Evidence map›Paper›PMID 40672308›Full record

ArticlebioRxiv : the preprint server for biology2025

Total, not isoform-specific, Lyn expression by macrophages promotes TLR activation and restricts proliferation.

Anders J Lindstedt, Joseph T Greene, Tanya S Freedman

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Anders J LindstedtMedical Scientist Training Program, University of Minnesota, Minneapolis, MN 55455, United States.ORCID 0000-0003-1988-5163
Joseph T GreeneDepartment of Pharmacology, University of Minnesota, Minneapolis, MN 55455, United States.ORCID 0000-0003-3482-0958
Tanya S FreedmanDepartment of Pharmacology, University of Minnesota, Minneapolis, MN 55455, United States.ORCID 0000-0001-5168-5829

Funding

TRAINING-PULMONARY CELL &MOLECULAR BIOLOGY &PHYSIOLOGYT32HL007741 · NHLBI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI DUDLEY, R. ADAMS, INGBAR, DAVID H · 1994 to 2023
$13.9M
TRAINING GRANT IN MICROBIOLOGY/CANCER RESEARCHT32CA009138 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Scott M. Dehm · 1985 to 2026
$11.3M
Medical Scientist Training ProgramT32GM156735 · NIGMS · UNIVERSITY OF MINNESOTA · PI YOJI SHIMIZU · 2025 to 2026
$2.6M
Roles of the Src-Family Kinases LynA and LynB in Macrophage Inflammatory SignalingR01AR073966 · NIAMS · UNIVERSITY OF MINNESOTA · PI FREEDMAN, TANYA S. · 2018 to 2022
$2.2M
Functions of LynA and LynB kinases in dendritic-cell pro-inflammatory signaling and lupusR56AR084525 · NIAMS · UNIVERSITY OF MINNESOTA · PI FREEDMAN, TANYA S. · 2024 to 2024
$300k
Generating LynA-/- and LynB-/- mice by CRISPR/Cas9 genome editingR03AI130978 · NIAID · UNIVERSITY OF MINNESOTA · PI FREEDMAN, TANYA S. · 2017 to 2018
$153k
NCI NIH HHS T32 CA009138NHLBI NIH HHS T32 HL007741NIAID NIH HHS R03 AI130978NIAMS NIH HHS R01 AR073966NIAMS NIH HHS R56 AR084525NIGMS NIH HHS T32 GM156735
6 · The paper itself

Abstract

Toll-like receptor (TLR) signaling is vital to antimicrobial macrophage function, and its dysregulation is associated with many disease states, including lupus, multiple sclerosis, pulmonary fibrosis, and cancer. The Src-family kinase Lyn plays activating and inhibitory roles downstream of TLRs, yet distinct functions of the Lyn splice variants LynA and LynB in TLR signaling had not been investigated. We used isoform-specific Lyn knockout mice (LynA

Indexed as

extracellular-matrix remodelinginflammationmyeloid-cell signalingSrc-family kinasetranscriptomics

Identifiers

PMID40672308
PMCPMC12265556

What OpenQuestion holds

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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.