Article in Journal of neuroimmunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 33% 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
1 citing paper in PubMed, 3 citations in OpenAlex.
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
6 authors at 2 institutions in 1 country.
Mercedes PriegoDepartment of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America.
Lorena NoriegaDepartment of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America.
Sergey KalininDepartment of Research, Jesse Brown VA Medical Center, Chicago, IL 60612, United States of America.
Lisa M HoffmanDepartment of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America.
Douglas L FeinsteinDepartment of Research, Jesse Brown VA Medical Center, Chicago, IL 60612, United States of America; Department of Anesthesiology, University of Illinois, Chicago, IL 60612, United States of America. Electronic address: dlfeins@uic.edu.
Gerardo MorfiniDepartment of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612, United States of America. Electronic address: gmorfini@uic.edu.
University of Illinois Chicago · USJesse Brown VA Medical Center · US
Funding
Mechanisms of SPG4 Hereditary Spastic ParaplegiaR01NS118177 · NINDS · DREXEL UNIVERSITY · PI BAAS, PETER W., MORFINI, GERARDO ANDRES · 2020 to 2024
$3.2M
Role of p38alpha signaling in mutant SOD1-linked motor neuron diseaseR21NS120126 · NINDS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI BOSCO, DARYL ANGELA, MORFINI, GERARDO ANDRES · 2020 to 2020
$458k
Liver Kinase B1, a genetic risk factor for multiple sclerosisI01BX002625 · VA · JESSE BROWN VA MEDICAL CENTER · PI FEINSTEIN, DOUGLAS L. · 2016 to 2023
–
Accelerating remyelination using lanthionine ketimine derivativesI01RX003955 · VA · JESSE BROWN VA MEDICAL CENTER · PI FEINSTEIN, DOUGLAS L. · 2022 to 2025
–
Characterization of the oral microbiome of patients with Multiple SclerosisI21BX005914 · VA · JESSE BROWN VA MEDICAL CENTER · PI FEINSTEIN, DOUGLAS L. · 2023 to 2024
–
BLR&D Research Career Scientist Award ApplicationIK6BX004852 · VA · JESSE BROWN VA MEDICAL CENTER · PI Douglas L. Feinstein · 2020 to 2026
–
BLRD VA I01 BX002625BLRD VA I21 BX005914BLRD VA IK6 BX004852NINDS NIH HHS R01 NS118177NINDS NIH HHS R21 NS120126RRD VA I01 RX003955
6 · The paper itself
Abstract
The c-Jun amino terminal kinases (JNKs) regulate transcription, and studies suggest they contribute to neuropathology in the EAE model of MS. To examine the role of the JNK3 isoform, we compared EAE in JNK3 null mice to wild type (WT) littermates. Although disease severity was similar in female mice, in male JNK3 null mice the day of onset and time to reach 100% incidence occurred sooner, and disease severity was increased. While glial activation in spinal cord was similar, white matter lesions were increased in JNK3 null mice. These results suggest JNK3 normally limits EAE disease in a sex-dependent manner.
Indexed as
Mitogen-Activated Protein Kinase 10Multiple SclerosisAnimalsFemaleJNK Mitogen-Activated Protein KinasesMaleMicePatient AcuityPhosphorylationSex FactorsJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 10AstrocytesEAEJNK3MicrogliaMultiple sclerosisSpinal cord
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 Socratic graph.
Genetic deletion of c-Jun amino-terminal kinase 3 (JNK3) modestly increases disease severity in a mouse model of multiple sclerosis. · full record | Socratic