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2007 ; 117
(8
): 2086-9
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When EGF is offside, magnesium is wasted
#MMPMID17671646
Muallem S
; Moe OW
J Clin Invest
2007[Aug]; 117
(8
): 2086-9
PMID17671646
show ga
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.
|*Mutation
[MESH]
|Animals
[MESH]
|Antibodies, Monoclonal, Humanized
[MESH]
|Antibodies, Monoclonal/adverse effects/therapeutic use
[MESH]
|Antineoplastic Agents/adverse effects/therapeutic use
[MESH]
free
free
free
