PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 17204094-9 2007 Biochemical characterization of the p200 molecule revealed a noncollagenous N-glycosylated acidic protein with an isoelectric point of approximately 5.5. Nitrogen 76-77 AT-rich interaction domain 2 Homo sapiens 36-40 17637825-5 2008 We show that the target antigen p200 is synthesized by both keratinocytes and fibroblasts, is disulfide-bonded, and participates in calcium-dependent molecular interactions. Disulfides 94-103 AT-rich interaction domain 2 Homo sapiens 32-36 17637825-5 2008 We show that the target antigen p200 is synthesized by both keratinocytes and fibroblasts, is disulfide-bonded, and participates in calcium-dependent molecular interactions. Calcium 132-139 AT-rich interaction domain 2 Homo sapiens 32-36 17381449-0 2007 Anti-p200 pemphigoid in a 17-year-old girl successfully treated with systemic corticosteroid and dapsone. Dapsone 97-104 AT-rich interaction domain 2 Homo sapiens 5-9 16360882-2 2006 Alcohol slowed the decision time (DT) component of reaction time, lengthened the latency of the P200 and P300 components, reduced N200 amplitude, increased P300 amplitude at parietal sites, and modified the effect of sagittal site on N500 difference wave peak amplitude. Alcohols 0-7 AT-rich interaction domain 2 Homo sapiens 96-100 10048585-5 1999 The 200 kDa protein (p200) is dephosphorylated within 2.5 min after heparin treatment with an IC50 that closely parallels the IC50 for growth inhibition. Heparin 68-75 AT-rich interaction domain 2 Homo sapiens 21-25 14675190-4 2003 Differential extraction experiments demonstrated that efficient recovery of p200 from the dermis was strongly dependent on the presence of reducing agents, suggesting that it forms highly insoluble oligomers and/or is extensively cross-linked to other extracellular matrix components by disulfide bonding. Disulfides 287-296 AT-rich interaction domain 2 Homo sapiens 76-80 14675190-9 2003 These data suggest that the p200 molecule contains N-glycans but lacks O-linked oligosaccharides and chondroitin/heparan sulfate side chains. n-glycans 51-60 AT-rich interaction domain 2 Homo sapiens 28-32 14675190-9 2003 These data suggest that the p200 molecule contains N-glycans but lacks O-linked oligosaccharides and chondroitin/heparan sulfate side chains. o-linked oligosaccharides 71-96 AT-rich interaction domain 2 Homo sapiens 28-32 14675190-9 2003 These data suggest that the p200 molecule contains N-glycans but lacks O-linked oligosaccharides and chondroitin/heparan sulfate side chains. Chondroitin 101-112 AT-rich interaction domain 2 Homo sapiens 28-32 14675190-9 2003 These data suggest that the p200 molecule contains N-glycans but lacks O-linked oligosaccharides and chondroitin/heparan sulfate side chains. Heparitin Sulfate 113-128 AT-rich interaction domain 2 Homo sapiens 28-32 12004326-4 2002 We describe the clinical, histologic, and immunopathologic features in a patient with anti-p200 pemphigoid, as well as his favorable response to treatment with systemic glucocorticosteroids and dapsone. glucocorticosteroids 169-189 AT-rich interaction domain 2 Homo sapiens 91-95 12004326-4 2002 We describe the clinical, histologic, and immunopathologic features in a patient with anti-p200 pemphigoid, as well as his favorable response to treatment with systemic glucocorticosteroids and dapsone. Dapsone 194-201 AT-rich interaction domain 2 Homo sapiens 91-95 16281877-6 2004 Biochemical characterization of the p200 molecule revealed a noncollagenous N-glycosylated acidic protein with an isoelectric point of approximately 5.5. Nitrogen 76-77 AT-rich interaction domain 2 Homo sapiens 36-40 10852920-2 2000 Previously, we reported the isolation of a heparan sulfate-binding collagenous protein, p200, that is expressed by Schwann cells in developing peripheral nerves ((1996) J. Biol. Heparitin Sulfate 43-58 AT-rich interaction domain 2 Homo sapiens 88-92 10048585-6 1999 Studies using the tyrosine phosphatase inhibitor, sodium orthovanadate, indicate that heparin blocks p200 phosphorylation by inhibiting a kinase. Sodium orthovanadate 50-70 AT-rich interaction domain 2 Homo sapiens 101-105 10048585-6 1999 Studies using the tyrosine phosphatase inhibitor, sodium orthovanadate, indicate that heparin blocks p200 phosphorylation by inhibiting a kinase. Heparin 86-93 AT-rich interaction domain 2 Homo sapiens 101-105 10048585-7 1999 Phosphorylation of p200 is not altered in heparin-resistant cells, supporting a role for p200 in mediating the antiproliferative effect of heparin. Heparin 139-146 AT-rich interaction domain 2 Homo sapiens 19-23 10048585-7 1999 Phosphorylation of p200 is not altered in heparin-resistant cells, supporting a role for p200 in mediating the antiproliferative effect of heparin. Heparin 139-146 AT-rich interaction domain 2 Homo sapiens 89-93 9042220-6 1996 RESULTS: Consistent with its parent MAb 29-13, purified and renatured scFV2913 showed affinity and specificity to the SAA p200 according to the immuno-histochemical staining study of 99 specimens of human sarcomas and other tissues. saa 118-121 AT-rich interaction domain 2 Homo sapiens 122-126 9656995-7 1998 Site-directed mutagenesis of the Cys-1151 residue (one of the catalytic dyad residues of the viral protease) and of the Gly-1300 residue (the viral protease cleavage site) abrogated protease activity and p200 precursor cleavage, respectively. Cysteine 33-36 AT-rich interaction domain 2 Homo sapiens 204-208 9656995-7 1998 Site-directed mutagenesis of the Cys-1151 residue (one of the catalytic dyad residues of the viral protease) and of the Gly-1300 residue (the viral protease cleavage site) abrogated protease activity and p200 precursor cleavage, respectively. Glycine 120-123 AT-rich interaction domain 2 Homo sapiens 204-208 7577143-5 1995 The N200 latency and the P300 latency were prolonged significantly by the intravenous injection of acetazolamide in the lacunar cerebral infarction group and in the healthy subject group but the N100 latency and the P200 latency did not show any significant changes. Acetazolamide 99-112 AT-rich interaction domain 2 Homo sapiens 216-220 33794742-10 2022 Manganese was associated with hypermethylation at four DNA methylation sites (FDR q-value <0.1), one of which was near the gene ARID2. Manganese 0-9 AT-rich interaction domain 2 Homo sapiens 128-133 8608441-5 1995 Bromocriptine increased the latencies of N100, P200 and P300 in the respective short-latency subject group, and decreased the latency of N200 in the long-latency subject group. Bromocriptine 0-13 AT-rich interaction domain 2 Homo sapiens 47-51 8528449-2 1995 The modified gel filtration media (Bio-Gel P-200) has a high capacity for Ag(I) (20 mumol/ml) and Pt(II) (8 mumol/ml) and has been shown to be stable and useful even in the presence of relatively high chloride (up to 1 M NaCl) and phosphate concentrations (0.25 M). Chlorides 201-209 AT-rich interaction domain 2 Homo sapiens 43-48 8528449-2 1995 The modified gel filtration media (Bio-Gel P-200) has a high capacity for Ag(I) (20 mumol/ml) and Pt(II) (8 mumol/ml) and has been shown to be stable and useful even in the presence of relatively high chloride (up to 1 M NaCl) and phosphate concentrations (0.25 M). Sodium Chloride 221-225 AT-rich interaction domain 2 Homo sapiens 43-48 8528449-2 1995 The modified gel filtration media (Bio-Gel P-200) has a high capacity for Ag(I) (20 mumol/ml) and Pt(II) (8 mumol/ml) and has been shown to be stable and useful even in the presence of relatively high chloride (up to 1 M NaCl) and phosphate concentrations (0.25 M). Phosphates 231-240 AT-rich interaction domain 2 Homo sapiens 43-48 8528449-4 1995 Bio-Gel P-200 modified using glutaraldehyde/thiourea and in the Ag(I) and Pt(II) form selectively binds biotinylated BSA (b-BSA) over BSA. Glutaral 29-43 AT-rich interaction domain 2 Homo sapiens 8-13 8528449-4 1995 Bio-Gel P-200 modified using glutaraldehyde/thiourea and in the Ag(I) and Pt(II) form selectively binds biotinylated BSA (b-BSA) over BSA. Thiourea 44-52 AT-rich interaction domain 2 Homo sapiens 8-13 2740657-2 1989 Results suggest that surface SP and SN1-2 and components V, VI and VII of ABSP and component P3 and P300 result from specific auditory system activation, while components N1-P2 of P200 and N2-N4 of P300 result from nonspecific systems. TFF2 protein, human 29-31 AT-rich interaction domain 2 Homo sapiens 180-184 34817398-7 2021 Electrophysiologically, a P200 (150-220 ms) enhancement was present in response to sexual images compared with neutral ones, which was absent in the low TCA group. Trichloroacetic Acid 153-156 AT-rich interaction domain 2 Homo sapiens 26-30 35045748-14 2022 A deleterious mutation in the SWItch/Sucrose Non-Fermentable (SWI/SNF) gene ARID2 was discovered in the patient without enhanced RAI avidity after therapy and an RAI-resistant tumor from another patient that was sampled off-study. Sucrose 37-44 AT-rich interaction domain 2 Homo sapiens 76-81 35144623-0 2022 Concomitant novel ALK-SSH2, EML4-ALK and ARID2-ALK, EML4-ALK double-fusion variants and confer sensitivity to crizotinib in two lung adenocarcinoma patients, respectively. Crizotinib 110-120 AT-rich interaction domain 2 Homo sapiens 41-46 35087963-7 2022 The presence of W, W3C as well as the Fe amount variation determined two different micro-galvanic corrosion mechanisms significantly changing the CR of coatings, 0.26 +- 0.02, 59.68 +- 1.21 and 59.06 +- 1.16 mum/year for P100, P200 and P400, respectively. Iron 38-40 AT-rich interaction domain 2 Homo sapiens 227-231 31075894-8 2019 Finally, the antiviral effects of IFITM1 on cell proliferation and HBV replication were found to be partially restored when HBc was co-transfected with BAF200. hbc 124-127 AT-rich interaction domain 2 Homo sapiens 152-158 994299-2 1976 Appearance of p200 was accompanied by a decrease in the synthesis of viral structural proteins, but [35S]methionine tryptic peptides from p200 were different from those derived from a 140,000-molecular-weight polypeptide that contains the amino acid sequences of viral structural proteins. Sulfur-35 101-104 AT-rich interaction domain 2 Homo sapiens 138-142 994299-2 1976 Appearance of p200 was accompanied by a decrease in the synthesis of viral structural proteins, but [35S]methionine tryptic peptides from p200 were different from those derived from a 140,000-molecular-weight polypeptide that contains the amino acid sequences of viral structural proteins. Peptides 124-132 AT-rich interaction domain 2 Homo sapiens 138-142 32113157-9 2020 The TAM subclass, which comprised 31% of liver cancers, showed a poor survival, expressed elevated levels of extracellular matrix genes, and was associated with somatic mutations of chromatin regulator ARID2. tam 4-7 AT-rich interaction domain 2 Homo sapiens 202-207 6435477-1 1984 In the separation of the triplet components of neurofilament (P 200, P 160, and P 68) by DE-52 column chromatography in the presence of urea, it was revealed that the efficiency of separation depended upon urea concentration. Urea 136-140 AT-rich interaction domain 2 Homo sapiens 62-84 6435477-1 1984 In the separation of the triplet components of neurofilament (P 200, P 160, and P 68) by DE-52 column chromatography in the presence of urea, it was revealed that the efficiency of separation depended upon urea concentration. Urea 206-210 AT-rich interaction domain 2 Homo sapiens 62-84 6223283-3 1982 Gel-filtration on Bio-Gel P-200 was the last step of purification; it gave the protein which was homogeneous on disc polyacrylamide gel electrophoresis. polyacrylamide 117-131 AT-rich interaction domain 2 Homo sapiens 26-31 33415090-5 2020 The central portion of Ro52 (p200), more than the full amino-acid sequence of Ro-52, is recognized to be the fine specificity of anti-Ro associated to the highest risk of cardiac damage. ro-52 78-83 AT-rich interaction domain 2 Homo sapiens 29-33 32958952-0 2020 ARID2 is a pomalidomide-dependent CRL4CRBN substrate in multiple myeloma cells. pomalidomide 11-23 AT-rich interaction domain 2 Homo sapiens 0-5 32958952-3 2020 Here we show that ARID2, a component of the polybromo-associated BAF (PBAF) chromatin-remodeling complex, is a pomalidomide-induced neosubstrate of CRL4CRBN. pomalidomide 111-123 AT-rich interaction domain 2 Homo sapiens 18-23 32958952-4 2020 BRD7, another subunit of PBAF, is critical for pomalidomide-induced ARID2 degradation. pomalidomide 47-59 AT-rich interaction domain 2 Homo sapiens 68-73 32958952-5 2020 ARID2 is involved in transcriptional regulation of pomalidomide target genes including MYC. pomalidomide 51-63 AT-rich interaction domain 2 Homo sapiens 0-5 32958952-6 2020 Pomalidomide is more effective than lenalidomide in degrading ARID2 and is capable of inhibiting MYC expression and proliferation in lenalidomide-resistant cell lines. pomalidomide 0-12 AT-rich interaction domain 2 Homo sapiens 62-67 32958952-6 2020 Pomalidomide is more effective than lenalidomide in degrading ARID2 and is capable of inhibiting MYC expression and proliferation in lenalidomide-resistant cell lines. Lenalidomide 36-48 AT-rich interaction domain 2 Homo sapiens 62-67 32958952-8 2020 These findings suggest that ARID2 is a promising target for overcoming lenalidomide resistance in patients with multiple myeloma. Lenalidomide 71-83 AT-rich interaction domain 2 Homo sapiens 28-33 33051312-1 2021 BACKGROUND: ARID2 belongs to the Switch/sucrose non-fermenting complex, in which the genetic defects have been found in patients with dysmorphism, short stature and intellectual disability (ID). Sucrose 40-47 AT-rich interaction domain 2 Homo sapiens 12-17 30535613-5 2019 We report the complete backbone 1H, 13C, and 15N chemical shift assignment and secondary structure of hBAF200 ARID domain. Hydrogen 32-34 AT-rich interaction domain 2 Homo sapiens 102-109 30838730-2 2019 ARID2 encodes a member of the SWItch/sucrose non-fermentable chromatin remodeling complex. Sucrose 37-44 AT-rich interaction domain 2 Homo sapiens 0-5 30535613-5 2019 We report the complete backbone 1H, 13C, and 15N chemical shift assignment and secondary structure of hBAF200 ARID domain. 13c 36-39 AT-rich interaction domain 2 Homo sapiens 102-109 30535613-5 2019 We report the complete backbone 1H, 13C, and 15N chemical shift assignment and secondary structure of hBAF200 ARID domain. 15n 45-48 AT-rich interaction domain 2 Homo sapiens 102-109 30529289-11 2019 These results confirm the N250 and LN as correlates of the processing of the identity of known faces, and show for the first time that the face-sensitive P200 is primarily modulated by DTN of a face in nMDFS. dtn 185-188 AT-rich interaction domain 2 Homo sapiens 154-158 30529289-11 2019 These results confirm the N250 and LN as correlates of the processing of the identity of known faces, and show for the first time that the face-sensitive P200 is primarily modulated by DTN of a face in nMDFS. nmdfs 202-207 AT-rich interaction domain 2 Homo sapiens 154-158 30529289-7 2019 ERPs showed pronounced DTN effects in the occipitotemporal P200 (190-260 ms), with progressively smaller amplitudes for faces with higher DTN, for all face types. dtn 23-26 AT-rich interaction domain 2 Homo sapiens 59-63 29303768-11 2018 CONCLUSIONS: The p200-free assay with respect to the biotin-based method was more specific in detecting p200 antibodies in women positive for anti-SSA/Ro52 antibodies. Biotin 53-59 AT-rich interaction domain 2 Homo sapiens 104-108 29020372-6 2017 Tolcapone reduced false alarm rate (d=0.8) and enhanced frontal P200 amplitude during correctly identified nontarget trials (d=0.6) in low-baseline 5 Choice-Continuous Performance Test performers and had opposite effects in high performers (d=0.5 and d=0.25, respectively). Tolcapone 0-9 AT-rich interaction domain 2 Homo sapiens 64-68 29020372-7 2017 Tolcapone"s effect on frontal P200 amplitude and false alarm rate was correlated (rs=-0.4, P=.05). Tolcapone 0-9 AT-rich interaction domain 2 Homo sapiens 30-34 28381560-4 2017 We used cytological and biochemical approaches to show that Baf200 plays an important function by facilitating homologous recombination-dependent processes, such as recruitment of Rad51 (a key component of homologous recombination) to DSBs, homology-directed repair, and cell survival after DNA damage. dsbs 235-239 AT-rich interaction domain 2 Homo sapiens 60-66 25803753-1 2014 The purpose of the current study was to determine the effects of three different pulse durations (200, 350, and 500 microseconds [P200, P350, and P500, respectively]) on oxygen uptake (VO2), cycling performance, and energy expenditure (EE) percentage of fatigue of the knee extensor muscle group immediately and 48 to 72 h after cycling in persons with spinal cord injury (SCI). Oxygen 170-176 AT-rich interaction domain 2 Homo sapiens 130-134 28124119-10 2017 Hence, this study identifies mutations in the ARID2 gene as a novel and rare cause for a CSS-like phenotype and enlarges the list of CSS-like genes. thiocysteine 89-92 AT-rich interaction domain 2 Homo sapiens 46-51 28124119-10 2017 Hence, this study identifies mutations in the ARID2 gene as a novel and rare cause for a CSS-like phenotype and enlarges the list of CSS-like genes. thiocysteine 133-136 AT-rich interaction domain 2 Homo sapiens 46-51 28066224-8 2016 Results: BNA intraclass correlation values of repeatability ranged between 0.51 and 0.82 for the known ERP components N100, P200, and P300. 2-Naphthylamine 9-12 AT-rich interaction domain 2 Homo sapiens 124-128 26257698-5 2015 The electrophysiological results showed that the dispositional NFC modified early perceptual components (N170, N200, and P200). NI-FE ACTIVE CENTER A-FORM 63-66 AT-rich interaction domain 2 Homo sapiens 121-125 28238438-1 2017 BACKGROUND & AIMS: Recent genomic studies have identified frequent mutations of AT-rich interactive domain 2 (ARID2) in hepatocellular carcinoma (HCC), but it is not still understood how ARID2 exhibits tumor suppressor activities. Adenosine Monophosphate 12-15 AT-rich interaction domain 2 Homo sapiens 84-112 28238438-1 2017 BACKGROUND & AIMS: Recent genomic studies have identified frequent mutations of AT-rich interactive domain 2 (ARID2) in hepatocellular carcinoma (HCC), but it is not still understood how ARID2 exhibits tumor suppressor activities. Adenosine Monophosphate 12-15 AT-rich interaction domain 2 Homo sapiens 114-119 28238438-4 2017 ARID2 depletion attenuated nucleotide excision repair (NER) of DNA damage sites introduced by exposure to UV as well as chemical compounds known as carcinogens for HCC, benzo[a]pyrene and FeCl3, since xeroderma pigmentosum complementation group G (XPG) could not accumulate without ARID2. pyrene 177-183 AT-rich interaction domain 2 Homo sapiens 0-5 28238438-4 2017 ARID2 depletion attenuated nucleotide excision repair (NER) of DNA damage sites introduced by exposure to UV as well as chemical compounds known as carcinogens for HCC, benzo[a]pyrene and FeCl3, since xeroderma pigmentosum complementation group G (XPG) could not accumulate without ARID2. ferric chloride 188-193 AT-rich interaction domain 2 Homo sapiens 0-5 28238438-9 2017 LAY SUMMARY: Recent genomic studies have identified frequent mutations of ARID2, a component of the SWItch/Sucrose Non-Fermentable (SWI/SNF) complex, in hepatocellular carcinoma, but it is not still understood how ARID2 exhibits tumor suppressor activities. Sucrose 107-114 AT-rich interaction domain 2 Homo sapiens 74-79 27413115-3 2016 Recurrent mutations arise in genes encoding several BAF/PBAF subunits, including ARID1A, ARID2, PBRM1, SMARCA4, and SMARCB1 These subunits share some degree of conservation with subunits from related adenosine triphosphate (ATP)-dependent chromatin remodeling complexes in model organisms, in which a large body of work provides insight into their roles in cancer. Adenosine Triphosphate 200-222 AT-rich interaction domain 2 Homo sapiens 89-94 27413115-3 2016 Recurrent mutations arise in genes encoding several BAF/PBAF subunits, including ARID1A, ARID2, PBRM1, SMARCA4, and SMARCB1 These subunits share some degree of conservation with subunits from related adenosine triphosphate (ATP)-dependent chromatin remodeling complexes in model organisms, in which a large body of work provides insight into their roles in cancer. Adenosine Triphosphate 224-227 AT-rich interaction domain 2 Homo sapiens 89-94 21822264-1 2011 Through exomic sequencing of ten hepatitis C virus (HCV)-associated hepatocellular carcinomas (HCC) and subsequent evaluation of additional affected individuals, we discovered novel inactivating mutations of ARID2 in four major subtypes of HCC (HCV-associated HCC, hepatitis B virus (HBV)-associated HCC, alcohol-associated HCC and HCC with no known etiology). Alcohols 305-312 AT-rich interaction domain 2 Homo sapiens 208-213