CSF2RB is the shared beta chain of the GM-CSF, IL-3 and IL-5 receptors. Its core role combines cooperative ligand/receptor assembly with recruitment of signaling machinery. The compact core records coreceptor activity and contribution to cytokine-receptor activity, the three ligand-specific pathways, and plasma-membrane location. This does not assign intrinsic kinase activity to the beta chain or make the private alpha chains dispensable. Original receptor reconstitution establishes PMID:1702217, and beta-chain mutagenesis supports PMID:7957082. Both originals were read in the bounded core consultation; the former directly measures binding, not downstream phosphorylation.
The 2024 structural and cellular study qualifies a universal requirement for a dodecamer. It reports signaling through paired private-alpha/beta intracellular domains, PMID:38614096. The actual assays use extracellular zipper/GFP constructs, tagged receptors in HeLa cells, JAK FERM–SH2 recruitment constructs and engineered HEK signaling chimeras. These do not establish one compulsory native stoichiometry in every cell, nor exclude minor higher-order populations or complexes elsewhere in the cell. The older 2008/2016 structures and mutagenesis remain positive evidence for cooperative receptor function. The 2008 supplement and selected 2016 original windows/supplement were read; access is not described as a complete read of both main papers.
The two official products reconstruct exactly as 897 and 903 amino acids. VSP_032798 replaces canonical Gly285 with GSAVLLR. This extracellular difference is recorded without claiming that the longer product has equivalent ligand affinity or signaling output, or mapping legacy constructs to a numbered product without sequence evidence. The existing annotation source objects retain their original product omissions and ordinary qualifiers.
Specific binding judgments preserve assay scope. JAK2 association is supported by independent receptor co-immunoprecipitation and newer recruitment experiments; the 2006 Figure 2D phosphorylated-JAK2 lysate panel is not itself a receptor–JAK2 pull-down. IL-5-receptor binding is a binding-class assertion, not an assertion that CSF2RB is an IL-5 agonist. The integrin source used human EPC co-immunoprecipitation and extracellular-domain Fc pull-down from lysates, not purified binary proteins. Blocking the interaction altered IL-3 responses PMID:20802515, so ordinary integrin binding is supported without assigning the more specific cell–matrix-adhesion binding class. The positive CBAP/TMEM102 interaction remains non-core generic binding where a defensible narrower molecular activity has not been established. This follows the standing campaign policy for supported generic binding.
The rat lipopolysaccharide response is retained as non-core at its actual expression-pattern scope. The available abstract reports PMID:7643220 in rat microglia/brain. It is explicitly truncated, and full Methods were not recovered. The response assertion does not require a demonstrated receptor-dependent protective mechanism; it also does not imply one. The 2021 IL-3/CXCL12 work measures plasmacytoid-dendritic-cell recruitment and inflammatory context, while independent receptor studies provide the proliferation evidence used for the existing broad proliferation assertion and its leukocyte refinement.
The immunoglobulin-production IBA is unresolved for CSF2RB. Its actual ancestral node lies on the human path and the mouse IL9R donor experiment is real: IL9R-deficient memory B cells show PMID:30082831. Those experiments concern IL9R-alpha/common-gamma signaling, including adoptive transfer and mixed chimeras. They support the donor claim but do not resolve whether CSF2RB performs a step in the broad annotated antibody process. Neither donor count, self-support, an off-path loss record nor general absence of immune function is used to reject it.
Pulmonary alveolar proteinosis evidence is retained as important receptor/macrophage physiology. The original clinical source reports PMID:9410898 and examines receptor expression and hematopoietic responses. It does not demonstrate that CSF2RB performs the diffusion/transport step of gas exchange, so that specific process assertion is marked over-annotated. This does not deny the clinical pulmonary phenotype or downstream effects on oxygenation.
The complete target phylogeny, exact MSA, eight on-path IBD joins and literal donor records are recorded in the source evidence index. Target experimental support legitimately appears among the PAINT descendant evidence. Current ARBA00028236 branches 0 and 50 match; ARBA00027801 has no matching current branch, although the plasma-membrane biology is independently supported. The current rule mismatch remains a provenance limitation rather than a biological negative. All 28 Reactome source rows have an explicit P32927-containing component path. Event titles do not transfer JAK, PI3K, GEF or phosphatase catalytic activity to CSF2RB. The mouse-JAK2/human-beta chimera is explicitly separated from wholly human events.
The current GO:0005895 label denotes the IL-5 receptor complex, but the first clause of its retrieved definition says IL-3. The source ID is preserved, and this internal ontology wording discrepancy is disclosed rather than silently repaired. The other specific binding terms were checked against their actual definitions and typed ancestry; plain cytokine ligand binding is not equated with binding to a GM-CSF complex.
Genuine fetch and parallel publication caching completed. The configured Falcon attempt timed out and the genuine perplexity-lite fallback failed with insufficient quota; no provider-authored report was fabricated. Primary evidence was subsequently assessed manually with explicit original/abstract/supplement limits. All 78 raw GOA records reconcile to 77 seeded source identities: two raw records differ in provenance metadata while yielding the same preserved plasma-membrane/NAS assertion. No new annotation is proposed. Existing main caches and the eight byte-identical sources also proposed by pending CSF2RA PR #4980 remain distinct preservation categories; pending additions are not represented as already present on main.
The public index is authored provenance, not independent biological evidence. It retains literal records, source locators, access limits, product reconstruction, current tree/rule/donor/interaction projections and GO-CAM roles. Quotes are intentionally short; the conservative aggregate includes repeated YAML and notes occurrences and remains at most 24 words per source.
The GM-CSF interaction retains its original PMID:18692472 and P04141 source identity. A proposed GM-CSF-binding term now records its ligand specificity. The previous cytokine-binding fallback was biologically valid; the request resolves missing precision rather than retracting the positive experiment. Current GO:0042021 explicitly names a GM-CSF complex, unlike the IL-3 and IL-5 ligand-binding terms. The proposed term and expert question ask whether that wording should be clarified or a distinct child is needed. No new biological annotation is created.
The two cytokine-receptor assertions remain accepted because beta performs ligand-contact and signaling work in an assembled receptor. Neither the receptor definition nor the biology requires a single autonomous chain. The signaling-receptor-to-coreceptor refinement describes the cooperative shared-beta role more precisely; it does not negate the compatible cytokine-receptor activity. The compact core continues to represent contribution to the assembled activity. Literal source relationships remain unchanged under the annotation-reviewer policy; this is not a qualifier-driven action change.
The IL-5 binding row now has a short exact target-contact anchor from the cached 2024 primary in addition to the original crosslinking experiment. The same primary's strongest JAK1 association is stated at its actual tagged HeLa receptor/JAK FERM–SH2 assay scope, with positive JAK2 and TYK2 association retained. The structure uses human ectodomains with zipper/GFP constructs, and its recruitment ranking does not establish a universal native receptor stoichiometry or kinase preference. See PMID:38614096(https://pmc.ncbi.nlm.nih.gov/articles/PMC11102305/), the IL-5 complex Results and Figure 1, JAK-association Results and Figure 4, and construct/micropatterning Methods.
Eleven rows now point directly to the portable source evidence, whose primary_access entries give the public original/supplement URLs, named assay or figure context, read limits and saved-source hashes. For PMID:9516124 the Figure 1A locator remains database/abstract provenance rather than a claim of full-paper access. No cached source is overwritten, and no authored sidecar prose is treated as primary evidence. The old journal is preserved in full; the finite index addition preserves all existing literal data. Quotes remain within the aggregate source budget, including the unchanged earlier notes.