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Exploring Retrograde Trafficking: Mechanisms and Consequences in Cancer and Disease.
Bingham, Rachel; McCarthy, Helen; Buckley, Niamh.
Afiliação
  • Bingham R; School of Pharmacy, Queen's University Belfast, Belfast, UK.
  • McCarthy H; School of Pharmacy, Queen's University Belfast, Belfast, UK.
  • Buckley N; School of Pharmacy, Queen's University Belfast, Belfast, UK.
Traffic ; 25(2): e12931, 2024 Feb.
Article em En | MEDLINE | ID: mdl-38415291
ABSTRACT
Retrograde trafficking (RT) orchestrates the intracellular movement of cargo from the plasma membrane, endosomes, Golgi or endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC) in an inward/ER-directed manner. RT works as the opposing movement to anterograde trafficking (outward secretion), and the two work together to maintain cellular homeostasis. This is achieved through maintaining cell polarity, retrieving proteins responsible for anterograde trafficking and redirecting proteins that become mis-localised. However, aberrant RT can alter the correct location of key proteins, and thus inhibit or indeed change their canonical function, potentially causing disease. This review highlights the recent advances in the understanding of how upregulation, downregulation or hijacking of RT impacts the localisation of key proteins in cancer and disease to drive progression. Cargoes impacted by aberrant RT are varied amongst maladies including neurodegenerative diseases, autoimmune diseases, bacterial and viral infections (including SARS-CoV-2), and cancer. As we explore the intricacies of RT, it becomes increasingly apparent that it holds significant potential as a target for future therapies to offer more effective interventions in a wide range of pathological conditions.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Retículo Endoplasmático / Neoplasias Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Retículo Endoplasmático / Neoplasias Limite: Humans Idioma: En Ano de publicação: 2024 Tipo de documento: Article