CXCR3

Summary: negative regulation of endothelial cell proliferation: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Reason: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Summary: regulation of leukocyte migration: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: G protein-coupled receptor activity: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: chemokine receptor activity: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: chemokine receptor activity: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: protein binding: The PMID:23170857 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Reason: The PMID:23170857 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Summary: protein binding: The PMID:32296183 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Reason: The PMID:32296183 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Summary: protein binding: The PMID:32296183 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Reason: The PMID:32296183 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Summary: protein binding: The PMID:32296183 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Reason: The PMID:32296183 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Summary: protein binding: The PMID:39083597 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Reason: The PMID:39083597 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Summary: protein binding: The PMID:39083597 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Reason: The PMID:39083597 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Summary: protein binding: The PMID:39083597 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Reason: The PMID:39083597 interaction annotation does not by itself identify a molecular role for CXCR3. The relevant bait/prey or complex evidence must be examined before choosing a more informative binding/regulatory term; no wrong-gene inference is made from a high-throughput study title.

Summary: cytoplasm: The available evidence examined for CXCR3 does not resolve the exact claim of cytoplasm. The specific experiment or traced orthology/phylogenetic inference behind PMID:10903743 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Reason: The available evidence examined for CXCR3 does not resolve the exact claim of cytoplasm. The specific experiment or traced orthology/phylogenetic inference behind PMID:10903743 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: chemotaxis: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: chemotaxis: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: inflammatory response: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: immune response: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: cell adhesion: The available evidence examined for CXCR3 does not resolve the exact claim of cell adhesion. The specific experiment or traced orthology/phylogenetic inference behind PMID:10942362 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Reason: The available evidence examined for CXCR3 does not resolve the exact claim of cell adhesion. The specific experiment or traced orthology/phylogenetic inference behind PMID:10942362 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Summary: cell surface receptor signaling pathway: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: G protein-coupled receptor signaling pathway: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: adenylate cyclase-activating G protein-coupled receptor signaling pathway: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Reason: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Summary: positive regulation of cytosolic calcium ion concentration: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: positive regulation of cytosolic calcium ion concentration: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: positive regulation of cytosolic calcium ion concentration: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: external side of plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: external side of plasma membrane: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: cell surface: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: cell surface: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: T cell chemotaxis: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: membrane: A membrane location is correct but much less informative than plasma membrane for this seven-pass receptor.

Reason: A membrane location is correct but much less informative than plasma membrane for this seven-pass receptor.

Summary: C-C chemokine receptor activity: The inspected CXCR3-B paper supports CXC ligands and explicitly reports no competition from multiple CC chemokines. A broad C-C claim cannot be settled by receptor name or by this one ligand panel, and the PAINT ancestral assertion or exact supporting assay needs to be traced before generalizing or rejecting all C-C interactions.

Reason: The inspected CXCR3-B paper supports CXC ligands and explicitly reports no competition from multiple CC chemokines. A broad C-C claim cannot be settled by receptor name or by this one ligand panel, and the PAINT ancestral assertion or exact supporting assay needs to be traced before generalizing or rejecting all C-C interactions.

Summary: C-C chemokine receptor activity: The inspected CXCR3-B paper supports CXC ligands and explicitly reports no competition from multiple CC chemokines. A broad C-C claim cannot be settled by receptor name or by this one ligand panel, and the PAINT ancestral assertion or exact supporting assay needs to be traced before generalizing or rejecting all C-C interactions.

Reason: The inspected CXCR3-B paper supports CXC ligands and explicitly reports no competition from multiple CC chemokines. A broad C-C claim cannot be settled by receptor name or by this one ligand panel, and the PAINT ancestral assertion or exact supporting assay needs to be traced before generalizing or rejecting all C-C interactions.

Summary: C-X-C chemokine receptor activity: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: negative regulation of angiogenesis: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Reason: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Summary: calcium-mediated signaling: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: calcium-mediated signaling: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: chemokine binding: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: C-C chemokine binding: The inspected CXCR3-B paper supports CXC ligands and explicitly reports no competition from multiple CC chemokines. A broad C-C claim cannot be settled by receptor name or by this one ligand panel, and the PAINT ancestral assertion or exact supporting assay needs to be traced before generalizing or rejecting all C-C interactions.

Reason: The inspected CXCR3-B paper supports CXC ligands and explicitly reports no competition from multiple CC chemokines. A broad C-C claim cannot be settled by receptor name or by this one ligand panel, and the PAINT ancestral assertion or exact supporting assay needs to be traced before generalizing or rejecting all C-C interactions.

Summary: C-X-C chemokine binding: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: regulation of cell adhesion: The available evidence examined for CXCR3 does not resolve the exact claim of regulation of cell adhesion. The specific experiment or traced orthology/phylogenetic inference behind PMID:19703720 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Reason: The available evidence examined for CXCR3 does not resolve the exact claim of regulation of cell adhesion. The specific experiment or traced orthology/phylogenetic inference behind PMID:19703720 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Summary: signaling receptor activity: The available evidence examined for CXCR3 does not resolve the exact claim of signaling receptor activity. The specific experiment or traced orthology/phylogenetic inference behind PMID:12782716 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Reason: The available evidence examined for CXCR3 does not resolve the exact claim of signaling receptor activity. The specific experiment or traced orthology/phylogenetic inference behind PMID:12782716 is needed; the annotation is not rejected from absence in a summary or from a different main focus of the paper.

Summary: positive regulation of transcription by RNA polymerase II: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Reason: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Summary: cell chemotaxis: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: chemokine-mediated signaling pathway: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Reason: CXCR3 ligand binding and receptor signaling recruit immune cells. The human receptor/isoform experiments support this membrane chemokine-receptor function; calcium signaling and chemotaxis are mechanistic components rather than unrelated downstream associations.

Summary: positive regulation of execution phase of apoptosis: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.

Reason: The CXCR3-B isoform experiments support endothelial growth inhibition, cAMP-linked signaling and apoptosis. These are real isoform/context-dependent activities but do not describe the principal lymphocyte-trafficking function of CXCR3-A. The experimental isoform context should accompany interpretation.