1. Academic Validation
  2. ZAKβ antagonizes and ameliorates the cardiac hypertrophic and apoptotic effects induced by ZAKα

ZAKβ antagonizes and ameliorates the cardiac hypertrophic and apoptotic effects induced by ZAKα

  • Cell Biochem Funct. 2016 Dec;34(8):606-612. doi: 10.1002/cbf.3234.
Chien-Yao Fu 1 2 3 Wei-Wen Kuo 4 Tsung-Jung Ho 5 6 Su-Ying Wen 7 8 Ling-Chun Lin 9 Yan-Shen Tseng 9 Hui-Chuan Hung 10 Vijaya Padma Viswanadha 11 Jaw-Ji Yang 12 Chih-Yang Huang 9 13 14
Affiliations

Affiliations

  • 1 Graduate Institute of Aging Medicine, China Medical University, Taichung, Taiwan.
  • 2 Orthopaedic Department, Armed Forces General Hospital, Taichung, Taiwan.
  • 3 Department of Emergency Medicine, China Medical University Hospital, Taichung, Taiwan.
  • 4 Department of Biological Science and Technology, China Medical University, Taichung, Taiwan.
  • 5 School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan.
  • 6 Chinese Medicine Department, China Medical University Beigang Hospital, Taiwan.
  • 7 Department of Dermatology, Taipei City Hospital, Renai Branch, Taipei, Taiwan.
  • 8 Center for General Education, Mackay Junior College of Medicine, Nursing, and Management, Taipei, Taiwan.
  • 9 Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
  • 10 Department of Nursing, National Taichung University of Science and Technology, Taichung, Taiwan.
  • 11 Department of Biotechnology, Bharathiar University, Coimbatore, India.
  • 12 School of Dentistry, Institute of Medicine, Chung Shan Medical University, Taichung, Taiwan.
  • 13 Graduate Institute of Chinese Medical Science, China Medical University, Taichung, Taiwan.
  • 14 Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan.
Abstract

ZAK (sterile alpha motif and leucine zipper containing kinase AZK), a serine/threonine kinase with multiple biochemical functions, has been associated with various cell processes, including cell proliferation, cell differentiation, and cardiac hypertrophy. In our previous reports, we found that the activation of ZAKα signaling was critical for cardiac hypertrophy. In this study, we show that the expression of ZAKα activated Apoptosis through both a FAS-dependent pathway and a mitochondria-dependent pathway by subsequently inducing Caspase-3. ZAKβ, an isoform of ZAKα, is dramatically expressed during cardiac hypertrophy and Apoptosis. The interaction between ZAKα and ZAKβ was demonstrated here using immunoprecipitation. The results show that ZAKβ has the ability to diminish the expression level of ZAKα. These findings reveal an inherent regulatory role of ZAKβ to antagonize ZAKα and to subsequently downregulate the cardiac hypertrophy and Apoptosis induced by ZAKα.

Keywords

ZAKα; ZAKβ; cardiac apoptosis; cardiac hypertrophy; sterile alpha motif and leucine zipper containing kinase.

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