Evidence map›Paper›PMID 23376999›Full record

ArticleExperimental hematology2013

Mice lacking the sodium-dependent phosphate import protein, PiT1 (SLC20A1), have a severe defect in terminal erythroid differentiation and early B cell development.

Li Liu, Marilyn Sánchez-Bonilla, Matthew Crouthamel, Cecilia Giachelli, Siobán Keel

Open access · bronzeAbstract read
In one paragraph

Article in Experimental hematology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

14 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Npt2a as a target for treating hyperphosphatemia.Biochemical Society transactions · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Mouse Models of Erythropoiesis and Associated Diseases.Methods in molecular biology (Clifton, N.J.) · 2018
    Review
  11. Article
  12. Article
  13. Renal phosphate transporters.Current opinion in nephrology and hypertension · 2014
    Review
  14. 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

5 authors at 1 institution in 1 country.

Li LiuDepartment of Medicine, University of Washington, Seattle, WA 98195, USA.
Marilyn Sánchez-Bonilla
Matthew Crouthamel
Cecilia Giachelli
Siobán Keel
University of Washington · US

Funding

CARDIOVASCULAR RESEARCH TRAINING PROGRAMT32HL007828 · NHLBI · UNIVERSITY OF WASHINGTON · PI Francis Kim, Farid Moussavi-Harami · 1997 to 2026
$10.2M
Vascular Calcification MechanismR01HL062329 · NHLBI · UNIVERSITY OF WASHINGTON · PI GIACHELLI, CECILIA M · 1999 to 2017
$5.3M
Recruitment of a translational researcher for leukemiaP30CA147883 · NCI · UNIVERSITY OF WASHINGTON · PI ABKOWITZ, JANIS L · 2009 to 2010
$1.5M
NCI NIH HHS P30 CA147883NHLBI NIH HHS R01 HL062329NHLBI NIH HHS T32 HL007828NHLBI NIH HHS T32 HL07828
6 · The paper itself

Abstract

Phosphate is critical in multiple biological processes (phosphorylation reactions, ATP production, and DNA structure and synthesis). It remains unclear how individual cells initially sense changes in phosphate availability and the cellular consequences of these changes. PiT1 (or SLC20A1) is a constitutively expressed, high-affinity sodium-dependent phosphate import protein. In vitro data suggest that PiT1 serves a direct role in mediating cellular proliferation; its role in vivo is unclear. We have discovered that mice lacking PiT1 develop a profound underproduction anemia characterized by mild macrocytosis, dyserythropoiesis, increased apoptosis, and a near complete block in terminal erythroid differentiation. In addition, the animals are severely B cell lymphopenic because of a defect in pro-B cell development and mildly neutropenic. The phenotype is intrinsic to the hematopoietic system, is associated with a defect in cell cycle progression, and occurs in the absence of changes in serum phosphate or calcium concentrations and independently of a change in cellular phosphate uptake. The severity of the anemia and block in terminal erythroid differentiation and B cell lymphopenia are striking and suggest that PiT1 serves a fundamental and nonredundant role in murine terminal erythroid differentiation and B cell development. Intriguingly, as the anemia mimics the ineffective erythropoiesis in some low-grade human myelodysplastic syndromes, this murine model might also provide pathologic insight into these disorders.

Indexed as

AnemiaAnimalsApoptosisBlotting, WesternCell CycleCell DifferentiationErythroid CellsErythropoiesisFlow CytometryHematologic DiseasesHumansLymphopeniaMiceMice, KnockoutNeutropeniaPrecursor Cells, B-LymphoidSlc20a1 protein, mouseSodium-Phosphate Cotransporter Proteins, Type III

Identifiers

PMID23376999
PMCPMC3948150
OpenAlexW2018677032

What OpenQuestion holds

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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.