Evidence map›Paper›PMID 17671646›Full record

ArticleThe Journal of clinical investigation2007

When EGF is offside, magnesium is wasted.

Shmuel Muallem, Orson W Moe

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.8field-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

12 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Epidermal growth factor, from gene organization to bedside.Seminars in cell & developmental biology · 2014
    Review
  9. Drug-induced impairment of renal function.International journal of nephrology and renovascular disease · 2014
    Review
  10. Chemotherapy-associated renal dysfunction.Nature reviews. Nephrology · 2009
    Review
  11. Regulation of magnesium reabsorption in DCT.Pflugers Archiv : European journal of physiology · 2009
    Review
  12. Molecular determinants of magnesium homeostasis: insights from human disease.Journal of the American Society of Nephrology : JASN · 2008
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 2 countries.

Shmuel MuallemDepartment of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. shmuel.muallem@utsouthwestern.edu
Orson W Moe
Southwestern Medical Center · US

Funding

RENAL BASIS OF HYPOCITRATURIAP01DK020543 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MOE, ORSON W · 1986 to 2008
$12.7M
MOLECULAR MECHANISMS OF ION TRANSPORT BY THE SMGR01DE012309 · NIDCR · UT SOUTHWESTERN MEDICAL CENTER · PI THOMAS, PHILIP J · 1997 to 2011
$4.4M
HORMONE REGULATION OF CA++ I- IN PANCREATIC ACINAR CELLSR01DK038938 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI STULL, JAMES TRAVIS · 1987 to 2010
$3.7M
Acute Regulation of the Renal Na/H Exchanger NHE-3R01DK048482 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MOE, ORSON W · 2001 to 2005
$1.3M
REGULATION OF RENAL NA+/H+ EXCHANGER BY PROTEIN KINASE AR29DK048482 · NIDDK · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI MOE, ORSON W · 1995 to 1999
–
NIDCR NIH HHS DE12309NIDCR NIH HHS R01 DE012309NIDDK NIH HHS DK20543NIDDK NIH HHS DK38938NIDDK NIH HHS DK48482NIDDK NIH HHS P01 DK020543NIDDK NIH HHS R01 DK038938NIDDK NIH HHS R01 DK048482NIDDK NIH HHS R29 DK048482
6 · The paper itself

Abstract

Our understanding of magnesium (Mg(2+)) regulation has recently been catapulted forward by the discovery of several disease loci for monogenic disorders of Mg(2+) homeostasis. In this issue of the JCI, Groenestege et al. report that their study of a rare inherited Mg(2+) wasting disorder in consanguineous kindred shows that EGF acts as an autocrine/paracrine magnesiotropic hormone (see the related article beginning on page 2260). EGF stimulates Mg(2+) reabsorption in the renal distal convoluted tubule (DCT) via engagement of its receptor on the basolateral membrane of DCT cells and activation of the Mg(2+) channel TRPM6 (transient receptor potential cation channel, subfamily M, member 6) in the apical membrane. These authors show that a point mutation in pro-EGF retains EGF secretion to the apical but not the basolateral membrane, disrupting this cascade and causing renal Mg(2+) wasting. This work is another seminal example of the power of the study of monogenic disorders in the quest to understand human physiology.

Indexed as

MutationAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCetuximabColorectal NeoplasmsEpidermal Growth FactorErbB ReceptorsFemaleHumansKidneyMagnesiumMalePedigreeProtein PrecursorsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCetuximabEGFR protein, humanEpidermal Growth Factorepidermal growth factor precursorErbB ReceptorsMagnesiumProtein PrecursorsTRPM6 protein, humanTRPM Cation Channels

Identifiers

PMID17671646
PMCPMC1934592
OpenAlexW2164188937

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.