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Shows that inhibition of Sec61 by mycolactone drives rapid and broad translational reprogramming of a subset of genes involved in stress responses that is initially protective but ultimately leads to cell death
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Unpicking the central dogma of molecular biology step-by-step identifies the Sec61 translocon as the target of anti-inflammatory activity of mycolactone, explaining why production of Sec61-dependent proteins (secretory, ER resident and membrane bound) is lost even though transcription and translation are unaffected.
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The direct contribution of Sec61 to antigen cross-presentation, endosome-to-cytosol export, and endoplasmic reticulum-to-cytosol export.
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The authors propose that the Sec61-IRE1alpha complex defines the extent of IRE1alpha activity and may determine cell fate decisions during endoplasmic reticulum stress conditions.
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EPO (7q22) and SEC-61(7p11) emerged as new candidate genes susceptible to genetic losses with 57.7% deletions identified in regions on chromosome 7.
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Tomography densities at subnanometer resolution revealed an intricate network of interactions between the ribosome, Sec61 and accessory translocon components that assist in protein transport, membrane insertion and maturation
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The discovery of export-specific sec61 mutants and of mammalian ER-associated degradation (ERAD) substrates whose export is dependent on the 19S regulatory particle suggest that dismissal of a role of Sec61 in export may have been premature.
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the effect of mycolactone on transmembrane protein biogenesis depends on how the nascent chain initially engages the Sec61 complex.
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data provide definitive genetic evidence that Sec61 is the host receptor mediating the diverse immunomodulatory effects of mycolactone and identify Sec61 as a novel regulator of immune cell functions.
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findings provide a mechanism by which mutations in SEC61A1 lead to an autosomal-dominant syndromic form of progressive chronic kidney disease; we highlight protein translocation defects across the endoplasmic reticulum membrane, the principal role of the SEC61 complex, as a contributory pathogenic mechanism for autosomal-dominant tubulo-interstitial kidney disease
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Nuclear envelope associated endosome-mediated transfer depends on the nuclear envelope proteins SUN1 and SUN2, as well as the Sec61 translocon complex.
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Cotransin, a substrate-selective Sec61 inhibitor, traps nascent transmembrane domains in the cytosolic vestibule, permitting detailed interrogation of an early pre-integration intermediate.
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BiP facilitates Sec61 channel closure (i.e. limits ER Ca(2+) leakage) via the Sec61 channel with the help of ERj3 and ERj6
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Sec61 complex is calcium permeable, the Sec61 complex is tightly regulated in its equilibrium between the closed and open conformations, or "gated", by ligands, such as signal peptides of the transport substrates
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Short secretory proteins appear to be ubiquitously transported across the ER membrane through the Sec61 translocon.
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The human SEC61A1 gene is essential for cell growth and viability.
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BiP limits ER Ca(2+) leakage through the Sec61 complex by binding to the ER lumenal loop 7 of Sec61alpha in the vicinity of tyrosine 344.
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The present study indicates that Sec61alpha is a host protein involved in Ebola virus (EBOV) replication, specifically in EBOV genome transcription and replication.
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Silencing the SEC61A1 gene using two different siRNAs in HeLa cells for 96 hours had little effect on cell growth and viability. However, calcium leakage from the ER was greatly decreased in the SEC61A1-silenced cells.
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At the cellular level, two different calmodulin antagonists stimulated calcium release from the endoplasmic reticulum through SEC61 channels.
