CD19

Summary: CD19 costimulation supports antigen-dependent B-cell proliferation.

Reason: The cited coligation study supports a proliferative output of receptor sensitization; proliferation is downstream of the core adaptor function.

Summary: Family mapping captures a downstream proliferative response.

Reason: The CD19-family mapping is consistent with B-cell activation evidence. It does not make the protein part of the cell-cycle machinery.

Summary: Human CD19 deficiency impairs antigen-driven responses.

Reason: Patient B-cell responses support this immune phenotype, which is downstream of receptor signaling.

Summary: The plasma membrane is the principal site of CD19 signaling.

Reason: The coligation experiment depends on cell-surface CD19.

Summary: The plasma membrane is the principal site of CD19 signaling.

Reason: Human cell-surface patching and receptor-complex coprecipitation support this localization.

Summary: The plasma membrane is the principal site of CD19 signaling.

Reason: Raji and recombinant K562 receptor-complex experiments support a membrane location.

Summary: The plasma membrane is the principal site of CD19 signaling.

Reason: The study explicitly describes CD19 on human B-lineage cells.

Summary: The plasma membrane is the principal site of CD19 signaling.

Reason: The transgenic-mouse study supports membrane targeting of the CD19 extracellular/transmembrane construct. Human surface localization is also established independently; the original EXP row is preserved.

Summary: The plasma membrane is the principal site of CD19 signaling.

Reason: Human CD19 constructs were expressed on mouse plasmacytoma cells; this is a membrane-localization experiment, not a primary-human-cell assay.

Summary: The inherited plasma-membrane assignment matches direct CD19 biology.

Reason: Retain the PAINT curator's ancestral inference. Human CD19 appearing among its own experimental descendants is expected, not circular. The IBD placement and alignment were not independently inspected.

Summary: The plasma membrane is the principal site of CD19 signaling.

Reason: Patient/control flow cytometry establishes the cell-surface context of CD19 expression.

Summary: The UniProt localization mapping captures the cell-surface protein.

Reason: The mapped plasma-membrane term agrees with the single-pass topology and direct surface-localization evidence.

Summary: The Reactome assembly places CD19 at the plasma membrane.

Reason: The reaction places the CD19-containing complex at the plasma membrane; C3d recognition is assigned to CR2/CD21.

Summary: The Reactome assembly places CD19 at the plasma membrane.

Reason: The CD19 signalosome is membrane-associated. PI3K performs the lipid phosphorylation; this row asserts location only.

Summary: The Reactome assembly places CD19 at the plasma membrane.

Reason: The PI3K reaction supplies membrane context for the CD19-containing assembly, not CD19 catalytic activity.

Summary: The Reactome assembly places CD19 at the plasma membrane.

Reason: The inhibitor reaction retains a membrane-associated assembly; it does not establish that CD19 is an enzyme or direct inhibitor target.

Summary: The Reactome assembly places CD19 at the plasma membrane.

Reason: The curated CR2-complement/CD19-CD81 assembly supports the cell-surface location.

Summary: The Reactome assembly places CD19 at the plasma membrane.

Reason: Recruitment of PI3K and GRB2 to the phosphorylated CD19-VAV assembly occurs at the membrane.

Summary: The extracellular domain of CD19 is exposed on the B-cell surface.

Reason: The original IDA is retained with curator deference and independent human surface evidence. The FcRL6-focused cached abstract does not expose the CD19-specific assay, and its title is not evidence of misattribution.

Summary: Cell-surface exposure is consistent with CD19 topology and antibody detection.

Reason: Retain the experimental localization using independent surface evidence. The selected microRNA-study cache is abstract-only; its CD19 target assay was not inspected and is not inferred from its title.

Summary: The cited CD19 association experiment supports recruitment of an intracellular signaling adaptor rather than the complete messenger-binding coreceptor activity.

Reason: In human DG75 B cells, GRB2-SH2 affinity purification with WT, R86L and GST controls detects CD19 by immunoblot after BCR stimulation. This demonstrates a signaling-complex association; it does not assay CD19 combining with a messenger and cooperating with another receptor to initiate signaling, as GO:0015026 requires. The source-specific molecular-function attribution is therefore broader than the demonstrated CD19 activity. Signaling receptor complex adaptor activity is independently supported and already retained. This assessment is limited to the inspected target experiment and does not claim that CD19 lacks every possible physiological ligand.

Summary: CD19 supports effective antibody-mediated immunity.

Reason: The human deficiency phenotype supports the immune response term as an organism-level consequence of impaired B-cell signaling.

Summary: CD19 supplies a noncatalytic platform for receptor signaling.

Reason: The patient study supports the signaling role. Complex-association and recruitment experiments supply complementary mechanistic evidence for the adaptor function.

Summary: The inherited receptor-complex adaptor assignment captures the core function.

Reason: Retain the PAINT judgment, consistent with direct CD19 complex and recruitment evidence. The target's own experimental evidence in WITH/FROM is legitimate descendant support. No new claim about an independently inspected IBD or ancestral gain is made.

Summary: CD19 participates in a signaling protein complex.

Reason: The richer authenticated extraction describes stimulated CD19-IKAROS-SYK association in human FL112 pro-B cells. The broad complex term is supported but does not identify a constitutive core complex or prove direct binary binding. The cited supplementary figure was not inspected.

Summary: The orthology-based proliferation assignment describes a downstream response.

Reason: Mouse evidence and human CD19-deficiency data agree on a role in B-cell activation. Proliferation is a physiological output, not the protein's immediate molecular function.

Summary: Membrane-raft association is a conditional membrane context.

Reason: Retain the conservative UniProt mapping without making raft residence obligatory or treating detergent-resistant fractions as a separate molecular function.

Summary: The mouse-derived raft localization is compatible with CD19 organization.

Reason: Retain the orthology-based localization with its original source, without asserting that human raft localization was directly tested by this ISS row.

Summary: The experimentally described pathway is B-cell receptor signaling.

Reason: The original study concerns CD19 costimulation of B lymphocytes; the B-cell-specific child term preserves that supported scope.

Proposed replacements: B cell receptor signaling pathway

Summary: CD19 participates in B-cell receptor signaling.

Reason: The inherited process assignment agrees with its signal-organizing role and experimental activation studies. The PAINT node placement has not been independently re-audited.

Summary: Conserved CD19 function supports participation in B-cell receptor signaling.

Reason: Retain the mouse-to-human transfer, corroborated by human patient and complex-assembly evidence; it remains ISS rather than a relabeled human experiment.

Summary: CD19 modulates antigen-receptor signaling.

Reason: WT/mutant comparisons support signaling regulation in a mouse-cell host expressing human CD19.

Summary: CD19 controls the threshold for B-cell activation.

Reason: Receptor coligation lowers the activation threshold, consistent with the core signaling-modulator role.

Summary: The CD19-family mapping captures regulation of B-cell activation.

Reason: The family-level transfer agrees with direct CD19 signaling evidence; it adds no claim that every family member was individually assayed.

Summary: CD19 signaling supports intracellular calcium mobilization.

Reason: Retain the curated human-study calcium assignment with supporting signaling evidence. Calcium release is an output of adaptor-mediated signaling, not channel activity by CD19.

Summary: CD19-dependent signaling promotes calcium release.

Reason: IP3 and calcium assays support this downstream output; CD19 is not the calcium-release channel.

Summary: CD19 promotes the PI3K arm of receptor signaling.

Reason: Human WT and Y484F/Y515F CD19 constructs in mouse J558L cells connect CD19 to antigen-stimulated PI3K activity and calcium responses. PI3K recruitment is a proximal mechanism of the receptor-complex adaptor core. This broader PI3K/protein-kinase-B pathway annotation is retained as a signaling arm rather than a separately defining core process. AKT was discussed rather than assayed; that access limit does not negate the measured PI3K contribution.

Summary: Exosomal detection is a secondary localization context.

Reason: Retain the curated high-throughput detection without promoting exosome biogenesis to a CD19 function. The cached abstract describes B-cell exosome proteomics; its CD19 target table was not independently inspected.