DDHD1, but Not DDHD2, Suppresses Neurite Outgrowth in SH-SY5Y and PC12 Cells by Regulating Protein Transport From Recycling Endosomes

Maemoto, Yuki; Maruyama, Toru; Nemoto, Kazuaki; Baba, Takashi; Motohashi, Manae; Ito, Akihiro; Tagaya, Mitsuo; Tani, Kazuhide

doi:10.3389/fcell.2020.00670

Cited by 2 publications

(1 citation statement)

References 53 publications

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“…Two scientists independently observed homozygous and compound heterozygous mutation in adaptor-related protein complex 4 subunit sigma 1 (SPG52/AP4S1) at 14q21 in Syrian [87] and Caucasian families [88], which induces HSP phenotypes due to defective endosomes trafficking. Maemoto et al [89] showed that DDHD1 protein depletion negatively affects neurite growth due to defective endosomal protein recruitment other than tubular recycling endosome. Another gene, Zinc Finger FYVE-Type Containing 26 (SPG15/ZFYVE26) at 14q24.1, is linked with [90] spatizin, and its mutations lead to HSPs.…”

Section: Chromosome 14mentioning

confidence: 99%

Hereditary Spastic Paraplegia: An Update

Meyyazhagan

Orlacchio

2022

IJMS

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Hereditary spastic paraplegia (HSP) is a rare neurodegenerative disorder with the predominant clinical manifestation of spasticity in the lower extremities. HSP is categorised based on inheritance, the phenotypic characters, and the mode of molecular pathophysiology, with frequent degeneration in the axon of cervical and thoracic spinal cord’s lateral region, comprising the corticospinal routes. The prevalence ranges from 0.1 to 9.6 subjects per 100,000 reported around the globe. Though modern medical interventions help recognize and manage the disorder, the symptomatic measures remain below satisfaction. The present review assimilates the available data on HSP and lists down the chromosomes involved in its pathophysiology and the mutations observed in the respective genes on the chromosomes. It also sheds light on the treatment available along with the oral/intrathecal medications, physical therapies, and surgical interventions. Finally, we have discussed the related diagnostic techniques as well as the linked pharmacogenomics studies under future perspectives.

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Section: Chromosome 14mentioning

confidence: 99%

Hereditary Spastic Paraplegia: An Update

Meyyazhagan

Orlacchio

2022

IJMS

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From Classical to Alternative Pathways of 2-Arachidonoylglycerol Synthesis: AlterAGs at the Crossroad of Endocannabinoid and Lysophospholipid Signaling

Briand-Mésange,

Gennero,

Salles

et al. 2024

Molecules

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2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid (EC), acting as a full agonist at both CB1 and CB2 cannabinoid receptors. It is synthesized on demand in postsynaptic membranes through the sequential action of phosphoinositide-specific phospholipase Cβ1 (PLCβ1) and diacylglycerol lipase α (DAGLα), contributing to retrograde signaling upon interaction with presynaptic CB1. However, 2-AG production might also involve various combinations of PLC and DAGL isoforms, as well as additional intracellular pathways implying other enzymes and substrates. Three other alternative pathways of 2-AG synthesis rest on the extracellular cleavage of 2-arachidonoyl-lysophospholipids by three different hydrolases: glycerophosphodiesterase 3 (GDE3), lipid phosphate phosphatases (LPPs), and two members of ecto-nucleotide pyrophosphatase/phosphodiesterases (ENPP6–7). We propose the names of AlterAG-1, -2, and -3 for three pathways sharing an ectocellular localization, allowing them to convert extracellular lysophospholipid mediators into 2-AG, thus inducing typical signaling switches between various G-protein-coupled receptors (GPCRs). This implies the critical importance of the regioisomerism of both lysophospholipid (LPLs) and 2-AG, which is the object of deep analysis within this review. The precise functional roles of AlterAGs are still poorly understood and will require gene invalidation approaches, knowing that both 2-AG and its related lysophospholipids are involved in numerous aspects of physiology and pathology, including cancer, inflammation, immune defenses, obesity, bone development, neurodegeneration, or psychiatric disorders.

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DDHD1, but Not DDHD2, Suppresses Neurite Outgrowth in SH-SY5Y and PC12 Cells by Regulating Protein Transport From Recycling Endosomes

Cited by 2 publications

References 53 publications

Hereditary Spastic Paraplegia: An Update

Hereditary Spastic Paraplegia: An Update

From Classical to Alternative Pathways of 2-Arachidonoylglycerol Synthesis: AlterAGs at the Crossroad of Endocannabinoid and Lysophospholipid Signaling

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