Evidence map›Paper›PMID 26774856›Full record

ArticleThe American journal of pathology2016

Far Upstream Element Binding Protein Plays a Crucial Role in Embryonic Development, Hematopoiesis, and Stabilizing Myc Expression Levels.

Weixin Zhou, Yang Jo Chung, Edgardo R Parrilla Castellar, Ying Zheng, Hye-Jung Chung, Russell Bandle, Juhong Liu, Lino Tessarollo, Eric Batchelor, Peter D Aplan and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

30 citing papers in PubMed, 37 citations in OpenAlex.

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  16. Developmental Roles of FUSE Binding Protein 1 (International journal of molecular sciences · 2020
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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

11 authors at 2 institutions in 1 country.

Weixin ZhouLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Yang Jo ChungLaboratory of Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Edgardo R Parrilla CastellarLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Ying ZhengLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Hye-Jung ChungLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Russell BandleLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Juhong LiuLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Lino TessarolloMouse Genetics Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland.
Eric BatchelorLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
Peter D AplanLaboratory of Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.
David LevensLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Electronic address: levens@helix.nih.gov.
Center for Cancer Research · USNational Cancer Institute · US

Funding

Activation of Proto-Oncogenes by Chromosomal TranslocationZIASC010378 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI APLAN, PETER · 2009 to 2025
$8.4M
Systems-level analysis of the regulation and function of MYCZIABC011487 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI BATCHELOR, ERIC · 2013 to 2020
$1.2M
Intramural NIH HHS
6 · The paper itself

Abstract

The transcription factor far upstream element binding protein (FBP) binds and activates the MYC promoter when far upstream element is via TFIIH helicase activity early in the transcription cycle. The fundamental biology and pathology of FBP are complex. In some tumors FBP seems pro-oncogenic, whereas in others it is a tumor suppressor. We generated an FBP knockout (Fubp1(-/-)) mouse to study FBP deficiency. FBP is embryo lethal from embryonic day 10.5 to birth. A spectrum of pathology is associated with FBP loss; besides cerebral hyperplasia and pulmonary hypoplasia, pale livers, hypoplastic spleen, thymus, and bone marrow, cardiac hypertrophy, placental distress, and small size were all indicative of anemia. Immunophenotyping of hematopoietic cells in wild-type versus knockout livers revealed irregular trilineage anemia, with deficits in colony formation. Despite normal numbers of hematopoietic stem cells, transplantation of Fubp1(-/-) hematopoietic stem cells into irradiated mice entirely failed to reconstitute hematopoiesis. In competitive transplantation assays against wild-type donor bone marrow, Fubp1(-/-) hematopoietic stem cells functioned only sporadically at a low level. Although cultures of wild-type mouse embryo fibroblasts set Myc levels precisely, Myc levels of mouse varied wildly between fibroblasts harvested from different Fubp1(-/-) embryos, suggesting that FBP contributes to Myc set point fixation. FBP helps to hold multiple physiologic processes to close tolerances, at least in part by constraining Myc expression.

Indexed as

Gene Expression RegulationAnimalsDNA-Binding ProteinsEmbryonic DevelopmentFemaleFibroblastsHematopoiesisHematopoietic Stem CellsMiceMice, KnockoutPregnancyPromoter Regions, GeneticProto-Oncogene Proteins c-mycDNA-Binding ProteinsFubp protein, mouseMyc protein, mouseProto-Oncogene Proteins c-myc

Identifiers

PMID26774856
PMCPMC4816710
OpenAlexW2234357922

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.