Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.7.7.6 (
RNA polymerase
)
34,946
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Phospholipase A2, group IIA, gene expression has been analyzed in primary heart tumors. High expression has been demonstrated through several ways: reverse-
transcriptase
chain polymerase chain, Northern blotting hybridization at the RNA level and immunoblotting, immunohistochemical assay at the protein level. Human cardiac myxoma exhibits highly positive
phospholipase A2, group IIA
, immunophenotype (100% positive cases). The immunophenotype is unique among human primary cardiac tumors. Phospholipase A2, group IIA, can be proposed as a tissue marker for pathological examination after heart tumor resection.
...
PMID:[Phospholipase A2, group IIa, as an earlier unknown immunohistological marker of cardiac myxoma]. 1854 Apr 39
It is commonly observed that onset or release of transcriptional gene silencing (TGS) correlates with alteration of repressive epigenetic marks. The TGS regulator
MOM1
in Arabidopsis is exceptional since it regulates transcription in intermediate heterochromatin with only minor changes in epigenetic marks. We have isolated an enhancer of the mom1 mutation that points towards regulatory interplay between
MOM1
and
RNA polymerase
-V (Pol-V). Pol-V transcribes heterochromatic loci, which seems to be required for maintenance of their silencing; however, it is still not clear how Pol-V is targeted to heterochromatin. We now provide evidence that Pol-V is required for
MOM1
-mediated suppression of transcription at a subset of its chromosomal targets. Thus, Pol-V genetically interacts with
MOM1
in the control of gene silencing. Interestingly, functional cooperation of
MOM1
and Pol-V not only broadens the range of the controlled loci in comparison to each individual factor, but also determines the degree of TGS.
...
PMID:MOM1 and Pol-IV/V interactions regulate the intensity and specificity of transcriptional gene silencing. 2008 85