ArticleMolecular therapy : the journal of the American Society of Gene Therapy2004
The angiostatic activity of interferon-inducible protein-10/CXCL10 in human melanoma depends on binding to CXCR3 but not to glycosaminoglycan.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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.
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.
Who cites it
47 citing papers in PubMed, 116 citations in OpenAlex.
- Pharmacological stabilization of hypoxia-inducible factor 1-α dampens the interferon response and promotes glycolysis in Aicardi-Goutières syndrome.Nature communications · 2026Article
- Dual role of CXCL10 in cancer progression: implications for immunotherapy and targeted treatment.Cancer biology & therapy · 2025Review
- The role of CXC chemokines and receptors in breast cancer.Clinical and experimental medicine · 2025Review
- Novel Hemodynamic, Vascular Lesion, and Cytokine/Chemokine Differences Regarding Sex in a Pulmonary Arterial Hypertension Model.American journal of respiratory cell and molecular biology · 2024Article
- Concordant and Discordant Cerebrospinal Fluid and Plasma Cytokine and Chemokine Responses in Mild Cognitive Impairment and Early-Stage Alzheimer's Disease.Biomedicines · 2023Article
- A novel inflammatory response-related signature predicts the prognosis of cutaneous melanoma and the effect of antitumor drugs.World journal of surgical oncology · 2022Article
- Cytokine responses of immunosuppressed and immunocompetent patients with Neoehrlichia mikurensis infection.Medical microbiology and immunology · 2022Article
- Human innate lymphoid cell activation by adenoviruses is modified by host defense proteins and neutralizing antibodies.Frontiers in immunology · 2022Article
- Article
- Microfluidic model with air-walls reveals fibroblasts and keratinocytes modulate melanoma cell phenotype, migration, and metabolism.Lab on a chip · 2021Article
- The Effect of Hypoxia on the Expression of CXC Chemokines and CXC Chemokine Receptors-A Review of Literature.International journal of molecular sciences · 2021Review
- Targeting Chemokine-Glycosaminoglycan Interactions to Inhibit Inflammation.Frontiers in immunology · 2020Review
- The Role of Chemokines in the Pathogenesis of HTLV-1.Frontiers in microbiology · 2020Review
- Enhanced cytotoxic T lymphocytes recruitment targeting tumor vasculatures by endoglin aptamer and IP-10 plasmid presenting liposome-based nanocarriers.Theranostics · 2019Article
- Interferon-inducible CXC-chemokines are crucial immune modulators and survival predictors in colorectal cancer.Oncotarget · 2017Article
- Article
- Overview of the Mechanisms that May Contribute to the Non-Redundant Activities of Interferon-Inducible CXC Chemokine Receptor 3 Ligands.Frontiers in immunology · 2017Review
- TNF-α augments CXCR2 and CXCR3 to promote progression of renal cell carcinoma.Journal of cellular and molecular medicine · 2016Article
- Association between preeclampsia and the CXC chemokine family (Review).Experimental and therapeutic medicine · 2015Article
- Role of Chemokines in Non-Small Cell Lung Cancer: Angiogenesis and Inflammation.Journal of Cancer · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Human interferon-inducible protein 10 (IP-10; HGMW-approved gene symbol CXCL10) is an ELR(-) CXC chemokine that contains binding domains for both the chemokine receptor CXCR3 and glycosaminoglycans. IP-10 has been recently demonstrated to be a potent angiostatic protein in vivo. Whether IP-10 exerts its angiostatic function through binding to CXCR3, glycosaminoglycans, or both, is not clear. To clarify this issue, we created expression constructs for mutants of IP-10 that exhibit partial (IP-10C) or total (IP-10C22) loss of binding to CXCR3 or loss of binding to glycosaminoglycans (IP-10H and IP-10C22H). The A375 human melanoma cell line was transfected with these expression vectors, and stable clones were selected and inoculated subcutaneously into nude mice. As expected, tumor cells secreting wild-type IP-10 showed remarkable reduction in tumor growth compared to control vector-transfected tumor cells. Surprisingly, mutation of IP-10 resulting in partial loss of receptor binding (IP-10C), or loss of GAG binding (IP-10H), did not significantly alter the ability to inhibit tumor growth. This tumor growth inhibition was associated with a reduction in microvessel density, leading to the observed increase in both tumor cell apoptosis and necrosis. In contrast, expression of the IP-10C22 mutant failed to inhibit melanoma tumor growth. These data suggest that CXCR3 receptor binding, but not glycosaminoglycan binding, is essential for the tumor angiostatic activity of IP-10. We conclude that the arginine 22 amino acid residue of IP-10 is essential for both CXCR3 binding and angiostasis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.