9bde: Difference between revisions
Jump to navigation
Jump to search
New page: '''Unreleased structure''' The entry 9bde is ON HOLD Authors: Description: Category: Unreleased Structures |
No edit summary |
||
| (2 intermediate revisions by the same user not shown) | |||
| Line 1: | Line 1: | ||
The entry | ==Middle Region of Apolipoprotein B 100 bound to Low Density Lipoprotein Receptor== | ||
<StructureSection load='9bde' size='340' side='right'caption='[[9bde]], [[Resolution|resolution]] 4.18Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[9bde]] is a 6 chain structure with sequence from [https://en.wikipedia.org/wiki/Camelus_bactrianus Camelus bactrianus], [https://en.wikipedia.org/wiki/Escherichia_coli Escherichia coli], [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens], [https://en.wikipedia.org/wiki/Mus_musculus Mus musculus], [https://en.wikipedia.org/wiki/Staphylococcus_aureus Staphylococcus aureus] and [https://en.wikipedia.org/wiki/Streptococcus_sp._'group_G' Streptococcus sp. 'group G']. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=9BDE OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=9BDE FirstGlance]. <br> | |||
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 4.18Å</td></tr> | |||
[[Category: | <tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=CA:CALCIUM+ION'>CA</scene>, <scene name='pdbligand=NAG:N-ACETYL-D-GLUCOSAMINE'>NAG</scene></td></tr> | ||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=9bde FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=9bde OCA], [https://pdbe.org/9bde PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=9bde RCSB], [https://www.ebi.ac.uk/pdbsum/9bde PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=9bde ProSAT]</span></td></tr> | |||
</table> | |||
== Disease == | |||
[https://www.uniprot.org/uniprot/APOB_HUMAN APOB_HUMAN] Homozygous familial hypercholesterolemia. The disease is caused by variants affecting the gene represented in this entry. Most cases of FHBL1 result from nonsense mutations in the APOB gene that lead to a premature stop codon, which generate prematurely truncated apo B protein products (PubMed:21981844).<ref>PMID:21981844</ref> The disease is caused by variants affecting the gene represented in this entry. Defects in APOB associated with defects in other genes (polygenic) can contribute to hypocholesterolemia. | |||
== Function == | |||
[https://www.uniprot.org/uniprot/APOB_HUMAN APOB_HUMAN] Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 functions as a recognition signal for the cellular binding and internalization of LDL particles by the apoB/E receptor. | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Camelus bactrianus]] | |||
[[Category: Escherichia coli]] | |||
[[Category: Homo sapiens]] | |||
[[Category: Large Structures]] | |||
[[Category: Mus musculus]] | |||
[[Category: Staphylococcus aureus]] | |||
[[Category: Streptococcus sp. 'group G']] | |||
[[Category: Dearborn AD]] | |||
[[Category: Graziano G]] | |||
[[Category: Kumar A]] | |||
[[Category: Lei H]] | |||
[[Category: Marcotrigiano J]] | |||
[[Category: Neufeld EB]] | |||
[[Category: Reimund M]] | |||
[[Category: Remaley AT]] | |||
Latest revision as of 12:30, 25 December 2024
Middle Region of Apolipoprotein B 100 bound to Low Density Lipoprotein ReceptorMiddle Region of Apolipoprotein B 100 bound to Low Density Lipoprotein Receptor
Structural highlights
DiseaseAPOB_HUMAN Homozygous familial hypercholesterolemia. The disease is caused by variants affecting the gene represented in this entry. Most cases of FHBL1 result from nonsense mutations in the APOB gene that lead to a premature stop codon, which generate prematurely truncated apo B protein products (PubMed:21981844).[1] The disease is caused by variants affecting the gene represented in this entry. Defects in APOB associated with defects in other genes (polygenic) can contribute to hypocholesterolemia. FunctionAPOB_HUMAN Apolipoprotein B is a major protein constituent of chylomicrons (apo B-48), LDL (apo B-100) and VLDL (apo B-100). Apo B-100 functions as a recognition signal for the cellular binding and internalization of LDL particles by the apoB/E receptor. References
|
| ||||||||||||||||||