Evidence map›Paper›PMID 23770287›Full record

ReviewCellular signalling2013

Rit subfamily small GTPases: regulators in neuronal differentiation and survival.

Geng-Xian Shi, Weikang Cai, Douglas A Andres

Abstract readReview
In one paragraph

Review in Cellular signalling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

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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.

Geng-Xian ShiDepartment of Molecular and Cellular Biochemistry, University of Kentucky College of Medicine, BBSRB, 741S. Limestone St., Lexington, KY 40536-0509, USA.
Weikang Cai
Douglas A Andres
University of Kentucky · US

Funding

UNDERSTANDING THE MOLECULAR BASIS OF EPIGENETIC TRANSCRIPTIONAL SILENCINGP20RR020171 · NCRR · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2004 to 2011
$16.5M
Center for Biomedical Research Excellence in the Molecular Basis of Human DiseaseP20GM103486 · NIGMS · UNIVERSITY OF KENTUCKY · PI LOUIS HERSH, LOUIS HERSH LOUIS HERSH · 2012 to 2013
$4.2M
Regulation of Neuronal Survival by the Rit GTPaseR01NS045103 · NINDS · UNIVERSITY OF KENTUCKY · PI ANDRES, DOUGLAS ALLEN · 2003 to 2012
$2.7M
Regulation of Neuronal Survival by the Rit GTPaseR56NS045103 · NINDS · UNIVERSITY OF KENTUCKY · PI ANDRES, DOUGLAS ALLEN · 2008 to 2008
$366k
NCRR NIH HHS 2P20 RR020171NCRR NIH HHS P20 RR020171NIGMS NIH HHS P20 GM103486NINDS NIH HHS R01 NS045103NINDS NIH HHS R56 NS045103
6 · The paper itself

Abstract

Ras family small GTPases serve as binary molecular switches to regulate a broad array of cellular signaling cascades, playing essential roles in a vast range of normal physiological processes, with dysregulation of numerous Ras-superfamily G-protein-dependent regulatory cascades underlying the development of human disease. However, the physiological function for many "orphan" Ras-related GTPases remain poorly characterized, including members of the Rit subfamily GTPases. Rit is the founding member of a novel branch of the Ras subfamily, sharing close homology with the neuronally expressed Rin and Drosophila Ric GTPases. Here, we highlight recent studies using transgenic and knockout animal models which have begun to elucidate the physiological roles for the Rit subfamily, including emerging roles in the regulation of neuronal morphology and cellular survival signaling, and discuss new genetic data implicating Rit and Rin signaling in disorders such as cancer, Parkinson's disease, autism, and schizophrenia.

Indexed as

AnimalsCell DifferentiationCell SurvivalDrosophilaHumansMAP Kinase Signaling SystemMiceMonomeric GTP-Binding ProteinsNeuronsras ProteinsSignal TransductionMonomeric GTP-Binding Proteinsras ProteinsRIT1 protein, humanCAcalmodulinCaMcAMPcAMP response element binding proteinCCICdc42/Rac interactive bindingc-Jun N-terminal protein kinaseconstitutively activecontrolled cortical impactCREBCRIBcyclic adenosine monophosphateDADATDNdominant negativedopaminedopamine transporterEGFEpacepidermal growth factorERKexchange protein directly activated by cAMPextracellular-signal regulated protein kinaseGAPGEFGPCRG protein coupled receptorGTPaseGTPase activating proteinguanine nucleotide exchange factorguanosine triphosphataseheat shock protein 27HSP27IFNγinterferon-γJNKMAPKMAPK-activated protein kinase 2 (MAPKAPK2)MAPK kinase (also MAP2K)MEFsmitogen-activated protein kinasemitogen- and stress-activated protein kinase 1/2MK2MKKmouse embryonic fibroblastsMSK1/2nerve growth factorNeuronNGFPACAP38Parkinson's diseasePDphorbol 12-myristate 13-acetatephosphatidylinositol 3-kinasePI3Kpituitary adenylate cyclase activated polypeptide 38PKAPKCPMAprotein kinase Aprotein kinase CRalGDS-like 3Ras GTPaseRas-related protein which interacted with calmodulinreactive oxygen speciesreceptor tyrosine kinaseRGL3RicRic (Ras)-related gene expressed in neural tissuesRic (Ras)-related gene expressed throughout the organismRinRitROSRTKSignalingson of sevenlessSOSTBITNFαtraumatic brain injuryTrkAtropomyosin receptor kinase Atumor necrosis factor α

Identifiers

PMID23770287
PMCPMC3774011
OpenAlexW2024431122

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.