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MICALs in control of the cytoskeleton, exocytosis, and cell death

Journal

CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 68, Issue 24, Pages 4033-4044

Publisher

SPRINGER BASEL AG
DOI: 10.1007/s00018-011-0787-2

Keywords

Apoptosis; Axon guidance; Cytoskeleton; Exocytosis; NDR kinase; Plexin; Rab GTPase; Semaphorin

Funding

  1. Netherlands Organization for Health Research and Development (ZonMW-VIDI)
  2. Netherlands Organization for Health Research and Development (ZonMW-TOP)
  3. HFSP-CDA
  4. Genomics Center Utrecht

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MICALs form an evolutionary conserved family of multidomain signal transduction proteins characterized by a flavoprotein monooxygenase domain. MICALs are being implicated in the regulation of an increasing number of molecular and cellular processes including cytoskeletal dynamics and intracellular trafficking. Intriguingly, some of these effects are dependent on the MICAL monooxygenase enzyme and redox signaling, while other functions rely on other parts of the MICAL protein. Recent breakthroughs in our understanding of MICAL signaling identify the ability of MICALs to bind and directly modify the actin cytoskeleton, link MICALs to the docking and fusion of exocytotic vesicles, and uncover MICALs as anti-apoptotic proteins. These discoveries could lead to therapeutic advances in neural regeneration, cancer, and other diseases.

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