Evidence map›Paper›PMID 19217427›Full record

ArticleDevelopmental cell2009

AMP-activated protein kinase phosphorylates retinoblastoma protein to control mammalian brain development.

Biplab Dasgupta, Jeffrey Milbrandt

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

73 citing papers in PubMed, 134 citations in OpenAlex.

  1. Article
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  4. Sugar signaling modulates SHOOT MERISTEMLESS expression and meristem function inProceedings of the National Academy of Sciences of the United States of America · 2024
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  20. Involvement of AMP-activated protein kinase in neuroinflammation and neurodegeneration in the adult and developing brain.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2019
    Review

13 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Biplab DasguptaDepartment of Pathology, Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 63110, USA.
Jeffrey Milbrandt
Hope Center for Neurological Disorders · US

Funding

PHYSIOLOGY AND GENETICS OF THE GDNF HOMOLOG NEURTURINR01AG013730 · NIA · WASHINGTON UNIVERSITY · PI JEFFREY D MILBRANDT · 1996 to 2026
$10.6M
Washington University Center for Translational NeuroscienceP30NS057105 · NINDS · WASHINGTON UNIVERSITY · PI HOLTZMAN, DAVID M. · 2006 to 2011
$8.7M
ROLE OF EGR2 MUTATIONS IN PERIPHERAL MYELINOPATHIESR01NS040745 · NINDS · WASHINGTON UNIVERSITY · PI MILBRANDT, JEFFREY D · 2001 to 2009
$3.3M
Regulating NAD Metabolism to Inhibit Axon Degeneration in Neurodegenerative DiseasesRF1AG013730 · NIA · WASHINGTON UNIVERSITY · PI MILBRANDT, JEFFREY D · 2017 to 2017
$2.8M
NIA NIH HHS AG13730NIA NIH HHS R01 AG013730NINDS NIH HHS NS040745NINDS NIH HHS NS057105NINDS NIH HHS P30 NS057105NINDS NIH HHS R01 NS040745
6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) is an evolutionarily conserved metabolic sensor that responds to alterations in cellular energy levels to maintain energy balance. While its role in metabolic homeostasis is well documented, its role in mammalian development is less clear. Here we demonstrate that mutant mice lacking the regulatory AMPK beta1 subunit have profound brain abnormalities. The beta1(-/-) mice show atrophy of the dentate gyrus and cerebellum, and severe loss of neurons, oligodendrocytes, and myelination throughout the central nervous system. These abnormalities stem from reduced AMPK activity, with ensuing cell cycle defects in neural stem and progenitor cells (NPCs). The beta1(-/-) NPC deficits result from hypophosphorylation of the retinoblastoma protein (Rb), which is directly phosphorylated by AMPK at Ser(804). The AMPK-Rb axis is utilized by both growth factors and energy restriction to increase NPC growth. Our results reveal that AMPK integrates growth factor signaling with cell cycle control to regulate brain development.

Indexed as

AMP-Activated Protein KinasesAnimalsApoptosisBrainCentral Nervous SystemMiceMice, TransgenicMutationMyelin SheathNeuronsOligodendrogliaPhosphorylationRetinoblastoma ProteinStem CellsAMP-Activated Protein KinasesRetinoblastoma Protein

Identifiers

PMID19217427
PMCPMC2662481
OpenAlexW2087840427

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.