4v6m

<table><tr><td colspan='2'>[[4v6m]] is a 60 chain structure with sequence from [http://en.wikipedia.org/wiki/Escherichia_coli Escherichia coli], [http://en.wikipedia.org/wiki/Escherichia_coli_536 Escherichia coli 536], [http://en.wikipedia.org/wiki/Escherichia_coli_dh1 Escherichia coli dh1], [http://en.wikipedia.org/wiki/Escherichia_coli_k-12 Escherichia coli k-12] and [http://en.wikipedia.org/wiki/Escherichia_coli_o157:h7 Escherichia coli o157:h7]. This structure supersedes the now removed PDB entries [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=3j00 3j00] and [http://oca.weizmann.ac.il/oca-bin/send-pdb?obs=1&id=3j01 3j01]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4V6M OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4V6M FirstGlance]. <br>

</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=PEV:(1S)-2-{[(2-AMINOETHOXY)(HYDROXY)PHOSPHORYL]OXY}-1-[(PALMITOYLOXY)METHYL]ETHYL+STEARATE'>PEV</scene>, <scene name='pdbligand=PGV:(1R)-2-{[{[(2S)-2,3-DIHYDROXYPROPYL]OXY}(HYDROXY)PHOSPHORYL]OXY}-1-[(PALMITOYLOXY)METHYL]ETHYL+(11E)-OCTADEC-11-ENOATE'>PGV</scene></td></tr>

<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4v6m FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4v6m OCA], [http://pdbe.org/4v6m PDBe], [http://www.rcsb.org/pdb/explore.do?structureId=4v6m RCSB], [http://www.ebi.ac.uk/pdbsum/4v6m PDBsum], [http://prosat.h-its.org/prosat/prosatexe?pdbcode=4v6m ProSAT]</span></td></tr>

== Disease ==

[[http://www.uniprot.org/uniprot/APOA1_HUMAN APOA1_HUMAN]] Defects in APOA1 are a cause of high density lipoprotein deficiency type 2 (HDLD2) [MIM:[http://omim.org/entry/604091 604091]]; also known as familial hypoalphalipoproteinemia (FHA). Inheritance is autosomal dominant.<ref>PMID:8240372</ref> <ref>PMID:8282791</ref> Defects in APOA1 are a cause of the low HDL levels observed in high density lipoprotein deficiency type 1 (HDLD1) [MIM:[http://omim.org/entry/205400 205400]]; also known as analphalipoproteinemia or Tangier disease (TGD). HDLD1 is a recessive disorder characterized by the absence of plasma HDL, accumulation of cholesteryl esters, premature coronary artery disease, hepatosplenomegaly, recurrent peripheral neuropathy and progressive muscle wasting and weakness. In HDLD1 patients, ApoA-I fails to associate with HDL probably because of the faulty conversion of pro-ApoA-I molecules into mature chains, either due to a defect in the converting enzyme activity or a specific structural defect in Tangier ApoA-I.<ref>PMID:8240372</ref> <ref>PMID:8282791</ref> Note=A mutation in APOA1 is the cause of amyloid polyneuropathy-nephropathy Iowa type (AMYLIOWA); also known as amyloidosis van Allen type or familial amyloid polyneuropathy type III. AMYLIOWA is a hereditary generalized amyloidosis due to deposition of amyloid mainly constituted by apolipoprotein A1. The clinical picture is dominated by neuropathy in the early stages of the disease and nephropathy late in the course. Death is due in most cases to renal amyloidosis. Severe peptic ulcer disease can occurr in some and hearing loss is frequent. Cataracts is present in several, but vitreous opacities are not observed.<ref>PMID:8240372</ref> <ref>PMID:8282791</ref> <ref>PMID:3142462</ref> <ref>PMID:2123470</ref> Defects in APOA1 are a cause of amyloidosis type 8 (AMYL8) [MIM:[http://omim.org/entry/105200 105200]]; also known as systemic non-neuropathic amyloidosis or Ostertag-type amyloidosis. AMYL8 is a hereditary generalized amyloidosis due to deposition of apolipoprotein A1, fibrinogen and lysozyme amyloids. Viscera are particularly affected. There is no involvement of the nervous system. Clinical features include renal amyloidosis resulting in nephrotic syndrome, arterial hypertension, hepatosplenomegaly, cholestasis, petechial skin rash.<ref>PMID:8240372</ref> <ref>PMID:8282791</ref> <ref>PMID:1502149</ref>

<div style="background-color:#fffaf0;">

The ubiquitous SecY-Sec61 complex translocates nascent secretory proteins across cellular membranes and integrates membrane proteins into lipid bilayers. Several structures of mostly detergent-solubilized Sec complexes have been reported. Here we present a single-particle cryo-EM structure of the SecYEG complex in a membrane environment, bound to a translating ribosome, at subnanometer resolution. Using the SecYEG complex reconstituted in a so-called Nanodisc, we could trace the nascent polypeptide chain from the peptidyltransferase center into the membrane. The reconstruction allowed for the identification of ribosome-lipid interactions. The rRNA helix 59 (H59) directly contacts the lipid surface and appears to modulate the membrane in immediate vicinity to the proposed lateral gate of the protein-conducting channel (PCC). On the basis of our map and molecular dynamics simulations, we present a model of a signal anchor-gated PCC in the membrane.

 

Cryo-EM structure of the ribosome-SecYE complex in the membrane environment.,Frauenfeld J, Gumbart J, Sluis EO, Funes S, Gartmann M, Beatrix B, Mielke T, Berninghausen O, Becker T, Schulten K, Beckmann R Nat Struct Mol Biol. 2011 May;18(5):614-21. Epub 2011 Apr 17. PMID:21499241<ref>PMID:21499241</ref>

 

<div class="pdbe-citations 4v6m" style="background-color:#fffaf0;"></div>

*[[Preprotein translocase|Preprotein translocase]]

== References ==

<references/>

[[Category: Escherichia coli 536]]

[[Category: Escherichia coli dh1]]

[[Category: Escherichia coli k-12]]

[[Category: Escherichia coli o157:h7]]

[[Category: Beatrix, B]]

[[Category: Becker, T]]

[[Category: Beckmann, R]]

[[Category: Berninghausen, O]]

[[Category: Frauenfeld, J]]

[[Category: Funes, S]]

[[Category: Gartmann, M]]

[[Category: Gumbart, J]]

[[Category: Mielke, T]]

[[Category: Schulten, K]]

[[Category: Sluis, E O.van der]]

[[Category: Zinc-finger]]