Evidence map›Paper›PMID 26395334›Full record

ReviewHuman genomics2015

Eyeing the Cyr61/CTGF/NOV (CCN) group of genes in development and diseases: highlights of their structural likenesses and functional dissimilarities.

Izabela Krupska, Elspeth A Bruford, Brahim Chaqour

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Human genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.6field-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

39 citing papers in PubMed, 64 citations in OpenAlex.

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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

3 authors at 3 institutions in 2 countries.

Izabela KrupskaDepartment of Cell Biology, Downstate Medical Center, Brooklyn, NY, 11203, USA.
Elspeth A BrufordHUGO Gene Nomenclature Committee, European Molecular Biology Laboratory, European Bioinformatics Institute, Wellcome Genome Campus, Hinxton, Cambridge, CB10 1SD, UK.
Brahim ChaqourDepartment of Cell Biology, Downstate Medical Center, Brooklyn, NY, 11203, USA. bchaqour@downstate.edu.
European Bioinformatics Institute · GBState University of New York · USSUNY Downstate Health Sciences University · US

Funding

Nomenclature of Human and Vertebrate GenesU41HG003345 · NHGRI · EUROPEAN MOLECULAR BIOLOGY LABORATORY · PI BIRNEY, EWAN, BRUFORD, ELSPETH · 2013 to 2017
$2.4M
Regulation and Function of the Matricellular Protein CCN1 in Ischemic RetinopathyR01EY022091 · NEI · SUNY DOWNSTATE MEDICAL CENTER · PI CHAQOUR, BRAHIM · 2012 to 2017
$2.0M
NEI NIH HHS R01 EY022091NEI NIH HHS R01EY022091NHGRI NIH HHS U41 HG003345NHGRI NIH HHS U41HG003345Wellcome TrustWellcome Trust 099129/Z/12/Z
6 · The paper itself

Abstract

"CCN" is an acronym referring to the first letter of each of the first three members of this original group of mammalian functionally and phylogenetically distinct extracellular matrix (ECM) proteins [i.e., cysteine-rich 61 (CYR61), connective tissue growth factor (CTGF), and nephroblastoma-overexpressed (NOV)]. Although "CCN" genes are unlikely to have arisen from a common ancestral gene, their encoded proteins share multimodular structures in which most cysteine residues are strictly conserved in their positions within several structural motifs. The CCN genes can be subdivided into members developmentally indispensable for embryonic viability (e.g., CCN1, 2 and 5), each assuming unique tissue-specific functions, and members not essential for embryonic development (e.g., CCN3, 4 and 6), probably due to a balance of functional redundancy and specialization during evolution. The temporo-spatial regulation of the CCN genes and the structural information contained within the sequences of their encoded proteins reflect diversity in their context and tissue-specific functions. Genetic association studies and experimental anomalies, replicated in various animal models, have shown that altered CCN gene structure or expression is associated with "injury" stimuli--whether mechanical (e.g., trauma, shear stress) or chemical (e.g., ischemia, hyperglycemia, hyperlipidemia, inflammation). Consequently, increased organ-specific susceptibility to structural damages ensues. These data underscore the critical functions of CCN proteins in the dynamics of tissue repair and regeneration and in the compensatory responses preceding organ failure. A better understanding of the regulation and mode of action of each CCN member will be useful in developing specific gain- or loss-of-function strategies for therapeutic purposes.

Indexed as

Gene Expression Regulation, DevelopmentalGenetic Predisposition to DiseaseAmino Acid SequenceAnimalsCCN Intercellular Signaling ProteinsDiseaseExonsHumansIntronsMolecular Sequence DataCCN Intercellular Signaling Proteins

Identifiers

PMID26395334
PMCPMC4579636
OpenAlexW1910037588

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.