Strain-specific complementation between NRIF1 and NRIF2, two zinc finger proteins sharing structural and biochemical properties

被引：19

作者：

Benzel, I ^{[1
]}

Barde, YA ^{[1
]}

Casademunt, E ^{[1
]}

机构：

[1] Max Planck Inst Neurobiol, Dept Neurobiochem, D-82152 Martinsried, Germany

来源：

GENE | 2001年 / 281卷 / 1-2期

关键词：

KRAB domain; SCAN domain; embryonic lethality; genetic background; cell cycle arrest;

D O I：

10.1016/S0378-1119(01)00730-2

中图分类号：

Q3 [遗传学];

学科分类号：

071007 ; 090102 ;

摘要：

The zinc finger protein NRIF (neurotrophin receptor interacting factor) was originally identified by virtue of its interaction with the neurotrophin receptor p75(NTR) and its participation in embryonic apoptosis. Targeted deletion of the nrif gene in mice is embryonically lethal in the C57BL6 genetic background, where it blocks cell cycle progression, but not in the Sv129 strain. We have now identified a second, highly homologous nrif gene, designated nrif2, encoding a protein with similar structural and biochemical properties as well as subcellular distribution as NRIF1, and whose over-expression in transfected fibroblasts also correlates with impaired BrdU incorporation. Unexpectedly, the nrij2 transcript becomes significantly upregulated in nrif1-/- mice only in Sv129, the genetic background where the mutants are viable, suggesting that the functional complementation of the two nrif genes may be strain-specific. (C) 2001 Elsevier Science B.V. All rights reserved.

引用

页码：19 / 30

页数：12

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