Limb and Skin Abnormalities in Mice Lacking IKKα

Author:

Takeda Kiyoshi1,Takeuchi Osamu1,Tsujimura Tohru2,Itami Satoshi3,Adachi Osamu1,Kawai Taro1,Sanjo Hideki1,Yoshikawa Kunihiko3,Terada Nobuyuki2,Akira Shizuo1

Affiliation:

1. Department of Biochemistry and Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation,

2. Department of Pathology, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan.

3. Department of Dermatology, Osaka University Medical School, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan.

Abstract

The gene encoding inhibitor of kappa B (IκB) kinase α (IKKα; also called IKK1) was disrupted by gene targeting. IKKα-deficient mice died perinatally. In IKKα-deficient fetuses, limb outgrowth was severely impaired despite unaffected skeletal development. The epidermal cells in IKKα-deficient fetuses were highly proliferative with dysregulated epidermal differentiation. In the basal layer, degradation of IκB and nuclear localization of nuclear factor kappa B (NF-κB) were not observed. Thus, IKKα is essential for NF-κB activation in the limb and skin during embryogenesis. In contrast, there was no impairment of NF-κB activation induced by either interleukin-1 or tumor necrosis factor–α in IKKα-deficient embryonic fibroblasts and thymocytes, indicating that IKKα is not essential for cytokine-induced activation of NF-κB.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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