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Study data suggest that SAR1A and SAR1B are the critical regulators of trafficking of Nav1.5. Moreover, SAR1A and SAR1B interact with MOG1, and are required for MOG1-mediated cell surface expression and function of Nav1.5.
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Study shows that the bona fide nonglycoprotein Nox5, a transmembrane superoxide-producing NADPH oxidase, is transported to the cell surface in a manner resistant to co-expression of Sar1 (H79G), a GTP-fixed mutant of the small GTPase Sar1, which blocks COPII vesicle fission from the endoplasmic reticulum.
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No associations were observed between any of the secretion associated Ras related GTPase 1A (SAR1a) promoter variants and baseline fetal hemoglobin HbF among sickle cell disease (SCD) patients.
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Sar1 is a novel regulator of endoplasmic reticulum-mitochondrial contact sites in the metazoans.
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SAR1A gene silencing in hepatocytes mimics the effect of ethanol: dedimerization of giantin, arresting PDIA3 in the endoplasmic reticulum (ER) and large-scale alterations in Golgi architecture.
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Data indicate that hydroxyurea (HU) induces SAR1 protein expression, which in turn activates gamma-globin expression, predominantly through the Gialpha/JNK/Jun pathway.
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although Sar1A antagonizes the lipoprotein secretion-promoting activity of Sar1B, both isoforms modulate the expression of genes encoding cholesterol biosynthetic enzymes and the synthesis of cholesterol de novo.
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Sar1 mutant proteins added to metaphase-arrested Xenopus laevis egg extracts cause dramatic effects on membrane organization.
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the behavior of the human of Sar1A and Sar1B, a key component of the COPII family of vesicle coat proteins, was examined.
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Sedlin bound and promoted efficient cycling of Sar1, a guanosine triphosphatase that can constrict membranes, and thus allowed nascent carriers to grow and incorporate procollagen prefibrils.
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lipid-directed and tether-assisted Sar1 organization controls membrane constriction to regulate ER export.
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the intracellular trafficking of hCaR from the endoplasmic reticulum is Sar1-dependent via coat protein complex-II vesicles.
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The Sec31 fragment stimulates GAP activity of Sec23/24, and a convergence of Sec31 and Sec23 residues at the Sar1 GTPase active site explains how GTP hydrolysis is triggered leading to COPII coat disassembly.
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Sar 1 H79G mutants efficiently blocked the plasma membrane trafficking of the Kir3.1/Kir3.4 complex however they did not block the Gbeta1gamma2/Kir3.1 interaction.
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Kir6.2 contains a di-acidic endoplasmic reticulum exit signal, which promotes endoplasmic reticulum exit via a process that requires Sar1.
