Diacylglycerol Kinase α Regulates Tubular Recycling Endosome Biogenesis and Major Histocompatibility Complex Class I Recycling

Xie, Shuwei; Naslavsky, Naava; Caplan, Steve

doi:10.1074/jbc.m114.594291

Cited by 25 publications

(27 citation statements)

References 35 publications

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“…An interaction between DGKa and the protein MICAL-L1 (microtubule-associated monooxygenase, calponin, and LIM domain containing-like 1) is proposed to facilitate the biogenesis of tubular recycling endosomes and the recycling of MHC I in HeLa cells (65). This function of DGKa in endosome recycling correlates with its regulation of integrin recycling and tumor invasiveness through the PA-dependent tethering of the Rab11 effector RCP (Rab-coupling protein) to invasive pseudopods (66).…”

Section: Dgk-mediated Generation Of Pa and Its Contribution To T Cellmentioning

confidence: 97%

Redundant and specialized roles for diacylglycerol kinases α and ζ in the control of T cell functions

et al. 2015

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The diacylglycerol kinases (DGKs) attenuate diacylglycerol (DAG)-mediated signals by catalyzing the conversion of DAG to phosphatidic acid. In T lymphocytes, the antigen-stimulated generation of DAG links signal strength to the intensity and duration of signaling by the Ras-extracellular signal-regulated kinase (ERK) and protein kinase C (PKC)-dependent pathways. The generation of DAG at the plasma membrane of T cells lies at the core of the mechanisms that delimit T cell functions. DGKα and DGKζ are the two main isoforms that are found in T cells, and several approaches define their precise contribution to T cell responses. Each of these isoforms has specialized and redundant functions that limit the intensity of DAG-regulated signals downstream of antigenic stimulation. This ability, which in normal T cells contributes to maintaining homeostasis and function, is exploited by tumors to evade immune surveillance. Modification of DGK activity offers new perspectives for the therapeutic manipulation of T cell functions for treatment of autoimmune pathologies, or for overcoming tumor-induced T cell tolerance. Precise knowledge of the mechanisms that sustain DGK isoform-specific regulation in T lymphocytes is indispensable for the development of new tools for pharmacological intervention.

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Section: Dgk-mediated Generation Of Pa and Its Contribution To T Cellmentioning

confidence: 97%

Redundant and specialized roles for diacylglycerol kinases α and ζ in the control of T cell functions

et al. 2015

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“…Tubulation of the Rab8a-dependent recycling system, which is responsible for recycling of non-clathrin-dependent endocytosed cargoes, such as MHC Class I, is regulated by MICAL-L1 [7,8]. MICAL-L1 recruits both Arf6 and EHD1 to recycling membranes and promotes tubulation [7,9,10 • ,11]. The association of MICAL-L1 with tubular endosomes is regulated by Rab35 [8,12].…”

Section: The Recycling Endosome Is a Dynamic Structurementioning

confidence: 99%

Recycling endosomes

Goldenring

2015

Current Opinion in Cell Biology

128

118

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The endosomal membrane recycling system represents a dynamic conduit for sorting and re-exporting internalized membrane constituents. The recycling system is composed of multiple tubulovesicular recycling pathways that likely confer distinct trafficking pathways for individual cargoes. In addition, elements of the recycling system are responsible for assembly and maintenance of apical membrane specializations including primary cilia and apical microvilli. The existence of multiple intersecting and diverging recycling tracks likely accounts for specificity in plasma membrane recycling trafficking.

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“…A decreased recycling rate results from either enhanced intracellular retentions or increased degradation. For example, when the lipid modifier diacylglycerol kinase a is depleted from cells, the MHC I recycling rate is dramatically decreased (Xie, Naslavsky, & Caplan, 2014). The shunting of receptors from recycling to degradation pathways, or vice versa, is not uncommon.…”

Section: Remarksmentioning

confidence: 99%