Evidence map›Paper›PMID 15040449›Full record

ArticleMolecular biology reports2004

A conserved sequence upstream of the B29 (Ig beta, CD79b) gene interacts with YY1.

Lisa Patrone, Sarah E Henson, Randolph Wall, Cindy Sue Malone

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 43% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Lisa PatroneDepartment of Microbiology, Immunology, & Molecular Genetics, University of California, Los Angeles, CA 90095, USA.
Sarah E Henson
Randolph Wall
Cindy Sue Malone
University of California, Los Angeles · US

Funding

TUMOR CELL SURFACES AND CHROMOSOMEST32CA009056 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Gay M Crooks, David A. Nathanson · 1985 to 2026
$10.5M
UCLA Tumor Immunology Training ProgramT32CA009120 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Steven M. Dubinett, MICHAEL A TEITELL · 1985 to 2026
$10.3M
CONTROL OF LYMPHOCYTE DEVELOPMENTR01GM040185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WALL, RANDOLPH · 1988 to 2005
$1.7M
NOVEL MECHANISMS IN B CELL LEUKEMOGENESISR01CA085841 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI WALL, RANDOLPH · 2001 to 2005
$1.3M
NCI NIH HHS 2-T32-CA09120-23NCI NIH HHS 2-T32-CA09120-25NCI NIH HHS CA85841NCI NIH HHS T32-CA09056NIGMS NIH HHS GM07185NIGMS NIH HHS GM40185
6 · The paper itself

Abstract

The human, murine, and rat B29 (Ig beta, CD79b) genes are highly conserved in sequence and organization and exhibit strict B cell-specific expression. In the human and rat genomes, the B29 gene is located between the skeletal muscle-specific Na-channel alpha subunit (SCN4A) gene and the pituitary-specific growth hormone (GH-N) gene. The human pituitary-specific GH-N gene is controlled by a tissue-specific locus control region (LCR) located just upstream of the B29 promoter that mediates tissue-specific enhancement, histone acetylation, and an open chromatin conformation across the B29 gene in growth hormone (GH)-expressing pituitary cells. Here we show that B29 mRNA is not detected in a GH-expressing pituitary cell line and that GH-N mRNA is not detected in B cells. This differential expression suggests that the B29 gene is insulated or otherwise protected from the regulatory influences of the closely proximal GH LCR. We searched available sequences upstream of the human, mouse, and rat B29 genes and found a highly conserved sequence that fulfills the criteria recently established for non-coding DNA elements potentially involved in gene control. This B29 conserved sequence (BCS) bound ubiquitously expressed nuclear protein complexes. DNase I protection analysis of the BCS revealed a central 'footprinted' core which was confirmed to bind the multifunctional transcription factor, YY1. However, neither the BCS nor the YY1-binding core motif exhibited silencer or enhancer activity in transient transfections or position-independent insulator activity in enhancer-blocking assays. Thus, the BCS may function as a tissue-specific LCR or position-dependent insulator specifically countering the influences of the 5' GH LCR and controlling B29 gene expression.

Indexed as

5' Flanking RegionAnimalsAntigens, CDBase SequenceBinding SitesB-LymphocytesCD79 AntigensCell LineConserved SequenceDeoxyribonuclease IEnhancer Elements, GeneticErythroid-Specific DNA-Binding FactorsGrowth HormoneHumansLocus Control RegionMiceAntigens, CDCD79 AntigensCD79B protein, humanCd79b protein, mouseCd79b protein, ratDeoxyribonuclease IErythroid-Specific DNA-Binding FactorsGrowth HormoneTranscription FactorsYY1 protein, humanYy1 protein, mouseYy1 protein, ratYY1 Transcription Factor

Identifiers

PMID15040449
OpenAlexW1983666965

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.