Evidence map›Paper›PMID 28942122›Full record

ArticleBone2017

Clcn7

J Caetano-Lopes, S G Lessard, S Hann, K Espinoza, K S Kang, K E Lim, D J Horan, H R Noonan, D Hu, R Baron and 2 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Bone, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
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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

12 authors at 3 institutions in 1 country.

J Caetano-LopesOrthopaedic Research Laboratories, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
S G LessardOrthopaedic Research Laboratories, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
S HannOrthopaedic Research Laboratories, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA.
K EspinozaHoward Hughes Medical Institute, Boston Children's Hospital, Boston, MA, USA.
K S KangDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
K E LimDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
D J HoranDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
H R NoonanBBS Program, Harvard Medical School, Boston, MA, USA.
D HuDivision of Bone and Mineral Research, Harvard School of Dental Medicine, Boston, MA, USA.
R BaronDivision of Bone and Mineral Research, Harvard School of Dental Medicine, Boston, MA, USA.
A G RoblingDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
M L WarmanOrthopaedic Research Laboratories, Boston Children's Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA; Howard Hughes Medical Institute, Boston Children's Hospital, Boston, MA, USA. Electronic address: matthew.warman@childrens.harvard.edu.
Boston Children's Hospital · USIndiana University School of MedicineHarvard University · US

Funding

Lrp5 signaling in bone mechanotransduction and metabolismR01AR053237 · NIAMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI ALEXANDER G ROBLING, Matthew L Warman · 2005 to 2026
$9.4M
Lrp5 and Lrp6 signaling in bone mechanotransduction and metabolismR56AR053237 · NIAMS · INDIANA UNIVERSITY INDIANAPOLIS · PI ROBLING, ALEXANDER G, WARMAN, MATTHEW L · 2023 to 2023
$349k
BLRD Research Career Scientist Award ApplicationIK6BX003783 · VA · RLR VA MEDICAL CENTER · PI ALEXANDER G ROBLING · 2017 to 2026
–
BLRD VA I01 BX001478BLRD VA IK6 BX003783Howard Hughes Medical InstituteNIAMS NIH HHS R01 AR053237NIAMS NIH HHS R56 AR053237
6 · The paper itself

Abstract

Dominant negative mutations in CLCN7, which encodes a homodimeric chloride channel needed for matrix acidification by osteoclasts, cause Albers-Schönberg disease (also known as autosomal dominant osteopetrosis type 2). More than 25 different CLCN7 mutations have been identified in patients affected with Albers-Schönberg disease, but only one mutation (Clcn7

Indexed as

AllelesAnimalsBone and BonesCancellous BoneCell CountChloride ChannelsDisease Models, AnimalGene Knock-In TechniquesGenes, DominantHeterozygoteHomozygoteInterferon-gammaLoss of Function MutationMiceOrgan SizeOsteoclastsChloride ChannelsClcn7 protein, mouseInterferon-gammaAlbers-Schönberg diseaseinterferon-gammaosteoclastOsteopetrosis

Identifiers

PMID28942122
PMCPMC5752150
OpenAlexW2757524584

What OpenQuestion holds

Textmetadata
LicenceTDM
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.