Results 21 to 30 of about 10,678 (163)

Accumulation of Ubiquitin and Sequestosome-1 Implicate Protein Damage in Diacetyl-Induced Cytotoxicity [PDF]

The American Journal of Pathology, 2016
Inhaled diacetyl vapors are associated with flavorings-related lung disease, a potentially fatal airway disease. The reactive α-dicarbonyl group in diacetyl causes protein damage in vitro. Dicarbonyl/l-xylulose reductase (DCXR) metabolizes diacetyl into acetoin, which lacks this α-dicarbonyl group.
Ann F. Hubbs, Kara Fluharty, Rebekah J. Edwards, Jamie L. Barnabei, John T. Grantham, Scott M. Palmer, Francine L. Kelly, Linda M. Sargent, Steven H. Reynolds, Robert R. Mercer, Madhusudan P. Goravanahally, Michael L. Kashon, John Honaker, Mark C. Jackson, Amy Cumpston, William T. Goldsmith, Walter McKinney, Jeffrey S. Fedan, Lori Battelli, Tiffany Munro, Winnie Bucklew-Moyers, Kimberly McKinstry, Diane Schwegler‐Berry, Sherri Friend, Alycia K. Knepp, Samantha L. Smith, Krishnan Sriram   +26 more
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Essential Role of Sequestosome 1/p62 in Regulating Accumulation of Lys63-ubiquitinated Proteins [PDF]

Journal of Biological Chemistry, 2008
Sequestosome 1 (SQSTM1)/p62 is an interacting partner of the atypical protein kinase C zeta/iota and serves as a scaffold for cell signaling and ubiquitin binding, which is critical for several cell functions in vivo such as osteoclastogenesis, adipogenesis, and T cell activation.
Marie W. Wooten, Thangiah Geetha, Jeganathan Ramesh Babu, M. Lamar Seibenhener, Junmin Peng, Nancy R. Cox, María T. Díaz‐Meco, Jorge Moscat   +7 more
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Lipotoxicity induces hepatic protein inclusions through TANK binding kinase 1–mediated p62/sequestosome 1 phosphorylation [PDF]

Hepatology, 2017
Obesity commonly leads to hepatic steatosis, which often provokes lipotoxic injuries to hepatocytes that cause nonalcoholic steatohepatitis (NASH). NASH, in turn, is associated with the accumulation of insoluble protein aggregates that are composed of ubiquitinated proteins and ubiquitin adaptor p62/sequestosome 1 (SQSTM1).
Chun‐Seok Cho, Hwan‐Woo Park, Allison Ho, Ian Semple, Bo Young Kim, Insook Jang, Haeli Park, Shannon M. Reilly, Alan R. Saltiel, Jun Hee Lee   +9 more
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NIMA-related kinase 9–mediated phosphorylation of the microtubule-associated LC3B protein at Thr-50 suppresses selective autophagy of p62/sequestosome 1

Journal of Biological Chemistry, 2020
Human ATG8 family proteins (ATG8s) are active in all steps of the macroautophagy pathway, and their lipidation is essential for autophagosome formation. Lipidated ATG8s anchored to the outer surface of the phagophore serve as scaffolds for binding of other core autophagy proteins and various effector proteins involved in trafficking or fusion events ...
Birendra Kumar Shrestha, Mads Skytte Rasmussen, Yakubu Princely Abudu, Jack‐Ansgar Bruun, Kenneth Bowitz Larsen, Endalkachew A. Alemu, Eva Sjøttem, Trond Lamark, Terje Johansen   +8 more
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Sequestosome 1 (SQSTM1/p62) maintains protein folding capacity under endoplasmic reticulum stress in mouse hypothalamic organotypic culture [PDF]

Neuroscience Letters, 2017
Sequestosome 1 (SQSTM1) also known as ubiquitin-binding protein p62 (p62) is a cargo protein involved in the degradation of misfolded proteins via selective autophagy. Disruption of autophagy and resulting accumulation of misfolded proteins in the endoplasmic reticulum (ER) leads to ER stress.
隆史 富永, Takashi Tominaga
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The ICP0 Protein of Herpes Simplex Virus 1 (HSV-1) Downregulates Major Autophagy Adaptor Proteins Sequestosome 1 and Optineurin during the Early Stages of HSV-1 Infection [PDF]

Journal of Virology, 2019
Autophagy is a homeostatic mechanism of cells to recycle components, as well as a defense mechanism to get rid of pathogens. Strategies that HSV-1 has developed to counteract autophagy have been described and involve inhibition of autophagosome formation or indirect mechanisms.
Hope Waisner, Maria Kalamvoki
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Sequestering sequestosome 1 via S-acylation in autophagy, Huntington disease, and beyond [PDF]

Autophagy Reports
Protein mislocalization and aggregation are hallmark features in neurodegeneration. As proteins mislocalize, proteostasis deficiency and protein aggregation typically follow.
Y Alshehabi, F Abrar, D.D.O Martin
doaj   +2 more sources

Functional interaction between Sequestosome-1/p62 and Autophagy-Linked FYVE-containing protein WDFY3 in human osteoclasts [PDF]

Biochemical and Biophysical Research Communications, 2010
Paget's disease of bone (PDB) is a late-onset disorder characterised by focal areas of increased bone resorption, with osteoclasts that are increased in size, multinuclearity, number and activity. PDB-causing missense and nonsense variants in the gene encoding Sequestosome-1/p62 (SQSTM1) have been identified, all of which cluster in and around the ...
Lynne J. Hocking, David Mellis, Paul S. McCabe, Miep Helfrich, Michael J. Rogers   +4 more
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Paget's disease-causing mutations in sequestosome-1 affect autophagic protein degradation

Frontiers in Endocrinology, 2011
Hocking LJ
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Accumulation of autophagic adaptor protein, p62/sequestosome 1, in the brains of Alzheimer�s disease

Frontiers in Immunology, 2013
Kunikazu Tanji, Maruyama Atsushi, Saori Odagiri, Fumiaki Mori, Ken Itoh, Akiyoshi Kakita, Takahashi Hitoshi, Wakabayashi Koichi   +7 more
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