Evidence map›Paper›PMID 11274051›Full record

ArticleGenes & development2001

A mutation in a mitochondrial transmembrane protein is responsible for the pleiotropic hematological and skeletal phenotype of flexed-tail (f/f) mice.

M D Fleming, D R Campagna, J N Haslett, C C Trenor, N C Andrews

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
–field-weighted citation impact
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

48 citing papers in PubMed, 112 citations in OpenAlex.

  1. Review
  2. From the cytosol to the inner membrane: biogenesis of the mitochondrial carrier family.Protein science : a publication of the Protein Society · 2026
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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

5 authors at 3 institutions in 1 country.

M D FlemingDepartment of Pathology, Children's Hospital, Boston, Massachusetts 02115, USA.
D R Campagna
J N Haslett
C C Trenor
N C Andrews
Harvard University · USBoston Children's Hospital · USHoward Hughes Medical Institute · US

Funding

EPIDEMIOLOGY STUDIES OF DIETARY FIBER AND BLOOD PRESSURER01HL060300 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI HE, JIANG · 1997 to 2001
$234k
NHLBI NIH HHS K08 HL60300
6 · The paper itself

Abstract

We have studied the flexed-tail (f) mouse to gain insight into mammalian mitochondrial iron metabolism. Flexed-tail animals have axial skeletal abnormalities and a transient embryonic and neonatal anemia characterized by pathologic intramitochondrial iron deposits in erythrocytes. Mitochondrial iron accumulation is the hallmark of sideroblastic anemias, which typically result from defects in heme biosynthesis or other pathways that lead to abnormal erythroid mitochondrial iron utilization. To clone the f gene, we used positional cloning techniques, and identified a frameshift mutation in a mitochondrial transmembrane protein. The mutated gene, Sfxn1, is the prototype of a novel family of evolutionarily conserved proteins present in eukaryotes.

Indexed as

Cation Transport ProteinsAmino Acid SequenceAnimalsBlotting, NorthernBlotting, WesternBone and BonesCell LineCell MembraneCloning, MolecularDNA, ComplementaryDNA Mutational AnalysisFrameshift MutationHumansMembrane ProteinsMiceMice, Inbred BALB CCation Transport ProteinsDNA, ComplementaryMembrane ProteinsSfxn1 protein, mouse

Identifiers

PMID11274051
PMCPMC312659
OpenAlexW2097958807

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.