Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
Compound
Query: EC:3.1.30.1 (
S1 nuclease
)
3,660
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Three primary isoforms of the dimeric glycolytic enzyme,
triosephosphate isomerase
(TPI; EC 5.3.1.1), are detected in proliferating human cells. The electrophoretically separable isoforms result from the three possible combinations of constitutive subunits and subunits expressed only in proliferating cells. Only a single primary isoform is observed in quiescent cells. The two subunits, which differ by covalent modification (s), are product of the single structural locus for this enzyme. Expression of the proliferation specific subunit (TPI-2) is detected within 6-10 hr following mitogen stimulation of quiescent human cells, requires RNA synthesis and is inhibited by agents which inhibit interleukin 2 expression or function. Only the constitutive subunit (TPI-1) is detected in proliferating cells from nonhominoid primate species. A single class of
TPI mRNA
, which is increased greater than 10 fold following stimulation of quiescent cells, is detected on northern blot analysis and
S1 nuclease
digestion analysis of RNA from quiescent and proliferating human cells. It is similar in size to the
TPI mRNA
from proliferating cells of the African green monkey, a primate species not expressing TPI-2. Comparison of the structure of the TPI gene from rhesus monkey (nonexpressing species) to the gene from expressing species does not suggest a mechanism for generating TPI-2. Thus, the regulation of the expression of the hominoid restricted, proliferation specific subunit of TPI has been further defined, although the mechanism for generating TPI-2 remains elusive.
...
PMID:Hominoid triosephosphate isomerase: regulation of expression of the proliferation specific isozyme. 255 Jul 87
To examine the functional organization of the human
triosephosphate isomerase
(
TPI
) promoter, deletion, insertion, and linker scanning mutations were introduced into the
TPI
promoter of hybrid
TPI
/beta-globin genes. These genes were transiently expressed in mouse L and human HeLa cells, and the effect of each mutation on the frequency and position of transcription initiation was assayed by
S1 nuclease
transcript mapping. Multiple positive regulatory elements reside between positions -595 and +1 in L cells and -920 and -7 in HeLa cells and coordinately promote maximum hybrid gene transcription. These elements include an array of GC boxes (positions -126 to -48) that variably conform to the consensus Sp1-binding site, and a canonical TATA box (positions -27 to -21) that is essential for detectable levels of transcription. In an additive yet position-dependent fashion, the GC boxes function in cis to the TATA box to control both the frequency and position of transcription initiation. Additional positive elements reside upstream of position -131 and are required for full promoter function. Also, an inhibitory element(s) residing between position -7200 and either -2800 in L cells or -920 in HeLa cells reduces transcription approximately 7-fold relative to the level of transcription achieved with the maximally active promoter.
...
PMID:Transcriptional regulatory sequences of the housekeeping gene for human triosephosphate isomerase. 292 88