TRIM16 controls turnover of protein aggregates by modulating NRF2, ubiquitin system, and autophagy: implication for tumorigenesis.

Jena, Kautilya Kumar; Kolapalli, Srinivasa Prasad; Mehto, Subhash; Chauhan, Swati; Chauhan, Santosh

Jena, Kautilya Kumar; Kolapalli, Srinivasa Prasad; Mehto, Subhash; Chauhan, Swati; Chauhan, Santosh.

Affiliation

Jena KK; Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Kolapalli SP; School of Biotechnology, KIIT University, Bhubaneswar, India.
Mehto S; Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Chauhan S; Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.
Chauhan S; Cell Biology and Infectious Diseases Unit, Institute of Life Sciences, Bhubaneswar, India.

Mol Cell Oncol ; 5(6): e1532251, 2018.

Article de En | MEDLINE | ID: mdl-30525100

Mots clés

NRF2/NFE2L2; TRIM16; aggrephagy; autophagy. Protein aggregates; cancer; oxidative stress; p62/SQSTM1; protein homeostasis; protein quality control; proteotoxic stress

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Texte intégral: 1 Collection: 01-internacional Base de données: MEDLINE Langue: En Journal: Mol Cell Oncol Année: 2018 Type de document: Article Pays d'affiliation: Inde Pays de publication: États-Unis d'Amérique

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