Protein quality control machinery supports primary ciliogenesis by eliminating GDP-bound Rab8-family GTPases

Takahashi, Tetsuya; Shirai, Jun; Matsuda, Miyo; Nakanaga, Sae; Matsushita, Shin; Wakita, Kei; Hayashishita, Mizuki; Suzuki, Rigel; Noguchi, Aya; Yokota, Naoto; Kawahara, Hiroyuki

doi:10.1016/j.isci.2023.106652

Cited by 2 publications

(2 citation statements)

References 76 publications

(142 reference statements)

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“…In accordance with this notion, proper assembly of the SNARE family tail-anchored proteins into the organelle membranes was disturbed under depletion of TRC components [ 73–75 ]. BAG6 is also known as a regulator of membrane trafficking in mammalian cells [ 74 , 76 , 77 ]. Therefore, defective endosomal trafficking induced by long polyQ tract accumulations may be partly explained by defective BAG6–UBL4A complex formation.…”

Section: Discussionmentioning

confidence: 99%

Proteotoxic stresses stimulate dissociation of UBL4A from the tail-anchored protein recognition complex

Hagiwara,

Minami,

Ushio

et al. 2023

Biochemical Journal

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Inclusion body formation is associated with cytotoxicity in a number of neurodegenerative diseases. However, the molecular basis of the toxicity caused by the accumulation of aggregation-prone proteins remains controversial. In this study, we found that disease-associated inclusions induced by elongated polyglutamine chains disrupt the complex formation of BAG6 with UBL4A, a mammalian homologue of yeast Get5. UBL4A also dissociated from BAG6 in response to proteotoxic stresses such as proteasomal inhibition and mitochondrial depolarization. These findings imply that the cytotoxicity of pathological protein aggregates might be attributed in part to disruption of the BAG6-UBL4A complex that is required for the biogenesis of tail-anchored proteins.

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Section: Discussionmentioning

confidence: 99%

Proteotoxic stresses stimulate dissociation of UBL4A from the tail-anchored protein recognition complex

Hagiwara,

Minami,

Ushio

et al. 2023

Biochemical Journal

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“…Active in the presence of GTP and inactive in the presence of GDP, they are associated with practically all stages of vesicular transport, including the Golgi stages. Rab8 is involved in the anterograde direction for the delivery of newly synthetized ion channels ( 155 ). Rab4 and Rab5 are associated with vesicles following ion channel internalization ( 156 , 157 ).…”

Section: Ion Channel Traffickingmentioning

confidence: 99%

Ion channel trafficking implications in heart failure

Reisqs,

Qu,

Boutjdir

2024

Front. Cardiovasc. Med.

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Heart failure (HF) is recognized as an epidemic in the contemporary world, impacting around 1%–2% of the adult population and affecting around 6 million Americans. HF remains a major cause of mortality, morbidity, and poor quality of life. Several therapies are used to treat HF and improve the survival of patients; however, despite these substantial improvements in treating HF, the incidence of HF is increasing rapidly, posing a significant burden to human health. The total cost of care for HF is USD 69.8 billion in 2023, warranting a better understanding of the mechanisms involved in HF. Among the most serious manifestations associated with HF is arrhythmia due to the electrophysiological changes within the cardiomyocyte. Among these electrophysiological changes, disruptions in sodium and potassium currents’ function and trafficking, as well as calcium handling, all of which impact arrhythmia in HF. The mechanisms responsible for the trafficking, anchoring, organization, and recycling of ion channels at the plasma membrane seem to be significant contributors to ion channels dysfunction in HF. Variants, microtubule alterations, or disturbances of anchoring proteins lead to ion channel trafficking defects and the alteration of the cardiomyocyte's electrophysiology. Understanding the mechanisms of ion channels trafficking could provide new therapeutic approaches for the treatment of HF. This review provides an overview of the recent advances in ion channel trafficking in HF.

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Protein quality control machinery supports primary ciliogenesis by eliminating GDP-bound Rab8-family GTPases

Cited by 2 publications

References 76 publications

Proteotoxic stresses stimulate dissociation of UBL4A from the tail-anchored protein recognition complex

Proteotoxic stresses stimulate dissociation of UBL4A from the tail-anchored protein recognition complex

Ion channel trafficking implications in heart failure

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