Ubiquitylation by Trim32 causes coupled loss of desmin, Z-bands, and thin filaments in muscle atrophy

During muscle atrophy induced by fasting, Trim32 promotes degradation of desmin cytoskeleton, which is linked to the loss of Z-bands and thin filaments.

[1]  A. Wilde,et al.  Desmin mutations as a cause of right ventricular heart failure affect the intercalated disks. , 2010, Heart rhythm.

[2]  Mi-Sung Kim,et al.  Myosin accumulation and striated muscle myopathy result from the loss of muscle RING finger 1 and 3. , 2007, The Journal of clinical investigation.

[3]  K. Weber,et al.  Intermediate filament forming ability of desmin derivatives lacking either the amino-terminal 67 or the carboxy-terminal 27 residues. , 1985, Journal of molecular biology.

[4]  C. Gregorio,et al.  A myopathy-linked desmin mutation perturbs striated muscle actin filament architecture. , 2008, Molecular biology of the cell.

[5]  F. Slack,et al.  A novel repeat domain that is often associated with RING finger and B-box motifs. , 1998, Trends in biochemical sciences.

[6]  A. Goldberg,et al.  Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[7]  C. Greenberg,et al.  Limb-girdle muscular dystrophy type 2H associated with mutation in TRIM32, a putative E3-ubiquitin-ligase gene. , 2002, American journal of human genetics.

[8]  W. Mitch,et al.  Activation of caspase-3 is an initial step triggering accelerated muscle proteolysis in catabolic conditions. , 2004, The Journal of clinical investigation.

[9]  M. Solomon,et al.  A Predictive Scale for Evaluating Cyclin-dependent Kinase Substrates , 1996, The Journal of Biological Chemistry.

[10]  Thomas L Casavant,et al.  Homozygosity mapping with SNP arrays identifies TRIM32, an E3 ubiquitin ligase, as a Bardet-Biedl syndrome gene (BBS11). , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[11]  Masahide Takahashi,et al.  Functional significance of the specific sites phosphorylated in desmin at cleavage furrow: Aurora-B may phosphorylate and regulate type III intermediate filaments during cytokinesis coordinatedly with Rho-kinase. , 2003, Molecular biology of the cell.

[12]  M. Inagaki,et al.  Site-specific phosphorylation induces disassembly of vimentin filaments in vitro , 1987, Nature.

[13]  Y. Capetanaki,et al.  Disruption of muscle architecture and myocardial degeneration in mice lacking desmin , 1996, The Journal of cell biology.

[14]  T. Hunter,et al.  The tyrosine kinase negative regulator c-Cbl as a RING-type, E2-dependent ubiquitin-protein ligase. , 1999, Science.

[15]  F. Chen,et al.  Caspase Proteolysis of Desmin Produces a Dominant-negative Inhibitor of Intermediate Filaments and Promotes Apoptosis* , 2003, The Journal of Biological Chemistry.

[16]  E. Kudryashova,et al.  Trim32 is a ubiquitin ligase mutated in limb girdle muscular dystrophy type 2H that binds to skeletal muscle myosin and ubiquitinates actin. , 2005, Journal of molecular biology.

[17]  K. Fröhlich,et al.  AAA-ATPase p97/Cdc48p, a Cytosolic Chaperone Required for Endoplasmic Reticulum-Associated Protein Degradation , 2002, Molecular and Cellular Biology.

[18]  A. Goldberg,et al.  FoxO3 coordinately activates protein degradation by the autophagic/lysosomal and proteasomal pathways in atrophying muscle cells. , 2007, Cell metabolism.

[19]  C. Côté,et al.  Remodeling of the cytoskeletal lattice in denervated skeletal muscle , 1996, Muscle & nerve.

[20]  E. Lazarides,et al.  Immunological characterization of the subunit of the 100 A filaments from muscle cells. , 1976, Proceedings of the National Academy of Sciences of the United States of America.

[21]  D J Glass,et al.  Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy , 2001, Science.

[22]  A. Goldberg,et al.  FoxO3 controls autophagy in skeletal muscle in vivo. , 2007, Cell metabolism.

[23]  J. Shay,et al.  The association of desmin with the developing myofibrils of cultured embryonic rat heart myocytes. , 1982, Developmental biology.

[24]  E. Lazarides.  The distribution of desmin (100 A) filaments in primary cultures of embryonic chick cardiac cells. , 1978, Experimental cell research.

[25]  S. Novak,et al.  Properties of easily releasable myofilaments: are they the first step in myofibrillar protein turnover? , 2009, American journal of physiology. Cell physiology.

[26]  Marco Sandri,et al.  Foxo Transcription Factors Induce the Atrophy-Related Ubiquitin Ligase Atrogin-1 and Cause Skeletal Muscle Atrophy , 2004, Cell.

[27]  E. Kudryashova,et al.  Deficiency of the E3 ubiquitin ligase TRIM32 in mice leads to a myopathy with a neurogenic component. , 2009, Human molecular genetics.

[28]  S. Fukuda,et al.  Tripartite motif protein 32 facilitates cell growth and migration via degradation of Abl-interactor 2. , 2008, Cancer research.

[29]  A. Goldberg,et al.  Coordinate activation of autophagy and the proteasome pathway by FoxO transcription factor , 2008, Autophagy.

[30]  A. Goldberg,et al.  Protein degradation by the ubiquitin-proteasome pathway in normal and disease states. , 2006, Journal of the American Society of Nephrology : JASN.

[31]  K Kosaka,et al.  Brain site‐specific gene expression analysis in Alzheimer's disease patients , 2006, European journal of clinical investigation.

[32]  G. Lozano,et al.  RING protein Trim32 associated with skin carcinogenesis has anti-apoptotic and E3-ubiquitin ligase properties. , 2003, Carcinogenesis.

[33]  A. Goldberg,et al.  Importance of the ATP-Ubiquitin-Proteasome Pathway in the Degradation of Soluble and Myofibrillar Proteins in Rabbit Muscle Extracts* , 1996, The Journal of Biological Chemistry.

[34]  S. Cannon,et al.  The common missense mutation D489N in TRIM32 causing limb girdle muscular dystrophy 2H leads to loss of the mutated protein in knock-in mice resulting in a Trim32-null phenotype. , 2011, Human molecular genetics.

[35]  A. Goldberg,et al.  Peroxisome Proliferator-activated Receptor γ Coactivator 1α or 1β Overexpression Inhibits Muscle Protein Degradation, Induction of Ubiquitin Ligases, and Disuse Atrophy* , 2010, The Journal of Biological Chemistry.

[36]  K. Weber,et al.  The amino acid sequence of chicken muscle desmin provides a common structural model for intermediate filament proteins. , 1982, The EMBO journal.

[37]  A. Goldberg,et al.  Rapid disuse and denervation atrophy involve transcriptional changes similar to those of muscle wasting during systemic diseases , 2007, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[38]  A. Goldberg,et al.  Multiple types of skeletal muscle atrophy involve a common program of changes in gene expression , 2004, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[39]  M. Inagaki,et al.  Visualization of protein kinase activities in single cells by antibodies against phosphorylated vimentin and GFAP , 1996, Neurochemical Research.

[40]  S. Kandarian,et al.  The molecular basis of skeletal muscle atrophy. , 2004, American journal of physiology. Cell physiology.

[41]  A. Goldberg,et al.  Effects of food deprivation on protein synthesis and degradation in rat skeletal muscles. , 1976, The American journal of physiology.

[42]  S. Rakhilin,et al.  The E3 Ligase MuRF1 degrades myosin heavy chain protein in dexamethasone-treated skeletal muscle. , 2007, Cell metabolism.

[43]  M. Tisdale,et al.  Induction of protein degradation in skeletal muscle by a phorbol ester involves upregulation of the ubiquitin-proteasome proteolytic pathway. , 2006, Life sciences.

[44]  K. Weber,et al.  Phosphorylation of desmin in vitro inhibits formation of intermediate filaments; identification of three kinase A sites in the aminoterminal head domain. , 1988, The EMBO journal.

[45]  M. Kulesz-Martin,et al.  Regulation of the psoriatic chemokine CCL20 by E3 ligases Trim32 and Piasy in keratinocytes. , 2010, The Journal of investigative dermatology.

[46]  S. Gygi,et al.  During muscle atrophy, thick, but not thin, filament components are degraded by MuRF1-dependent ubiquitylation , 2009, The Journal of cell biology.

[47]  T. Helliwell,et al.  Lectin binding and desmin expression during necrosis, regeneration, and neurogenic atrophy of human skeletal muscle , 1989, The Journal of pathology.

[48]  J. Tidball,et al.  Expression of a calpastatin transgene slows muscle wasting and obviates changes in myosin isoform expression during murine muscle disuse , 2002, The Journal of physiology.

[49]  M. Woo,et al.  Absence of caspase-3 protects against denervation-induced skeletal muscle atrophy. , 2009, Journal of applied physiology.

[50]  D. Blake,et al.  TRIM32 is an E3 ubiquitin ligase for dysbindin , 2009, Human molecular genetics.

[51]  S. Sze,et al.  Myostatin induces degradation of sarcomeric proteins through a Smad3 signaling mechanism during skeletal muscle wasting. , 2011, Molecular endocrinology.

[52]  G. Butler-Browne,et al.  Desmin Is Essential for the Tensile Strength and Integrity of Myofibrils but Not for Myogenic Commitment, Differentiation, and Fusion of Skeletal Muscle , 1997, The Journal of cell biology.