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he present study demonstrated that DANCR/miR-634/RAB1A axis plays crucial roles in the progression of glioma, and DANCR might potentially serve as a therapeutic target for the treatment of glioma patients.
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Rab1 is regulated by the host in a similar fashion, and that the innate immunity kinase TAK1 and Legionella effectors compete to regulate Rab1 by switch II modifications during infection.
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Rab1A may be involved in the pathogenesis of human lung cancer in an mTOR- and MAPK-independent manner.
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In clinical samples, the expression of Rab1A or DHX33 was reversely correlated with miR-634. Re-expression of Rab1A or DHX33 abrogated the miR-634-mediated inhibition of cell proliferation and migration. Collectively, our data suggest a tumor suppressor role of miR-634 in hepatocellular carcinoma.
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New Rab1 binding sites have been discovered using an ensemble of clustering methods.
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Leucine-rich repeat kinase 2 (LRRK2) can interact with several Rab proteins, and such ractions may serve to recruit LRRK2 to distinct subcellular organelles to phosphorylate select substrate proteins involved in membrane trafficking events.
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As a Rab1a effector, C9orf72 controls initiation of autophagy by regulating the Rab1a-dependent trafficking of the ULK1 autophagy initiation complex to the phagophore.
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our data indicate that miR-1202 suppresses proliferation and induces endoplasmic reticulum stress and apoptosis through targeting and inhibiting Rab1A in glioma cells. These results suggest miR-1202 as a potential therapeutic target for the treatment of glioma patients.
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Upregulation of RAB1A is associated with triple-negative breast cancer.
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For RAB1A, a high accuracy for the discrimination of human hepatocellular carcinoma and nontumorous liver tissue was observed.
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The ability of Rab1 to regulate WHAMM and the Arp2/3 complex represents a distinct strategy for membrane remodeling in which a Rab G-protein recruits the actin nucleation machinery but dampens its activity.
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Rab1A isoform 3 shows enhanced basal activity and is not controlled by accessory proteins
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Results demonstrate that ALS-mutant forms of TDP-43, FUS, and SOD1 all perturb protein transport in the early secretory pathway between ER and Golgi compartments, and imply that restoring Rab1-mediated ER-Golgi transport is a novel ALS therapeutic target
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Rab1A-dependent activation of mTORC1 has as role in amino acid signaling promotes growth and metastasis of hepatocellular carcinomas
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Overexpression of RAB1A is associated with hepatocellular carcinoma.
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Rab1A regulates anterograde melanosome transport by recruiting kinesin-1 to melanosomes through interaction with SKIP
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Rab1A knockdown induced cell death by inhibition of autophagosome formation.
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Vaccinia virus can be added to the growing list of viruses which require RAB1A for optimal replication, highlighting this protein as a broadly proviral host factor.
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hyperactive amino acid signaling through Rab1A overexpression drives oncogenesis and renders cancer cells prone to mTORC1-targeted therapy.
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A major biological consequence of upregulation of miR-221 is reprogramming of androgen receptor signaling via downregulation of HECTD2 and RAB1A.
