Evidence map›Paper›PMID 10645947›Full record

ArticleGenome research2000

Uterine dysfunction and genetic modifiers in centromere protein B-deficient mice.

K J Fowler, D F Hudson, L A Salamonsen, S R Edmondson, E Earle, M C Sibson, K H Choo

Open access · greenAbstract read
In one paragraph

Article in Genome research, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
6.2field-weighted citation impact, top 4% 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

16 citing papers in PubMed, 55 citations in OpenAlex.

  1. CENP-A and centromere evolution in equids.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. FBXO38 Ubiquitin Ligase Controls Centromere Integrity via ZXDA/B Stability.Frontiers in cell and developmental biology · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Centromeres of filamentous fungi.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2012
    Review
  11. Article
  12. Article
  13. Partially functional Cenpa-GFP fusion protein causes increased chromosome missegregation and apoptosis during mouse embryogenesis.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2003
    Article
  14. Jerky, a protein deficient in a mouse epilepsy model, is associated with translationally inactive mRNA in neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  15. Article
  16. 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

7 authors at 1 institution in 1 country.

K J FowlerThe Murdoch Institute, Royal Children's Hospital, Parkville 3052, Australia.
D F Hudson
L A Salamonsen
S R Edmondson
E Earle
M C Sibson
K H Choo
Royal Children's Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Centromere protein B (CENP-B) binds constitutively to mammalian centromere repeat DNA and is highly conserved between humans and mouse. Cenpb null mice appear normal but have lower body and testis weights. We demonstrate here that testis-weight reduction is seen in male null mice generated on three different genetic backgrounds (denoted R1, W9.5, and C57), whereas body-weight reduction is dependent on the genetic background as well as the gender of the animals. In addition, Cenpb null females show 31%, 33%, and 44% reduced uterine weights on the R1, W9.5, and C57 backgrounds, respectively. Production of "revertant" mice lacking the targeted frameshift mutation but not the other components of the targeting construct corrected these differences, indicating that the observed phenotype is attributable to Cenpb gene disruption rather than a neighbouring gene effect induced by the targeting construct. The R1 and W9.5 Cenpb null females are reproductively competent but show age-dependent reproductive deterioration leading to a complete breakdown at or before 9 months of age. Reproductive dysfunction is much more severe in the C57 background as Cenpb null females are totally incompetent or are capable of producing no more than one litter. These results implicate a further genetic modifier effect on female reproductive performance. Histology of the uterus reveals normal myometrium and endometrium but grossly disrupted luminal and glandular epithelium. Tissue in situ hybridization demonstrates high Cenpb expression in the uterine epithelium of wild-type animals. This study details the first significant phenotype of Cenpb gene disruption and suggests an important role of Cenpb in uterine morphogenesis and function that may have direct implications for human reproductive pathology.

Indexed as

AutoantigensDNA-Binding ProteinsAnimalsBody WeightCell LineCentromereCentromere Protein BChimeraChromosomal Proteins, Non-HistoneEpitheliumFemaleFrameshift MutationHumansMaleMiceMice, Inbred C57BLAutoantigensCENPB protein, humanCenpb protein, mouseCentromere Protein BChromosomal Proteins, Non-HistoneDNA-Binding Proteins

Identifiers

PMID10645947
PMCPMC310504
OpenAlexW1770659658

What OpenQuestion holds

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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.