Evidence map›Paper›PMID 11404423›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Neuronal expression of synaptotagmin-related gene 1 is regulated by thyroid hormone during cerebellar development.

G B Potter, F Facchinetti, G M Beaudoin, C C Thompson

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Novel biomarkerFuture science OA · 2018
    Article
  3. Article
  4. Article
  5. Article
  6. Thyroid hormone and cerebellar development.Cerebellum (London, England) · 2008
    Review
  7. Three distinct kinetic groupings of the synaptotagmin family: candidate sensors for rapid and delayed exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2005
    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

4 authors at 2 institutions in 1 country.

G B PotterKennedy Krieger Research Institute and Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
F Facchinetti
G M Beaudoin
C C Thompson
Johns Hopkins University · USKennedy Krieger Institute · US

Funding

TARGETS OF THYROID HORMONE ACTION IN DEVELOPING BRAINR29DK046074 · NIDDK · HUGO W. MOSER RES INST KENNEDY KRIEGER · PI THOMPSON, CATHERINE C · 1995 to 1999
–
NIDDK NIH HHS DK46074
6 · The paper itself

Abstract

Thyroid hormone (TH) is essential for proper brain development, acting through nuclear receptors that modulate the expression of specific genes in response to hormone binding. In a screen for genes regulated by TH in the rat cerebellum, we recently identified a novel gene, synaptotagmin-related gene 1 (Srg1). The Srg1 protein is structurally similar to synaptotagmins, a family of proteins involved in regulating neurotransmission. To elucidate a potential role of Srg1 in brain development, we have investigated the developmental and TH-regulated expression of Srg1 in the neonatal rat brain. We show that expression of both Srg1 RNA and protein is detected only in the brain and specifically in neurons. Srg1 mRNA and protein levels increase postnatally, nearing adult levels after the third postnatal week. Neonatal TH deficiency results in a significant reduction and delay in expression of both Srg1 RNA and protein. Using immunohistochemistry, we were able to detect Srg1 protein in numerous brain regions. In the cerebellum, Srg1 protein is localized to the molecular layer, indicating that it is highly expressed in granule cell axons. To further examine Srg1 expression in cerebellar granule cells (CGCs), we used an in vitro cell culture model. In primary cultures of CGCs, Srg1 expression is significantly reduced in the absence of TH. Srg1 mRNA is rapidly upregulated in cultured CGCs, suggesting a direct response to TH. Neuronal and TH-regulated expression of Srg1, together with its localization to neurites, implicates Srg1 as an important component of the program of gene expression induced by TH in the developing brain.

Indexed as

Gene Expression Regulation, DevelopmentalAgingAnimalsAnimals, NewbornAxonsBrainCells, CulturedCerebellumFemaleHypothyroidismImmunohistochemistryIn Situ HybridizationMaleMembrane ProteinsMethimazoleNeuronsMembrane ProteinsMethimazoleRNA, MessengerSynaptotagminsSyt12 protein, ratSytl1 protein, mouseThyroid HormonesVesicular Transport Proteins

Identifiers

PMID11404423
PMCPMC6762732
OpenAlexW2144490903

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.