Evidence map›Paper›PMID 17322928›Full record

ReviewNature clinical practice. Nephrology2007

Mechanisms of disease: regulation of RANTES (CCL5) in renal disease.

Alan M Krensky, Yong-Tae Ahn

Open access · greenAbstract readReview
In one paragraph

Review in Nature clinical practice. Nephrology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

83 citing papers in PubMed, 141 citations in OpenAlex.

  1. Trial
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  5. CCL5 mRNA-enriched small extracellular vesicles from renal tubular epithelial cells enhance macrophage inflammatory responses in diabetic nephropathy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  6. Single-cell profiling reveals clonal CD8Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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23 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Alan M KrenskyDivision of Immunology and Transplantation Biology in the Department of Pediatrics at Stanford University School of Medicine, Stanford, CA, USA. krensky@stanford.edu
Yong-Tae Ahn
Stanford Medicine · USStanford University · US

Funding

ANTIGENS IN CTL MEDIATED TRANSPLANT REJECTIONR37DK035008 · NIDDK · STANFORD UNIVERSITY · PI KRENSKY, ALAN MICHAEL · 1997 to 2006
$2.8M
NIDDK NIH HHS R37 DK035008NIDDK NIH HHS R37 DK35008-23
6 · The paper itself

Abstract

Chemokines (chemoattractant cytokines) are fundamental regulators of immune cell movement from the bloodstream into tissues. Regulating expression of chemokines might, therefore, alleviate inflammation in autoimmune diseases and transplant rejection, or augment immune responses in cancer and immunodeficiency. RANTES (regulated upon activation, normal T cell expressed and secreted [also known as CCL5]) is a model chemokine of relevance to a myriad of diseases. Regulation of RANTES expression is complex. In fibroblasts and monocytes, rel proteins alone suffice to induce transcription of RANTES. By contrast, expression of RANTES in T lymphocytes 3-5 days after activation requires the development of a molecular complex (enhancesome) including KLF13 (Krueppel-like factor 13), rel proteins p50 and p65, and scaffolding proteins. This complex recruits enzymes involved in acetylation, methylation and phosphorylation of chromatin, and ultimately in the expression of RANTES. In addition, KLF13-the lynchpin for recruitment of this molecular complex-is itself translationally regulated. Such complex regulation of biological systems has major implications for the rational design of drugs aimed at increasing or decreasing inflammatory responses in patients.

Indexed as

Gene Expression RegulationCell Cycle ProteinsChemokine CCL5Chromatin Assembly and DisassemblyHumansKidney DiseasesKruppel-Like Transcription FactorsPromoter Regions, GeneticRepressor ProteinsT-LymphocytesTranscription, GeneticCell Cycle ProteinsChemokine CCL5KLF13 protein, humanKruppel-Like Transcription FactorsRepressor Proteins

Identifiers

PMID17322928
PMCPMC2702760
OpenAlexW2021165859

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.