| 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. |