Ablation of the Kell/Xk complex alters erythrocyte divalent cation homeostasis.
Ablation of the Kell/Xk complex alters erythrocyte divalent cation homeostasis.
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DOI：
10.1016/j.bcmd.2012.10.002
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发表时间：
2013-02
影响因子：
2.3
通讯作者：
Lee, Soohee
中科院分区：
文献类型：
--
作者：
Rivera, Alicia;Kam, Siok Yuen;Ho, Mengfatt;Romero, Jose R.;Lee, Soohee
XK is a putative transporter of unknown function that is ubiquitously expressed and linked through disulfide bonds to Kell protein, an endothelin-3 (ET-3)-converting enzyme. We generated three knockout (KO) mice that lacked either Xk, Kell or both proteins and characterized erythrocyte cation levels, transport and hematological parameters. Absence of Xk or Kell was accompanied by changes in erythrocyte K+, Mg2+, Na+ and Ca2+ transport that were associated with changes in mean cellular volume and corpuscular hemoglobin concentration mean. Baseline Ca2+-ATPase activity was undetected in erythrocytes from all three mouse types but was restored upon pre-incubation with ET-3. Consistent with these alterations in Ca2+ handling, we observed increased Gardos channel activity in Kel and Xk KO mice. In addition Kel deletion was associated with increased Mg2+ permeability while Xk deletion blocked Na/Mg exchanger activity. Our results provide evidence that cellular divalent cation regulation is functionally coupled to the Kell/XK system in erythrocytes and loss of this complex may contribute to acanthocytosis formation in McLeod syndrome.
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影响因子：
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通讯作者：
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