Evidence map›Paper›PMID 34902552›Full record

ArticleNeurobiology of disease2022

KLF15 overexpression in myocytes fails to ameliorate ALS-related pathology or extend the lifespan of SOD1G93A mice.

Ryan Massopust, Devin Juros, Dillon Shapiro, Mikayla Lopes, Saptarsi M Haldar, Thomas Taetzsch, Gregorio Valdez

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurobiology of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Article
  2. Review
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

7 authors at 3 institutions in 1 country.

Ryan MassopustDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA.
Devin JurosDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA.
Dillon ShapiroMolecular Biology, Cell Biology, & Biochemistry Graduate Program, Brown University, Providence, RI, USA.
Mikayla LopesDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA.
Saptarsi M HaldarGladstone Institutes, San Francisco, CA, USA; Department of Medicine, Cardiology Division, UCSF School of Medicine, San Francisco, CA, USA.
Thomas TaetzschDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA.
Gregorio ValdezDepartment of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI, USA; Center for Translational Neuroscience, Robert J. and Nancy D. Carney Institute for Brain Science and Brown Institute for Translational Science, Brown University, Providence, RI, USA; Department of Neurology, Warren Alpert Medical School of Brown University, Providence, United States. Electronic address: gregorio_valdez@brown.edu.
Brown University · USAllen Institute for Brain Science · USGladstone Institutes · US

Funding

Predoctoral Training in the Molecular Biology of AgingT32AG041688 · NIA · BROWN UNIVERSITY · PI NICOLA NERETTI, John M Sedivy · 2012 to 2026
$3.5M
Targeting the fibroblast growth factor binding protein-1 to slow degeneration of neuromuscular junctionsR01AG055545 · NIA · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI VALDEZ, GREGORIO · 2017 to 2021
$2.2M
Analysis of Sensory Neurons to Understand and Identify Factors to Treat ALSR21NS106313 · NINDS · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI VALDEZ, GREGORIO · 2018 to 2019
$433k
Synaptic FGFs are required and sufficient to maintain and repair aged NMJsR56AG051501 · NIA · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI VALDEZ, GREGORIO · 2015 to 2015
$377k
NIA NIH HHS R01 AG055545NIA NIH HHS R56 AG051501NIA NIH HHS T32 AG041688NINDS NIH HHS R21 NS106313
6 · The paper itself

Abstract

Amyotrophic Lateral Sclerosis (ALS) is a currently incurable disease that causes progressive motor neuron loss, paralysis and death. Skeletal muscle pathology occurs early during the course of ALS. It is characterized by impaired mitochondrial biogenesis, metabolic dysfunction and deterioration of the neuromuscular junction (NMJ), the synapse through which motor neurons communicate with muscles. Therefore, a better understanding of the molecules that underlie this pathology may lead to therapies that slow motor neuron loss and delay ALS progression. Kruppel Like Factor 15 (KLF15) has been identified as a transcription factor that activates alternative metabolic pathways and NMJ maintenance factors, including Fibroblast Growth Factor Binding Protein 1 (FGFBP1), in skeletal myocytes. In this capacity, KLF15 has been shown to play a protective role in Duchenne muscular dystrophy (DMD) and spinal muscular atrophy (SMA), however its role in ALS has not been evaluated. Here, we examined whether muscle-specific KLF15 overexpression promotes the health of skeletal muscles and NMJs in the SOD1

Indexed as

Amyotrophic Lateral SclerosisKruppel-Like Transcription FactorsAnimalsDisease Models, AnimalIntercellular Signaling Peptides and ProteinsLongevityMiceMice, TransgenicMotor NeuronsMuscle CellsMuscle, SkeletalNeuromuscular JunctionSuperoxide Dismutase-1Fgfbp1 protein, mouseIntercellular Signaling Peptides and ProteinsKlf15 protein, mouseKruppel-Like Transcription FactorsSuperoxide Dismutase-1ALSFGFBP1KLF15NMJ

Identifiers

PMID34902552
PMCPMC8750438
OpenAlexW4200167402

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.