8bbf

From Proteopedia

(Difference between revisions)
Jump to: navigation, search
Current revision (06:47, 24 July 2024) (edit) (undo)
 
Line 4: Line 4:
== Structural highlights ==
== Structural highlights ==
<table><tr><td colspan='2'>[[8bbf]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8BBF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8BBF FirstGlance]. <br>
<table><tr><td colspan='2'>[[8bbf]] is a 3 chain structure with sequence from [https://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=8BBF OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=8BBF FirstGlance]. <br>
-
</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=8bbf FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8bbf OCA], [https://pdbe.org/8bbf PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8bbf RCSB], [https://www.ebi.ac.uk/pdbsum/8bbf PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8bbf ProSAT]</span></td></tr>
+
</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">Electron Microscopy, [[Resolution|Resolution]] 8&#8491;</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=8bbf FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=8bbf OCA], [https://pdbe.org/8bbf PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=8bbf RCSB], [https://www.ebi.ac.uk/pdbsum/8bbf PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=8bbf ProSAT]</span></td></tr>
</table>
</table>
== Disease ==
== Disease ==
-
[https://www.uniprot.org/uniprot/WDR19_HUMAN WDR19_HUMAN] Jeune syndrome;Senior-Loken syndrome;Juvenile nephronophthisis;Cranioectodermal dysplasia. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry. The disease is caused by variants affecting the gene represented in this entry.
+
[https://www.uniprot.org/uniprot/IF122_HUMAN IF122_HUMAN] Cranioectodermal dysplasia;Short rib-polydactyly syndrome, Beemer-Langer type. The disease is caused by variants affecting the gene represented in this entry.
== Function ==
== Function ==
-
[https://www.uniprot.org/uniprot/WDR19_HUMAN WDR19_HUMAN] As component of the IFT complex A (IFT-A), a complex required for retrograde ciliary transport and entry into cilia of G protein-coupled receptors (GPCRs), it is involved in cilia function and/or assembly (PubMed:20889716). Essential for functional IFT-A assembly and ciliary entry of GPCRs (PubMed:20889716). Associates with the BBSome complex to mediate ciliary transport (By similarity).[UniProtKB:Q3UGF1]<ref>PMID:20889716</ref>
+
[https://www.uniprot.org/uniprot/IF122_HUMAN IF122_HUMAN] As a component of the IFT complex A (IFT-A), a complex required for retrograde ciliary transport and entry into cilia of G protein-coupled receptors (GPCRs), it is required in ciliogenesis and ciliary protein trafficking (PubMed:27932497, PubMed:29220510). Involved in cilia formation during neuronal patterning. Acts as a negative regulator of Shh signaling. Required to recruit TULP3 to primary cilia (By similarity).[UniProtKB:Q6NWV3]<ref>PMID:27932497</ref> <ref>PMID:29220510</ref>
 +
<div style="background-color:#fffaf0;">
 +
== Publication Abstract from PubMed ==
 +
Intraflagellar transport (IFT) trains are massive molecular machines that traffic proteins between cilia and the cell body. Each IFT train is a dynamic polymer of two large complexes (IFT-A and -B) and motor proteins, posing a formidable challenge to mechanistic understanding. Here, we reconstituted the complete human IFT-A complex and obtained its structure using cryo-EM. Combined with AlphaFold prediction and genome-editing studies, our results illuminate how IFT-A polymerizes, interacts with IFT-B, and uses an array of beta-propeller and TPR domains to create "carriages" of the IFT train that engage TULP adaptor proteins. We show that IFT-A⋅TULP carriages are essential for cilia localization of diverse membrane proteins, as well as ICK-the key kinase regulating IFT train turnaround. These data establish a structural link between IFT-A's distinct functions, provide a blueprint for IFT-A in the train, and shed light on how IFT evolved from a proto-coatomer ancestor.
 +
 
 +
IFT-A structure reveals carriages for membrane protein transport into cilia.,Hesketh SJ, Mukhopadhyay AG, Nakamura D, Toropova K, Roberts AJ Cell. 2022 Dec 22;185(26):4971-4985.e16. doi: 10.1016/j.cell.2022.11.010. Epub , 2022 Dec 2. PMID:36462505<ref>PMID:36462505</ref>
 +
 
 +
From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
 +
</div>
 +
<div class="pdbe-citations 8bbf" style="background-color:#fffaf0;"></div>
== References ==
== References ==
<references/>
<references/>

Current revision

Structure of the IFT-A complex; IFT-A1 module

PDB ID 8bbf

Drag the structure with the mouse to rotate

Proteopedia Page Contributors and Editors (what is this?)

OCA

Personal tools