The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index; none of the 14 sources its claims cite is checked for support yet.
Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning
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Development of surface folds of the human brain is controlled in sections. [Also see Perspective by Rash and Rakic ]
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“Dominant-negative RFX abrogates normal, but not mutant, e1m promoter activity on embryonic day 13.5 (E13.5) in mouse cortical cultures”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The two Irish-American families carry the mutation on the same chromosomal haplotype, which reflects a common founder.”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The element is located <150 bp upstream of the transcriptional start site of noncoding exon 1m (e1m) of GPR56”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, the 23-kb construct containing the 15-bp deletion drives expression in medial, but not lateral, cortex or lateral ganglionic eminence”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we performed yeast one-hybrid (Y1H) screening of a mouse forebrain cDNA library with the human cis-regulatory element as bait and obtained multiple yeast colonies encoding members of the regulatory factor X (Rfx) transcription factor family”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“RFX1 and GPR56 colocalize in germinal zones of fetal human brain”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Chromatin immunoprecipitation sequencing confirmed RFX3 binding to the element”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This construct drives GFP expression in the entire central nervous system, including neocortex, and recapitulates the location and relative amount of expression of endogenous mouse GPR56 protein”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“we sequenced 38 conserved non-exonic elements (table S2), in one of which we identified a small deletion in all five individuals. The mutated element normally contains two copies of a 15–base pair (bp) tandem repeat, but all affected individuals have a homozygous deletion of one 15-bp repeat”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mouse e1m promoter drives β-gal expression broadly in the nervous system in diverse cell types”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 16
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In the paper
“The diverse noncoding first exons have distinct expression profiles, with e1m being the most robustly transcribed first exon in fetal human brain but with several other alternative transcripts also expressed in fetal and adult brain”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The deletion is heterozygous in parents of the affected individuals, who manifest no obvious clinical signs, and is absent from thousands of control chromosomes in the Single-Nucleotide Polymorphism Database and 1000 Genomes database.”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“RFX1 and RFX3 bind the normal element in vitro, with binding decreased 60 to 70% by the 15-bp deletion”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“It is noteworthy that the Turkish family carries the same deletion on a distinct haplotype, which indicates that the mutation arose independently”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“RFX and GPR56 expression patterns are correlated (fig. S5, A and B) (15), with RFX3 and RFX7 most prominent in human ventrolateral prefrontal cortex, the region affected in perisylvian polymicrogyria”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
What the sources say
- Not checked yetcites [15] Kang HJ Nature 478 483 489 2011 22031440 PMC3566780 source
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In the paper
“Another noncoding GPR56 exon (exon 2), present only in primates, derives from a primate-specific Alu insertion”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Gpr56 knockout mice show fewer phosphohistone H3 (PH3)–positive mitotic progenitor cells and TBR2-positive intermediate progenitors than wild-type mice in the neocortex at E14.5.”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The cis-regulatory element upstream of GPR56 e1m is found in genomes of all placental mammals, but not monotremes, marsupials, or non-mammals”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“the corresponding human e1m promoter has a variety of deletions and single-nucleotide variants, relative to the mouse sequence (fig. S6A), and drives much more limited expression in rostral-lateral cortex”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“GPR56 expression in developing human and marmoset neocortex is highest in the ventricular zone, as well as in the outer subventricular zone, which is expanded in mammals with larger brains”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data suggest that the cis-regulatory element upstream of e1m drives GPR56 expression in the perisylvian and lateral cortex, whereas disruption of the element, with consequent impairment of e1m expression, causes the perisylvian malformation.”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“GPR56 encodes an adhesion heterotrimeric guanine nucleotide–binding protein (G protein)–coupled receptor that is highly expressed in cortical progenitors (7, 16) and binds extracellular matrix proteins (17).”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
What the sources say
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Loss of GPR56 disrupts radial glia and causes breaches in the pial basement membrane, through which some neurons over-migrate (9, 16).”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Postmortem analysis of a human with biallelic GPR56 coding mutations showed a very thin cortex, which suggested potential roles of GPR56 in neurogenesis as well (9).”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
What the sources say
- Not checked yetcites [9] Bahi-Buisson N Brain 133 3194 3209 2010 20929962 source
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The elaboration of the GPR56 locus in gyrencephalic mammals, and especially humans, to produce many alternative splice forms with diverse expression patterns presents GPR56 as a key target that could influence the dramatic changes in shape and folding that characterize the forebrain of many mammals.”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, GPR56 acquired many noncoding upstream exons and generated alternative splice forms with distinct expression patterns (fig. S2, B and D), in the lineage leading to humans. Transposable element insertion played a role in generating this diversity.”
§ Evolutionarily Dynamic Alternative Splicing of GPR56 Regulates Regional Cerebral Cortical Patterning > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
The mechanisms of cortical gyrification and the formation of specialized cortical regions are poorly understood.
“the genetic and evolutionary mechanisms of cortical gyrification are poorly understood”
“it is unsolved how these cortical regions form and how human cortical regions evolved from those of prehuman ancestors.”
The paper relies on this without support.
Abnormal gyrification invariably indicates abnormal cortical development.
“Abnormal gyrification, such as polymicrogyria (too many small gyri), invariably signals abnormal cortical development”
The paper relies on this without support.
Placental and nonplacental mammals diverged 85 to 100 million years ago.
“diverged 85 to 100 million years ago”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“For example, extensive variation in the cis-regulation of GPR56, a gene that promotes neural progenitor proliferation (Bae et al., 2014), is observed due to the expansion of the number of transcriptional start sites present in human GPR56 (17 start sites) as compared to its mouse ortholog Gpr56 (5 start sites; Figure 7A).”
From The Cellular and Molecular Landscapes of the Developing Human Central Nervous System (2016) · cites this paper as Bae et al., 2014
In the citing paper
“In addition to evolutionary changes in transcription factor binding sites, human-specific expansion, deletion, and de novo emergence of regulatory elements are also observed (Bae et al., 2014).”
From The Cellular and Molecular Landscapes of the Developing Human Central Nervous System (2016) · cites this paper as Bae et al., 2014
In the citing paper
“The cis-element of one of these human alternative transcriptional start sites (E1m) can drive expression of a reporter gene in RG cells throughout the embryonic neocortex of a transgenic mouse (Figure 7B).”
From The Cellular and Molecular Landscapes of the Developing Human Central Nervous System (2016) · cites this paper as Bae et al., 2014
In the citing paper
“Moreover, a 15 base pair deletion of the E1m cis-element caused perysylvian microgyria in humans and affected rostro-lateral GPR56 expression in mouse (Figures 7C and D).”
From The Cellular and Molecular Landscapes of the Developing Human Central Nervous System (2016) · cites this paper as Bae et al., 2014
In the citing paper
“Further experiments with sequences found in other mammals with a prominent sylvian fissure and gyrencephalic brain recapitulated this pattern of expression, suggesting that GPR56 was important for the evolutionary expansion of the perisylvian neocortex, a region involved in the processing of language and speech and other higher-order cognitive functions.”
From The Cellular and Molecular Landscapes of the Developing Human Central Nervous System (2016) · cites this paper as Bae et al., 2014
In the citing paper
“Intriguingly, the human noncoding element directs gene expression in a highly restricted pattern, whereas the mouse element directs more diffuse expression.”
From Genetic Changes Shaping the Human Brain (2015) · cites this paper as Bae et al., 2014
In the citing paper
“It turned out that the human GPR56 has at least 17 alternative promoters, whereas mouse Gpr56 has only a handful.”
From Genetic Changes Shaping the Human Brain (2015) · cites this paper as Bae et al., 2014
In the citing paper
“For example, many of the complex alternative promoters and exons of human GPR56 were derived from LINEs and SINEs (Bae et al., 2014).”
From Genetic Changes Shaping the Human Brain (2015) · cites this paper as Bae et al., 2014
In the citing paper
“Recently, polymicrogyria restricted to the neocortical areas surrounding the Sylvian fissure including Broca’s area, the primary language area, was identified (Bae et al., 2014). The causative mutation is found in the GPR56 locus, but disrupts a noncoding element, which constitutes a strong neural promoter during development, in the 5’-upstream regulatory region of GPR56.”
From Genetic Changes Shaping the Human Brain (2015) · cites this paper as Bae et al., 2014
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Metadata
- Authors
- Bae, B.-I., Tietjen, I., Atabay, K. D., Evrony, G. D., Johnson, M. B., Asare, E., Wang, P. P., Murayama, A. Y., Im, K., Lisgo, S. N., Overman, L., Šestan, N., Chang, B. S., Barkovich, A. J., Grant, P. E., Topçu, M., Politsky, J., Okano, H., Piao, X., & Walsh, C. A.
- Affiliations
- Broad Institute (US)
- Keio University (JP)
- Boston Children's Hospital (US)
- Centre for Life (GB)
- Yale University (US)
- Beth Israel Deaconess Medical Center (US)
- University of California, San Francisco (US)
- Hacettepe University (TR)
- Augusta University (US)
- Corresponding author
- Bae, Byoung-Il
- Tietjen, Ian
- Politsky, Jeffrey
- Walsh, Christopher A.
- ORCID
- Venue
- Science
- Published
- 2014-02-14
- Volume
- 343
- Issue
- 6172
- Pages
- 764-768
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC4480613
- OpenAlex
- W1979208523
- Semantic Scholar
- ab78a1227d69c6090e8a819cd5935b59848b1f92
- Cited by
- 229
- References
- 40
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 10 · 2023: 8 · 2022: 11 · 2021: 18 · 2020: 44 · 2019: 21 · 2018: 20 · 2017: 18 · 2016: 21 · 2015: 26 · 2014: 14
- FWCI
- 9.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Hacettepe University Institutional Repository (hacettepe.edu.tr) (submittedVersion, other-oa)
- Funders
- Howard Hughes Medical Institute
- Wellcome Trust (GR082557)
- Medical Research Council (MC_PC_15004)
- National Institute of Mental Health (U01MH081896)
- National Institute of Neurological Disorders and Stroke (R01NS035129)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (HHSN275200900011C, P30HD018655, N01-HD-90011)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- GPR56, alternative splicing, alternative promoters, cortical development, Broca's area, Sylvian fissure, RFX transcription factors, G protein-coupled receptors, cortical progenitor cells, stem cell proliferation, neocortex evolution, laterality
- MeSH terms
- Animals, Base Sequence, Cats, Cerebral Cortex, Biological Evolution, Frontal Lobe, Haplotypes, Humans, Molecular Sequence Data, Pedigree, Promoter Regions, Genetic, Genetic Variation, Sequence Deletion, Alternative Splicing, Codon, Nonsense, Body Patterning, Receptors, G-Protein-Coupled, Cell Proliferation, Mice, Neural Stem Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-07, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-07 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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