Evidence map›Paper›PMID 18508528›Full record

ReviewFrontiers in bioscience : a journal and virtual library2008

Regulation of neurite outgrowth by G(i/o) signaling pathways.

Kenneth D Bromberg, Ravi Iyengar, John Cijiang He

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience : a journal and virtual library, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. GαJournal of neurochemistry · 2025
    Article
  3. Article
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  6. Article
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  9. Phosphodiesterase Inhibitors Revert Axonal Dystrophy in Friedreich's Ataxia Mouse Model.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  10. Article
  11. Review
  12. Review
  13. CBAdvances in pharmacology (San Diego, Calif.) · 2017
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Amyloid precursor proteins interact with the heterotrimeric G protein Go in the control of neuronal migration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    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.

Kenneth D BrombergDepartment of Pharmacology and Systems Therapeutics, Mount Sinai School of Medicine, New York, NY 10029, USA. Kenneth.Bromberg@mssm.edu
Ravi Iyengar
John Cijiang He
Icahn School of Medicine at Mount Sinai · US

Funding

MOLECULAR MECHANISM OF DESENSITIZATIONR01GM054508 · NIGMS · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI IYENGAR, SRINIVAS RAVI V · 1995 to 2016
$8.0M
SIGNALING PATHWAYS INTERACTIONS AND MAMMARY TUMORR01CA081050 · NCI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI IYENGAR, SRINIVAS RAVI V · 2000 to 2004
$1.8M
Pathogenesis of HIVAN: the role of NefK08DK065495 · NIDDK · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI HE, JOHN C · 2003 to 2007
$640k
NCI NIH HHS CA-81050NCI NIH HHS R01 CA081050NIDDK NIH HHS DK-65495NIDDK NIH HHS K08 DK065495NIGMS NIH HHS GM-54508NIGMS NIH HHS R01 GM054508
6 · The paper itself

Abstract

Neurogenesis is a long and winding journey. A neural progenitor cell migrates long distances, differentiates by forming a single axon and multiple dendrites, undergoes maturation, and ultimately survives. The initial formation of neurites during neuronal differentiation, commonly referred to as "neurite outgrowth," can be induced by a large repertoire of signals that stimulate an array of receptors and downstream signaling pathways. The G(i/o) family of heterotrimeric G-proteins are abundantly expressed in the brain and enriched at neuronal growth cones. Recent evidence has uncovered several G(i/o)-coupled receptors that induce neurite outgrowth and has begun to elucidate the underlying molecular mechanisms. Emerging data suggests that signals from several G(i/o)-coupled receptors converge at the transcription factor STAT3 to regulate neurite outgrowth and at Rac1 and Cdc42 to regulate cytoskeletal reorganization. Physiologically, signaling through G(i/o)-coupled cannabinoid receptors is critical for pro percentral nervous system development. As the mechanisms by which G(i/o)-coupled receptors regulate neurite outgrowth are clarified, it is becoming evident that modulating signals from G(i/o) and their receptors has great potential for the treatment of neurodegenerative diseases.

Indexed as

AnimalsCannabinoidsCell DifferentiationCell DivisionGrowth ConesGTP-Binding Protein alpha Subunits, Gi-GoNerve DegenerationNeuritesSignal TransductionCannabinoidsGTP-Binding Protein alpha Subunits, Gi-Go

Identifiers

PMID18508528
PMCPMC3068557
OpenAlexW1982822508

What OpenQuestion holds

Textmetadata
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.