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Lanosterol elevates cytoprotective response through induced-proteasomal degradation of aberrant proteins.
Kinger, Sumit; Jagtap, Yuvraj Anandrao; Dubey, Ankur Rakesh; Kumar, Prashant; Choudhary, Akash; Dhiman, Rohan; Prajapati, Vijay Kumar; Chitkara, Deepak; Poluri, Krishna Mohan; Mishra, Amit.
Afiliación
  • Kinger S; Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan 342037, India.
  • Jagtap YA; Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan 342037, India.
  • Dubey AR; Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan 342037, India.
  • Kumar P; Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan 342037, India.
  • Choudhary A; Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan 342037, India.
  • Dhiman R; Laboratory of Mycobacterial Immunology, Department of Life Science, National Institute of Technology, Rourkela 769008, India.
  • Prajapati VK; Department of Biochemistry, University of Delhi South Campus, Benito Juarez Road, Dhaula Kuan, New Delhi 110021, India.
  • Chitkara D; Department of Pharmacy, Birla Institute of Technology and Science, Pilani (BITS-Pilani), Vidya Vihar Campus, Pilani 333031, India.
  • Poluri KM; Department of Biosciences and Bioengineering, Indian Institute of Technology Roorkee, Roorkee 247667, Uttarakhand, India.
  • Mishra A; Cellular and Molecular Neurobiology Unit, Indian Institute of Technology Jodhpur, Rajasthan 342037, India. Electronic address: amit@iitj.ac.in.
Biochim Biophys Acta Mol Cell Res ; 1871(2): 119631, 2024 02.
Article en En | MEDLINE | ID: mdl-37967794
Efficient protein synthesis is a basic requirement of our cells to replace the old or defective proteins from the intrinsic crowded biomolecular environment. The interconnection among synthesis, folding, and degradation of proteins represents central paradigm to proteostasis. Failure of protein quality control (PQC) mechanisms results in the disturbance and inadequate functions of proteome. The consequent misfolded protein accumulation can form the basis of neurodegeneration onset and largely represents imperfect aging. Understanding how cells improve the function of deregulated PQC mechanisms to establish and maintain proteostasis against the unwanted sequestration of normal proteins with misfolded proteinaceous inclusions is a major challenge. Here we show that treatment of Lanosterol, a cholesterol synthesis pathway intermediate, induces Proteasome proteolytic activities and, therefore, supports the PQC mechanism for the elimination of intracellular aberrant proteins. The exposure of Lanosterol not only promotes Proteasome catalytic functions but also elevates the removal of both bona fide and neurodegenerative diseases associated toxic proteins. Our current study suggests that increasing Proteasome functions with the help of small molecules such as Lanosterol could serve as a cytoprotective therapeutic approach against abnormal protein accumulation. Cumulatively, based on findings in this study, we can understand the critical importance of small molecules and their potential therapeutic influence in re-establishing disturbed proteostasis linked with neurodegeneration.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pliegue de Proteína / Complejo de la Endopetidasa Proteasomal Idioma: En Revista: Biochim Biophys Acta Mol Cell Res Año: 2024 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Pliegue de Proteína / Complejo de la Endopetidasa Proteasomal Idioma: En Revista: Biochim Biophys Acta Mol Cell Res Año: 2024 Tipo del documento: Article País de afiliación: India Pais de publicación: Países Bajos