Evidence map›Paper›PMID 24960694›Full record

ArticleDevelopmental cell2014

Dynamic control of excitatory synapse development by a Rac1 GEF/GAP regulatory complex.

Kyongmi Um, Sanyong Niu, Joseph G Duman, Jinxuan X Cheng, Yen-Kuei Tu, Brandon Schwechter, Feng Liu, Laura Hiles, Anjana S Narayanan, Ryan T Ash and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  9. MARCKS and PI(4,5)PMolecular biology of the cell · 2024
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  19. Rho Signaling in Synaptic Plasticity, Memory, and Brain Disorders.Frontiers in cell and developmental biology · 2021
    Review
  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

14 authors at 1 institution in 1 country.

Kyongmi UmDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Sanyong NiuDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Joseph G DumanDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Jinxuan X ChengDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Yen-Kuei TuDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Integrative Molecular and Biomedical Sciences Program, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Brandon SchwechterDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Feng LiuDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Laura HilesDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Anjana S NarayananDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Ryan T AshDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Shalaka MulherkarDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Kannan AlpadiVerna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Stelios M SmirnakisDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Kimberley F ToliasDepartment of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Verna and Marrs McLean Department of Biochemistry and Molecular Biology, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA; Integrative Molecular and Biomedical Sciences Program, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. Electronic address: tolias@bcm.edu.
Baylor College of Medicine · US

Funding

UNDERSTANDING FXTAS AMONG MALES WITH THE FMR1 PREMUTATIONP30HD024064 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI ZOGHBI, HUDA Y · 1988 to 2013
$29.4M
Signaling Mechanisms Regulating Rho GTPase-Dependent Synaptic Plasticity Underlying Memory in Health and DiseaseR01NS062829 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI TOLIAS, KIMBERLY R · 2009 to 2025
$4.4M
Mechanisms of Brain-specific Angiogenesis Inhibitor 1 (BAI1) in neural developmenK01MH086119 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI DUMAN, JOSEPH G · 2010 to 2013
$506k
Rapid and Quantitative Point Of Care Stool Assays For The Diagnosis And Monitoring Of Inflammatory Bowel DiseaseR43DK131680 · NIDDK · PREDICT HEALTH, LLC, THE · PI ALPADI, KANNAN · 2022 to 2022
$280k
NICHD NIH HHS P30 HD024064NICHD NIH HHS P30HD024064NIDDK NIH HHS R43 DK131680NIMH NIH HHS K01 MH086119NIMH NIH HHS K01MH089112NINDS NIH HHS R01 NS062829NINDS NIH HHS R01NS062829
6 · The paper itself

Abstract

The small GTPase Rac1 orchestrates actin-dependent remodeling essential for numerous cellular processes including synapse development. While precise spatiotemporal regulation of Rac1 is necessary for its function, little is known about the mechanisms that enable Rac1 activators (GEFs) and inhibitors (GAPs) to act in concert to regulate Rac1 signaling. Here, we identify a regulatory complex composed of a Rac-GEF (Tiam1) and a Rac-GAP (Bcr) that cooperate to control excitatory synapse development. Disruption of Bcr function within this complex increases Rac1 activity and dendritic spine remodeling, resulting in excessive synaptic growth that is rescued by Tiam1 inhibition. Notably, EphB receptors utilize the Tiam1-Bcr complex to control synaptogenesis. Following EphB activation, Tiam1 induces Rac1-dependent spine formation, whereas Bcr prevents Rac1-mediated receptor internalization, promoting spine growth over retraction. The finding that a Rac-specific GEF/GAP complex is required to maintain optimal levels of Rac1 signaling provides an important insight into the regulation of small GTPases.

Indexed as

AnimalsBlotting, WesternDendritic SpinesElectrophysiologyEndocytosisGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsImmunoenzyme TechniquesImmunoprecipitationMiceMice, KnockoutNeuritesProto-Oncogene Proteins c-bcrrac1 GTP-Binding ProteinReceptors, Eph FamilyRNA, Small InterferingAbr protein, mouseBcr protein, mouseGTPase-Activating ProteinsGuanine Nucleotide Exchange FactorsProto-Oncogene Proteins c-bcrrac1 GTP-Binding ProteinReceptors, Eph FamilyRNA, Small InterferingTiam1 protein, mouseT-Lymphoma Invasion and Metastasis-inducing Protein 1

Identifiers

PMID24960694
PMCPMC4111230
OpenAlexW2003944475

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.