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PubMed:9920778 JSONTXT 18 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
TextSentencer_T1 0-174 Sentence denotes Imbalanced expression of the glucocorticoid receptor isoforms in cultured lymphocytes from a patient with systemic glucocorticoid resistance and chronic lymphocytic leukemia.
T1 0-174 Sentence denotes Imbalanced expression of the glucocorticoid receptor isoforms in cultured lymphocytes from a patient with systemic glucocorticoid resistance and chronic lymphocytic leukemia.
TextSentencer_T2 175-285 Sentence denotes The human glucocorticoid receptor (GR) is expressed as two alternatively spliced isoforms, GRalpha and GRbeta.
T2 175-285 Sentence denotes The human glucocorticoid receptor (GR) is expressed as two alternatively spliced isoforms, GRalpha and GRbeta.
TextSentencer_T3 286-472 Sentence denotes Whereas GRalpha is a hormone-activated transcription factor, GRbeta does not bind glucocorticoids (GCs), is transcriptionally inactive, and is a potential inhibitor of activated GRalpha.
T3 286-472 Sentence denotes Whereas GRalpha is a hormone-activated transcription factor, GRbeta does not bind glucocorticoids (GCs), is transcriptionally inactive, and is a potential inhibitor of activated GRalpha.
TextSentencer_T4 473-576 Sentence denotes Differential expression of GR isoforms may play a role in generalized or tissue-specific GC resistance.
T4 473-576 Sentence denotes Differential expression of GR isoforms may play a role in generalized or tissue-specific GC resistance.
TextSentencer_T5 577-720 Sentence denotes GCs induce apoptosis in neoplastic lymphoid cells; and, defective apoptosis is implicated in the genesis of chronic lymphocytic leukemia (CLL).
T5 577-720 Sentence denotes GCs induce apoptosis in neoplastic lymphoid cells; and, defective apoptosis is implicated in the genesis of chronic lymphocytic leukemia (CLL).
TextSentencer_T6 721-781 Sentence denotes We studied a patient with generalized GC resistance and CLL.
T6 721-781 Sentence denotes We studied a patient with generalized GC resistance and CLL.
TextSentencer_T7 782-959 Sentence denotes GR number in the patient's transformed lymphocytes was approximately one half that of control cells with a approximately 10-fold reduction in binding affinity for dexamethasone.
T7 782-959 Sentence denotes GR number in the patient's transformed lymphocytes was approximately one half that of control cells with a approximately 10-fold reduction in binding affinity for dexamethasone.
TextSentencer_T8 960-1070 Sentence denotes In vitro apoptosis induction in CLL cells was delayed in response to GCs, but not to other apoptosis inducers.
T8 960-1070 Sentence denotes In vitro apoptosis induction in CLL cells was delayed in response to GCs, but not to other apoptosis inducers.
TextSentencer_T9 1071-1267 Sentence denotes Sequencing of the GR cDNA and gene including the 2.3-kb coding region, the intron/exon junctions, the known 5'-regulatory region, and approximately 300 bp of the 3'-region revealed no alterations.
T9 1071-1267 Sentence denotes Sequencing of the GR cDNA and gene including the 2.3-kb coding region, the intron/exon junctions, the known 5'-regulatory region, and approximately 300 bp of the 3'-region revealed no alterations.
TextSentencer_T10 1268-1497 Sentence denotes Western blot with an N-terminal antibody showed normal levels of immunoreactive GR, but quantitative analysis with isoform-specific C-terminal antibodies revealed a markedly reduced GRalpha expression, and high GRbeta expression.
T10 1268-1497 Sentence denotes Western blot with an N-terminal antibody showed normal levels of immunoreactive GR, but quantitative analysis with isoform-specific C-terminal antibodies revealed a markedly reduced GRalpha expression, and high GRbeta expression.
TextSentencer_T11 1498-1676 Sentence denotes These findings indicate that imbalanced expression of the GR isoforms may be a mechanism of GC resistance, and may have implications for tumorigenesis by enhancing cell survival.
T11 1498-1676 Sentence denotes These findings indicate that imbalanced expression of the GR isoforms may be a mechanism of GC resistance, and may have implications for tumorigenesis by enhancing cell survival.