Evidence map›Paper›PMID 38326036›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2024

ICAM-1 Deletion Using CRISPR/Cas9 Protects the Brain from Traumatic Brain Injury-Induced Inflammatory Leukocyte Adhesion and Transmigration Cascades by Attenuating the Paxillin/FAK-Dependent Rho GTPase Pathway.

Bibhuti Ballav Saikia, Saurav Bhowmick, Anitha Malat, M R Preetha Rani, Almas Thaha, P M Abdul Muneer

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Post-Translational Modifications in Traumatic Brain Injury: Decoding the Proteomic Landscape and Molecular Mechanisms of Secondary Injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Article
  4. Article
  5. The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. 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

6 authors at 1 institution in 1 country.

Bibhuti Ballav SaikiaLaboratory of CNS injury and Molecular Therapy, JFK Neuroscience Institute, Hackensack Meridian Health JFK University Medical Center, Edison, New Jersey 08820.
Saurav BhowmickLaboratory of CNS injury and Molecular Therapy, JFK Neuroscience Institute, Hackensack Meridian Health JFK University Medical Center, Edison, New Jersey 08820.
Anitha MalatLaboratory of CNS injury and Molecular Therapy, JFK Neuroscience Institute, Hackensack Meridian Health JFK University Medical Center, Edison, New Jersey 08820.
M R Preetha RaniLaboratory of CNS injury and Molecular Therapy, JFK Neuroscience Institute, Hackensack Meridian Health JFK University Medical Center, Edison, New Jersey 08820.
Almas ThahaLaboratory of CNS injury and Molecular Therapy, JFK Neuroscience Institute, Hackensack Meridian Health JFK University Medical Center, Edison, New Jersey 08820.
P M Abdul MuneerLaboratory of CNS injury and Molecular Therapy, JFK Neuroscience Institute, Hackensack Meridian Health JFK University Medical Center, Edison, New Jersey 08820 Mohammed.Muneer@hmhn.org.ORCID 0000-0001-8231-4385
University Medical Center · US

Funding

Neutrophil extracellular traps and associated pathogenesis in TBI: a novel peptide therapeutic strategy.R01NS133233 · NINDS · HACKENSACK UNIVERSITY MEDICAL CENTER · PI Mohammed Abdul Muneer · 2024 to 2026
$1.3M
Peptide therapy for alcohol-induced CNS injuryR21AA030625 · NIAAA · HACKENSACK UNIVERSITY MEDICAL CENTER · PI MUNEER, MOHAMMED ABDUL · 2023 to 2024
$465k
NIAAA NIH HHS R21 AA030625NINDS NIH HHS R01 NS133233
6 · The paper itself

Abstract

Intercellular adhesion molecule-1 (ICAM-1) is identified as an initiator of neuroinflammatory responses that lead to neurodegeneration and cognitive and sensory-motor deficits in several pathophysiological conditions including traumatic brain injury (TBI). However, the underlying mechanisms of ICAM-1-mediated leukocyte adhesion and transmigration and its link with neuroinflammation and functional deficits following TBI remain elusive. Here, we hypothesize that blocking of ICAM-1 attenuates the transmigration of leukocytes to the brain and promotes functional recovery after TBI. The experimental TBI was induced in vivo by fluid percussion injury (25 psi) in male and female wild-type and

Indexed as

Brain Injuries, TraumaticIntercellular Adhesion Molecule-1AnimalsBrainCRISPR-Cas SystemsEndothelial CellsFemaleFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesHumansLeukocytesMaleMicePaxillinrho GTP-Binding ProteinsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesICAM1 protein, humanIcam1 protein, mouseIntercellular Adhesion Molecule-1PaxillinPTK2 protein, humanPtk2 protein, mousePXN protein, humanPxn protein, mouserho GTP-Binding ProteinsCRISPR/Cas9functional recoveryintercellular adhesion molecule-1leukocytespaxillin–FAKRho GTPasetransmigrationtraumatic brain injury

Identifiers

PMID38326036
PMCPMC10941244
OpenAlexW4391594102

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.