Concept
Cell signalling
7 studies1 discovery
Cell signalling is how cells detect cues and transmit information through receptors and intracellular pathways to change behaviour.
Signalling pathways explain how cells decide; students meet them in every physiology and development course.
Studies
7
Findings
5
7 supporting · 0 challenging · 0 qualifying citations
Open tensions
1
Currently
What we know
- Multiple empirical papers in this library examine cell signalling with mechanistic biological findings.
- A 34-residue-pair pathway across layers; comparisons used 142 inactive and 27 active structures (p<0.001).
- USP8 prevents Smo ubiquitination and enhances signaling; Hh promotes Smo–USP8 interaction; USP8 is required for Hh-induced surface accumulation and keeps Smo out of Rab5 early endosomes.
- LOX1 is guard-cell expressed; lox1 mutants show >10-fold more Pst growth and impaired flg22/Pst-induced stomatal closure.
- 103 genes on 32 genomes (87 functional, 16 pseudogenes); vertebrates have the largest counts; Archaea nearly lack HSP90.
Largest unresolved question
Systems and scales differ across cell signalling studies (species, tissues, methods), so mechanisms should not be over-generalised.
Common misconceptions
Cell signalling findings from one model organism always transfer to humans.
Model systems teach mechanism; transfer to other species is a separate empirical claim.
Related
Claim ledger
What the evidence shows
Drawn from 7 studies in this library. Mix labels say which citation roles are present; they are not a strength score. Supports means evidence for a finding; Challenges means evidence against a stated position; Qualifies marks scope.
Multiple empirical papers in this library examine cell signalling with mechanistic biological findings.
- Shared class A GPCR activation path
- How does USP8 turn on Smoothened?
- LOX1 oxylipins close stomata in defense
Study Role Design N Population Outcome Shared class A GPCR activation path Supports Computational / modellingResidue–residue contact score comparison across inactive and active Class A GPCR structures N=169 · 142 inactive and 27 active structures compared Class A GPCR crystal/cryo-EM structures Conserved 34-residue-pair activation contact pathway How does USP8 turn on Smoothened? Supports Animal / in-vitroRNAi screen of Drosophila DUBs in wings and S2 cells focused on USP8–Smo regulation Drosophila genetics and S2 cell assays — no single sample N Drosophila tissues and S2 cells USP8 prevention of Smoothened ubiquitination promoting Hedgehog signaling LOX1 oxylipins close stomata in defense Supports Animal / in-vitroArabidopsis LOX1 mutants tested for stomatal immunity and Pst colonization Plant mutant phenotyping; no single primary analytic N in stored text Arabidopsis thaliana (lox1 mutants vs wild type/complemented lines) Stomatal closure and Pst leaf colonization controlled by LOX1/oxylipins A 34-residue-pair pathway across layers; comparisons used 142 inactive and 27 active structures (p<0.001).
USP8 prevents Smo ubiquitination and enhances signaling; Hh promotes Smo–USP8 interaction; USP8 is required for Hh-induced surface accumulation and keeps Smo out of Rab5 early endosomes.
LOX1 is guard-cell expressed; lox1 mutants show >10-fold more Pst growth and impaired flg22/Pst-induced stomatal closure.
103 genes on 32 genomes (87 functional, 16 pseudogenes); vertebrates have the largest counts; Archaea nearly lack HSP90.
Debates
Tensions and limits
Some items are genuine disagreements on the same question. Others mark different assays, populations, or outcomes.
Systems and scales differ across cell signalling studies (species, tissues, methods), so mechanisms should not be over-generalised.
Systems and scales differ across cell signalling studies (species, tissues, methods), so mechanisms should not be over-generalised.
- Shared class A GPCR activation path
- How does USP8 turn on Smoothened?
- LOX1 oxylipins close stomata in defense
Study Role Design N Population Outcome Shared class A GPCR activation path Supports Computational / modellingResidue–residue contact score comparison across inactive and active Class A GPCR structures N=169 · 142 inactive and 27 active structures compared Class A GPCR crystal/cryo-EM structures Conserved 34-residue-pair activation contact pathway How does USP8 turn on Smoothened? Supports Animal / in-vitroRNAi screen of Drosophila DUBs in wings and S2 cells focused on USP8–Smo regulation Drosophila genetics and S2 cell assays — no single sample N Drosophila tissues and S2 cells USP8 prevention of Smoothened ubiquitination promoting Hedgehog signaling LOX1 oxylipins close stomata in defense Supports Animal / in-vitroArabidopsis LOX1 mutants tested for stomatal immunity and Pst colonization Plant mutant phenotyping; no single primary analytic N in stored text Arabidopsis thaliana (lox1 mutants vs wild type/complemented lines) Stomatal closure and Pst leaf colonization controlled by LOX1/oxylipins
PaperFren reads this as a limit on how far one study travels — different assays, populations, or outcomes — not a forced fight between papers.
Timeline
How understanding moved
Study years are when the paper was published. Evidence edits are dated changes to this page's claims. Explanations are when PaperFren added a Discovery — not a claim that the science happened that day.
2026
Concept page published
Cell signalling
- The same Wnt protein switches β-catenin signaling on or off, depending on the receptor
Change log
What changed
Dated edits to this page's evidence: studies added or removed from a claim, claims added or withdrawn, and new explanations tagged here. Coverage edits are distinct from reviewed research changes and corrections. Dates record PaperFren updates; study publication dates appear in the timeline.
- The same Wnt protein switches β-catenin signaling on or off, depending on the receptorEvidence: Strengthening
- Coverage updated · Concept page published
Papers
7 studies in this library bear on Cell signalling, ordered by citations.
- When does Wnt5a turn β-catenin signaling on or off?
Purified Wnt5a can activate or inhibit β-catenin–TCF signaling depending on which Frizzled/receptor context is present.
- Shared class A GPCR activation path
Class A GPCRs share a conserved residue-contact rearrangement pathway from ligand pocket to G-protein site.
- CPK3/6 mediate ABA guard-cell signaling
Calcium-dependent kinases CPK3 and CPK6 act in ABA control of guard-cell anion/Ca²⁺ channels and stomatal closure.
- How specific are bacterial two-component pathways?
Caulobacter histidine kinases prefer their cognate response regulators in vitro; phosphotransfer profiling reveals conserved pathways controlling growth.
- HSP90 family across kingdoms
Comparative genomics maps 103 HSP90-family genes across 32 genomes and deep phylogenetic diversity.
- LOX1 oxylipins close stomata in defense
Guard-cell LOX1 drives ABA-independent stomatal closure that limits Pseudomonas colonization.
- How does USP8 turn on Smoothened?
USP8 deubiquitinates Smoothened, promoting Hh-dependent cell-surface accumulation and signaling while limiting early-endosome localization.
Compare studies
Select 2–10 studies. Design and N are labels, not a ranking.
Nothing selected yet.
Questions
What is still open
Systems and scales differ across cell signalling studies (species, tissues, methods), so mechanisms should not be over-generalised.
Ask PaperFren about Cell signalling
Study this conceptflashcards and short-answer questions
What is Cell signalling?
Cell signalling is how cells detect cues and transmit information through receptors and intracellular pathways to change behaviour.
Why does Cell signalling matter for biology undergraduates?
Signalling pathways explain how cells decide; students meet them in every physiology and development course.