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PubMed:24916015 JSONTXT 8 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-86 Sentence denotes Corneal dystrophy-causing SLC4A11 mutants: suitability for folding-correction therapy.
T1 0-86 Sentence denotes Corneal dystrophy-causing SLC4A11 mutants: suitability for folding-correction therapy.
TextSentencer_T2 87-301 Sentence denotes SLC4A11 mutations cause some cases of the corneal endothelial dystrophies, congenital hereditary endothelial corneal dystrophy type 2 (CHED2), Harboyan syndrome (HS), and Fuchs endothelial corneal dystrophy (FECD).
T2 87-301 Sentence denotes SLC4A11 mutations cause some cases of the corneal endothelial dystrophies, congenital hereditary endothelial corneal dystrophy type 2 (CHED2), Harboyan syndrome (HS), and Fuchs endothelial corneal dystrophy (FECD).
TextSentencer_T3 302-386 Sentence denotes SLC4A11 protein was recently identified as facilitating water flux across membranes.
T3 302-386 Sentence denotes SLC4A11 protein was recently identified as facilitating water flux across membranes.
TextSentencer_T4 387-492 Sentence denotes SLC4A11 point mutations usually cause SLC4A11 misfolding and retention in the endoplasmic reticulum (ER).
T4 387-492 Sentence denotes SLC4A11 point mutations usually cause SLC4A11 misfolding and retention in the endoplasmic reticulum (ER).
TextSentencer_T5 493-617 Sentence denotes We set about to test the feasibility of rescuing misfolded SLC4A11 protein to the plasma membrane as a therapeutic approach.
T5 493-617 Sentence denotes We set about to test the feasibility of rescuing misfolded SLC4A11 protein to the plasma membrane as a therapeutic approach.
TextSentencer_T6 618-859 Sentence denotes Using a transfected HEK293 cell model, we measured functional activity present in cells expressing SLC4A11 variants in combinations representing the state found in CHED2 carriers, affected CHED2, FECD individuals, and unaffected individuals.
T6 618-859 Sentence denotes Using a transfected HEK293 cell model, we measured functional activity present in cells expressing SLC4A11 variants in combinations representing the state found in CHED2 carriers, affected CHED2, FECD individuals, and unaffected individuals.
TextSentencer_T7 860-983 Sentence denotes These cells manifest respectively about 60%, 5%, and 25% of the water flux activity, relative to the unaffected (WT alone).
T7 860-983 Sentence denotes These cells manifest respectively about 60%, 5%, and 25% of the water flux activity, relative to the unaffected (WT alone).
TextSentencer_T8 984-1116 Sentence denotes ER-retained CHED2 mutant SLC4A11 protein could be rescued to the plasma membrane, where it conferred 25%-30% of WT water flux level.
T8 984-1116 Sentence denotes ER-retained CHED2 mutant SLC4A11 protein could be rescued to the plasma membrane, where it conferred 25%-30% of WT water flux level.
TextSentencer_T9 1117-1234 Sentence denotes Further, some ER-retained CHED2 mutants expressed at 30°C supported increased water flux compared with 37°C cultures.
T9 1117-1234 Sentence denotes Further, some ER-retained CHED2 mutants expressed at 30°C supported increased water flux compared with 37°C cultures.
TextSentencer_T10 1235-1366 Sentence denotes Caspase activation and cell vitality assays revealed that expression of SLC4A11 mutants in HEK293 cells does not induce cell death.
T10 1235-1366 Sentence denotes Caspase activation and cell vitality assays revealed that expression of SLC4A11 mutants in HEK293 cells does not induce cell death.
TextSentencer_T11 1367-1517 Sentence denotes We conclude that therapeutics able to increase cell surface localization of ER-retained SLC4A11 mutants hold promise to treat CHED2 and FECD patients.
T11 1367-1517 Sentence denotes We conclude that therapeutics able to increase cell surface localization of ER-retained SLC4A11 mutants hold promise to treat CHED2 and FECD patients.