Evidence map›Paper›PMID 15688008›Full record

ArticleOncogene2005

KSHV-GPCR and CXCR2 transforming capacity and angiogenic responses are mediated through a JAK2-STAT3-dependent pathway.

Meike Burger, Tanja Hartmann, Jan A Burger, Ingrid Schraufstatter

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.2field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 102 citations in OpenAlex.

  1. Lnk Governs chemokine-directed trafficking of CD8Molecular therapy. Oncology · 2026
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  19. A C-X-C Chemokine Receptor Type 2-Dominated Cross-talk between Tumor Cells and Macrophages Drives Gastric Cancer Metastasis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2019
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Meike BurgerDepartment of Internal Medicine, Freiburg University Hospital, Freiburg, Germany. burgerm@mm11.uk1.uni-freiburg.de
Tanja Hartmann
Jan A Burger
Ingrid Schraufstatter
University Medical Center Freiburg · DEInstitute for Molecular Medicine · USUniversity of Freiburg · DE

Funding

Role of IL-8 in Cell Migration and ProliferationR01HL055657 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI SCHRAUFSTATTER, INGRID U · 1996 to 2004
$1.5M
NHLBI NIH HHS HL55657
6 · The paper itself

Abstract

The Kaposi's sarcoma herpesvirus encodes a G-protein-coupled chemokine receptor termed KSHV-GPCR. Expression of this constitutively active GPCR leads to cell transformation and vascular overgrowth characteristic of Kaposi's sarcoma. Previously, we have shown that CXCR2, the closest human homolog, is similarly able to transform cells if continuously stimulated or constitutively activated by amino-acid exchange D138V of the DRY sequence. Here, we demonstrate that STAT3 activation is a prerequisite for transformation in KSHV-GPCR and CXCR2 transfected NIH 3T3 cells. In KSHV-GPCR and D138V transfected cells, STAT-3 is constitutively phosphorylated on Tyr705. In CXCR2 transfected NIH 3T3 cells and human microvascular endothelial cells (HMEC), which express the CXCR2 constitutively, STAT3 is phosphorylated upon stimulation with IL-8 (CXCL8). Focus formation in NIH 3T3 cells transfected with the KSHV-GPCR, CXCR2, or the D138V mutant, was blocked by the specific JAK2 inhibitor AG490. Typical functions of the CXCR2 including actin stress fiber formation, haptotaxis, and the angiogenic response in HMEC shown by tube formation in Matrigel were blocked by AG490. These data suggest that the transforming capacity and migratory responses that are involved in tumor development, metastasis, and angiogenesis in KSHV or CXCR2-expressing cells is at least partially mediated through a JAK2-STAT3 dependent pathway.

Indexed as

3T3 CellsActinsAnimalsCell Transformation, NeoplasticDNA-Binding ProteinsHerpesvirus 8, HumanHumansJanus Kinase 2MiceNeovascularization, PathologicPhosphorylationProtein-Tyrosine KinasesProto-Oncogene ProteinsReceptors, ChemokineReceptors, Interleukin-8BRecombinant ProteinsActinsDNA-Binding ProteinsG protein-coupled receptor, Human herpesvirus 8JAK2 protein, humanJak2 protein, mouseJanus Kinase 2Protein-Tyrosine KinasesProto-Oncogene ProteinsReceptors, ChemokineReceptors, Interleukin-8BRecombinant ProteinsSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription FactorTrans-ActivatorsViral Proteins

Identifiers

PMID15688008
OpenAlexW2039000698

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.