ArticleDevelopment (Cambridge, England)2014
The splicing factor PQBP1 regulates mesodermal and neural development through FGF signaling.
Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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.
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.
Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- Disrupted PQBP1-HNRNPU-LINE-1 axis underlies aberrant neurodevelopment in renpenning syndrome.Molecular psychiatry · 2026Article
- Loss of wbp11 causes multi-system developmental defects: a zebrafish model of VACTERL association.Frontiers in cell and developmental biology · 2026Article
- Review
- The splicing factor WBP11 mediates MCM7 intron retention to promote the malignant progression of ovarian cancer.Oncogene · 2024Article
- Molecular consequences of PQBP1 deficiency, involved in the X-linked Renpenning syndrome.Molecular psychiatry · 2024Article
- Complex haploinsufficiency in pluripotent cells yields somatic cells with DNA methylation abnormalities and pluripotency induction defects.Stem cell reports · 2023Article
- Identification of a DNA methylation signature for Renpenning syndrome (RENS1), a spliceopathy.European journal of human genetics : EJHG · 2023Article
- Prostate cancer resistance leads to a global deregulation of translation factors and unconventional translation.NAR cancer · 2022Article
- The emerging significance of splicing in vertebrate development.Development (Cambridge, England) · 2022Review
- Recognition of HIV-1 capsid by PQBP1 licenses an innate immune sensing of nascent HIV-1 DNA.Molecular cell · 2022Article
- The atypical RNA-binding protein Taf15 regulates dorsoanterior neural development through diverse mechanisms in Xenopus tropicalis.Development (Cambridge, England) · 2021Article
- Heterozygous loss of WBP11 function causes multiple congenital defects in humans and mice.Human molecular genetics · 2020Article
- The miR-29c-KIAA1199 axis regulates gastric cancer migration by binding with WBP11 and PTP4A3.Oncogene · 2019Article
- Expanding the genetic toolkit in Xenopus: Approaches and opportunities for human disease modeling.Developmental biology · 2017Review
- An optimized method for cryogenic storage of Xenopus sperm to maximise the effectiveness of research using genetically altered frogs.Theriogenology · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alternative splicing of pre-mRNAs is an important means of regulating developmental processes, yet the molecular mechanisms governing alternative splicing in embryonic contexts are just beginning to emerge. Polyglutamine-binding protein 1 (PQBP1) is an RNA-splicing factor that, when mutated, in humans causes Renpenning syndrome, an X-linked intellectual disability disease characterized by severe cognitive impairment, but also by physical defects that suggest PQBP1 has broader functions in embryonic development. Here, we reveal essential roles for PQBP1 and a binding partner, WBP11, in early development of Xenopus embryos. Both genes are expressed in the nascent mesoderm and neurectoderm, and morpholino knockdown of either causes defects in differentiation and morphogenesis of the mesoderm and neural plate. At the molecular level, knockdown of PQBP1 in Xenopus animal cap explants inhibits target gene induction by FGF but not by BMP, Nodal or Wnt ligands, and knockdown of either PQBP1 or WBP11 in embryos inhibits expression of fgf4 and FGF4-responsive cdx4 genes. Furthermore, PQBP1 knockdown changes the alternative splicing of FGF receptor-2 (FGFR2) transcripts, altering the incorporation of cassette exons that generate receptor variants (FGFR2 IIIb or IIIc) with different ligand specificities. Our findings may inform studies into the mechanisms underlying Renpenning syndrome.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.