Evidence map›Paper›PMID 15798188›Full record

ArticleMolecular and cellular biology2005

Scaffold attachment factor B1 functions in development, growth, and reproduction.

Margarita Ivanova, Klaudia M Dobrzycka, Shiming Jiang, Kai Michaelis, Rene Meyer, Kaiyan Kang, Brian Adkins, Oleg A Barski, Simeen Zubairy, Jana Divisova and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. CDK2 regulates the NRF1/The Journal of cell biology · 2019
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Co-repressor activity of scaffold attachment factor B1 requires sumoylation.Biochemical and biophysical research communications · 2011
    Article
  15. Article
  16. Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2010
    Article
  17. Article
  18. Article
  19. Article
  20. 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

12 authors at 2 institutions in 1 country.

Margarita IvanovaDepartment of Medicine, Baylor College of Medicine, Breast Center, One Baylor Plaza, Houston, TX 77030, USA.
Klaudia M Dobrzycka
Shiming Jiang
Kai Michaelis
Rene Meyer
Kaiyan Kang
Brian Adkins
Oleg A Barski
Simeen Zubairy
Jana Divisova
Adrian V Lee
Steffi Oesterreich
Methodist Hospital · USBaylor College of Medicine · US

Funding

TRANSFORMING GROWTH FACTOR ALPHA IN PATHOGENESIS OF BREAST CANCERP01CA030195 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI OESTERREICH, STEFFI · 1985 to 2009
$16.8M
IRS1 and 2 Signaling in Mammary Development and CancerR01CA094118 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LEE, ADRIAN V · 2002 to 2015
$3.0M
Coordination of Proliferation and ApoptosisR03CA092713 · NCI · MONTEFIORE MEDICAL CENTER (BRONX, NY) · PI AUGENLICHT, LEONARD H. · 2001 to 2002
$126k
NCI NIH HHS P01 CA030195NCI NIH HHS R01 CA094118NCI NIH HHS R01 CA92713NCI NIH HHS R01 CA94118
6 · The paper itself

Abstract

Scaffold attachment factor B1 (SAFB1) is a multifunctional protein that can bind both DNA and RNA and is involved in RNA processing and stress response. In addition, SAFB1 contains a transcriptional repression domain and can bind certain hormone receptors and repress their activity. To assess the role of SAFB1 in vivo, we generated SAFB1 mutant mice through targeted deletion in embryonic stem cells. While viable homozygous mutant (SAFB1-/-) mice were obtained, genotypic distribution indicated that homozygous deficiency resulted in both prenatal and neonatal lethality. Mice lacking SAFB1 exhibited dwarfism, as a result of in utero growth retardation, and had low serum insulin-like growth factor 1 (IGF1) levels. In agreement with the previous characterization of SAFB1 as a corepressor for hormone receptors, we found that SAFB1-/- mice displayed dramatic defects in the development and function of the reproductive system. Male SAFB1 null mice were infertile, apparently because of low circulating levels of testosterone. SAFB1-/- testes were small and showed progressive degeneration of the germinal epithelium, increased apoptosis of germ cells, and Leydig cell hyperplasia. SAFB-/- female mice were subfertile and showed progressive infertility, in part because of defects in oviductal transport and reduced numbers of follicles. Immortalized SAFB1-/- mouse embryonic fibroblasts showed cell-intrinsic defects including increased transcriptional estrogen receptor alpha activity and enhanced responsiveness to IGF1. Together, these in vivo findings establish a critical role for SAFB1 in development, growth regulation, and reproduction.

Indexed as

Genes, LethalAnimalsApoptosisCell Line, TransformedDNA-Binding ProteinsDwarfismEmbryonic DevelopmentEstrogen Receptor alphaFemaleFetal Growth RetardationFibroblastsGonadal Steroid HormonesInfertility, FemaleInfertility, MaleInsulin-Like Growth Factor ILeydig CellsDNA-Binding ProteinsEstrogen Receptor alphaGonadal Steroid HormonesInsulin-Like Growth Factor IRNA-Binding Proteinsscaffold attachment factor B1, mouse

Identifiers

PMID15798188
PMCPMC1069606
OpenAlexW2103243951

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.