Evidence map›Paper›PMID 36102617›Full record

ReviewDevelopment (Cambridge, England)2022

Calcium and activity-dependent signaling in the developing cerebral cortex.

Arpana Arjun McKinney, Ralitsa Petrova, Georgia Panagiotakos

Open access · hybridAbstract readReview
In one paragraph

Review in Development (Cambridge, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Calcium and CaBrain sciences · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
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  15. Article
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  18. Polymorphisms inGenes · 2025
    Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Arpana Arjun McKinneyGraduate Program in Developmental and Stem Cell Biology, University of California, San Francisco, CA 94143, USA.
Ralitsa PetrovaEli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, University of California, San Francisco, CA 94143, USA.ORCID 0000-0001-5586-6192
Georgia PanagiotakosGraduate Program in Developmental and Stem Cell Biology, University of California, San Francisco, CA 94143, USA.ORCID 0000-0001-9444-2480
University of California, San Francisco · US

Funding

Calcium-Dependent Regulation of Neural Fate in Development and DiseaseR01MH125004 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PANAGIOTAKOS, GEORGIA · 2021 to 2025
$2.0M
Cell type signaling specificity of the neurodevelopmental disease-associated DYRK1A kinaseR01MH127075 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PANAGIOTAKOS, GEORGIA · 2022 to 2025
$1.9M
Cell type signaling specificity of the neurodevelopmental disease-associated DYRK1A kinaseR56MH127075 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PANAGIOTAKOS, GEORGIA · 2021 to 2021
$378k
NIMH NIH HHS R01 MH125004NIMH NIH HHS R01 MH127075NIMH NIH HHS R56 MH127075
6 · The paper itself

Abstract

Calcium influx can be stimulated by various intra- and extracellular signals to set coordinated gene expression programs into motion. As such, the precise regulation of intracellular calcium represents a nexus between environmental cues and intrinsic genetic programs. Mounting genetic evidence points to a role for the deregulation of intracellular calcium signaling in neuropsychiatric disorders of developmental origin. These findings have prompted renewed enthusiasm for understanding the roles of calcium during normal and dysfunctional prenatal development. In this Review, we describe the fundamental mechanisms through which calcium is spatiotemporally regulated and directs early neurodevelopmental events. We also discuss unanswered questions about intracellular calcium regulation during the emergence of neurodevelopmental disease, and provide evidence that disruption of cell-specific calcium homeostasis and/or redeployment of developmental calcium signaling mechanisms may contribute to adult neurological disorders. We propose that understanding the normal developmental events that build the nervous system will rely on gaining insights into cell type-specific calcium signaling mechanisms. Such an understanding will enable therapeutic strategies targeting calcium-dependent mechanisms to mitigate disease.

Indexed as

CalciumNervous System DiseasesCalcium SignalingCerebral CortexHumansCalciumCalcium signalingCortical developmentNeurodevelopmental disorders

Identifiers

PMID36102617
PMCPMC9578689
OpenAlexW4295654268

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.