Myosin 1c: A novel regulator of glucose uptake in brown adipocytes

Åslund, Alice; Bokhari, Muhammad Hamza; Wetterdal, Erika; Martin, René; Knölker, Hans‐Joachim; Bengtsson, Tore

doi:10.1016/j.molmet.2021.101247

Cited by 3 publications

(2 citation statements)

References 66 publications

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“…Finally, MYO1C (OMIM*606538), which is downregulated in male and female cohorts with MDS, is a myosin involved in cytoskeletal organisation and vesicle trafficking and when depleted, induces fragmentation of the Golgi complex, the loss of cellular F‐actin and a delay in transport (Capmany et al, 2019). MYO1C is also involved in the recycling of glucose transporters in response to insulin (Åslund et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Multi‐omics in MECP2 duplication syndrome patients and carriers

Pascual‐Alonso,

Xiol,

Smirnov

et al. 2024

Eur J of Neuroscience

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MECP2 duplication syndrome (MDS) is an X‐linked neurodevelopmental disorder caused by the gain of dose of at least the genes MECP2 and IRAK1 and is characterised by intellectual disability (ID), developmental delay, hypotonia, epilepsy and recurrent infections. It mainly affects males, and females can be affected or asymptomatic carriers. Rett syndrome (RTT) is mainly triggered by loss of function mutations in MECP2 and is a well described syndrome that presents ID, epilepsy, lack of purposeful hand use and impaired speech, among others. As a result of implementing omics technology, altered biological pathways in human RTT samples have been reported, but such molecular characterisation has not been performed in patients with MDS. We gathered human skin fibroblasts from 17 patients with MDS, 10 MECP2 duplication carrier mothers and 21 patients with RTT, and performed multi‐omics (RNAseq and proteomics) analysis. Here, we provide a thorough description and compare the shared and specific dysregulated biological processes between the cohorts. We also highlight the genes TMOD2, SRGAP1, COPS2, CNPY2, IGF2BP1, MOB2, VASP, FZD7, ECSIT and KIF3B as biomarker and therapeutic target candidates due to their implication in neuronal functions. Defining the RNA and protein profiles has shown that our four cohorts are less alike than expected by their shared phenotypes.

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Section: Discussionmentioning

confidence: 99%

Multi‐omics in MECP2 duplication syndrome patients and carriers

Pascual‐Alonso,

Xiol,

Smirnov

et al. 2024

Eur J of Neuroscience

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show abstract

“…STK17B is upregulated in MDS males but downregulated in females. Finally, MYO1C (OMIM*606538), which is downregulated in male and female MDS cohorts, is a myosin involved in cytoskeletal organisation and vesicle trafficking and when depleted, induces fragmentation of the Golgi complex, the loss of cellular F-actin and a delay in transport 42 .MYO1C is also involved in the recycling of glucose transporters in response to insulin 43 . MDS male and female cohorts share some biological pathways, such as cellular adhesion, vesicular activity and synapses; which are downregulated.…”

Section: Comparison Between Female and Male Mds Patientsmentioning

confidence: 99%

Multi-omics in MECP2 duplication syndrome patients and carriers.

Pascual-Alonso,

Xiol,

Smirnov

et al. 2024

Preprint

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MECP2 duplication syndrome (MDS) is an X-linked neurodevelopmental disorder caused by the gain of dose of at least the genes MECP2 and IRAK1 and is characterised by intellectual disability (ID), developmental delay, hypotonia, epilepsy and recurrent infections. It mainly affects males, and females can be affected or asymptomatic carriers. Rett syndrome (RTT) is mainly triggered by loss of function mutations in MECP2 and is a well described syndrome that presents ID, epilepsy, lack of purposeful hand use and impaired speech, among others. As a result of implementing omics technology, altered biological pathways in human RTT samples have been reported, but such molecular characterisation has not been performed in MDS patients. We gathered human skin fibroblasts from 17 patients with MDS, 10 MECP2 duplication carrier mothers and 21 RTT patients, and performed multi-omics (RNAseq and proteomics) analysis. Here, we provide a thorough description and compare the shared and specific dysregulated biological processes between the cohorts. We also highlight the genes TMOD2, SRGAP1, COPS2, CNPY2, IGF2BP1, MOB2, VASP, FZD7, ECSIT andKIF3B as biomarker and therapeutic target candidates due to their implication in neuronal functions. Defining the RNA and protein profiles has shown that our four cohorts are less alike than expected by their shared phenotypes.

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Sortilin-mediated translocation of ACSL1 impairs non-shivering thermogenesis

Chen

Yang

Zhu

et al. 2023

Preprint

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Obesity and its related metabolic disorders are caused by an imbalance between homeostatic energy consumption and expenditure. Brown and beige adipose tissues have been shown to be protective against these diseases due to their critical roles in non-shivering thermogenesis; additionally, adrenergic innervation of these cells promotes lipolysis and fatty acid oxidation1. A key enzyme promoting fatty acid oxidation in adipose tissues, particularly in response to cold-stimulus, is mitochondrial acyl-CoA synthetase long-chain family member 1(ACSL1)2 However, the regulatory mechanism of the subcellular localization of ACSL1 in adipocytes remains poorly understood. Here, we identify an endosomal trafficking component sortilin (encoded by Sort1) in adipose tissues that facilitates the translocation of ACSL1 from mitochondria to lysosome for further degradation. In brown and beige adipose tissues, sortilin is downregulated upon adrenergic stimulation but its levels are restored to baseline after the stimulus is withdrawn. Depletion of Sort1 in adipocytes results in an increase in whole body energy expenditure. Moreover, mice with adipose-specific Sort1 depletion are resistant to high-fat diet (HFD)-induced obesity and insulin resistance. Collectively, our findings identify sortilin as a promising therapeutic target that negatively regulates non-shivering thermogenesis in adipocytes by promoting the translocation of ACSL1 from the mitochondria to lysosome.

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Myosin 1c: A novel regulator of glucose uptake in brown adipocytes

Cited by 3 publications

References 66 publications

Multi‐omics in MECP2 duplication syndrome patients and carriers

Multi‐omics in MECP2 duplication syndrome patients and carriers

Multi-omics in MECP2 duplication syndrome patients and carriers.

Sortilin-mediated translocation of ACSL1 impairs non-shivering thermogenesis

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