170-173	TCPT	Homo sapiens	12-16
34631707-6	2021	Herein, we aimed at preventing PCH during CCS via modulating adaptive cardiac and inflammatory responses by inhibiting GRK5 and/or stimulating ACs.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	31-34	G protein-coupled receptor kinase 5	Mus musculus	119-123
35390228-2	2022	Therefore, we conducted experiments to investigate whether GATA4 accumulation induces SA-PCH, and whether Bmi-1-RING1B promotes GATA4 ubiquitination and its selective autophagic degradation to prevent SA-PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	204-207	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	106-111
35390228-2	2022	Therefore, we conducted experiments to investigate whether GATA4 accumulation induces SA-PCH, and whether Bmi-1-RING1B promotes GATA4 ubiquitination and its selective autophagic degradation to prevent SA-PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	204-207	ring finger protein 2	Homo sapiens	112-118
35390228-2	2022	Therefore, we conducted experiments to investigate whether GATA4 accumulation induces SA-PCH, and whether Bmi-1-RING1B promotes GATA4 ubiquitination and its selective autophagic degradation to prevent SA-PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	204-207	GATA binding protein 4	Homo sapiens	128-133
35390228-12	2022	Downregulated GATA4 ameliorated SA-PCH and cardiac dysfunction by reducing GATA4-dependent hypertrophy and SASP-related molecules.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	35-38	GATA binding protein 4	Homo sapiens	14-19
35390228-12	2022	Downregulated GATA4 ameliorated SA-PCH and cardiac dysfunction by reducing GATA4-dependent hypertrophy and SASP-related molecules.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	35-38	GATA binding protein 4	Homo sapiens	75-80
12505264-8	2002	The absence of the HMGA2-LPP fusion in small populations of tumors with a normal karyotype suggests the primary nature of chromosomal rearrangements in the development of PCH affected by those aberrations.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	171-174	high mobility group AT-hook 2	Homo sapiens	19-24
12505264-8	2002	The absence of the HMGA2-LPP fusion in small populations of tumors with a normal karyotype suggests the primary nature of chromosomal rearrangements in the development of PCH affected by those aberrations.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	171-174	LIM domain containing preferred translocation partner in lipoma	Homo sapiens	25-28
11434565-9	2001	The difference in the melanin content between PCH and PCA subspecies is most likely related to tyrosinase levels, as suggested by the presence of unpigmented muzzle in the PCH subspecies compared with the black muzzle in the PCA subspecies.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	46-49	tyrosinase	Papio anubis	95-105
10881205-5	2000	ADH2 1 allele frequencies in alcoholics compared to their controls groups were: PP, .56 vs.62 (P =.66); PCA,.75 vs.56 (P =.09); PCH,.78 vs.32 (P =.009).	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	128-131	alcohol dehydrogenase 1B (class I), beta polypeptide	Homo sapiens	0-4
33741347-9	2021	All cases of PCh and CCh showed diffuse immunopositivities for cytokeratin 8, pan-cytokeratin and brachyury.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	13-16	T-box transcription factor 1	Homo sapiens	98-107
29166597-5	2017	In contrast, HP1beta is functionally associated with Suv4-20h2 and H4K20me3, and its loss induces global chromatin decompaction and an abnormal enrichment of CTCF in PCH and other genomic regions.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	166-169	chromobox 1	Homo sapiens	13-20
33296675-4	2020	Moreover, MeCP2 contributes to maintenance of PCH by promoting deposition of H3K9me3 and H4K20me3.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	46-49	methyl CpG binding protein 2	Mus musculus	10-15
32565793-8	2020	TCH and PCH have equal shares in patients with mutated DUOX2 or DUOXA2.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	8-11	dual oxidase 2	Homo sapiens	55-60
32565793-8	2020	TCH and PCH have equal shares in patients with mutated DUOX2 or DUOXA2.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	8-11	dual oxidase maturation factor 2	Homo sapiens	64-70
29166597-5	2017	In contrast, HP1beta is functionally associated with Suv4-20h2 and H4K20me3, and its loss induces global chromatin decompaction and an abnormal enrichment of CTCF in PCH and other genomic regions.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	166-169	CCCTC-binding factor	Homo sapiens	158-162
29095837-4	2017	We found that resveratrol suppressed, similar to anti-TNF-beta, TNF-beta-induced increased adhesiveness in an inflammatory microenvironment of T-lymphocytes and PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	161-164	lymphotoxin alpha	Homo sapiens	64-72
29095837-10	2017	Ultrastructural and cell viability assay investigations revealed that resveratrol revoked TNF-beta-induced dose-dependent degradative/apoptotic morphological changes, cell viability and proliferation in PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	203-206	lymphotoxin alpha	Homo sapiens	90-98
29095837-11	2017	Taken together, suppression of TNF-beta-induced inflammatory microenvironment in PCH by resveratrol/Sirt1 might be a novel therapeutic approach for targeting inflammation during rheumatoid arthritis.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	81-84	lymphotoxin alpha	Homo sapiens	31-39
29095837-11	2017	Taken together, suppression of TNF-beta-induced inflammatory microenvironment in PCH by resveratrol/Sirt1 might be a novel therapeutic approach for targeting inflammation during rheumatoid arthritis.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	81-84	sirtuin 1	Homo sapiens	100-105
27885439-11	2017	Loss of HER2 was also correlated to ER conversion in PCH cohort.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	53-56	erb-b2 receptor tyrosine kinase 2	Homo sapiens	8-12
28915617-1	2017	OBJECTIVE: This study was performed to investigate the proportion as well as the predictive factors of pathologic complete response in HER2-positive and axillary lymph node positive breast cancer after neoadjuvant paclitaxel, carboplatin plus with trastuzumab (PCH).	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	261-264	erb-b2 receptor tyrosine kinase 2	Homo sapiens	135-139
28915617-8	2017	CONCLUSIONS: Preoperative PCH regimen was an effective neoadjuvant therapy in HER2 positive and axillary lymph node positive patients, and patients coexisting with HR-negative and high Ki67 index may benefit more from this regimen.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	26-29	erb-b2 receptor tyrosine kinase 2	Homo sapiens	78-82
28273705-11	2017	Conclusion: TPO and DUOX2 variants are the common molecular pathogenesis in children with PCH suspected dyshormonogenesis.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	90-93	thyroid peroxidase	Homo sapiens	12-15
28273705-11	2017	Conclusion: TPO and DUOX2 variants are the common molecular pathogenesis in children with PCH suspected dyshormonogenesis.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	90-93	dual oxidase 2	Homo sapiens	20-25
28273705-12	2017	Monoallelic variants in TPO, DUOX2 or DUOXA2 are associated with PCH and showed wide variability in their phenotypes.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	65-68	thyroid peroxidase	Homo sapiens	24-27
28273705-12	2017	Monoallelic variants in TPO, DUOX2 or DUOXA2 are associated with PCH and showed wide variability in their phenotypes.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	65-68	dual oxidase 2	Homo sapiens	29-34
28273705-12	2017	Monoallelic variants in TPO, DUOX2 or DUOXA2 are associated with PCH and showed wide variability in their phenotypes.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	65-68	dual oxidase maturation factor 2	Homo sapiens	38-44
27108200-11	2016	Most one or two DUOX2 pathogenic variants turned out to be SCH or TCH, whereas patients with three or more DUOX2 pathogenic variants were mostly associated with PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	161-164	dual oxidase 2	Homo sapiens	107-112
26300654-4	2015	Mutations in the eukaryotic translation initiation factor 2alpha kinase 4 (EIF2AK4) gene were identified in familial and idiopathic PCH cases, suggesting EIF2AK4 is a genetic risk factor for PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	132-135	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	17-73
26872260-18	2016	Compared to control, total enzyme activity (SOD, POD, CAT, APX and GR) and soluble protein content increased, malonaldehyde (MDA) and hydrogen peroxide (H2O2) content reduced in PCH-treated plants.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	178-181	ascorbate peroxidase 2	Zea mays	59-62
27213000-5	2016	The effect of the two fetal cardiac genes, atrial natriuretic factor (ANF) and beta-myosin heavy chain (beta-MHC), on PCH was reversed by FP.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	118-121	natriuretic peptide type A	Mus musculus	43-68
27213000-5	2016	The effect of the two fetal cardiac genes, atrial natriuretic factor (ANF) and beta-myosin heavy chain (beta-MHC), on PCH was reversed by FP.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	118-121	natriuretic peptide type A	Mus musculus	70-73
27213000-5	2016	The effect of the two fetal cardiac genes, atrial natriuretic factor (ANF) and beta-myosin heavy chain (beta-MHC), on PCH was reversed by FP.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	118-121	myosin, heavy polypeptide 7, cardiac muscle, beta	Mus musculus	79-102
27213000-5	2016	The effect of the two fetal cardiac genes, atrial natriuretic factor (ANF) and beta-myosin heavy chain (beta-MHC), on PCH was reversed by FP.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	118-121	myosin, heavy polypeptide 7, cardiac muscle, beta	Mus musculus	104-112
26356361-3	2016	The aim of present study was to investigate tshr gene mutations in patients with primary congenital hypothyroidism, analyzing a sample of 106 patients that were diagnosed with PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	176-179	thyroid stimulating hormone receptor	Homo sapiens	44-48
26349762-11	2015	Monoallelic and biallelic DUOX2 pathogenic variants were mainly associated with TCH, while triallelic DUOX2 pathogenic variants were associated with PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	149-152	dual oxidase 2	Homo sapiens	102-107
26300654-4	2015	Mutations in the eukaryotic translation initiation factor 2alpha kinase 4 (EIF2AK4) gene were identified in familial and idiopathic PCH cases, suggesting EIF2AK4 is a genetic risk factor for PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	191-194	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	75-82
26300654-4	2015	Mutations in the eukaryotic translation initiation factor 2alpha kinase 4 (EIF2AK4) gene were identified in familial and idiopathic PCH cases, suggesting EIF2AK4 is a genetic risk factor for PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	191-194	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	154-161
26300654-5	2015	EIF2AK4 mutations were identified in 100% (6/6) of autosomal recessively inherited familial PCH and 20% (2/10) of sporadic PCH cases.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	92-95	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	0-7
26300654-8	2015	Bone morphogenetic protein receptor 2 (BMPR2) is a major genetic risk factor in pulmonary arterial hypertension and EIF2AK4 potentially connects with BMPR2 to cause PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	165-168	bone morphogenetic protein receptor type 2	Homo sapiens	0-37
26300654-8	2015	Bone morphogenetic protein receptor 2 (BMPR2) is a major genetic risk factor in pulmonary arterial hypertension and EIF2AK4 potentially connects with BMPR2 to cause PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	165-168	bone morphogenetic protein receptor type 2	Homo sapiens	39-44
26300654-8	2015	Bone morphogenetic protein receptor 2 (BMPR2) is a major genetic risk factor in pulmonary arterial hypertension and EIF2AK4 potentially connects with BMPR2 to cause PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	165-168	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	116-123
26300654-8	2015	Bone morphogenetic protein receptor 2 (BMPR2) is a major genetic risk factor in pulmonary arterial hypertension and EIF2AK4 potentially connects with BMPR2 to cause PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	165-168	bone morphogenetic protein receptor type 2	Homo sapiens	150-155
26300654-4	2015	Mutations in the eukaryotic translation initiation factor 2alpha kinase 4 (EIF2AK4) gene were identified in familial and idiopathic PCH cases, suggesting EIF2AK4 is a genetic risk factor for PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	132-135	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	75-82
26300654-4	2015	Mutations in the eukaryotic translation initiation factor 2alpha kinase 4 (EIF2AK4) gene were identified in familial and idiopathic PCH cases, suggesting EIF2AK4 is a genetic risk factor for PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	132-135	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	154-161
26300654-4	2015	Mutations in the eukaryotic translation initiation factor 2alpha kinase 4 (EIF2AK4) gene were identified in familial and idiopathic PCH cases, suggesting EIF2AK4 is a genetic risk factor for PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	191-194	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	17-73
25801166-3	2015	In contrast, maternal PCH (mat-PCH) is enriched for H3 lysine 9 tri-methylation (H3K9me3) and Hp1beta.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	22-25	chromobox 1	Mus musculus	94-101
26022890-4	2015	Possible interactions of 5-FU with PCH were pointed out using different characterization methods like spectroscopic techniques (FT-IR, UV-vis, XPS), thermogravimetrical and BET analysis.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	35-38	delta/notch like EGF repeat containing	Homo sapiens	173-176
26022890-11	2015	BET results confirmed the PCH synthesis and drug loading capacity.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	26-29	delta/notch like EGF repeat containing	Homo sapiens	0-3
25886868-5	2015	We detail the pathologic findings of PCH, describe the differential diagnosis, and present a review of the literature on the possible association of PCH with CTD.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	149-152	CTD	Homo sapiens	158-161
25801166-8	2015	Loss-of-function studies show that Hp1beta and not H3K9me3 prevents PRC1 targeting to mat-PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	90-93	chromobox 1	Mus musculus	35-42
25609374-7	2015	FCS with PCH revealed molecular brightness values for native 5-HT2C receptors equivalent to the molecular brightness of a homodimer.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	9-12	5-hydroxytryptamine receptor 2C	Homo sapiens	61-67
25006453-2	2014	Platelet-derived growth factor and its receptor (PDGFR) have been implicated in the pathogenesis of pulmonary hypertension in PAH and PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	134-137	platelet derived growth factor receptor beta	Homo sapiens	49-54
25134515-3	2014	We assembled a quantitative map for the abundance and interactions of 16 factors related to PCH in living cells and found that stably bound complexes of the histone methyltransferase SUV39H1/2 demarcate the PCH state.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	92-95	suppressor of variegation 3-9 1	Mus musculus	183-192
25134515-3	2014	We assembled a quantitative map for the abundance and interactions of 16 factors related to PCH in living cells and found that stably bound complexes of the histone methyltransferase SUV39H1/2 demarcate the PCH state.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	207-210	suppressor of variegation 3-9 1	Mus musculus	183-192
22299646-4	2012	The active species to react with O(2) in the catalytic reaction is switched from Co(II)(Ph(8)Pc) to protonated Co(I)(Ph(8)PcH), depending on the reducing ability of ferrocene derivatives employed.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	122-125	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	81-87
25174386-5	2014	Morphology of THP-1 cells in normal serum group was observed at post culture hour (PCH) 24, and that in burn serum group at PCH 3, 6, 24.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	83-86	GLI family zinc finger 2	Homo sapiens	14-19
22408001-6	2013	In addition to these findings, expression of osteocalcin and runt-related gene 2 (RUNX2) mRNA, both markers of bone formation, was lower in the PCH-treated defects than in the controls.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	144-147	RUNX family transcription factor 2	Rattus norvegicus	82-87
22408001-7	2013	In contrast, collagen type 1alpha2 and alpha-smooth muscle actin (alpha-SMA) mRNA levels were significantly higher in the PCH-treated defects after 1 week.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	122-125	actin gamma 2, smooth muscle	Rattus norvegicus	39-64
22408001-7	2013	In contrast, collagen type 1alpha2 and alpha-smooth muscle actin (alpha-SMA) mRNA levels were significantly higher in the PCH-treated defects after 1 week.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	122-125	actin gamma 2, smooth muscle	Rattus norvegicus	66-75
22408001-6	2013	In addition to these findings, expression of osteocalcin and runt-related gene 2 (RUNX2) mRNA, both markers of bone formation, was lower in the PCH-treated defects than in the controls.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	144-147	bone gamma-carboxyglutamate protein	Rattus norvegicus	45-56
22322243-1	2012	In a novel template synthesis of carbodiphosphoranes (CDPs), the phosphine functionalized CDP ligand C(dppm)(2) (dppm = Ph(2)PCH(2)PPh(2)) is formed in the coordination sphere of group 10 metals from CS(2) and 4 equivalents of dppm.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	125-128	cut like homeobox 1	Homo sapiens	54-57
22299646-5	2012	The protonation of Co(II)(Ph(8)Pc) inhibits the direct reduction of O(2); however, the proton-coupled electron transfer from Me(10)Fc to Co(II)(Ph(8)Pc) and the protonated [Co(II)(Ph(8)PcH)](+) occurs to produce Co(I)(Ph(8)PcH) and [Co(I)(Ph(8)PcH(2))](+), respectively, which react immediately with O(2).	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	185-188	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	137-143
22299646-5	2012	The protonation of Co(II)(Ph(8)Pc) inhibits the direct reduction of O(2); however, the proton-coupled electron transfer from Me(10)Fc to Co(II)(Ph(8)Pc) and the protonated [Co(II)(Ph(8)PcH)](+) occurs to produce Co(I)(Ph(8)PcH) and [Co(I)(Ph(8)PcH(2))](+), respectively, which react immediately with O(2).	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	185-188	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	212-217
22299646-5	2012	The protonation of Co(II)(Ph(8)Pc) inhibits the direct reduction of O(2); however, the proton-coupled electron transfer from Me(10)Fc to Co(II)(Ph(8)Pc) and the protonated [Co(II)(Ph(8)PcH)](+) occurs to produce Co(I)(Ph(8)PcH) and [Co(I)(Ph(8)PcH(2))](+), respectively, which react immediately with O(2).	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	185-188	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	233-238
22299646-6	2012	The rate-determining step is a proton-coupled electron-transfer reduction of O(2) by Co(II)(Ph(8)Pc) in the Co(II)(Ph(8)Pc)-catalyzed cycle with Me(2)Fc, whereas it is changed to the electron-transfer reduction of [Co(II)(Ph(8)PcH)](+) by Me(10)Fc in the Co(I)(Ph(8)PcH)-catalyzed cycle with Me(10)Fc.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	227-230	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	85-91
22299646-6	2012	The rate-determining step is a proton-coupled electron-transfer reduction of O(2) by Co(II)(Ph(8)Pc) in the Co(II)(Ph(8)Pc)-catalyzed cycle with Me(2)Fc, whereas it is changed to the electron-transfer reduction of [Co(II)(Ph(8)PcH)](+) by Me(10)Fc in the Co(I)(Ph(8)PcH)-catalyzed cycle with Me(10)Fc.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	227-230	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	108-114
22299646-6	2012	The rate-determining step is a proton-coupled electron-transfer reduction of O(2) by Co(II)(Ph(8)Pc) in the Co(II)(Ph(8)Pc)-catalyzed cycle with Me(2)Fc, whereas it is changed to the electron-transfer reduction of [Co(II)(Ph(8)PcH)](+) by Me(10)Fc in the Co(I)(Ph(8)PcH)-catalyzed cycle with Me(10)Fc.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	227-230	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	108-114
22299646-6	2012	The rate-determining step is a proton-coupled electron-transfer reduction of O(2) by Co(II)(Ph(8)Pc) in the Co(II)(Ph(8)Pc)-catalyzed cycle with Me(2)Fc, whereas it is changed to the electron-transfer reduction of [Co(II)(Ph(8)PcH)](+) by Me(10)Fc in the Co(I)(Ph(8)PcH)-catalyzed cycle with Me(10)Fc.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	227-230	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	255-260
22299646-4	2012	The active species to react with O(2) in the catalytic reaction is switched from Co(II)(Ph(8)Pc) to protonated Co(I)(Ph(8)PcH), depending on the reducing ability of ferrocene derivatives employed.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	122-125	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	111-116
22299646-5	2012	The protonation of Co(II)(Ph(8)Pc) inhibits the direct reduction of O(2); however, the proton-coupled electron transfer from Me(10)Fc to Co(II)(Ph(8)Pc) and the protonated [Co(II)(Ph(8)PcH)](+) occurs to produce Co(I)(Ph(8)PcH) and [Co(I)(Ph(8)PcH(2))](+), respectively, which react immediately with O(2).	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	185-188	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-25
22299646-5	2012	The protonation of Co(II)(Ph(8)Pc) inhibits the direct reduction of O(2); however, the proton-coupled electron transfer from Me(10)Fc to Co(II)(Ph(8)Pc) and the protonated [Co(II)(Ph(8)PcH)](+) occurs to produce Co(I)(Ph(8)PcH) and [Co(I)(Ph(8)PcH(2))](+), respectively, which react immediately with O(2).	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	185-188	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	137-143
22455844-11	2012	Increased number of mast cell and the up-regulation of PDGFR-beta may suggest mechanism for PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	92-95	platelet derived growth factor receptor beta	Homo sapiens	55-65
21971046-3	2011	Here we report that NFATc4 expression is also up-regulated by newly expressed protein kinase D3 (PKD3) to induce PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	113-116	nuclear factor of activated T cells 4	Homo sapiens	20-26
21971046-3	2011	Here we report that NFATc4 expression is also up-regulated by newly expressed protein kinase D3 (PKD3) to induce PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	113-116	protein kinase D3	Homo sapiens	78-95
21971046-3	2011	Here we report that NFATc4 expression is also up-regulated by newly expressed protein kinase D3 (PKD3) to induce PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	113-116	protein kinase D3	Homo sapiens	97-101
21971046-7	2011	Therefore, PKD3 is a pivotal mediator of the CaN-NFATc1/c3-PKD3-NFATc4 hypertrophic signaling cascade and a potential new drug target for the PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	142-145	protein kinase D3	Homo sapiens	11-15
21971046-7	2011	Therefore, PKD3 is a pivotal mediator of the CaN-NFATc1/c3-PKD3-NFATc4 hypertrophic signaling cascade and a potential new drug target for the PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	142-145	nuclear factor of activated T cells 1	Homo sapiens	49-55
21971046-7	2011	Therefore, PKD3 is a pivotal mediator of the CaN-NFATc1/c3-PKD3-NFATc4 hypertrophic signaling cascade and a potential new drug target for the PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	142-145	nuclear factor of activated T cells 4	Homo sapiens	64-70
19208733-10	2009	Peak and 6-h postprandial area under the curve glucose, insulin, and lipids were higher in PCH subjects, who also had higher fasting and postprandial levels of plasminogen activator inhibitor-1.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	91-94	insulin	Homo sapiens	56-63
19208733-10	2009	Peak and 6-h postprandial area under the curve glucose, insulin, and lipids were higher in PCH subjects, who also had higher fasting and postprandial levels of plasminogen activator inhibitor-1.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	91-94	serpin family E member 1	Homo sapiens	160-193
17318017-1	2007	Thyroid transcription factor-2 (TTF-2/FOXE1) is a polyalanine domain protein that regulates thyroid embryogenesis, but very few patients with permanent primary congenital hypothyroidism (pCH) harbor germline mutations of this or other transcription factors that are involved in thyroid development that might explain the etiology of pCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	187-190	forkhead box E1	Homo sapiens	0-30
17318017-1	2007	Thyroid transcription factor-2 (TTF-2/FOXE1) is a polyalanine domain protein that regulates thyroid embryogenesis, but very few patients with permanent primary congenital hypothyroidism (pCH) harbor germline mutations of this or other transcription factors that are involved in thyroid development that might explain the etiology of pCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	187-190	transcription termination factor 2	Homo sapiens	32-37
17318017-1	2007	Thyroid transcription factor-2 (TTF-2/FOXE1) is a polyalanine domain protein that regulates thyroid embryogenesis, but very few patients with permanent primary congenital hypothyroidism (pCH) harbor germline mutations of this or other transcription factors that are involved in thyroid development that might explain the etiology of pCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	187-190	forkhead box E1	Homo sapiens	38-43
17318017-3	2007	Therefore, in this study we investigated whether alanine (Ala) length polymorphisms and non-polymorphic mutations of the TTF-2 gene in pCH patients might be involved in the pathogenesis of pCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	135-138	transcription termination factor 2	Homo sapiens	121-126
17318017-10	2007	Therefore, this study demonstrates that mutations in the TTF-2 gene are rare in pCH patients and suggests that variations in the length of the Ala-tract could at least partially explain the etiology of pCH but not that of extra-thyroidal malformations.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	80-83	transcription termination factor 2	Homo sapiens	57-62
16246326-5	2005	As NOS contributes to angiogenesis and is reduced in the hypertensive pulmonary microcirculation, we examined the expression of NOS-III protein in situ in the lungs of patients with PCH.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	182-185	nitric oxide synthase 3	Homo sapiens	128-135
16246326-6	2005	Reduced microvascular expression of NOS-III protein by endothelial cells was observed in 4/6 (67%) cases of PCH, and all of these showed concomitant pulmonary vascular hypertensive remodeling.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	108-111	nitric oxide synthase 3	Homo sapiens	36-43
16271958-8	2005	Thus, based on this one finding, a role of LPP-HMGA2 in PCH should be considered.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	56-59	LIM domain containing preferred translocation partner in lipoma	Homo sapiens	43-46
16271958-8	2005	Thus, based on this one finding, a role of LPP-HMGA2 in PCH should be considered.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	56-59	high mobility group AT-hook 2	Homo sapiens	47-52
21111744-9	2011	In conclusion, increasing I(Ca-L) is sufficient to induce PCH through the calcineurin/NFAT and CaMKII/HDAC pathways.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	58-61	calcium/calmodulin-dependent protein kinase II alpha	Mus musculus	95-101
18077328-6	2007	Using PCH, we show that cytosolic Ste5 were mostly monomers.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	6-9	Ste5p	Saccharomyces cerevisiae S288C	34-38
18077328-7	2007	Artificial dimerization of Ste5, as confirmed by PCH, using a dimerizing tag, stimulated the interaction between Ste5 and Fus3.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	49-52	Ste5p	Saccharomyces cerevisiae S288C	27-31
18077328-7	2007	Artificial dimerization of Ste5, as confirmed by PCH, using a dimerizing tag, stimulated the interaction between Ste5 and Fus3.	poly(ethylene oxide)-b-poly(alpha-cholesteryl carboxylate-epsilon-caprolactone) block copolymer	49-52	Ste5p	Saccharomyces cerevisiae S288C	113-117