Promoting Glucose Transporter-4 Vesicle Trafficking along Cytoskeletal Tracks: PAK-Ing Them Out

Tunduguru, Ragadeepthi; Thurmond, Debbie C.

doi:10.3389/fendo.2017.00329

Cited by 34 publications

(29 citation statements)

References 165 publications

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“…While some have suggested that an intact microtubule system is important for the insulin-induced actin remodeling prior to the transporter translocation, some studies using agents that inhibit microtubule polymerization has suggested against this (Fletcher et al, 2000; Olson et al, 2001; Liu et al, 2013). Nonetheless, it has been shown that GLUT4 storage vesicles travel along microtubules via kinesins and actin filaments, from the perinuclear region, bringing them into close proximity with the plasma membrane SNARE proteins (Tunduguru and Thurmond, 2017). Newly formed GLUT4 vesicles also are transported from the plasma membrane to the cell interior by the microtubule-based motor protein dynein.…”

Section: Tau Protein and Insulin Signaling In Peripheral Tissuesmentioning

confidence: 99%

The Link Between Tau and Insulin Signaling: Implications for Alzheimer’s Disease and Other Tauopathies

Gonçalves

Wijesekara

Fraser

et al. 2019

Front. Cell. Neurosci.

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The microtubule-associated protein tau (MAPT) is mainly identified as a tubulin binding protein essential for microtubule dynamics and assembly and for neurite outgrowth. However, several other possible functions for Tau remains to be investigated. Insulin signaling is important for synaptic plasticity and memory formation and therefore is essential for proper brain function. Tau has recently been characterized as an important regulator of insulin signaling, with evidence linking Tau to brain and peripheral insulin resistance and beta cell dysfunction. In line with this notion, the hypothesis of Tau pathology as a key trigger of impaired insulin sensitivity and secretion has emerged. Conversely, insulin resistance can also favor Tau dysfunction, resulting in a vicious cycle of these events. In this review article, we discuss recent evidence linking Tau pathology, insulin resistance and insulin deficiency. We further highlight the deleterious consequences of Tau pathology-induced insulin resistance to the brain and/or peripheral tissues, suggesting that these are key events mediating cognitive decline in Alzheimer’s disease (AD) and other tauopathies.

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Section: Tau Protein and Insulin Signaling In Peripheral Tissuesmentioning

confidence: 99%

The Link Between Tau and Insulin Signaling: Implications for Alzheimer’s Disease and Other Tauopathies

Gonçalves

Wijesekara

Fraser

et al. 2019

Front. Cell. Neurosci.

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“…Perturbation of glucose uptake into skeletal muscle causes hyperglycemia, which eventually damages vessels and organs, such as kidney and heart [10]. Intracellular GLUT4 localization is controlled by small G protein Rabs, such as Rab8a and Rab14, which are physically associated with GLUT4 vesicles, and GTP-bound active Rabs are necessary to facilitate translocation of GLUT4 [25,26]. TBC1D1 and TBC1D4 are Rab-GTPase-activating proteins (GAPs) that negatively control GLUT4 trafficking through their Rab-GAP activities under basal conditions [25,27,28].…”

Section: Discussionmentioning

confidence: 99%

Increased glucose metabolism in Arid5b−/− skeletal muscle is associated with the down-regulation of TBC1 domain family member 1 (TBC1D1)

et al. 2020

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Background Skeletal muscle has an important role in regulating whole-body energy homeostasis, and energy production depends on the efficient function of mitochondria. We demonstrated previously that AT-rich interactive domain 5b (Arid5b) knockout (Arid5b−/−) mice were lean and resistant to high-fat diet (HFD)-induced obesity. While a potential role of Arid5b in energy metabolism has been suggested in adipocytes and hepatocytes, the role of Arid5b in skeletal muscle metabolism has not been studied. Therefore, we investigated whether energy metabolism is altered in Arid5b−/− skeletal muscle. Results Arid5b−/− skeletal muscles showed increased basal glucose uptake, glycogen content, glucose oxidation and ATP content. Additionally, glucose clearance and oxygen consumption were upregulated in Arid5b−/− mice. The expression of glucose transporter 1 (GLUT1) and 4 (GLUT4) in the gastrocnemius (GC) muscle remained unchanged. Intriguingly, the expression of TBC domain family member 1 (TBC1D1), which negatively regulates GLUT4 translocation to the plasma membrane, was suppressed in Arid5b−/− skeletal muscle. Coimmunofluorescence staining of the GC muscle sections for GLUT4 and dystrophin revealed increased GLUT4 localization at the plasma membrane in Arid5b−/− muscle. Conclusions The current study showed that the knockout of Arid5b enhanced glucose metabolism through the downregulation of TBC1D1 and increased GLUT4 membrane translocation in skeletal muscle.

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“…Human erythroid progenitors (pro-EBLs, early basophilic EBLs) express the IGF1R, and not the InsR, which changes during differentiation when the InsR becomes the prominent receptor [57]. InsR signaling is particularly important to control trafficking of GLUT4 glucose transporters to the cell membrane [58]. Late EBLs and mature RBCs depend on glycolysis and EBLs express high levels of glucose transporters [59].…”

Section: Growth Factor-binding Tyrosine Kinase Receptorsmentioning

confidence: 99%

Erythropoiesis and Megakaryopoiesis in a Dish

Varga¹,

Hansen²,

Akker³

et al. 2019

Cell Culture

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Erythrocytes and platelets are the major cellular components of blood. Several hereditary diseases affect the production/stability of red blood cells (RBCs) and platelets (Plts) resulting in anemia or bleeding, respectively. Patients with such disorders may require recurrent transfusions, which bear a risk to develop alloantibodies and ultimately may result in transfusion product refractoriness. Cell culture models enable to unravel disease mechanisms, and to screen for alternative therapeutic products. Besides these applications, the ultimate goal is the large-scale production of blood effector cells for transfusion. Cultured RBCs that lack many of the common blood group antigens and Plts-lacking HLA expression would improve transfusion practice. Large numbers of RBCs and Plts can already be generated using hematopoietic stem cells derived from fetal liver, cord blood, peripheral blood, and bone marrow as starting material for cell culture. The recent advances to generate blood cells from induced pluripotent stem cells provide a donor-independent, immortal primary source for cell culture models. This enables us to study developmental switches during erythropoiesis/megakaryopoiesis and provides potential future therapeutic applications. In this review, we will discuss how erythropoiesis and megakaryopoiesis are mimicked in culture systems and how these models relate to the in vivo process.

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Promoting Glucose Transporter-4 Vesicle Trafficking along Cytoskeletal Tracks: PAK-Ing Them Out

Cited by 34 publications

References 165 publications

The Link Between Tau and Insulin Signaling: Implications for Alzheimer’s Disease and Other Tauopathies

The Link Between Tau and Insulin Signaling: Implications for Alzheimer’s Disease and Other Tauopathies

Increased glucose metabolism in Arid5b−/− skeletal muscle is associated with the down-regulation of TBC1 domain family member 1 (TBC1D1)

Erythropoiesis and Megakaryopoiesis in a Dish

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