Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.1 (S1 nuclease)
 3,660 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An abnormally sized 3.5 kb p53 transcript was detected in the KE-37R human leukemic T-cell line in which no p53 protein could be detected by immunoprecipitation. S1 nuclease protection experiments and sequencing analysis indicated conservation of the entire intron 4 (755 bp) in the 3.5 kb transcript and the presence of a G to A substitution in the last exonic nucleotide of the splice donor site. These data support the notion that p53 gene inactivation by point mutations in splice junctions also exists in hemopoietic neoplasia.
Leukemia 1991 Oct
PMID:Inactivation of the p53 gene expression by a splice donor site mutation in a human T-cell leukemia cell line. 196 Oct 27

Northern blot analysis of RNA isolated from HL-60 cells before and after differentiation induction by TPA and DMSO showed that four MPO mRNA species (3.3, 3.1, 2.7, and 2.5 kb, respectively designated alpha 1, beta 1, alpha 2, and beta 2) are expressed in HL-60 cells. However, alpha 2 and beta 2 lack part of the 3' end sequence due to different polyadenylation sites. The steady state levels of alpha 2 and beta 2 MPO mRNA increase significantly after 1 hr of induction, while all four MPO mRNA species decrease dramatically after 10 hr of induction. Our results demonstrate that MPO gene expression is developmentally and differentially regulated. Northern blot analysis of RNA isolated from blast samples of acute myelogenous leukemia (M0-M5) and chronic lymphocytic leukemia (CLL) patients indicate that four MPO mRNA species are expressed in M1-M4 but are undetectable in M5 and CLL. Primer extension and S1 nuclease protection analysis of the MPO mRNA revealed a single transcription initiation site for the MPO gene.
Leukemia 1990 Jul
PMID:Developmental and differential regulation of human MPO gene in leukemic cells. 216 3

We have examined the S1 nuclease sensitivity of supercoiled plasmids harboring the Moloney Murine Leukemia Virus (MoMuLV) long terminal repeat (LTR). S1 sensitivity was found within the LTR enhancer direct repeats. Transformation of E. coli DH5 cells with a construct containing most of the MoMuLV LTR yielded the precise deletion of one direct repeat and loss of S1 sensitivity. The dependence of S1 sensitivity on the presence of both direct repeats, together with the exact excision of one direct repeat by E. coli, suggests the presence of slipped DNA within the enhancer. Such structures may represent targets for effector proteins which mediate vital functions during viral propagation.
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PMID:Slipped DNA structures within the enhancer region of the Moloney murine leukemia virus. 305 52

Activation of transcription by the Moloney Murine Leukemia Virus (MLV) and Simian Virus (SV40) enhancers was compared by transfecting recombinants containing these enhancers in either mouse or human cell-lines, and analysing RNA 48 h later by quantitative S1 nuclease mapping. The enhancers share the following properties. They stimulate transcription in an orientation-independent manner from the same startsites on the natural heterologous conalbumin (+62 to -102) or SV40 early promoter elements as well as on substitute promoter elements. The enhancers are most efficient when they are located directly upstream from the conalbumin (+62 to -102) promoter element, but they still stimulate transcription when they are either immediately downstream from the promoter element, or further upstream. Increasing the distance by interposing DNA sequences between the enhancers and the conalbumin promoter fragment results in decreased activation. Both enhancers show some cell-line specificity for activation of transcription. However, in all cell-lines and constructions tested the MLV enhancer was always less efficient than the SV40 enhancer. These results suggest that the MLV and SV40 enhancers stimulate transcription by similar mechanisms.
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PMID:The MLV and SV40 enhancers have a similar pattern of transcriptional activation. 609 7