Id |
Subject |
Object |
Predicate |
Lexical cue |
TextSentencer_T1 |
0-214 |
Sentence |
denotes |
Preferential beta-hexosaminidase (Hex) A (alpha beta) formation in the absence of beta-Hex B (beta beta) due to heterozygous point mutations present in beta-Hex beta-chain alleles of a motor neuron disease patient. |
TextSentencer_T2 |
215-486 |
Sentence |
denotes |
Deficiency of the lysosomal enzyme beta-hexosaminidase B (beta-Hex B) (a homodimer, beta beta), caused by a defect in the HEX B gene encoding the beta-chain, is usually accompanied by an absence of beta-Hex A (a heterodimer, alpha beta), thereby causing Sandhoff disease. |
TextSentencer_T3 |
487-651 |
Sentence |
denotes |
However, we have earlier demonstrated the presence of partial beta-Hex A (30-50% of normal) even in the absence of beta-Hex B in an adult with motor neuron disease. |
TextSentencer_T4 |
652-793 |
Sentence |
denotes |
The patient is a compound heterozygote with normal beta-chain message and one HEX B point mutation originating from each asymptomatic parent. |
TextSentencer_T5 |
794-951 |
Sentence |
denotes |
Since the non-expression of beta-Hex B was post-transcriptional, we transfected COS-7 cells to understand the effect of each mutation on beta-Hex B activity. |
TextSentencer_T6 |
952-1126 |
Sentence |
denotes |
Transfection of the A1367-->C mutant (maternal allele) construct produced no overexpressed beta-Hex B, indicating that the encoded Tyr456-->Ser beta-chain was non-functional. |
TextSentencer_T7 |
1127-1295 |
Sentence |
denotes |
Chou-Fasman analysis predicted that the Tyr456-->Ser mutation would cause a dramatic change in beta-chain folding (which often inhibits formation of functional dimers). |
TextSentencer_T8 |
1296-1448 |
Sentence |
denotes |
This explains the complete lack of beta-Hex B in the transfectants and a partial deficiency of beta-Hex A and B (50% of normal) in the patient's mother. |
TextSentencer_T9 |
1449-1826 |
Sentence |
denotes |
Since immunoprecipitated beta-Hex A (alpha beta) protein from patient fibroblasts showed the presence of mature beta-chains even though there was no beta-Hex B (beta beta) protein, the mutant beta-chain inherited from the father (who has normal beta-Hex A and B) must undergo preferential association with the normal alpha-chains in the patient, thus producing only beta-Hex A. |
TextSentencer_T10 |
1827-2151 |
Sentence |
denotes |
Transient expression of the A619-->G mutant (paternal allele) construct produced beta-Hex B activity comparable to the wild type (approximately 10-20-fold over mock-transfected) whereas stable expression produced normal message but no beta-Hex B activity (wild type beta-Hex B expression: only 2-fold over mock-transfected). |
TextSentencer_T11 |
2152-2355 |
Sentence |
denotes |
The lack of increased beta-Hex B after stable expression of the Ile207-->Val beta-chains at a lower copy number indicates the absence of self-association at low concentrations of Ile207-->Val beta-chain. |
TextSentencer_T12 |
2356-2672 |
Sentence |
denotes |
In the patient who also has a non-functional Tyr456-->Ser allele, the effective concentration of beta-chains is reduced to 50% of normal and the remaining Ile207-->Val beta-chains fail to self-associate but can still dimerize with the abundant normal alpha-chains thus producing partial beta-Hex A and no beta-Hex B. |
T1 |
0-214 |
Sentence |
denotes |
Preferential beta-hexosaminidase (Hex) A (alpha beta) formation in the absence of beta-Hex B (beta beta) due to heterozygous point mutations present in beta-Hex beta-chain alleles of a motor neuron disease patient. |
T2 |
215-486 |
Sentence |
denotes |
Deficiency of the lysosomal enzyme beta-hexosaminidase B (beta-Hex B) (a homodimer, beta beta), caused by a defect in the HEX B gene encoding the beta-chain, is usually accompanied by an absence of beta-Hex A (a heterodimer, alpha beta), thereby causing Sandhoff disease. |
T3 |
487-651 |
Sentence |
denotes |
However, we have earlier demonstrated the presence of partial beta-Hex A (30-50% of normal) even in the absence of beta-Hex B in an adult with motor neuron disease. |
T4 |
652-793 |
Sentence |
denotes |
The patient is a compound heterozygote with normal beta-chain message and one HEX B point mutation originating from each asymptomatic parent. |
T5 |
794-951 |
Sentence |
denotes |
Since the non-expression of beta-Hex B was post-transcriptional, we transfected COS-7 cells to understand the effect of each mutation on beta-Hex B activity. |
T6 |
952-1126 |
Sentence |
denotes |
Transfection of the A1367-->C mutant (maternal allele) construct produced no overexpressed beta-Hex B, indicating that the encoded Tyr456-->Ser beta-chain was non-functional. |
T7 |
1127-1295 |
Sentence |
denotes |
Chou-Fasman analysis predicted that the Tyr456-->Ser mutation would cause a dramatic change in beta-chain folding (which often inhibits formation of functional dimers). |
T8 |
1296-1448 |
Sentence |
denotes |
This explains the complete lack of beta-Hex B in the transfectants and a partial deficiency of beta-Hex A and B (50% of normal) in the patient's mother. |
T9 |
1449-1826 |
Sentence |
denotes |
Since immunoprecipitated beta-Hex A (alpha beta) protein from patient fibroblasts showed the presence of mature beta-chains even though there was no beta-Hex B (beta beta) protein, the mutant beta-chain inherited from the father (who has normal beta-Hex A and B) must undergo preferential association with the normal alpha-chains in the patient, thus producing only beta-Hex A. |
T10 |
1827-2151 |
Sentence |
denotes |
Transient expression of the A619-->G mutant (paternal allele) construct produced beta-Hex B activity comparable to the wild type (approximately 10-20-fold over mock-transfected) whereas stable expression produced normal message but no beta-Hex B activity (wild type beta-Hex B expression: only 2-fold over mock-transfected). |
T11 |
2152-2355 |
Sentence |
denotes |
The lack of increased beta-Hex B after stable expression of the Ile207-->Val beta-chains at a lower copy number indicates the absence of self-association at low concentrations of Ile207-->Val beta-chain. |
T12 |
2356-2672 |
Sentence |
denotes |
In the patient who also has a non-functional Tyr456-->Ser allele, the effective concentration of beta-chains is reduced to 50% of normal and the remaining Ile207-->Val beta-chains fail to self-associate but can still dimerize with the abundant normal alpha-chains thus producing partial beta-Hex A and no beta-Hex B. |